text:
Tag Archives: The Ekphrastic Review
Summer bonanza at The High Window
Nothing says treat like a bumper pack of juicy goodies in The High Window. There are new poems from 36 writers (including 4 of my own); two featured poets (the American Steve Lambert, and Australian Kim Waters); a Russian poetry supplement edited and translated by Belinda Cooke; an essay about what it means to write by Feilim James; a raft of book reviews, plus poetry and artwork from The High Window's very own resident artist, Stella Wulf. How on earth does editor, David Cooke, pull this off single-handedly every three months?
I've been in love with the Russian language since I stumbled across my father's Teach Yourself Russian text book as a teenager. I dropped out before taking the 'A' level, but retain enough to be entranced by Belinda's wonderful translations of poems by Alexander Blok, Anna Akhmatova, Osip Mandelstam, Vladimir Mayakovksy and Marina Tsvetaeva plus several other poets less well known to the West.
"The Silver Age of Russian poetry includes early and late Symbolists, as well as the later Acmeism and Futurism, two movements that reacted against the otherworldly, often artificial language of Symbolism, bringing it back down to earth, with more concrete language. . . . But it is the younger generation: Mayakovsky, Mandelstam, Tsvetaeva, Pasternak and Akhmatova who were to create poetry that achieved international renown, as well as suffering the realities of attempting to maintain their art within the apocalyptic events of the Russian Revolution, Civil War and Stalin's Purges of the thirties."
On a more cheery note, this inquisitive little piggie (below) is one of many of Stella's drawings you can view by visiting The High Window.
Poets in the summer issue include Isabel Bermudez, Michael Bartholomew-Biggs, Claire Booker, Neil Elder, Oz Hardwick, Jill Learner, Dino Mahoney, Jane Lovell, Wendy Klein, Ilse Pedler, Jessica Mukherjee, Rachel Playforth, Graham Mort, Simon Williams, Robert Lindsay Wilson and Rodney Wood.
You can read their poems for free (like everything else on the website) by visiting https://thehighwindowpress.com/category/poetry/
And if you're still at a loose end, do click on the following link to read my poem 'Redacted' which was recently published by litzine The Ekphrastic Review. This poem is my response to seeing the stunning Bruegel interpretation of The Massacre of the Innocents in the Queen's Gallery, London. The painting was over-painted hundreds of years ago as literal political cover-up of a real life atrocity in the Spanish Netherlands. Once seen, never forgotten (the painting, I mean!).
https://www.ekphrastic.net/ekphrastic-journal/redacted-by-claire-booker
Tagged Belinda Cooke, Claire Booker, David Cooke, Ekphrastic poetry, Futurism, Graham Mort, Jessica Mukherjee, Kim Waters, new poetry, Pieter Bruegel the Elder, Russian poetry, Steve Lambert, Symbolists, The Ekphrastic Review, The High Window
High Window, Ekphrastic Review and Celebrating Change – why publish on-line?
A recent flurry of my poems being carried by The High Window (issue 15), The Ekphrastic Review (August 2019) and Celebrating Change (September 2019) has made me ponder the pros and cons of online publishing.
You write a poem, you re-write a poem, you workshop it, you work on it again, eventually you submit, sometimes it's accepted for publication. So far, so normal. Appearing in a magazine or anthology enables us to share our craft, our vision, our voice. Being published doffs its cap to posterity.
So what can online publication offer that printed books and magazines can't? Well, for a start, online magazines are usually free to read. This, together with the fact that content can be shared more easily via social media, means you potentially reach more readers. There can be greater immediacy too when you by-pass the laborious processes of printing and posting out. This is particularly relevant for political poems. Online is so handy for journeys – no more lugging heavy books around. Stuck in a jam? Pull out your mobile and get reading. Online magazines allow you to search for individual poet's work, often across many issues. At magazines like The Ekphrastic Review, you also get to see the painting or artwork that inspired the poem – a delight that books can usually only dream of. Online creative collaborations such as Celebrating Change can use film, music, written word or spoken word in ways that printed form simply can't deliver. Not least of all, online poetry saves trees!
For many writers (and readers) however, the printed book or magazine simply can't be beaten. There's something about the quietness of paper that conduces to contemplation and absorption. Bad habits of dipping and diving on-screen can be left behind and poems given the space (literal and metaphorical) they deserve. Many online magazines can't take unusual formats because line breaks get easily mangled. Goodbye concrete poetry! In terms of longevity, a book can be retrieved from your shelves and re-read in years to come, whereas online work tends to plunge into oblivion remarkably quickly (unless it's a bad review or embarrassing photo!)
There are no right or wrongs, of course. Clearly, online and print both have a place in our reading lives. It's fun to embrace them both. As far as I'm concerned, thank you for taking my work, and vive la difference!
The Ekphrastic Review, edited in Canada by Lorette C Luzajic, publishes poems on a daily basis and accepts reprints: "We're an online journal devoted entirely to writing inspired by visual art. Our objective is to promote ekphrastic writing, promote art appreciation, and experience how the two strengthen each other and bring enrichment to every facet of life. We want to inspire more ekphrastic writing and promote the best in ekphrasis far and wide." Check it out here at: The Ekphrastic Review
The High Window is published quarterly by David Cooke and includes reviews, guest poets, poems in translation, occasional articles, and new poems by established and up and coming poets. He has recently started releasing it in instalments to allow for less pressured reading. By clicking names on the contributors' list, you get taken straight to that person's poems. Poets in the autumn 2019 issue include Claire Booker, Rebecca Gethin, Rosie Jackson, Maitreyabandhu, Angela Topping and Gareth Writer Davis. The High Window (issue 15)
Celebrating Change is an ACE funded story-telling project based in Middlesbrough led by Laura Degnan and Kirsten Luckins, which combines film, poetry and writing workshops around social change. It releases a poem every ten days, and accepts reprints. Guest editors have included Amy Kinsman and Jess Green. Some of the poets published so far are Claire Booker, Rachel Burns, Sarah L Dixon, Catherine Fulkner, Moira Garland, Ye Min and Marka Rifat. Check it out here at: Celebrating Change
Tagged Amy Kinsman, Celebrating Change, Claire Booker, David Cooke, Jess Green, Kirsten Luckins, Laura Degnan, Lorette C Luzajic, Middlesbrough, new poems, new writing, Online poetry, Poetry from Art, The Ekphrastic Review, The High Window


ozgifts Great buyer to deal with!
shopoholicgirl Item delivered as described. Pleasant transaction!
Letting go pre-loved stuff which I don't use.
Pristine Condition Medium sized Gold hardware. Tote handles 4" drop; removable shoulder strap, 10" drop. Zip top. Front Givenchy logo. Black canvas lining; inside, two open and one zip pockets. Made in Italy.


My niece's sweet bundle of joy. I think that means I am her great-Aunt? 🙂 Yes, I quite like that term 🙂 She is quite a doll! Meet Arianna. Love this moment between mom and her little one. That one hand 🙂 She wasn't happy unless it was out 🙂 Precious. Her hair is so cute!
Oh, my! What a cutie! Such a dollbaby. You did a great job on the photos, as usual. 🙂 I love the way you did the announcements..so sweet. God is good, and there is nothing like a new little one to bring forth a fresh revelation of His goodness!
Thank you, Cheryl! Yes, God is good!
Aww how cute is she?!
Awww!!! She is adorable….great job on the pictures Jo.
Thank you , sweetie 😉 She is adorable!
Look at that hair! She is a doll. She looks almost too perfect to be real. I like the one in the basket. Great job capturing that innocent expression.


The lack of myostatin promotes growth of skeletal muscle, and blockade of its activity has been proposed as a treatment for various muscle-wasting disorders. Here, we have examined two independent mouse lines that harbor mutations in the myostatin gene, constitutive null (Mstn−/−) and compact (Berlin High Line, BEHc/c). We report that, despite a larger muscle mass relative to age-matched wild types, there was no increase in maximum tetanic force generation, but that when expressed as a function of muscle size (specific force), muscles of myostatin-deficient mice were weaker than wild-type muscles. In addition, Mstn−/− muscle contracted and relaxed faster during a single twitch and had a marked increase in the number of type IIb fibers relative to wild-type controls. This change was also accompanied by a significant increase in type IIB fibers containing tubular aggregates. Moreover, the ratio of mitochondrial DNA to nuclear DNA and mitochondria number were decreased in myostatin-deficient muscle, suggesting a mitochondrial depletion. Overall, our results suggest that lack of myostatin compromises force production in association with loss of oxidative characteristics of skeletal muscle.
Lack of myostatin function results in the excessive growth of skeletal muscle, demonstrating the existence of a powerful mechanism to control muscle size in normal individuals (1). The myostatin gene encodes a member of the TGF-β family of signaling molecules and has been highly conserved throughout vertebrate evolution (2). This finding, together with the extremely rare incidence of spontaneous mutations within the gene (3, 4), points to biological advantage and associated evolutionary constraints on muscle size by this pathway. In some respects, this is paradoxical, because muscularity has been positively associated with vigor and reproductive fitness. Such views may have neglected a critical evaluation of the functional aspects of muscle hypertrophy induced by the absence of myostatin. Doubts of this sort are indirectly supported by the observation that this increase in muscle mass is not accompanied by a proportionate increase in muscle force (5, 6). Furthermore, cattle with hereditary muscular hypertrophy (double-muscled cattle), many of which have been shown to harbor mutations in the myostatin (Mstn) gene, are actually prone to muscle damage after mild exercise (7–10). It is reported, however, that myostatin-deficient mice do not suffer from muscle fiber damage when subjected to brief periods of exercise (11).
Targeted inactivation or antibody blocking of myostatin in the dystrophin-deficient mdx mice, a model of Duchenne muscular dystrophy, demonstrated that dystrophic muscle could indeed be stimulated to grow (5, 12, 13). The effect on force development in these animal models differed depending on the methods of myostatin blockade. Whereas specific force output in mdx mice remained decreased after treatment with anti-myostatin antibody, treatment with stabilized myostatin propeptide resulted in an increase of specific force output (5, 12, 13). On a discordant note, targeted inactivation of myostatin in the dyw/dyw mouse, the animal model for merosin-deficient congenital muscular dystrophy, revealed no improvement of the muscle pathology and actually increased postnatal mortality (14).
Despite these uncertainties, the use of specific antibodies to block myostatin has now been proposed as a new therapeutic strategy to stimulate muscle growth, and a multicenter clinical trial on muscular dystrophy patients is in process. In this report, we analyzed the functional and structural characteristics of muscle from myostatin-null mice. Importantly, the main body of our study has been performed on the same line originally used to describe the myostatin knockout phenotype and to confer the beneficial value of blocking myostatin function in muscle-wasting disorders (1, 5).
Decreased Specific Force Generation in the Myostatin Knockout Mouse.
To examine the relationship between muscle size and improved function in Mstn−/− mice, we first performed a series of tests of force generation. The maximal isometric twitch force (Pt) and tetanic force (Po) of extensor digitorum longus (EDL) muscles of 7-month-old male Mstn−/− and age-matched C57BL/6 wild-type mice are presented in Table 1 and Fig. 1. Maximal Po was reached at 100 Hz in both Mstn−/− and C57BL/6 wild-type muscles and did not increase with stimulation at higher frequencies. We therefore compared values obtained at 100 Hz from wild-type and Mstn−/− mice (Fig. 1 a and b). Despite the increased muscle bulk in the myostatin-deficient animals, maximal Po was similar to that of wild-type mice of the same genetic background (P = 0.189; Table 1; Fig. 1 c and e). Moreover, when maximal Po was normalized for muscle weight (specific force), we found that Mstn−/− male mice generated only 53% of the force developed by wild-type animals (P < 0.001; Table 1; Fig. 1d). Similarly, normalization of Po for the cross-sectional area also revealed a reduction in specific force generation (P = 0.010; Table 1).
Physiological properties and size of EDL muscles from male adult Mstn−/− mice compared with age-matched C57BL/6 wild types. (a and b) Records of superimposed isometric contraction in response to direct muscle stimulation at 1, 10, 20, 50, 100, and 200 Hz are shown for EDL muscles from wild-type (a) and Mstn−/− (b) mice. (c) Maximal Po of EDL muscles from Mstn−/− mice (blue column) compared with wild types (yellow column) (P = 0.189). (d) Maximal Po expressed as a function of muscle weight of EDL muscles from Mstn−/− mice (blue column) compared with wild types (yellow column) (P < 0.001). (e) Wet weight of EDL muscles that were measured after force testing from Mstn−/− mice (blue column) compared with wild types (yellow column) (P < 0.001). (f) Records of isometric twitch contraction of EDL muscles from a Mstn−/− mouse (blue trace) and a wild-type mouse (black trace). (g) Contraction times after a single twitch stimulation of EDL muscles from Mstn−/− mice (blue column) compared with wild types (yellow column) (P < 0.001). (h) Relaxation times after a single twitch stimulation of EDL muscles from Mstn−/− mice (blue column) compared with wild types (yellow column) (P < 0.001).
The weight of 7-month-old male Mstn−/− EDL muscle was increased by 66% over wild-type values (P < 0.001; Table 1; Fig. 1e), and the total cross-sectional area of the Mstn−/− EDL exceeded control values by 53% (P = 0.035; Table 1).
We also performed contraction measurements on EDL muscles from 10-month-old female Mstn−/− mice and found a similar maximal Po (P = 0.106) and a marked reduction in specific force (P < 0.001) despite a >2-fold higher muscle mass (P < 0.001) than in age-matched female wild types (Table 1). Maximum and specific tetanic force was similar in male and female Mstn−/− mice.
Force measurements were performed on EDL muscles from young animals (2 months of age) and again gave similar maximal Po for the two genotypes (P = 0.5; Table 1). The wet weight of homozygous EDL muscle was increased to 191% compared with wild types (P = 0.003; Table 1), thus resulting in a decreased specific force for homozygous muscle (P = 0.001; Table 1), confirming data obtained from older mice. Reduction in specific force was 52% for 2-month-old and 53% for 7-month-old Mstn−/− male mice compared with age-matched male wild-type mice.
Additionally, muscles of the Mstn−/− EDL showed a decay of tension during tetanic stimulation at 100 and 200 Hz, whereas in the wild-type EDL, there was an increase in tension over the stimulation period (Fig. 1 a and b). Moreover, the maximal twitch force was slightly higher in the Mstn−/− than the wild-type EDL (P = 0.204), but the maximal tetanic force was slightly lower than the wild-type EDL (Table 1; Fig. 1f), resulting in a significant alteration of the twitch/tetanus ratio of 0.27 for Mstn−/− compared with 0.21 for wild-type EDL (Table 1).
Male Mstn−/− EDL muscles also showed significantly shorter time to peak tension (contraction time) (P < 0.001) and shorter time to half relaxation than wild-type muscles (P = 0.001; Table 1; Fig. 1 f–h). Similar results were also observed in female Mstn−/− vs. wild-type muscles (data not shown).
Decreased Specific Force Generation in the compact Mouse.
Essentially similar results were obtained from force measurements on skeletal muscle from the compact (Berlin High Line, BEH(C/C)) mouse that displays hypermuscularity but differs from Mstn−/− in both its genetic background and the nature of the mutation in the myostatin gene. We found a slightly higher maximal Po in EDL muscles from the 2-month-old homozygous compact females (BEH(C/C)), albeit statistically not significant (P = 0.64), which converted to a significant reduction in specific force (P < 0.025), allowing for the 2-fold higher muscle mass (P < 0.05) compared with EDL muscles from their wild-type controls [Table 2 and supporting information (SI) Fig. 5]. Thus, both Mstn−/− and compact mice have significantly smaller specific force values as compared with their wild-type littermates.
Lack of Myostatin Predisposes to Differentiation to Type IIB Fibers.
Functional studies revealed a shortening in contraction and relaxation time in Mstn−/− muscle. We therefore investigated the fiber-type distribution of the EDL muscle (Fig. 2), finding very few type I fibers (slow fibers) in either Mstn−/− or C57BL/6 wild-type muscles (data not shown). The total number of IIa fibers on midbelly sections was five times lower in the Mstn−/− EDLs than in wild-type mice (P < 0.001; Fig. 2e). IIa fibers were generally segregated in the deeper region of the muscle. Therefore, we determined the fiber-type distribution at this site (Fig. 2 a–d). We counted IIa, IIb, and non-IIa/non-IIb fibers in this region and expressed the distribution as percentage of relative frequency. Fibers negative for both isoforms were considered nonhybrid IIx fibers. We found a reduction in IIa and IIx fibers and a concomitant increase in IIb fibers in Mstn−/− EDL muscles (Fig. 2f). This shift in the fiber-type distribution in the myostatin-deficient EDL muscle is consistent with the shortening of contraction and relaxation time.
Muscle fiber-type profiles in EDL muscles from male Mstn−/−- and C57BL/6 wild-type mice. (a and b) Transverse sections of whole EDL (5× objective). The green fluorescence in a shows expression of MHC IIa in only a few fibers of Mstn−/− EDL compared with C57BL/6 wild-type EDL shown in b. IIa fibers can be seen to predominate in the deep muscle regions of the muscles, which are shown on the left side of the images. The white frames show areas of deep muscle region where the fiber type distribution was analyzed. The regions outlined in a and b are shown enlarged in c and d and show an overlay of staining for MHC IIa (green) and MHC IIb (red) by using ×20 objective. Asterisks depict non-IIa/non-IIb fibers. (e) Total number of IIa fibers in the whole EDL muscle sections from Mstn−/− mice (blue column) compared with wild types (yellow column) (P < 0.001). (f) Histogram showing the fiber-type distribution in the deep region of the EDL muscles. Fibers expressing MHC IIa and IIb and fibers negative for IIa/IIb were counted. Non-IIa/non-IIb fibers were considered as IIx fibers because there were hardly any fibers expressing slow MHC.
Oxidative Enzymes Are Decreased in Mstn−/− Muscle.
In view of the fiber-type bias toward fast glycolytic type IIb fibers, suggesting a concomitant decrease in mitochondrial activity, we performed staining for the mitochondrial enzymes succinate dehydrogenase (SDH), cytochrome oxidase (COX), and NADH reductase on sections of EDL muscles. Staining for SDH activity revealed markedly fewer strongly stained fibers (high activity) and an increase in a larger proportion of very pale fibers (low activity) in Mstn−/− than in wild-type mice (Fig. 3). Similarly, fibers from Mstn−/− EDL muscles showed a lower activity for COX and NADH paralleling that for SDH (data not shown).
Oxidative properties of adult EDL muscles from 7-month-old male Mstn−/− mice relative to age-matched C57BL/6 wild types. SDH staining of Mstn−/− EDL (a and c) and of control EDL (b and d) in the deep (a and b, respectively) and superficial (c and d, respectively) regions. Darkly stained fibers contain high SDH activity, and pale-stained fibers contain low SDH activity.
However, SDH activity in muscle from Mstn−/− mice seemed generally lower compared with control muscle and was difficult to explain solely by a fiber-type switch toward fast glycolytic fibers (Fig. 3).
mtDNA Depletion and Decreased Mitochondria Number in Mstn−/− Muscle.
The above results suggested a decreased number of mitochondria in myostatin-deficient muscle. We therefore determined the ratio of the number of mtDNA (MT-CO1) copies per single-copy nuclear gene (Ndufv1) by quantitative real-time PCR with gene-specific probes (SI Fig. 6). This assay has been controlled on rho0-cells, which are devoid of mtDNA, and did not yield a signal for the MT-CO1 probe (data not shown), thus excluding the possibility of amplification of nuclear pseudogenes. Half the copy number of the nuclear autosomal single-copy gene can thus be equaled with the number of myonuclei. In wild-type muscle, despite a different fiber-type composition of EDL (fast muscle) and soleus (slow muscle), the mtDNA/myonucleus ratios were similar between these two muscles (209.8 and 200.2, respectively; P = 0.754), suggesting that different fiber types contain about same number of mitochondria per myonucleus. Interestingly, we found a significantly lower mtDNA/myonucleus ratio in muscle from Mstn−/− mice compared with wild-type muscle (from 205.0 to 104.8; P = 0.007, if EDL and soleus were taken together). The decrease was more pronounced in EDL muscle (from average 209.8 to 75.2 P = 0.014) as compared with soleus muscle (from 200.2 to 134.4, P = 0.027), thus suggesting a mitochondrial depletion in muscle from Mstn−/− mice independent of fiber-type composition.
We additionally determined the number of mitochondria in muscle fibers of the EDL muscle from 2-month-old male Mstn−/− mice and male C57BL/6 wild-type mice by analyzing electron micrographs taken at the midbelly region. We found that the myofibers from male Mstn−/− mice, on average, had 30.3 mitochondria per unit area compared with 41.3 mitochondria for wild-type mice (P < 0.001; 455 fibers from four EDL muscles from Mstn−/− mice; 401 fibers from four EDL muscles from C57BL/6 wild-type mice; Table 1), thus confirming mitochondrial depletion in muscle from Mstn−/− mice.
Muscle from Mstn−/− Mice Accumulates Tubular Aggregates.
Histological examination by H&E and Gomori's trichrome stains revealed many cytoplasmic inclusions in the EDL of both male (7 months old; Fig. 4a and b) and female (10 months old) Mstn−/− mice. These were rare in age-matched C57BL/6 wild-type males and were never detected in wild-type females (SI Fig. 7). We also found similar inclusions in the tibialis anterior and gastrocnemius muscles, both of which contain a high proportion of type IIb fibers, but not in the soleus muscle (data not shown). Cytoplasmic inclusions were found predominantly in superficial regions of these muscles, which contain mainly IIb fibers. Electron microscopy revealed them to be a membranous accumulation of tubules and saccular dilatations, which defined them as tubular aggregates (Fig. 4c).
Histological analysis of tubular aggregates from adult EDL muscles of Mstn−/− mice. (a) Transverse sections of the EDL muscles from a 7-month-old male Mstn−/− mouse after staining with H&E showing the presence of numerous cytoplasmic inclusions (arrowheads) in many muscle fibers. (b) Transverse sections of the EDL from a 7-month-old male Mstn−/− mouse after Gomori's trichrome staining showing cytoplasmic inclusions in purple color (arrowheads). (c) Electron micrograph taken from an EDL of a 7-month-old male Mstn−/− mouse showing stacks of tubular and saccular formations (∗), which define tubular aggregates, between the contractile apparatus.
Cytoplasmic inclusions were not present in the EDL muscles from 2-month-old Mstn−/− mice, suggesting that they accumulated over time. Moreover, cytoplasmic inclusions were not present in EDL muscles from 2-month-old compact mice (BEHC/C) examined in this study (data not shown).
Immunolabeling showed that these inclusions accumulated SERCA1, the calcium-release channel of the sarcoplasmic reticulum of fast muscle fibers (SI Fig. 7). However, they were largely devoid of the dihydroxypyridine receptor (DHPR) of the transverse tubules desmin or myosin heavy chain, when stained with an antibody that detects all forms of MHC (data not shown). Triple staining for MHC type IIb, SERCA 1, and laminin-γ1 confirmed the presence of cytoplasmic inclusions in IIb fibers only (SI Fig. 7 and data not shown). Other abnormalities such as fiber necrosis or centrally located nuclei were rarely seen in the muscle of Mstn−/− or wild-type mice.
The frequency of tubular aggregates showed no correlation with specific force generation in the Mstn−/− mice (data not shown).
In this study, we have investigated the functional and cellular characteristics of enlarged skeletal muscle from mouse lines with mutations in the myostatin gene (Mstn−/− and BEHC/C). In accord with other reports, we found that a deficiency in myostatin resulted in increased muscle mass (1, 6, 15–18), but that this increase was not accompanied by a proportionate increase in force generation. It follows that specific tetanic tension was significantly decreased when normalized for muscle size, which was observed in both mouse lines. These findings clearly indicate that the increase in muscle mass of myostatin mutant animals confers no strength advantage over wild-type controls.
Although previous studies on the Mstn−/− mouse strain and on wild-type mice that were treated with antimyostatin antibodies revealed an increase in grip strength (5, 6, 11), the increase in force was disproportionately low when compared with the increase in muscle mass, suggesting a decrease in specific force generation. In light of our results, it is surprising that a blockade of myostatin in the mdx mouse, the animal model of Duchenne muscular dystrophy actually increased the total as well as specific force output (5, 12, 13).
A relevant comparison may be made with another form of inhibition of the myostatin-signaling pathway resulting in a similar physiological phenotype to the myostatin mutants. Overexpression of ski in MSVski transgenic mice resulted in Type IIb fiber hypertrophy accompanied by a 30% decrease in specific force generation (19). Ski negatively regulates Smad phosphorylation (20–22), thereby inhibiting signaling of TGF-β-like factors, such as myostatin. These findings contrast with muscle-specific overexpression of insulin-like growth factor 1, where fiber hypertrophy is accompanied by increased maximum force generation and maintained specific force levels (23). One may suggest that massive hypertrophy simply could alter the angle of pull on the muscle fibers during contraction, thereby reducing the ability to generate a higher force output. However, that hypertrophy increases force output after overexpression of IGF-1, but not after myostatin knockout, points to additional factors that cause the force problems in a lack of myostatin.
In agreement with previous findings on the Mstn−/− mouse line (24), we found a predominance of type IIb fibers in the EDL muscle from Mstn−/− mice together with a marked reduction in types IIa and IIx fibers, as well as preliminary evidence of a similar IIb fiber predominance for tibialis anterior and gastrocnemius muscles. We also noted a substantial deficit in the activity of oxidative enzymes in myostatin-deficient EDL muscle, in accord with the high proportion of fast glycolytic fibers that, in general, contain less mitochondria. However, the extent of loss of activity of oxidative enzymes is difficult to explain solely by a fiber-type switch toward fast glycolytic fibers. We found that the mtDNA copy number per myonucleus in muscles from Mstn−/− mice was lower than that seen even in fast glycolytic fibers of wild-type muscle, and we found a decreased number of mitochondria in muscles from Mstn−/− mice. We conclude that these findings truly reflect a mitochondrial depletion that cannot be explained by a simple switch of fiber types, and our data suggest a marked diminution in mitochondria per unit volume of cytoplasm.
This finding, together with previous reports of reduced capillary density in myostatin-deficient muscle (18), prompts the idea that myostatin may function to optimize aerobic metabolism in skeletal muscle. It has been reported that blockade of mitochondrial respiration in skeletal muscle resulted in decreased tetanic force generation (25, 26), and in patients with mitochondrial depletion syndrome, muscle weakness is one leading clinical feature (26, 27). Thus, the low specific force in hypertrophic muscle due to lack of myostatin, may be attributable to the associated mitochondrial depletion.
Our results do not specify whether the altered fiber-type composition in muscle of Mstn−/− mice arises during development, or whether fibers convert later in life. Nor is it evident whether they represent a direct effect on the muscle or whether the firing patterns of the innervating motorneurons are implicated (28), a topic for further investigation. Interestingly, a similar bias toward glycolytic myofiber phenotype has also been found in cattle with hereditary muscle hypertrophy associated with mutation of the myostatin gene (29). This predominance of fast glycolytic fibers may well explain the increase in contraction speed and shortening in relaxation time in myostatin-deficient muscle, but, given the normal association of IIb fibers with high force production, it is surprising that maximal stimulation hardly changed force production. Thus, Mstn−/− muscle does not seem to benefit from the high tetanic force generation to be expected of glycolytic fibers, and the mitochondrial depletion would suggest increased fatigability and exercise intolerance, a mark of derangement rather than orderly change in the differentiation process.
This view is sustained by the observed accumulation with age of tubular aggregates composed of sarcoplasmic reticulum components and located exclusively in type IIb fibers in Mstn−/− muscle. This feature has not been reported (1, 5, 6, 11). Although their presence may be associated with the source of the physiological problems, our data do not implicate tubular aggregates as the primary cause of reduced force generation. Thus, both young mice of Mstn−/− and compact mice (BEHC/C) genotypes exhibited low specific force production before they had developed tubular aggregates, and female Mstn−/− mice produced far fewer tubular aggregates than males but exhibited a low specific force output very similar to that of males. Moreover, within the male group, there was no correlation between the number of myofibers containing cytoplasmic inclusions and specific force output. Again, comparison is invited with the MSVski transgenic mouse model of fiber hypertrophy, which also exhibits a decrease of specific force generation in combination with increased and aggregated sarcoplasmic reticulum (30). It seems likely that aberrations of physiological function of sarcoplasmic reticular organization both arise, perhaps independently, as a result of physiological stresses associated with dysregulated fiber hypertrophy. One such explanation that springs to mind is that the disturbances may reflect different aspects of problems in calcium handling. The decay in tension during tetanic stimulation together with the increased maximum isomeric twitch force (Pt)/Po ratio and the proliferation of sarcoplasmic reticulum may both be mechanistically linked to an altered calcium homeostasis in myostatin-deficient muscle. This hypothesis fits well, too, with the dearth of mitochondria, which can act as fast calcium sinks in skeletal muscle (31) as well as providing ATP for calcium uptake into the sarcoplasmic reticulum; their lack in Mstn−/− might well stimulate a compensatory formation of the sarcoplasmic reticulum. Intriguingly, small numbers of tubular aggregates are found in muscles of older male wild-type mice of the reference wild type used here and of various inbred and outbred laboratory mouse strains (32, 33) but not in wild-type females, which correlates with the higher level of myostatin in wild-type female than male muscle (34).
Our twitch-force testings revealed an increase in contraction speed and shortening in relaxation time in myostatin-deficient muscle, which may sufficiently be explained by the fiber-type conversion toward fast glycolytic fibers observed in myostatin-deficient muscle. Alternatively, differences in the connective tissue between Mstn−/− and wild-type mice may lead to a more rapid uptake of the series elastic component and may act as an additional contributing factor to induce the more rapid twitch kinetics. Additionally, the expanded sarcoplasmic reticulum that morphologically became evident in the form of tubular aggregates might be responsible for a more rapid release and reuptake of calcium, thus accounting for the differences in twitch kinetics. However, its exact role remains to be determined.
Current interest in myostatin centers on the potential of therapeutic blockade of this cytokine to increase the size and strength of muscle as a means of counteracting muscle weakness associated with sarcopenia and muscular dystrophy. Although a number of studies have demonstrated some benefit from this strategy in mice carrying the mdx muscular dystrophy, the basis of the clinical improvements observed is unclear, and the experimental regimes have been fairly short term. Nonetheless, human trials of myostatin-blocking agents are being conducted currently. Our data on nonmyopathic mice, while not directly contradicting previous work on the mdx mouse, do raise questions as to the precise biological effects of myostatin blockade and suggest an urgent need for further elucidation of the mechanisms of muscle growth and differentiation that are affected by such treatments.
Mstn−/+ founder breeding pairs on a C57BL/6 background were a kind gift of Se-Jin Lee (Johns Hopkins University, Baltimore, MD) (1). Myostatin knockout and wild-type mice (C57BL/6) were bred in the animal facilities of Royal Veterinary College. After the establishment of the colony, mice were screened and shown to be free of common rodent infectious diseases. Studies were performed on 2- and 7-month-old male Mstn−/− and male C57BL/6 mice and 10-month-old female Mstn−/− and female C57BL/6 mice unless otherwise stated. All investigations on animals carried out for this study had prior approval of the institutional ethics approval committee (Royal Veterinary College). Animals were kept under guidelines set out by the Home Office (United Kingdom). Animals were kept under license PPL/70/5218 (Home Office, United Kingdom).
Additionally, mice from a subline of the BEH have been used (35). The BEH line is homozygous for the compact mutation (36) and is coded as MstnCompt−dl1ABC (37, 38). Mice from the BEH line were crossed with mice from the Berlin Low line (BEL) to introduce the wild type back into the BEH mice, to allow segregation of the wild-type and the compact allele in this subline, coded BEHC/+ (35). Heterozygous mice from BEHC/+ have been repeatedly backcrossed to mice from the BEH line to reestablish the high growth background of this line, which had been long-term selected for high growth (35). The mice used here were sampled after completion of five backcross generations (including F1), which had on average 98.44% of genetic background of the BEH line reestablished. Heterozygous mice of this generation were mated inter se to produce the experimental animals for this study [all three genotypes: homozygous compact (BEHC/C), heterozygous (BEHC/+), and homozygous for wild type (BEH+/+)].
All functional studies were performed in vitro on EDL muscles. The time to reach peak tension (contraction time) and the half-relaxation time (time between maximum and half-maximum force during the relaxation phase of the twitch, t½r) were determined. The maximal Po was determined from the plateau of the frequency-force relationship. For detailed information, see SI Table 3.
Relative Quantification of mtDNA Copy Numbers.
Four male Mstn−/− and five male C57BL/6 control mice were killed by cervical dislocation at 7 weeks. The EDL and soleus muscles of the right leg were immediately explanted in toto and flash-frozen in liquid nitrogen. DNA was extracted, and quantifications of the mtDNA encoded gene MT-CO1 (GenBank accession no. NC_001807) and of the single-copy nuclear gene Ndufv1 (GenBank accession no. NM_133666) were performed by using TaqMan chemistry (Applied Biosystems, Weiterstadt, Germany). A detailed protocol can be viewed in SI Text.
Each EDL muscle was weighed and then mounted in OCT (VWR, Poole, U.K.) and frozen in melting isopentane cooled in liquid nitrogen. Ten-micrometer transverse sections from the midbelly region were cut on a cryostat. Serial sections were stained for H&E, modified Gomori's trichrome, SDH, NADH–tetrazolium, and cytochrome oxidase.
A list of antibodies and concentrations used is in SI Text. Double staining was performed to depict expression of myosin heavy chain (MHC) IIa and IIb. Triple staining was performed to depict expression of MHC IIb, laminin-γ1, and SERCA1 or DHPR. For detailed immunohistochemistry protocols, see SI Table 3.
Samples (1 mm3) were initially fixed in 4% glutaraldehyde in 0.1 M cacodylate buffer (pH 7.2) for 1.5–2 h, followed by washing in buffer for 30 min and fixation for 1 h in 1% osmium tetroxide in 0.1 M cacodylate buffer. Samples were then dehydrated and infiltrated with propylene oxide followed by embedding in araldite. Semithin (1 μm) and ultrathin (70-nm) sections were cut by using a Leica Ultracut (Leica, Bensheim, Germany). Sections were stained with uranyl acetate and contrasted with lead citrate according to standard protocols and viewed on Jeol JEM-1011 (JEOL, Tokyo, Japan). The mitochondria number was determined by using a point-counting method on micrographs taken at ×3000 magnification according to previously published methods (39, 40).
The total cross-sectional area was determined from H&E-stained transverse sections from the midbelly region of EDL muscles by using imaging software (Leica QWin).
The number of each experiment is listed in SI Text.
We thank Elaine Shervill, Helen Smith, Lucy Feng, and Angelika Zwirner for excellent technical assistance. We are indebted to Prof. Se-Jin Lee for providing founder mice for our Mstn−/− colony and to Dr. Simon Hughes (King's College London) for providing antibodies. This work was funded by MDA USA (Grant MDA3870, to H.A.), the Wellcome Trust (Grants 066195 and 078649, to R.M. and K.P.), and l'Association Monégasque Contre les Myopathies and Duchenne Parent Project France (M.S.).
Author contributions: H.A., R.M., R.N., M.S., S.C.B., T.P., P.Z., L.B., and K.P. designed research; H.A., R.M., R.N., M.S., S.C.B., A.O., P.Z., and L.B. performed research; H.A., R.M., R.N., M.S., S.C.B., A.O., G.V., T.P., P.Z., L.B., and K.P. analyzed data; and H.A., R.M., R.N., M.S., S.C.B., T.V., F.M., G.V., T.P., P.Z., L.B., and K.P. wrote the paper.
This article contains supporting information online at http://www.pnas.org/cgi/content/full/0604893104/DC1.
(2004) Annu Rev Cell Dev Biol 20:61–86.
(2004) N Engl J Med 350:2682–2688.
(2003) Biochem Biophys Res Commun 300:965–971.
(1973) J Anim Sci 36:684–694.
(1997) Proc Natl Acad Sci USA 94:12457–12461.
(2005) Proc Natl Acad Sci USA 102:2519–2524.
(2005) Am J Pathol 166:491–497.
(2003) Proc Natl Acad Sci USA 100:15842–15846.
(2005) J Muscle Res Cell Motil 26:103–112.
(2002) Am J Physiol 283:C1228–C1241.
(1999) J Biol Chem 274:35269–35277.
(1991) Am J Hum Genet 48:492–501.
(2000) J Anim Sci 78:1485–1496.
(2005) Acta Physiol Scand 185:141–149.
(2005) Invest Ophthalmol Visual Sci 46:4541–4547.
(2000) Histochem Cell Biol 114:477–481.
(2003) Am J Physiol 284:E377–E381.
(1979) Stereological Methods (Academic, London).
(1980) Stereological Methods (Academic, London).


What product are you enquiring about?
We will at all times strive to provide you with and after sale service to all our products, Not just for 1 year but for all the years to come.
© Copyright 2019 - Solaris Interiors Ltd.


text:
Sport Champions Cup
Wasps sing after winning at Quins but Toner confident they won't sting Blues
Leinster's Devin Toner
David Kelly Twitter Email
January 19 2015 2:30 AM
IF Leinster are finding form at the business end of European qualification, their rivals for a potential home quarter-final Wasps, are also hitting their straps when it matters most.
http://indo.ie/3vN7s5
https://www.independent.ie/sport/rugby/champions-cup/article30917133.ece/7e0ff/AUTOCROP/h342/DevinToner_app.jpg
Both these sides warmed up for the Pool 2 decider at Coventry's Ricoh Arena next Saturday lunchtime with contrasting successes.
As Leinster effected their predicted turkey shoot with ease, Wasps, backboned by an incredible 199 tackles, staged a stunning smash and grab at the Stoop to almost certainly floor the last-eight hopes of Conor O'Shea's Harlequins.
"It will be a new match," declared James Haskell, the back-row forward who personifies a club who have come from five years of European exile to brink of a quarter-final.
This time last year, Haskell was a journeyman in Japan; now he is being touted for an England starting spot after his 28 tackles. Other business will come first.
"We can't allow a team to keep as much ball as they did tonight because Leinster are too dangerous. This will be a real test for us. We know what the occasion will be. If we can get the win then hopefully we will bring the house down."
Harlequins dominated all the stats but, after Danny Care's ambitious tap and go was intercepted by Christian Wade and then visiting scrum-half Joe Simpson sold a hatful of dummies to score a second try, there was no way back.
"We were tested by a good side," said Haskell. "I don't know how they didn't get through. The amount of passes they put together, the amount of tackles we had to make.
"That is what European rugby is about: going to a dark, dark place, playing until you can't play anymore and doing it again week in, week out and playing against the best opposition.
"I don't like to get too carried away. We had a sing song after the game but we haven't won anything yet. By Monday morning it will be back to business as usual.
"Leinster at home - that is what dreams are made of. It is a huge, huge occasion that some of these boys won't have experienced before."
The sides have met in Challenge Cup fare two seasons back; Leinster cruised to a quarter-final and the switch from that venue, Adams Park, to the more spacious Ricoh poses no fears for Leinster second-row Devin Toner (left).
"We have a good back-line and if we can get them a good bit of space, I'd back them against anyone," he said.
"I hope this was a red letter day for us. For these lads to get that experience today and to come out of that fashion, will really stand to them.
"It's hugely important that we have the confidence in them. We know they're very young and don't have a huge amount of experience, but to see lads come on and know they can do a job for you is massive.
"Everyone now wants to play every week. If we have everyone playing to the best of their ability, it's a hard team to get into.
"We're getting there. We had the confidence building and we knew we had it in us.
"Not getting those performances has been frustrating, but in the last couple of weeks the performances have been pretty positive.
"A lot of it had to do with the set-piece. Recently, we might have won the line-out but we wouldn't have used the ball as well as we would have liked.
"And we wouldn't be getting clean ball out of the scrum and then our breakdown has struggled too.
"So just to get that platform tonight was good. We took our chances tonight. It's going to be hugely different next week."
Analysis: Why the World Cup schedule could hurt the Irish provinces in next season's Champions...
Jonathan Bradley In two of the three opening seasons of the Heineken Cup, Irish teams failed to make it beyond the pool stages. Since then, it's happened only once.
Cian Tracey: 'Defending champions, Zebo factor and condensed schedule - many threats for...
Cian Tracey Back in February of last year when Simon Zebo was preparing for his French sojourn, the prospect of playing against Munster for Racing 92 was put to him.
'It's such a tough draw' - van Graan admits Munster face 'massive challenge' to emerge...
Cian Tracey Munster head coach Johann van Graan insists his side face a 'massive challenge' to emerge from a daunting Champions Cup pool that includes the defending champions Saracens, as well as Racing 92...
Late anguish for Munster as Racing snatch win but Euro destiny still in their own hands Champions Cup
Alan Quinlan: The Joe Schmidt show has permeated into all four provinces and... Champions Cup
'I'm bitterly disappointed for the lads' - Donnacha Ryan all class as he commiserates... Champions Cup
'One guy's got a broken jaw' - Munster set to face riled up Leicester at... Champions Cup
Holland: Paris outfit are fitter than they get credit for Champions Cup
'It's very hard to know what is going on with Tiger' - Paul McGinley questions Woods'...
Former Ryder Cup captain Paul McGinley is...

redpajama_set_name: RedPajamaCommonCrawl


So this post is a little different today. I want to tell you about my friend Saruuh. Saruuh writes two blogs (and updates them far more often than I update this one) and has still found the time to write and self publish multiple novels over the past two years! As someone who genuinely struggles to get literally anything done I find this absolutely amazing and honestly I am just totally in awe of her.
I've mentioned Saruuh's previous books The Forgotten and The Beast of Callaire a few times before on this blog. They're both genuinely great YA novels (and I promise I'm not only saying that because the author sometimes sends me cute presents) and what's even more amazing is that The Forgotten is available totally for free from all major ebook retailers and you can also sign up at her tumblr to receive a free paperback version!
Saruuh has chosen to give this series of novels away for free because she believes that stories should always be available to people who might not always be able to afford to buy books and I think that's an amazing thing for her to do. It's also her birthday this week and I think it would be absolutely amazing if she could reach her donation target before then. So if you can afford to donate even $1 then please do, or if you can't then please just help spread the word! Either way check out her blog post about it here for more details about the campaign and about all of the different goodies that she is giving away to people who donate!


If you're looking for people of color in your summer sci-fi blockbuster, you'll be waiting for a long time. A new infographic form Lee & Low Books details just how lacking fantasy films are in the diversity department: only 14 percent of movies feature a female protagonist and only 8 percent feature a protagonist of color. Read more.
Sporadic gunfire isn't an unusual sound in the Brewster Homes public housing complex in Detroit, but booming noises that shook Tenesha Higgins early Wednesday morning were way too close. Numerous shots were fired at an apartment building, with one piercing a wall and hitting an 8-year-old boy who was sleeping. The child — who Higgins described as a "good boy" who loved playing baseball — died 45 minutes later. Read more.
The Obama administration on Wednesday sought to join two ongoing lawsuits against voting laws in Wisconsin and Ohio. In the filings, the Justice Department argued that a federal judge was right to strike down Wisconsin's voter ID law and that Ohio is incorrectly interpreting its duties under a provision of the Voting Rights Act. Read more.
It's been almost two weeks since Eric Garner died on Staten Island after being put into a chokehold by NYPD officer Daniel Pantaleo. Since Garner's death, photo and video evidence has emerged showing New York City police officers using apparent chokeholds to apprehend two other suspects, both of whom were black, and both of whom allegedly resisted arrest over petty crimes. Read more.
Grammy award-winning songwriter and producer Carvin Haggins is spearheading a controversial drive to urge urban radio stations to clean up their acts. Haggins, 44, a respected industry heavyweight, is calling on territorial stations to stop playing violent, misogynistic and over-sexualized songs. Read more.
Staten Island police arrive at the scene of an alleged crime, where they find a middle-aged black man. He resists arrest, maybe, so they rough him up a bit. After a while, he complains that he's having difficulty breathing, but medical attention arrives too late, and he dies.
It's the story of Eric Garner, but also of Iriving Mizell, who died in police custody last year in the same precinct where Garner perished this month. Last week, the NYPD's Civilian Complaint Review Board ruled that Officers Megan Carroll and Earl Javellana did not seek medical attention for Mizzell, and that Officer Todd Craven used excessive force and gave a false statement regarding his arrest, the New York Daily News reports. And a lawsuit this week alleges Mizzell was "viciously" beaten and assaulted by cops before his death. Read more.


text:
Q: Entity property is null even with value entity framework So for some reason when I try to do db.SaveChanges it says the property Username is not allowed to have null value inserted yet it is not null when I use debugger. The item Username property has a string in it...
public void fvAddUser_InsertItem()
{
    var item = new InventarioCiclico.xUtilizador();

    TryUpdateModel(item);

    if (ModelState.IsValid)
    {
        using (InventarioCiclicoContext db = new InventarioCiclicoContext())
        {
            if (db.xUtilizador.Any(u => u.Username == item.Username))
            {
                Page.ClientScript
                    .RegisterStartupScript(
                        this.GetType(),
                        "ShowToast",
                        "ShowToast('Erro','topCenter','error', 'Utilizador já exsiste.', '2000')",
                        true
                    );
            }
            else
            {
                xColaborador c = new xColaborador();
                c.Nome = (fvAddUser.FindControl("txtNome") as TextBox).Text;
                c.Email = (fvAddUser.FindControl("txtEmail") as TextBox).Text;
                item.xColaborador.Add(c);

                db.xUtilizador.Add(item);
                db.SaveChanges();
                Page.ClientScript
                    .RegisterStartupScript(
                        this.GetType(),
                        "ShowToast",
                        "ShowToast('OK', 'topCenter','success', 'Utilizador adicionado com sucesso.', '2000')",
                        true
                    );
            }
        }
    }
}

I'm using database first, this is the xUtilizador class
public partial class xUtilizador
{
    [System.Diagnostics.CodeAnalysis.SuppressMessage("Microsoft.Usage", "CA2214:DoNotCallOverridableMethodsInConstructors")]
    public xUtilizador()
    {
        this.Activo = true;
        this.xAcesso = new HashSet<xAcesso>();
        this.xColaborador = new HashSet<xColaborador>();
    }

    public int UserID { get; set; }
    public string Username { get; set; }
    public bool Activo { get; set; }
    public Nullable<System.DateTime> UltimoAcesso { get; set; }

    [System.Diagnostics.CodeAnalysis.SuppressMessage("Microsoft.Usage", "CA2227:CollectionPropertiesShouldBeReadOnly")]
    public virtual ICollection<xAcesso> xAcesso { get; set; }
    [System.Diagnostics.CodeAnalysis.SuppressMessage("Microsoft.Usage", "CA2227:CollectionPropertiesShouldBeReadOnly")]
    public virtual ICollection<xColaborador> xColaborador { get; set; }
}

EDIT
I also had to create partial and metadata classes to update the default value in database
 [MetadataType(typeof(Metadata.UtilizadorMetadata))]
    public partial class xUtilizador
    {
        [DatabaseGenerated(DatabaseGeneratedOption.Computed)]
        public bool Activo { get; set; }
    }

 public class UtilizadorMetadata
    {
        [StringLength(8)]
        [Display(Name="Username")]
        public string Username;

        [DatabaseGenerated(DatabaseGeneratedOption.Computed)]
        public bool Active;
    }

EDIT
Also I just noticed the Username StoreGeneratedPattern is set to Computed for some reason and I never gave it any default values on database..

A: The problem was username was being set as Computed on the model on StoreGeneratedPattern. Make sure it is set to none to not give null exception on insert.

redpajama_set_name: RedPajamaStackExchange


The Aero Club of South Africa is the official representative for sport and recreational aviation in South Africa. The Aero Club has representation on various regulatory bodies the most important of which is the Civil Aviation Regulations Committee (CARCom) and the National Airspace Committee (NASCOM). SAPFA assists the Aero Club in raising objections against proposals that adversely affect recreational aviation. SAPFA also represents its members when making representations to other Governmental organisations and businesses on issues that affect them.
Are you aware of an issue affecting aviation in South Africa? Report it to Aviation Watch South Africa (AWSA) by completing a AWSA Report.This report will be distributed to all interested parties that have registered with AWSA.
The Gazette Containing Part 61 (Air crew licensing) and Part 136 (Balooning) can be downloaded Here1.46meg. Alternatively email us and we will mail you a copy.
The South African Civil Aviation Authority has issued a discussion paper on the future use of Non-Type Certified Aircraft (NTCA). This discussion paper proposes drastic changes to the use of NTCAs. SAPFA is co-ordinating a response to this document.
ATNS has released details of its new fee structure that will come into effect on 1 April 2005. To summarise the structure provides for an Aerodrome fee for departing from an ACSA airport, a TMA fee for every TMA that you fly in or through and an Area fee which is based on the distance you fly. Each fee is based mainly on the weight of the aircraft.
Aircraft below 1200kg are exempt except for flying in the CT, Dbn and Jhb TMAs.
The fees for aircraft over 1 200 kg are enormous. For example the fee for a single flight from PE via BLV to Lanseria in an aircraft weighing 1725kg (a C210) will be R365.90. Full details of the fees are on the ATNS web site.
For further developments on this issue - see Aviation Watch South Africa SAPFA and other industry actions will be recorded there.
After an incident at Pelindaba there was a perceived terrorism threat posed by aviation to the nuclear installation there. The South African Nuclear Energy Corporation now wanted to promulgate legislation to declare a no-fly zone over this and other facilities. After discussion the applicant was informed that the concept of no-fly zones is not acceptable but that they could work within the existing definitions of Prohibited or Restricted airspace. A Prohibited area up to 6 500 ft has been instituted.
During the year a draft bill on National Protected Areas was published in the Government Gazette in which it was suggested to raise the minimum over-flight height over National Parks and World Heritage Sites from 1 500 ft above ground level to 1km over the highest point of the particular area. This would effectively put an end to recreational flying in the Drakensburg area as the highest point would be in excess of 10 000 ft. Once again the Aero Club of South Africa was successful in persuading the CAA and NASCOM to take its rightful place and defend our position.
Currently FIR sector boundaries are not depicted on aeronautical charts. ATC do however require pilots to report at these boundaries as Air Traffic Control is still organised on a sector basis. It would be helpful for the sector boundaries to be depicted on aeronautical charts SAPFA is currently in negotiation with CAA to have this done. No change has yet been agreed.
CAA issued a notification to all licensed airfield owners that they are obliged to provide the new airfield position using the WGS84 datum. Their requirement was that this position be calculated and certified by a qualified land surveyor.
Airfield owners found that the fee for this requirement would be in the region of R20 000, a cost that would have to be passed on to aircraft users in the form of additional landing fees. Intervention by Aero Club resulted in CAA agreeing to allow a WGS84 position to be determined by the use of A GPS thereby eliminating the cost.
ATNS proposed to introduce fees for the aircraft that are currently exempt from approach fees. In addition there were also proposals for new service fees for flying through controlled airspace. After substantial negotiation between Aero Club and ATNS is has now been agreed that general aviation aircraft would continue to be exempt from fees and that the weight category for the exemption be increased from 900kg to 1 200kg. In addition certain "warbirds" would also be exempt. This is a significant relief for general aviation. The proposal by ATNS for fees for aircraft over 1 200kg will be received soon.
In February 2003 a proposal was made to CARCom that auto pilots be compulsory for VFR flights at night. There is no evidence that this would result in greater safety as it is the opinion of SAPFA that most accidents at night are in the take-off and landing stages where an auto pilot would be disconnected and controlled flight into terrain where the use of an auto pilot would not assist. The cost to general aviation would be enormous. The SAPFA objection, (see SAPFA Part 91.pdf ), was motivated at the CARCom meeting on 25 February 2004 by Aero Club's Neil de Lange and was successful. The proposal has been scrapped.
In January 2004 the SAWS published a regulation creating new charges for aircraft owners for weather services. Assisted by members D Lempp and R Wheeldon who pointed out errors in the proposed regulations, SAPFA has objected against the levy of these charges, (See South African Weather Services charges.pdf ). Up to now there has been no response to our submission.
In January 2004 a proposal was made to reduce the lower limit of Class A airspace from FL195 to FL145. This amendment would severely affect our members that fly jet warbirds. Due to the Aero Club submission at NASCOM this proposal was dropped.
When Part 61 of the Civil Aviation Regulations was issued SAPFA made comment and proposed a number of changes. The majority of these proposals were included in the second draft of the regulations. Some major issues were raised by SAPFA in a submission in November 2000.


text:
http://tvtropes.org/pmwiki/pmwiki.php/TearJerker/StreetFighter
This is based on opinion. Please don't list it on a work's trope example list.
Tear Jerker / Street Fighter
FanficRecs
TabletopGame
More Less - More - Es FrFranchise Memes Narm
Create New - Create New - Analysis FanWorks Haiku ImageLinks PlayingWith Recap ReferencedBy Synopsis Timeline
Somehow, even Street Fighter manages to get in on the heartstring tugging action.
open/close all folders
Almost all of the Street Fighter characters have tragic backstories, with most of them involving being affected by a member of Shadaloo in some way (Guile, Charlie, Chun-Li, T. Hawk, Juri, Dan, Cammy, the Dolls, etc.), but also involving broken homes (Remy, Vega), being survivors of tragic incidents (Blanka, Dhalsim, F.A.N.G, Kolin), being the results of experimentation (Necro, Abel), or being orphaned (Ryu).
In every game in the series Charlie has starred in, all of his storylines result in a Downer Ending where he dies. In the Alpha trilogy, he's shot down in II and blown up in III. In the crossover X-Men vs. Capcom, his ending consisted of him being captured by Shadaloo and turned into the secret character Shadow. The endings where he doesn't die are labeled "non-canon".
Guile's original ending in SFII was a big-ass tearjerker. His wife and pre-teen daughter practically have to beg Guile to not kill Bison because they don't want him to lower himself to commit deliberate murder and plead with him to return home with them. One single, simple phrase can still make many a player sniffle like a little child once in a while:
Guile: "A-Amy? Is that... my little Amy...?
Street Fighter Alpha I-III
The story ending for Juni was downright heartbreaking. She and fellow Doll Juli (aka Julia, T. Hawk's friend/girlfriend) hug each other in front of Bison's body as they become Empty Shells (and they won't get better for a LONG time.) The montage in which Charlie and Chun-Li discuss the project that made them borderline Robot Girls really doesn't help.
Juni: We are... we are... Always... Sir Bison's...
The story of how Bison's Dolls came to be is a big tearjerker, too. They are a bunch of once normal and innocent girls who were kidnapped and thoroughly brainwashed to become super-soldiers, to the point where nothing of their personalities or past lives remain save for being created to serve Bison. They are even mindlinked to Bison so if he dies, they die as well, so any chance of hope for these girls is shot to hell.
If the Doll's history won't make you tear up, then the callous way Bison commands them to die after they successfully locate and bring Ryu for him, like how a child grows tired of his new toys definitely will.
Charlie sacrificing himself at the end of Alpha 3. He, Chun-Li and Guile have just infiltrated Bison's base and are planting explosives to destroy the Psycho Drive. As they are doing so, Bison ambushes them and incapacitates the three of them. As he approaches Guile to kill him, Charlie tackles Bison and orders the others to leave while he holds Bison back. Several minutes later, the base explodes, taking Charlie and Bison down with it. Meanwhile, Guile is watching the explosion and is implied to be crying. Some time later, Guile holds Charlie's dogtags and swears to honor his memory, while at the same time holding some small hope that he is still alive somewhere.
There's a brief Moment of Awesome in there. Charlie manages to hold his own against Final Bison, explicitly stated to be the strongest Bison has ever been, for at least several minutes while already injured.
Cody's entire character development from Final Fight up until his reveal in Alpha III. In Final Fight, Cody and his best friend Guy fought to rid the city of the Mad Gear gang, and rescue Cody's girlfriend Jessica. And while both were lauded as heroes, Cody was thrown into prison by a corrupt cop he had defeated along the way. While in prison, he develops an addiction to fighting that he carried with him when he got out, resulting in him walking the streets, looking for even the slightest reason to fight. When he is thrown back into jail, everybody but his best friend Guy abandons him. Eventually, he breaks out of prison to enter the various World Warrior tournaments. And while deep down, Cody is still a hero who longs to return to what he once was, he seems to have mostly convinced himself that he can never be a hero again.
Cody: "I've saved the city, saved the girl, but couldn't save myself."
It's revealed here that since Street Fighter I, Sagat was completely driven by rage and hatred for Ryu, since the latter was responsible for both Sagat's loss of his title as a Muay Thai champion and the scar Sagat now carries on his chest. He joined Shadaloo for a chance to win against Ryu at all costs, but somewhere down the line he was confronted by Dan Hibiki, whose father Sagat killed before the events of Alpha. Seeing the intense desire for revenge in Dan's eyes reminded Sagat too much of himself, and the Heel Realization that resulted from their fight put him on the path of defecting from Shadaloo and becoming The Atoner.
One of Evil Ryu's win quotes is "It is too late to go back, now..."
Despite being a nihilistic Jerkass, Remy's backstory is incredibly tragic. His father walked out to become a martial artist, and shortly after that, his sister died, her body preserved in a block of ice underwater in the Bay of Biscay. His father's departure and the tragedy it resulted in emotionally broke Remy and caused him to develop a hatred for fighting and those who pursue such a lifestyle, as it is a reminder of the very thing that tore his family apart.
You can't help but feel bad for Necro, as he left his home to seek a better life, but ended up being tricked by the Illuminati and was kidnapped for their experiments and is now a mutant suffering Body Horror, is a fugitive on the run, has no home, is being hunted by Shapeshifter Weapon Twelve, and is implied to be self conscious about his appearance and abilities. Luckily for him, he's happily in love with his girlfriend Effie and has a very nice case of Earn Your Happy Ending.
A few endings are genuinely sad. A notable example would be T. Hawk's ending, where he finds Juli/a with Rose's help, but her experience with Shadaloo has totally traumatized her to the point of being put in a near-catatonic state, mute, and unresponsive to external stimuli, being unable to remember T. Hawk at all when she meets him again. It is probably one of the most depressing things you would ever see in a fighting game.
Guile's ending consists of him visiting Charlie's grave and having a toast on it, vowing to finish his takedown of Shadaloo so that Charlie can have closure. However, unlike T. Hawk's ending above, Guile's can put a bit of a glow in the heart knowing in hindsight that he succeeded, since Shadaloo is gone by Street Fighter III's events, so Charlie can rest in peace.
Guy's ending has him holding Rose in his arms after he rescues her from Bison, and begs her not to give into darkness, which is pretty heartwrenching. However, it's followed up by a Heartwarming Moments in Rose's own ending, since she hears his voice and manages to wake up, finally earning something similar to a happy ending.
Decapre's ending in Ultra Street Fighter IV. Knowing Bison is the only one that can save her life, Cammy allows her "younger sister" to be taken away.
Everything about Decapre is a serious punch to the heart and guts. Her prologue is completely heartbreaking, especially with flashbacks to her and the other Dolls being experimented on, and the young Cammy taking a protective older sister role towards her, and Decapre's confusion and rage that finishes with her getting out of the capsule she has been stashed inside, saying "Killer Be... kill... kill... kill... kill them all...! KILL ALL!".
All of the titles unlocked in the original edition of IV by using a character tell something deeply personal about them, when they aren't being funny in a cheeky way. What's one of Ryu's title cards? "Wish I had a family". If Street Fighter: Assassin's Fist and/or Street Fighter Alpha: Generations are canon, Gouken may be his biological father by Goutetsu's daughter Sayaka.
Many victory quotes against Evil Ryu in the Arcade Edition of IV, especially from friends and associates of Ryu, express severe shock, sadness, concern or disappointment at his fall from grace. Some are quite heartbreaking.
Ken: "Ryu... Is that really you!? What the hell happened? Ryu!"
Sakura: "Ryu-san! Wake up, please!"
Sagat: "I am so disappointed, Ryu! Is this the power you so desired?!"
Gouken: "Don't give in to this power, Ryu!"
Dhalsim:"I pray that the hatred inside of you is extinguished quietly..."
But perhaps the most painful quote comes from Gouken when he fights Evil Ryu as a hidden boss.
Gouken: "You are no pupil of mine."
Also from Gouken is his victory quote against Oni, the ultimate result of Akuma's descent into darkness.
Gouken: "Goodbye, brother."
Evil Ryu's win quote against Ken is "There is nothing you can say, Ken, and nothing you can do."
Remember Charlie's Heroic Sacrifice ending in Alpha III? Well, it turns out that Charlie did indeed survive the explosion that destroyed Shadaloo, but was mangled horribly as a result, so apparently he underwent extensive and horrific surgery that made him resemble a stitched-together monstrosity. Even worse, Charlie's body may have recovered, but his mind certainly has not. Gone is the cool-headed but passionate beacon of justice and mentor to Guile and occasional partner/almost boyfriend to Chun-Li from Alpha. In his stead is a cold-blooded, cynical, and ruthless assassin who will not hesitate to remove any obstacles in his way of his goal, even if said obstacles are people he once called friends.
His story mode manages to be an even bigger punch to the gut and heart by confirming that his Alpha 2 ending, the one where he's betrayed by his fellow Air Force unit and shot via helicopter before being sent careening off a Venezuelan waterfall, is his canon death. One has to wonder what was going through his mind during that moment. A paragon of justice and virtue, betrayed by those he once called comrades. To make it worse, it pretty much retroactively renders Charlie's Heroic Sacrifice in Alpha 3 null and void.
Hell, even the title of his story mode is one big Tear Jerker by appropriately naming it, "The Man Who Lost It All".
Even worse, after the events of Alpha, Charlie has gone so past the Despair Event Horizon that he has simply given up on saving others, knowing that he'll just be backstabbed in the end. Several of his win quotes suggest that he doesn't even place value in friendship and justice, things he used to treasure greatly, anymore, seeing them as useless things that only brought him betrayal and heartache. He only lives for himself and revenge now.
In the end, however, he does get a dignified Heroic Sacrifice after all, along with realizing the error of his ways when it's revealed that he can't kill Bison because he's a walking corpse and his hate is merely fuel for Bison's Psycho Power. Nash ends up using his newfound ability to absorb energy to de-power Bison as much as possible after his supply of Psycho Power via the Black Moons has been stopped so that Ryu can finish what he started. While he does end up weakening Bison severely, the energy is too much for him to handle and it results in an explosion that destroys his decaying body. Only his dog tags remain, which Bison promptly steps on.
With Guile confirmed as a DLC character for V, you can now experience the long-awaited yet saddest matchup in the series. Guile, who has gotten past his desire for revenge against Bison for killing his best friend, versus Charlie, said best friend who has been brought back from the dead and became what Guile stopped himself from becoming. Their win-quote dialogue to each other says it all.
Nash: "I have nothing left to say to you."
Guile: "Nash... What on earth happened to you?!"
F.A.N.G's backstory is tearjerking as it is horrific. He is the sole surviving member of a cartel that specialized in kidnapping young children and training them in the art of assassination through poison, called the "Poison Hands" technique, by constantly exposing the children to harmful poisons. F.A.N.G had watched so many fellow students die as the result of this harsh and cruel training that it turned him into a Determinator and eventually resulted in him gaining a Social Darwinist mindset. When the cartel attacked Bison and died in the attempt (due to Bison's immunity to poison), F.A.N.G was the only one who kept on fighting; despite knowing he'll die like the rest of his fellow assassins, he kept attacking Bison because he wanted to live another day.
In a very weird way, Bison's death. Yes, he totally deserves it, and his death scene is pretty awesome, but it's still a sight to see such an iconic villain who's been constantly kept alive finally die. What sells it is that he faces death with dignity and gives off one final Evil Laugh before his body and Psycho Power are dissolved away by the Power of Nothingness, while F.A.N.G cries out for him in anguish. Supplemental materials and other characters' stories reveal Bison is still alive as a spirit and F.A.N.G. is bent on resurrecting him, which adds another layer to the sadness as the fight the heroes thought was finally over isn't.
Rashid's entire storyline can count. He desperately tries to rescue his friend, a female scientist forced to work for Shadaloo. He even went so far as to work with the Illuminati, who clearly don't care about his dilemma. Tragically, he was too late as she was already murdered by F.A.N.G. Even worse, it happened just as Rashid was infiltrating the base, meaning he could have saved her if he didn't stop to rescue Li-Fen. Still, like Charlie above, he gets a Moment of Awesome when he avenges her death by beating the crap out of F.A.N.G and using her final command code to stop the Black Moons.
The Story Mode fight between Cammy and the again Brainwashed and Crazy Decapre is this, especially when Decapre starts to struggle and then when she leaves despite Cammy's pleas (flashback to Cammy's promise to protect her included), leaving her Iron Woobie of a "big sister" all heartbroken.
Kolin's Story Mode reveals her past, and it's not pretty. She was found by Gill when her whole homeland (a part from the Soviet Union) had already collapsed, her friends and family were dead, and she was so past the Despair Event Horizon that she was willing to let herself die in the middle of a snowy wasteland. Gill was the one who took her in after all of that, and that explains a LOT of her Undying Loyalty to him.
Gill: "What is thy name, child?"
Kolin: "I have none."
Gill: "Where is...thy country?"
Kolin: "It's gone..."
Gill: "Then I shall forge one. The country of God. It could be thy new home, siring every nameless flower, bringing forth a thousand years of peace and harmony to all...if you desire it.
Ed's story mode can best be described as "a father-son/brotherly relationship falling apart", and arguably sets him as one of the biggest woobies of the franchise (while giving Balrog, of all people, some Jerkass Woobie traits). During the Season 1 story, it's shown that Ed is constantly plagued by nightmares of Bison trying to take over his body, since him being a possible candidate as a vessel for Bison's soul is the reason he was kidnapped by Shadaloo in the first place, and he openly angsts over his Rapid Aging. While taking the chess piece from Guile and Zangief in India, Ed is visited within his mind by Menat, an Egyptian Fortune Teller who warns him that she foresees hard times for him and Balrog in the future. Sure enough, Ed's issues come to a head, and Balrog tries, in his own way, to reassure him that as long as Ed stays with him he'll be fine. Of course, since it's Balrog, his choice of words comes out wrong, causing Ed to lash out at him, saying that Balrog would be nothing without him. The two fight, and end up parting ways on a sour note. Balrog tells him to get lost, and Ed walks away with a deeply hurt expression on his face. The fact that Balrog sounded like he was gonna cry when he told Ed to get lost and refusal to recover to fight back just shows how much he used to care for the young man (and probably still does afterwards), unlike the indifference and hostility he has for everyone else.
Sakura's story might hit a little close to home for some people. Sakura is now an adult working a part-time job, and is coming to the realization that her passion for fighting is beginning to fade. She doesn't have the money to jet around the world the way Karin does, and she begins contemplating just how she's going to live the rest of her life. She's not sure whether to continue fighting or if she just wants to settle down and start a family. When she bumps into Ryu, she even brings up the inevitability of death, no matter how strong you get from training. The entire thing is basically her having an existential crisis.
Sagat's Arcade Mode ending is a combination of this and Nightmare Fuel. Some time after his story mode, he finds the village where he had been living and training in seclusion to conquer his demons in flames, having been set ablaze by a group of unknown thugs. He mercilessly attacks them, but the last frame has him crying Tears of Blood, implying not only that he flat-out killed them, but that he lost the people he came to care for from the village as well. That innocent little girl from his Story Mode who brought him his meals? She probably died in the fire.
Guile's (fake) death early on can qualify to those who watch the movie without much familiarity with the series, and end up getting the impression he was Killed Off for Real.
Raúl Juliá's whole performance, as he knew he didn't have much time left and wanted to secure a big paycheck for his family, plus do a role his kids wanted to see. And it was fucking awesome, too. Although the film as a whole is often ridiculed as being one of the sillier video game adaptations, Julia's final appearance is generally treated with well-deserved respect, to the point where he was even posthumously nominated for a Saturn Award.
Charlie is mutated and tortured halfway into insanity, and then he, and the man who tried to help him apparently die in an explosion. Talk about depressing.
Even more affecting is when Dhalsim tries to undo his brainwashing by filling his mind with love, hope for the future, and happiness.
When Guile finds his friend in this state, he barely manages to talk him out of killing him (using his first name), then attempts a Mercy Kill on Charlie. Dhalsim quietly stops him, saying he has no right to do so; Charlie still retains capacity for good as well as evil, and shouldn't be killed because he has difficulty understanding the difference.
Before the final battle, Guile reminisces on happy memories he had with Charlie with Worth Fighting For by Angelique Kidjo playing.
The dedication to Raul Julia at the start of the credits. "For Raul. ¡Vaya con Dios!" ("Go forth with God!") note Raúl Julia (who was from Puerto Rico , which has both Spanish and English as its official languages) died not too long after filming the movie.
The whole "But for Me, It Was Tuesday" scene in a strange sort of way. It's legitimately well-acted and staged; Chun-Li explains how Bison and his minions were stopped from destroying her village by Chun-Li's father. As Bison was forced into retreat, he had Chun-Li's dad shot by a sharpshooter, purely out of spite. She's wanted revenge/justice ever since and it's clearly driven her life. Bison then apologizes... and bluntly informs her that he doesn't know what she's talking about and can't remember the incident at all. And he doesn't mean it as a taunt, he sounds genuinely apologetic that he can't remember. It drives home how senseless Bison and his plans really are; he's done so much that it's all just blurring together for him.
Animated Media
Street Fighter II: The Animation
Fei Long starts having an intense and tearful Heroic BSoD when he thinks Chun-Li's father Dorai, who trained him and treated him like a son, is dead.
Charlie's death via strangulation at the hands of Bison.
Street Fighter (TV series)
In the episode "Eye of the Beholder", Blanka rescues the Japanese Prime Minister from an attack, only for the man to run away screaming that he's a monster. After this, Blanka deals with his angst over being mutated for the rest of the series.
Cammy declines Guile's offer to rejoin the Street Fighters following Bison's defeat, echoing the same words she told Guile when he got back together with Lucinda:
"A person can't live in the past, Colonel. The past is filled with pain."
Street Fighter Alpha: The Animation
Shun's death in his "older brother" Ryu's arms.
Street Fighter Alpha: Generations
Generations may not be fully canon, but damn it is depressing. Especially in the flashbacks to Akuma and Gouken's more or less happy lives before it went From Bad to Worse, and the Bittersweet Ending where Akuma recovers some parts of his humanity after almost killing Ryu in battle (and this particular Alternate Universe all but states that Ryu is Akuma's son) and later the Old Master that Ryu befriends passes away, and Ryu leaves after mourning him.
Street Fighter IV: The Ties That Bind
The scene where Ryu snaps massively upon seeing C. Viper torture Cammy, practically loses himself to the Satsui no Hado out of anger and a tearful Sakura has to give him a Cooldown Hug to stop him is surprisingly powerful, and it's not helped by how Ryu slumps to his knees in horror upon coming back to his senses, with poor Sakura still hugging him, and a Grey Rain of Depression falls on them both as well as on Ken and the injured Cammy.
Super Street Fighter IV: Juri OVA
Even after Bison's death, the nightmare doesn't end for the Dolls. While a Hope Spot was given in E. Honda's ending, where the aforementioned character took in a few Dolls and gave them a place to stay until they recovered from their Trauma-Induced Amnesia (while also teaching them sumo), here they were revealed to be kept in capsules since Seth plans to experiment on them all until they die, which is barely averted by the efforts of Cammy and Guile. But while Juni and Juli were rescued (without some repercussions, of course); it's unknown whether the rest of the Dolls were saved from their intended fate, leaving a lot of open questions...
The OVA reveals why Juri became so sadistic and batshit insane. She and her parents were killed by Shadaloo after her father, a lawyer, decided to prosecute the criminal organization, marking his family for death. During the incident, Juri survived, but at the cost of her left eye. It's implied that the loss of her parents and eye, combined with whatever Shadaloo (or SIN, its sister organization) did to her after that, drove her deep into madness, turning her into the person she is today.
It may not be canon, but Shadow is sure to make fans of Charlie shudder. Shadow is Charlie, after being captured by Bison post Alpha 3 and experimented on, tortured, and brainwashed. He is so far gone that he beats Guile to a bloody pulp without any hesitation, and is willing to attack Chun-Li, with whom Charlie was almost an Official Couple.
It becomes slightly heartwarming when Shadow breaks Bison's control and sacrifices himself to save Chun-li and Guile by destroying the cliff him and Bison are standing on with a Summersault Justice, which is specifically differentiated from Shadow Justice to show that for a brief moment, Charlie has regained control of himself.
In Legends: Chun-Li, we have the death of Go Hibiki, Dan's father. First alluded to in Street Fighter Alpha II, the creators of UDON did their take on the incident that cost Sagat his right eye and made Dan so deadset on getting revenge. Go and Dan were building their own martial arts dojo in a place that happened to be in Shadaloo territory, and were approached by a group of Shadaloo thugs demanding a protection racket fee. Go makes quick work of them, but later he is confronted by Sagat, who at the time was a member of Shadaloo. Go bests Sagat and tears out his right eye, after which things go downhill. Sagat, in a pain-induced fury, overpowers and brutalizes Go, reducing him to a bloody pulp, right in front of Dan.
What's more, when Chun-Li, Dorai, and Po Lin arrive with the police to question Dan at the crime scene, Dan is so traumatized that he refuses to out Sagat as his father's killer, instead claiming he was responsible and wanting to bring Sagat to justice himself.
Related to the issue, a variant cover drawn by UDON artist Jeffery "Chamba" Cruz shows a wounded Sagat clutching onto a bloodied Go Hibiki's head, while behind him, Dan screams for his father as Chun-Li struggles to hold him back. Never before has a Butt-Monkey Joke Character brought anyone to tears...
The incident was revisited in Unlimited where Dan finally corners Sagat. Sagat, regretting his past actions and how they affected Dan, offers up his head so Dan can find closure for Go's death. Though clearly tempted, Dan ultimately refuses the chance to take revenge and walks away in bitter tears, saying the only thing he wants is his father back. Ouch.
Juri's backstory, first revealed in the Super Street fighter IV: Juri OVA above, was expanded by UDON . She was a Taekwondo prodigy who was frequently pressured to uphold her family name, and her parents, while loving, were strict and demanding. Her father's decision to prosecute Shadaloo led to Juri's mother being killed, and him being ransomed and publicly executed on camera. Juri, however, survived, but she lost her left eye to a stray bullet when Shadaloo attacked and fell into a coma for a month. All of this left Juri with a very intense hatred of Shadaloo, Bison in particular; it's jarring to see the once innocent and shy Juri become a broken, angry teenager hell-bent on revenge, screaming at her Taekwondo master to "serve" her and make her into an instrument of revenge..
Street Fighter II: The Manga reveals that Guile was responsible for Charlie's death - Charlie was experimented on by Shadaloo to test a mind-controlling drug and he went insane from it. Guile intercepted him as Charlie was attacking unarmed villagers and was forced to perform a Mercy Kill on his best friend to prevent more lives from being endangered. While not canon, it certainly gave Guile a reason to hate Bison.
Ryu: Then and Now , an animated short made by Egoraptor (of Game Grumps and Awesome Series fame). The short begins with an idealistic Ryu during the SFII days, getting ready to take on the world. It then skips ahead to 20 years later, in which he is now a businessman. The short ends with him looking at a picture of his younger self and remembering the good ol' days, and starting to tear up as he does so. Anyone who grew up with the series is sure to shed a tear when watching this.
The two short movies made by ChubbyBoyFilms:
In the Balrog: Behind the Glory documentary, we see Balrog's father clearly torn up over how teaching his son to defend himself from bullies (the only time they ever really bonded, at that) was a misguided first step that led to him becoming a murderer and infamous criminal. Also, what caused him, the Heavyweight Champion of the World, to become said criminal: his trainer and the public drove him to become more and more vicious and fouling until he killed a challenger with a headbutt, and that got him banned from boxing and made into a joke.
While Vega's backstory is already sad enough, El Matador manage to make it worse by having young Vega try to intervene before his stepfather can murder his mother - only for both of them to fall out of the window, killing her instantly. And the end shows why he works for Bison: because he recognizes him as beautiful.
Story of Seasons (2014)
TearJerker/Video Games


text:
NM, United States
www.sandia.gov/isrc
Robotic Educator/Researcher
Sandia is a multiprogram National Laboratory operated by Sandia Corporation, a Lockheed Martin Company, for the United States Department of Energy. With many years of experience and hundreds of successful projects in designing, developing, and delivering complex micro- to macro-sized automated systems, Sandia's Intelligent Systems, Robotics, and Cybernetics (ISRC) organization responds to challenges impacting national security and US economic competitiveness.
The Lockheed Martin Corp. has managed Sandia since Oct. 1, 1993, for the U.S. Department of Energy. Most of Sandia's work is sponsored by DOE's National Nuclear Security Administration, but we also work for other federal agencies, including the Department of Defense, Department of Homeland Security, and others. We work cooperatively with a number of government, U.S. industry, and academic partners to accomplish our missions.
Choose a Section: Make a Selection Services Industry Insights Case Studies
Government Research Services
Offering Government Research Services


text:
Spartan Bioscience's rapid COVID-19 test approved by Health Canada
By Victoria Ahearn & Nicole Thompson | News | January 25th 2021
#1147 of 1611 articles from the Special Report: Coronavirus in Canada
Spartan Bioscience Inc. CEO Paul Lem holds one of his company's COVID-19 portable, rapid testing devices in a handout photo. Health Canada has approved the use of the device for testing for COVID-19. Handout photo by Spartan Bioscience Inc.
The federal government has approved an Ottawa company's made-in-Canada rapid COVID-19 test, Health Canada confirmed Saturday as the nation's top doctor warned the virus's impact on the health-care system showed no signs of abating.
The test developed by Spartan Bioscience is performed by a health-care professional and provides on-site results within an hour, a spokeswoman for the federal agency said.
Spartan bills the test as the first "truly mobile, rapid PCR test for COVID-19 for the Canadian market."
"The Spartan system will be able to provide quality results to remote communities, industries and settings with limited lab access, helping relieve the burden on overwhelmed healthcare facilities," the company said in a news release Saturday.
The company originally unveiled a rapid test for COVID-19 last spring but had to voluntarily recall it and perform additional studies after Health Canada expressed some reservations.
At the time, Spartan said Health Canada was concerned about the "efficacy of the proprietary swab" for the testing product.
The new version uses "any nasopharyngeal swab" rather than one of the company's own design, Health Canada said, and meets the agency's requirements for both safety and effectiveness.
The Spartan COVID-19 System was developed through clinical evaluation completed in Canada and the U.S., with the University of Ottawa Heart Institute as one of the testing locations.
The company said it has already started production on the rapid tests.
The news comes as Dr. Theresa Tam, Canada's chief public health officer, warned that COVID-19 continues to strain the health-care system even as daily case counts decline in several long-standing hot spots.
Health Canada approves #SpartanBioscience's previously recalled rapid #COVID19 test. #PCRTest #CovidTesting #RapidTest
"As severe outcomes lag behind increased disease activity, we can expect to see ongoing heavy impacts on our healthcare system and health workforce for weeks to come," she said in a written statement.
Surging new infection rates continued to show signs of easing in multiple provinces, though one jurisdiction was poised to impose new restrictions in a bid to stem the ongoing spread.
Public health officials in New Brunswick reported 17 new cases across the province, 10 of which were in the Edmundston region, which was set to go into a lockdown first thing Sunday morning.
Starting at midnight, non-essential travel is prohibited in and out of the area, which borders northern Maine and Quebec's Bas-St-Laurent region.
The health order forces the closure of all non-essential businesses as well as schools and public spaces, including outdoor ice rinks and ski hills. All indoor and outdoor gatherings among people of different households are prohibited.
Saskatchewan, meanwhile, logged 274 new cases of the virus and three new deaths, while Manitoba counted three more deaths and 216 new diagnoses.
Alberta logged 573 new cases and 13 virus-related deaths in the past 24 hours, while both Nova Scotia and Newfoundland and Labrador reported no new infections on Saturday.
Both Quebec and Ontario reported fewer cases Saturday — 1,685 and 2,359 respectively.
But officials in Ontario expressed concern about a highly contagious U.K. variant of the virus that was detected at a long-term care facility north of Toronto.
Simcoe Muskoka District Health Unit confirmed the variant was behind the outbreak at Roberta Place Retirement Lodge in Barrie, Ont., where 32 residents have died of COVID-19 and dozens of others have tested positive.
"Stringent and consistent efforts are needed to sustain a downward trend in case counts and strongly suppress COVID-19 activity across Canada," Tam said. "This will not only prevent more tragic outcomes, but will help to ensure that new virus variants of concern do not have the opportunity to spread."
Fears of variants that can circulate quickly come as the federal government considers a mandatory quarantine in hotels for travellers returning to Canada.
This report by The Canadian Press was first published Jan. 23, 2021.
Victoria Ahearn
Film and TV writer with The Canadian Press
@VictoriaAhearn
Reporter with The Canadian Press
Don't pressure Health Canada to approve rapid COVID-19 tests: Freeland
By Mia Rabson | News, Politics | September 25th 2020
Rapid COVID-19 test recalled after Health Canada has concerns
By The Canadian Press | News, Politics | May 4th 2020
Health Canada approves portable COVID-19 test kit
By Cassandra Szklarski | News, Politics | April 14th 2020


text:
Punjab ranks second in average monthly income per agricultural household: Center : The Tribune India
Leave a Comment / ECONOMY / By millssY
IANS Chandigarh, December 17 Punjab ranks second in the country in average monthly income per agricultural household. This fact came to light in a data provided by Union Minister of Agriculture and Farmers Welfare Narendra Singh Tomar in the ongoing session of Rajya Sabha. The minister was replying to a question by Aam Aadmi Party's Rajya Sabha member Sanjeev Arora. As per information, Meghalaya tops across the country with average monthly income per agricultural household (Rs 29,348). Punjab (Rs 26,701) is followed by Haryana (Rs 22,841), Arunachal Pradesh (Rs 19,225), Jammu and Kashmir (Rs 18,918), group of Union Territories (Rs 18,511), Mizoram (Rs 17,964), Kerala (Rs 17,915), group of northeastern states (Rs 16,863), Uttarakhand (Rs 13,552), Karnataka (Rs 13,441), Gujarat (Rs 12,631), Rajasthan (Rs 12,520), Sikkim (Rs 12,447) and Himachal Pradesh (Rs 12,153). Responding to the reply, Arora told the media, "If we consider states dependent the maximum on cash crops, Punjab would rank first with Meghalaya having major share of horticulture and fruits." He urged the Punjab farmers to go for more diversification of crops, horticulture and fruits. The prominent crops produced in Punjab include rice, wheat, maize, bajra, sugarcane, oilseeds, and cotton, but rice and wheat alone constitute 80 per cent of the total gross cropped area. Arora said Chief Minister Bhagwant Mann is trying his best to further improve condition of peasantry in the state. Citing an example, he said in October the Chief Minister had announced to increase the price of sugarcane to Rs 380 per quintal from Rs 360 per quintal. This was done with a view to supplementing the income of farmers. At present, sugarcane is cultivated on 1.25 lakh hectares in Punjab. The MP said the Chief Minister has assured to make the minimum support price (MSP) for crops a legal guarantee. #Agriculture


Point prevalence surveys of healthcare-associated infections (HAIs) provide for a national snapshot of this critical patient safety concern and complement the location- or infection-specific data that infection preventionists report to the National Healthcare Safety Network (NHSN). Utilizing 10 sites in the CDC Emerging Infections Program (EIP) which represents the major geographic sections of the U.S., an initial prevalence survey was conducted in 2011 of 11,282 patients in 183 hospitals and found that 4% of hospitalized patients had an HAI.
Heightened focus on the prevention of intraluminal contamination of intravascular devices to prevent bloodstream infections through disinfection of needleless connectors using chlorhexidine/alcohol (CHG/ALC), which was found to be superior to 70% alcohol alone and alcohol-impregnated caps.2 The immediate and sustained bactericidal activity of CHG/ALC makes it an attractive option for reducing culture contamination and improving the accuracy of BSI and UTI diagnosis.
C. difficile transmission reduction has been associated with the use of enhanced environmental cleaning practices6 along with antimicrobial stewardship efforts.
As healthcare facilities continue their efforts to eliminate HAIs, embracing the newer technologies and products that are supported by science in addition to process improvement activities should move the numbers in the right direction. The verdict will be clear when the next prevalence survey results are reported.
1 Magill SS, et al. Changes in Prevalence of Health Care– Associated Infections in U.S. Hospitals. N Engl J Med 2018; 379:1732-44. DOI: 10.1056/NEJMoa1801550.
2 Flynn JM, Rickard CM, Keogh S, Zhang L. Alcohol Caps or Alcohol Swabs With and Without Chlorhexidine: An In Vitro Study of 648 Episodes of Intravenous Device Needleless Connector Decontamination. Infect Control Hosp Epidemiol 2017; 38(5):617-18.
3 Phillips M, Rosenberg A, Shopsin B, et al. Preventing surgical site infections: a randomized, open-label trial of nasal mupirocin ointment and nasal povidone-iodine solution. Infect Control Hosp Epidemiol 2014;35(7):826-32.
4 Bebko SP, Green DM, Awad SS. Effect of a Preoperative Decontamination Protocol on Surgical Site Infections in Patients Undergoing Elective Orthopedic Surgery With Hardware Implantation. JAMA Surg 2015;150(5):390-395.
5 Maslow J, Hutzler L, Cuff G et al. Patient Experience with Mupirocin or Povidone-Iodine Nasal Decolonization. Orthopedics 2014;37(6):e576-e581.
6Anderson, DJ et al. for the CDC Prevention Epicenters Program. Enhanced terminal room disinfection and acquisition and infection caused by multidrug-resistant organisms and Clostridium difficile (BETR-D study): a cluster-randomised, multicentre, crossover study. Lancet 2017 http://dx.doi.org/10.1016/S0140-6736(16)31588-4.