text:
Sacramento weighs more film industry tax breaks…
Sacramento weighs more film industry tax breaks to keep movie, TV production in state
Tony Stark/Iron Man (Robert Downey Jr.) chats with a friend in "Iron Man 3." Iron Man 3 was filmed in North Carolina.
By Dakota Smith | dksmith@scng.com |
PUBLISHED: January 6, 2014 at 8:09 p.m. | UPDATED: August 28, 2017 at 7:48 a.m.
The MTV series "Teen Wolf" is set in Northern California, but filmed in Atlanta for its first two years to take advantage of Georgia's generous filming tax subsidy.
When the show won a $10 million tax break from California in 2012, it relocated to Los Angeles.
The cross-country move isn't unusual. Hollywood is on the go, as studios and networks leapfrog from state to state, lured by incentives. There are 42 states, in addition to countries like Canada and New Zealand, that offer a dizzying number of subsidies, increasing the competition to woo productions.
That's why Sacramento lawmakers are hatching an aggressive plan to expand the state's film tax credit, with Los Angeles-area Assemblyman Raul Bocanegra seeking to boost California's $100 million a year limit.
The Arleta Democrat maintains California needs to stay competitive with states like New York, which offers $420 million annually to entertainment companies.
Skeptics in Sacramento aren't sure the state's tax credits pay off. Some critics point out other states are scaling back their own programs amid concerns of their effectiveness.
But producers say that now more than any other time, incentives determine a shoot's location. The upcoming NBC drama "Crisis" is currently filming in Chicago, in part because of Illinois' film subsidy. "Iron Man 3" was shot in North Carolina, earning $20 million in incentives. And the latest "Hunger Games" installment was shot in Georgia.
Bocanegra said he wants to make California's program "substantially bigger." Big budget films or network dramas, currently ineligible for the credit, are also being considered for the state program.
"Every economic analysis says that it's a net economic generator," Bocanegra said of California's program.
Launched in 2009, the program — which allows films or television shows to receive a 20-25 percent tax credit toward expenses — has slowed runaway production, supporters say. The number of feature filming days rose 20 percent between 2009-2012, reversing a declining trend from the previous year, according to a California Film Commission report.
Still, studies are mixed on the program's economic benefits. A 2011 Los Angeles County Economic Development Corp. study claimed each tax credit dollar returned at least $1.13, though a 2012 UCLA analysis says the return is more like $1.04. And a 2012 review by the state's top budget analyst said the program results in a net loss.
LA Mayor Eric Garcetti defended the new program as "designed well."
"It doesn't take money away from the state budget, and it adds billions of dollars to our economy here locally," he said. "So the more they expand that credit, it doesn't do any damage to our state budget, but it provides a lot of help for our local economy."
Some plan to expand
While some states, like New Jersey, are weighing increasing their tax incentive programs, others have suspended their allotments. In New York, an independent commission recently recommended scaling back the state's $420 million annual program. "It is not clear from our analysis that there is sufficient justification for the size of the film credits," the commission concluded.
California state Sen. Lois Wolk, D-Davis, opposes Bocanegra's efforts to increase the tax credit program, stating she wants to wait until a state budget analysis of the program is completed in 2016. In a statement, Wolk said there is an "inherent problem in all of these tax credits that spend millions of dollars with little or no transparency or accountability."
Wolk also pointed to the recent FBI investigation of Sen. Ron Calderon, D-Montebello, who is accused of accepting bribes over the state's film credit program. Calderon, who has not been charged, is being investigated for allegedly taking money from an undercover agent in return for promises to expand the state's film tax program, according to a leaked FBI affidavit. Some supporters of incentives fear the association with Calderon may damage the effort politically.
In addition to Wolk, Northern California legislators and education groups like the powerful California Teachers Association, historically have opposed expanding the film program out of concern that it is taking money away from other state programs, such as schools.
Numerous studios and networks contacted declined to be interviewed on how their productions use the tax credit.
Benson R. Berro, a partner at the auditing and tax advisory firm KPMG, said incentives play a major role in financing production, with banks lending against the film tax credits, which ultimately can help greenlight a project.
Some states also allow the credits to be transferable, meaning a producer can sell a future credit to get a production launched.
"Teen Wolf" producer Joseph Genier said tax incentives reduce the bottom line of a film production, though he could provide few details on how specifically the tax subsidy is used by the MTV show.
Overall, California's tax incentive program, he said, allows him to shoot close to his Sherman Oaks residence.
"It's great to come home and work where you live," said Genier, who has two young sons.
"Teen Wolf" won another round of credits last year and will receive up to $11 million from the state for its fourth season.
Dakota Smith


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text:
New leadership for Boys and Girls Club of Atchison
(KAIR)--New leadership is on the job at the Boys and Girls Club of Atchison.
That follows the resignation of Executive Director Sean Crittendon, who cites his other roles of community involvement, as well as growth of his personal business, as reasons for his decision. In email correspondence with MSC News, Crittendon said due to those commitments, he is "unable to manage the day-to-day operations as necessary."
Crittendon, whose resignation was effective January 4, had been at the helm of the program for nearly five years, and will serve on the Boys and Girls Club Board.
Taking the reins as executive director is Jasmine Smith. Crittendon, in email correspondence with MSC News, called Smith his assistant, and said he trained her to take over the position.
A social media post from the Boys and Girls Club of Atchison said Crittendon's years of leadership and passion for youth success "has set a strong foundation for what the club is today."

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COVID-19, Furins & Hypoxia – The Vitamin C Connection
Scritto da Doris Loh
Categorie: Doris Loh | integratori | Nutrizione | Salute
Tag: Anthrax | ascorbic acid | cancer | Cleavage Site | Coronavirus | COVID-19 | Cytokines | EBOLA | Furin | HIF-1a Vitamin C | HIV | Prolyl Hydroxylase | S protein | SARS
By Doris Loh
The official documentation of an ASYMPTOMATIC carrier of COVID-19 (SARS-CoV-2) released by China on February 28, 2020 brings into serious question if the global concerted reaction and efforts to contain the coronavirus outbreak are justified.
According to the paper by Weng, Jianping et al. the subject is a 50-year old woman with no significant past medical history, and did not have any direct connections to Wuhan and adjacent areas. Apart from mild elevation of liver enzymes after a 10-day treatment course of antivirals after being confirmed positive for COVID-19 on February 6, she was asymptomatic, with all functions being normal, and free of signs of viral pneumonia. After the treatment course was completed, the patient was re-tested by throat and anal swabs and results still returned as POSITIVE for the COVID-19 coronavirus. The authors of the paper concluded that the discovery of a healthy carrier of the virus increases the difficulty in prevention of transmission [1]
Since the outbreak of the coronavirus in late 2019, the total death rate reported as of February 28, 2020 is 7% of total closed cases, or 3.42% of total confirmed cases reported globally. 43.9% of the confirmed infected recovered. Only 18% of the remaining patients still infected are in serious condition.
How is COVID-19 different from a normal garden-variety flu virus, and why are countries closing borders, placing cities and towns on quarantines; canceling public events; closing schools; suspending air travels; locking down resorts and refusing docking of cruise ships just to prevent the spread of a seemingly non-lethal flu virus? Why are investors around the globe selling off equities in such a panic? The Dow Jones Industrial Average registered its worst one-day point drop in history on February 27, 2020 [2]
Discovery of Furin Cleavage Site in COVID-19
The answer lies in a paper that was first released on Jan 27, 2020 in China by Jishou Ruan et al. from the prestigious Nankai University, Tianjin China. This study has since been revised twice, last edit was Feb 14, 2020 [3]. The authors of this study reported for the first time, that unlike all other betacoronavirus, an important mutation in the Spike (S) protein of COVID-19 allowed it to acquire a cleavage site for the furin enzyme. This furin cleavage site is NOT PRESENT in S proteins of ALL OTHER betacoronavirus, including the HIGHLY INFECTIOUS SARS coronavirus [4].
The furin cleavage allows efficient virus entry into cells, making the COVID-19 easily transmissible at rates up to 1,000 times greater than the virulent SARS coronavirus [3]. The authors compared the packing mechanism of the virus to other furin cleavage viruses like HIV, Ebola, as well as other highly transmissible avian influenza strains. The findings of Ruan and Gao et al. have been independently confirmed by a French team led by Decroly around the same time.
On February 10th, Decroly et al. reported the S-protein sequence of COVID-19 has a specific furin-like cleavage site that is absent in betacoronavirus including SARS-CoV. Importantly, the authors pointed out that this furin cleavage site could have significant implications for the viral life cycle and pathogenicity of COVID-19 [5].
Furins and Coronaviruses – What's the Big Deal?
In order to infect host cells after they enter the body, envelope viruses, like bacteria and viral exotoxins, remain dormant until they are activated. Common influenza viruses can be activated by proteases typically found in cells in the airway epithelium of the respiratory tract [6].
Coronaviruses are highly adaptive to the environments of the different cells they infect. Each coronavirus may be activated by a specific set of proteases. Proteases catalyzes the breakdown of proteins into smaller polypeptides or amino acids by cleaving the peptide bonds of those proteins.
The fact that COVID-19 has cleavage sites for furin enzymes means that this virus can be extremely pathogenic, with the capacity to replicate in MULTIPLE tissues and organs due to how furins are utilized and distributed in the human body [7].
Cleavage specificity can dictate the tropism and virulence of the virus. Furin-like cleavage in human coronaviruses have been associated with the development of neurological diseases where the invasiveness and efficient establishment of lower pathogenicity can result in persistent infection of the central nervous system [8].
HIV, human immunodeficiency virus, initiates infection by fusing the viral envelope with host cell membranes. Furin is used by HIV to cleave the glycoproteins in the viral envelope to complete the fusion process, gaining entry into various host cells and infecting them [9]. The ability of viruses such as Ebola to exploit furin may heavily influence their pathogenicity.
In addition, bioweapons such as Anthrax require furin to initiate toxicity. Furin has been identified as the cellular protease that cleaves the protective antigen protein of anthrax toxins that unleashes toxic activity [10].
If furins are essential to viral entry and replication, would it not be simple just to inhibit furin expression? That would indeed be an easy solution if only furins are not involved in a multitude of vital cellular processes. Basically all cell types have been observed to contain at least a small amount of furin exposed on their cell surface [10]. What are furins exactly?
Furins in Health & Disease
Two percent of the human genome encodes for more than 550 proteases [11]. Proteases are important because they play important roles in basically ALL physiological processes, including the digestion of proteins in our food and degradation of misfolded or discarded proteins [12].
Furin is a gene that encodes a type 1 membrane bound protease that is expressed in many tissues including neuroendocrine, liver, gut, and brain. Many important biological proteins are inactive when they are first synthesized. In order to become active, certain sections must be removed, or cleaved, by proteases.
Furin enzymes cleave their substrates in order to activate them. More than 100 furin cleavage sites in mammalian proteins have been identified to date. These proteins include growth factors; cytokines such as IGF1, IGF2, TGFβ, PDGFα, PDGFβ, VEGF‐C, NGF, CXCL10; hormones like PTH, TRH, GHRH; adhesion molecules including integrins, vitronectin; collagens, metalloproteinases; coagulation factors; receptors; membrane channels and albumin [13].
Once cleaved by furin enzymes, these proteins and peptides become bioactive, performing key functions in cell proliferation, immunity and inflammation. While most of the target substrates of furins are activated upon cleavage, furins can also inactivate substrates via cleavage [14]. Mutations in proteases like furins or dysregulation in furin activity have been associated with numerous pathological diseases including cardiovascular and neurological disorders; autoimmune diseases and cancer [15, 16, 8, 17, 18].
In a similar way, envelope proteins of viruses including HIV, influenza, dengue fever, ebola, and marburg virus, MUST be cleaved by furin or furin-like proteases to become fully active and functional. COVID-19, a novel coronavirus that originated from Wuhan, China, has now been identified to possess furin-cleavage sites in the S protein.
Thus COVID-19 and a host of important substrates found in the human body, including cytokines, hormones, growth factors and receptor all need to be cleaved by furin enzymes for activation. It is now becoming much clearer why furin-cleavage sites in viruses can increase their virulence and pathogenicity.
What is most interesting about furins, is that because it has pleiotropic properties, variations in furin expression levels and/or its enzymatic activity may result in the progression and pathogenesis of a wide array of disorders, including rheumatoid arthritis, amyloid dementia, but most of all, tumorigenesis [15].
Furins & Cancer
Furins hold the 'master switch' that controls tumor growth and development [19]. Furin expression levels are positively correlated with cancer aggressiveness, and are used as a prognostic biomarker for advanced cancers [20]. Aberrant expression or activation of furin promote formation and enhance malignancies of various tumors including colon, head and neck, lung, skin and brain cancers [20].
Since adhesion molecules are substrates of furin, this enzyme can promote migration and extravasation of malignant cells as it processes adhesion molecules that mediate cell to cell interactions. Furin mediated cleavage of integrins can regulate cell growth, division and survival [21]. Cancer metastasis is further increased by the activation of matrix metalloproteinases (MMP14) when they are cleaved by furin enzymes [20].
Furins are now widely accepted to be oncogenic and prometastatic, because they are able to cleave and activate proteins that promote cell proliferation, angiogenesis, migration and tissue invasion. These proteins include growth factors such as IGFs, PDGFs, NGF, or angiogenic factors like VEGF, all of which promote tumorigenesis [20].
The cancer microenvironment is extremely hypoxic. Tumor cells exhibit increased oxygen demand as a result of cell expansion in a background of decreased oxygen supply due to defective tumor vascularization [22]. In response to inadequate oxygen supply, complex mechanisms, like hypoxia-inducible factors (HIFs) and their downstream gene expression networks are activated to allow cells to adapt and survive in a hostile environment [23].
Hypoxia inducible factor 1α (HIF1α) is a transcription factor that can be activated under hypoxia. HIF1a is now regarded as an effective prognostic marker of cancer aggressiveness because it is considered to be the master regulator of neoangiogenesis in cancer development. HIF1a is able to control the expression of a wide array of genes involved in cancer progression.
It is therefore not surprising that furin expression is induced by hypoxia, and ALL THREE promoters for the FUR gene that encodes furin proteins have binding sites for HIF1 [24].
The Love-Hate Relationship Between Furins & HIF1a
During hypoxia, messenger RNA of the FUR gene are dramatically enhanced. Hypoxia activates both HIF-1a AND furin promoters. Expression of furin mRNA was found to be increased rapidly in oxygen-deprived cells by HIF-1, which binds to a sequence in the gene that promotes its rapid expression [25].
Hypoxia triggers the translocation of furins from the trans-Golgi network [26] to the cell surface where furins may further enhance the processing of growth factors and other extracellular cancer precursor proteins [27]. The relationship between HIF-1a and furins is further complicated by the negative feed-back loop between furins and HIF-1a.
As it turns out, although the expression of furins can be significantly increased by HIF-1a [25], furins can also turn around and suppress HIF-1a protein translation in a regulatory feed-back loop that is related to IGF (insulin-like growth factor) signaling [28].
Although furin inhibition is a promising target to treat COVID-19, the use of systemic inhibition will inevitably result in detrimental effects, as furins are involved in a multitude of important physiological activities. Furin knock-out mice die at day 11 during embryonic development due to cardial ventral closure defects and hemodynamic insufficiency [29, 36]. Eliminating furin-expression in endothelial cells of mice resulted in cardiac malformation and death shortly after birth [30].
Even mutations in the cleavage site of a single furin target protein have been shown to result in genetic disorders such as haemophilia B or X‐linked hypohidrotic ectodermal dysplasia [31, 32] Underexpression or knock-out of furin expression in retinal myeloid inhibit revascularization and angiogenesis [33]. Furin expression in the eyes is not only important for maintaining ocular health, it also allows transmission of viruses that have furin-cleavage sites. COVID-19 has recently been shown to be transmitted through ocular pathways [34].
Clearly the systemic inhibition of furins to control COVID-19 infection is fraught with obstacles. Yet there is one molecule that holds promise for the treatment of COVID-19
Vitamin C & Immunity
Clinical trials on the use of high-dose ascorbic acid (24 g), Vitamin C are currently underway in China [35]. One of the most obvious reasons for using Vitamin C is the effect on lymphocytes.
Infected patients in critical condition who were able to elevate lymphocyte counts during the third week of infection could usually escape death and recover. Whereas patients whose lymphocyte counts continue to plummet could not reverse the complete destruction of their immune systems. These patients inevitably die due to multiple organ failures [37].
During critical illness, lymphocytes (white blood cells) are the slowest to restore, endangering patients' chances for recovery. The regeneration of a subset of lymphocytes known as T-lymphocytes are especially important in the fight against viral infections [38].
Ascorbic acid (Vitamin C) has been found to enhance human T cell proliferation in vitro [39]. In addition, ascorbic acid promotes the maturation of T cells and has been found to be INDISPENSABLE for T cell development in vitro. Without ascorbic acid, a preT cell-stage arrest would occur, inhibiting development and maturation [40].
Ascorbic acid also speeds the regeneration and proliferation of natural killer (NK) cells [41]. Natural killer (NK) cells are unique lymphocytes without a clonally specific receptor and NK cells play a key role in our defense against viral infections [42]. NK cells are critical for the control of viral infections [43].
Ascorbic acid not only is able to protect mitochondria during viral infections [44], it can strengthen the immune system by protecting and regenerating critical lymphocytes [45, 46]. Yet in the context of furin cleavage sites, the importance of ascorbic acid cannot be understated.
Vitamin C, COVID-19 & Furins – The HIF-1a Connection
Hypoxia inducible factor 1α (HIF1α) is a transcription factor that can be activated under hypoxia. HIF-1a levels are normally kept low in the presence of oxygen. When there is adequate oxygen, HIF-1a is bound by the von Hippel-Lindau (VHL) protein, which then prepares HIF-1a for degradation [47].
If HIF-1a is not degraded properly, it will be able to bind with its heterodimeric component, HIF-1β, and becomes stabilized. Once HIF-1a is stabilized, it can activate the expression of a large number of genes associated with survival, apoptosis, and metabolic reprogramming, and of course, increase the expression of furins.
When a person is critically ill, oxidative stress levels are significantly elevated [48, 49]. Oxidative stress can activate HIF-1a [50, 51]. The activation of HIF-1a inevitably triggers the increased expression of furins, leading to cleavage and activation of COVID-19.
Ascorbic acid, Vitamin C has been convincingly demonstrated to modulate the HIF pathway in a dose dependent manner. Increased intracellular ascorbate dramatically elevated activity levels prolyl hydroxylase, which prevented the stabilization of HIF-1a [52].
Prolyl hydroxylase is an enzyme that can add a hydroxyl group (hydroxylation) to the α-subunits of HIF. This hydroxylation process allows HIF-1a to be bound to the von Hippel-Lindau protein (VHL), which then initiates the degradation process of HIF-1a. Prolyl hydroxylases are therefore, critical in preventing HIF-1a from activation and stabilization.
What is truly fascinating is that prolyl hydroxylases not only depend on ascorbic acid as substrates, but ascorbic acid MUST BE IN THE SPECIFIC MOLECULAR STRUCTURE of L-ASCORBATE in order to suppress HIF-1a [53]!!
These are the reasons why 50 tons of Vitamin C were sent to Wuhan to help citizens combat COVID-19 [54], and doctors from China are reporting excellent patient recovery rates from the use of Vitamin C in the treatment of COVID-19.
As of March 3rd, 2020, 80 countries around the world reported confirmed cases of COVID-19, that is a 100% increase from 40 countries that reported confirmed cases on February 25th [55]. The furin cleavage site of COVID-19 confers high transmissibility. We do not yet understand the true extent of the pathogenicity of this novel coronavirus from Wuhan. Only time will tell. In the meantime,
Have you had your AA today?
[1] Confirmed asymptomatic carrier of SARS-CoV-2 Luo, Sihui et al. http://www.chinaxiv.org/abs/202002.00078
[2] https://edition.cnn.com/2020/02/27/investing/dow-stock-market-selloff/index.html
[3] http://www.chinaxiv.org/abs/202002.00004
[4] A furin cleavage site was discovered in the S protein of the 2019 novel coronavirus https://www.researchgate.net/publication/338804501_A_furin_cleavage_site_was_discovered_in_the_S_protein_of_the_2019_novel_coronavirus
[5] The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade – https://www.ncbi.nlm.nih.gov/pubmed/32057769
[6] Activation of influenza viruses by proteases from host cells and bacteria in the human airway epithelium | Pathogens and Disease | Oxford Academic https://academic.oup.com/femspd/article/69/2/87/2399059
[7] Furin cleavage site in the SARS-CoV-2 coronavirus glycoprotein http://www.virology.ws/2020/02/13/furin-cleavage-site-in-the-sars-cov-2-coronavirus-glycoprotein/
[8] Cleavage of a Neuroinvasive Human Respiratory Virus Spike Glycoprotein by Proprotein Convertases Modulates Neurovirulence and Virus Spread within the Central Nervous System https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636366/
[9] Inhibition of furin-mediated cleavage activation of HIV-1 glycoprotein gp160. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/1360148
[10] Anthrax toxin protective antigen is activated by a cell surface protease with the sequence specificity and catalytic properties of furin. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC50321/
[11] Proteases as therapeutics. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/books/NBK9957/
[12] Research Applications of Proteolytic Enzymes in Molecular Biology https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030975/
[13] FurinDB: A database of 20-residue furin cleavage site motifs, substrates and their associated drugs. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/21541042?dopt=Abstract
[14] Proprotein convertases [corrected] are responsible for proteolysis and inactivation of endothelial lipase. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16109723?dopt=Abstract
[15] FURIN AT THE CUTTING EDGE: FROM PROTEIN TRAFFIC TO EMBRYOGENESIS AND DISEASE https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1964754/
[16] Influence of a Coronary Artery Disease–Associated Genetic Variant on FURIN Expression and Effect of Furin on Macrophage Behavior | Arteriosclerosis, Thrombosis, and Vascular Biology https://www.ahajournals.org/doi/10.1161/ATVBAHA.118.311030
[17] Protective role of systemic furin in immune response-induced arthritis. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/22605541
[18] The proprotein convertase furin in tumour progression. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/28369813
[19] Proprotein convertases: "master switches" in the regulation of tumor growth and progression. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/16167351?dopt=Abstract
[20] The proprotein convertase furin in tumour progression. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/28369813?dopt=Abstract
[21] Get a ligand, get a life: integrins, signaling and cell survival. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/12235283?dopt=Abstract
[22] Hypoxia-inducible factors and the response to hypoxic stress. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/20965423
[23] Hypoxia-Inducible Factors: Master Regulators of Cancer Progression. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/28741521
[24] Hypoxia-enhanced expression of the proprotein convertase furin is mediated by hypoxia-inducible factor-1: impact on the bioactivation of proproteins. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/15611046?dopt=Abstract
[25] Hypoxia-enhanced expression of the proprotein convertase furin is mediated by hypoxia-inducible factor-1: impact on the bioactivation of proproteins. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/15611046\
[26] Paired Basic/Furin-like Proprotein Convertase Cleavage of Pro-BMP-1 in the trans-Golgi Network https://www.jbc.org/content/278/20/18478.long
[27] Hypoxia enhances cancer cell invasion through relocalization of the proprotein convertase furin from the trans‐golgi network to the cell surface – Arsenault – 2012 – Journal of Cellular Physiology – Wiley Online Library https://onlinelibrary.wiley.com/doi/abs/10.1002/jcp.22792
[28] Regulation of HIF-1 alpha by the proprotein convertases furin and PC7 in human squamous carcinoma cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101078/
[29] Failure of ventral closure and axial rotation in embryos lacking the proprotein convertase Furin. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/9811571?dopt=Abstract
[30] Loss of endothelial furin leads to cardiac malformation and early postnatal death. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/22733989?dopt=Abstract
[31] Mutations within a furin consensus sequence block proteolytic release of ectodysplasin-A and cause X-linked hypohidrotic ectodermal dysplasia. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/11416205?dopt=Abstract
[32] Haemophilia B: database of point mutations and short additions and deletions. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pmc/articles/PMC331159/
[33] Furin deficiency in myeloid cells leads to attenuated revascularization in a mouse-model of oxygen-induced retinopathy – ScienceDirect https://www.sciencedirect.com/science/article/pii/S0014483517300052
[34] 2019-nCoV transmission through the ocular surface must not be ignored – The Lancet https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30313-5/fulltext
[35] Vitamin C Infusion for the Treatment of Severe 2019-nCoV Infected Pneumonia – Full Text View – ClinicalTrials.gov https://clinicaltrials.gov/ct2/show/NCT04264533
[36] Haemophilia B: database of point mutations and short additions and deletions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC331159/
[37] https://www.straitstimes.com/asia/east-asia/reporters-notebook-life-and-death-in-a-wuhan-coronavirus-icu
[38] Recovery of immune reactivity after T-cell-depleted bone marrow transplantation depends on thymic activity. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/10979980/
[39] Technical advance: ascorbic acid induces development of double-positive T cells from human hematopoietic stem cells in the absence of stromal cells. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/25157026/
[40] Vitamin C Promotes Maturation of T-Cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869442/
[41] Ascorbic acid promotes proliferation of natural killer cell populations in culture systems applicable for natural killer cell therapy. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/25747742/
[42] Natural Killer Cell Responses to Viral Infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128146/
[43] Keeping NK cells in highly regulated antiviral warfare. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/17466596/
[44] Mitochondria & The Coronavirus – The Vitamin C Connection Doris Loh https://www.evolutamente.it/mitochondria-the-coronavirus-the-vitamin-c-connection-part-3/
[45] A short overview of vitamin C and selected cells of the immune system | SpringerLink https://link.springer.com/article/10.2478/s11536-010-0066-x
[46] Influence of Vitamin C on Lymphocytes: An Overview https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5874527/
[47] Hypoxia-Inducible Factors in Physiology and Medicine https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437543/
[48] Oxidative stress in intensive care unit patients: a review of glutathione linked metabolism and lipid peroxidation | The Southwest Respiratory and Critical Care Chronicles https://pulmonarychronicles.com/index.php/pulmonarychronicles/article/view/511
[49] Oxidative Stress and Disease | IntechOpen https://www.intechopen.com/books/a-master-regulator-of-oxidative-stress-the-transcription-factor-nrf2/oxidative-stress-and-disease
[50] Identification of a functional antioxidant response element at the HIF1A locus – ScienceDirect https://www.sciencedirect.com/science/article/pii/S2213231718305391
[51] Relationship between oxidative stress and HIF-1 alpha mRNA during sustained hypoxia in humans. – PubMed – NCBI https://www.ncbi.nlm.nih.gov/pubmed/19028566
[52] Ascorbate modulates the hypoxic pathway by increasing intracellular activity of the HIF hydroxylases in renal cell carcinoma cells https://www.dovepress.com/ascorbate-modulates-the-hypoxic-pathway-by-increasing-intracellular-ac-peer-reviewed-fulltext-article-HP
[53] L-ascorbic acid: A true substrate for HIF prolyl hydroxylase? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460286/
[54] https://twitter.com/dsm?fbclid=IwAR2M_5xD7N2ccbVFM1iSvPfEjcOd110DljWWWq0bTgSo3PLTuS3k5DI8LfU
[55] https://www.worldometers.info/coronavirus/
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i dati sul tasso di natalità della Svezia rimangono gravemente soppressi in un modo pazzesco e senza precedenti. Si...
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Nei giorni appena trascorsi, hanno fatto scalpore le dichiarazione del primo Ministro giapponese: Nella sua apertura...
COVID UPDATE: 15/1/2023. Cose che in TV non ascolterete mai.
In quest'articolo scoprirete che le corsie dei reparti "covid" sono totalmente sgombre di "non vaccinati" e piene di...
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Lyle Clay Loughry, age 84 of Ravenna, Ohio, passed away Thursday, September 20, 2018. Lyle was born July 24, 1934 in Parsons, West Virginia to Howard Loughry and Fern (Carter) Loughry. He graduated from Parsons High School in 1952. Lyle loved the Lord, his family, sports, hunting, and consulting on health issues.
In addition to his parents, Lyle was preceded in death by his son, Keith Loughry.
Lyle is survived by his wife, Vera (Harner) Loughry, his children: Michael (Donna) Loughry, Linda (James) McNees, Cheryl (James) Poland, Howard (Kathy) Loughry, Kevin Loughry, Kathi (Michael) Smith, and Korey (Molly) Loughry; seventeen grandchildren and seventeen great-grandchildren.
Memorial service will be held on Thursday, September 27, 2018 at 7:00 p.m. at Grace Baptist Church, 5915 Rhodes Road, Kent, Ohio.
As I said on Facebook, Lyle's was one of my favorite faces to see at Grace when I attended, and later when I would be home in Ohio to visit. His voice was so soothing and his care and concern for my life were so genuine. I know he was part of a group of really special people who supported me and prayed without ceasing while I was in the hospital for months with a brain injury- and he continued to pray for me as I healed. That has touched my heart and I will cherish that. Thank you.
Lyle was a very genuine man with a good heart, and he loved the Lord with all his heart. He and his wife Vera prayed fervently for my older brother, when he was seriously sick with cancer. He was always a friend to me. Tonight in my prayers, I thanked the Lord for his life and for the hope we have in Christ that one day we shall see him again in Heaven.


WARWICK — The Warwick Valley Chorale will perform three concerts in December.
The concerts, directed by Stanley Curtis and accompanied by Gail Johnson, will present selections from Bach and Handel to Irving Berlin's "White Christmas." A new (2018) cantata by John Leavitt, "A Midnight Clear," highlighting traditional carols will be featured.
The concerts will be presented at 7 p.m. tonight at Grace Episcopal Church, 58 North St., Middletown; at 7 p.m. Dec. 14 at Goshen United Methodist Church, 115 Main St., Goshen; and at 4 p.m. Dec. 16 at St. Stephen's Roman Catholic Church, 75 Sanfordville Road, Warwick.
Admission is free; donations will be gratefully accepted.
For further information, visit WarwickValleyChorale.org and the Warwick Valley Chorale Facebook page.


text:
Home » Blogs » Margaret Reeves's blog
Strange bedfellows on immigration reform
Who'd have thought? United Farmworkers (UFW) and the California Farm Bureau Federation (CFBF) are on the same side of the table when it comes to farm labor and immigration reform. Since 2007 the Farm Bureau has been supporting and promoting AgJobs — a compromise bill negotiated by farmworker leaders and farmers.
This month CFBF took their message to Washington, D.C. to argue against introduction of E-Verify, a mandatory electronic verification program to determine an employee's eligibility for employment. E-Verify, the Bureau claims, would lead to the collapse of the agricultural industry. UFW agrees.
Herein lies the under-appreciated underbelly of immigration debates: our agricultural economy is flatly impossible without immigrant labor. And the Farm Bureau knows it.
E-Verify would not only cause major dislocations in the agricultural industry and serious economic losses, it would have truly terrible consequences for a half million farmworker children, most of whom are U.S. citizens whose parents are without legal status.
Farmworker policy reform overdue
Current government policies reinforce a power imbalance that leaves farmworkers with poor wages and horrendous working conditions. The following excerpt from a UFW letter to the House Judiciary Subcommittee clearly explains how reform of these policies would benefit both growers and workers:
The current situation is not good for farmworkers who want to be able to work legally and earn a decent living to support their families. It is not good for employers who want to hire people without worrying that they will be raided by the immigration service at the peak of the harvest of their perishable fruits and vegetables. It is not good for the government, which needs to know who is working in our economy and living among us.
But it is no answer to say we will deport them and start again. The growers need these experienced workers to cultivate and harvest their crops. In fact, many growers contend that there are labor shortages in some areas because undocumented workers are too fearful of immigration raids to come to the open fields.
Under AgJobs, undocumented workers in the country now would earn legal status by continuing to work in agriculture. It offers growers a legal and stable work force, ensures workers already in the U.S. receive jobs before foreign workers are brought in, and protects guest workers from being exploited. The proposed law has been embraced by leading Democrats and Republicans in Congress — but has yet to move forward and become law.
Immigration reform is one good example of how unusual alliances can help achieve policy change in Washington, D.C. Strange bedfellows may also be key in the upcoming swirl of negotiations on the 2012 Farm Bill — a large package of federal farm and food legislation, worth billions of dollars, that set the farm, food, and rural policy goals and priorities for the country.
We'll keep you posted here as these policy battles moves forward on the national stage.
Margaret Reeves
Margaret Reeves's blog
Margaret Reeves is a PAN Senior Scientist with expertise in agroecology and soil ecology. As a long-time farmworker advocate, Margaret serves on the Board of the Equitable Food Initiative and works with partners around the country to ensure worker-protective federal and state policy. Follow @MargaretatPAN
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This is a sequel to "The Nibelungen: Siegfried's Death". Following her husband's death, Kriemhild wanted to seek revenge on her husband's murder and plotted to do so after King Attila proposed to her.
King Attila had a very cool image and Kriemhild looked very scary with her vengeful eyes! Quite sad how the thought of revenge could destroy families and wreck havoc on entire nations. Liked how the contrast between the loyalty among the Nibelungens and the cold blooded actions of Kriemhild slowly built towards a grand finale in the end!


Yet perhaps even more troublesome than these errors is the phenomenon known as "mental accounting." Mental accounting refers to the tendency of humans to develop and make decisions based on purely mental categories. Although they seem rational, the categories we create are often wholly arbitrary — and in some cases, dangerously misleading. If we are not careful, mental accounting can sabotage our investment strategies or even our entire financial lives.
Here are eight pernicious examples of mental accounting — and how to see the fallacy behind each one.
In an in-depth article, the Washington Post found that where money comes from influences how we decide to spend it. A major example of this (as will be seen throughout) pertains to money we did not expect to get. Generally speaking, human beings are more likely to be impulsive or reckless with unexpected money because, they reason, it was never factored in to their serious financial plans to begin with. Tax refunds are a case in point.
Most of us know a tax refund is coming, but rarely know the exact amount. Therefore, we tend to forget about it until it arrives and then regard it as a sort of windfall whose eventual disposal means nothing to the broader financial picture of our lives. This is erroneous however, because as a fungible commodity, money is money. Where it came from should have no bearing on what it objectively makes sense to be spent on.
The same basic logic applies to birthday money. As kids (and perhaps still today), we all remember getting cards stuffed with cash from our relatives on each birthday. Other than a few young geniuses with the foresight to save some of it, most of us eagerly rushed out and bought the most outlandish and impractical things we could. The reasoning? We weren't expecting the money.
Sure, people can criticize your spending choices when it comes to recurring job income, but who could possibly second-guess what you did with a random, one-time birthday payoff?
Yet the same intractable reality applies: birthday money is in no way different than or inferior to job income, business profits, investment returns, or any other source. If you decided previously that the car payment was your most important bill, for instance, there is no logical justification for not using "birthday money" to pay it.
Bonuses are essentially an adult's version of "birthday money." The very name — "bonus" — suggests a sum of money meant to be seen in a different light than mere ordinary income. Unsurprisingly, many employees are seen spending their bonus money on things they would never be able to justify (to their spouses or to themselves) spending "regular" income on — boats, new cars, or lavish vacations, for instance. Of course, nothing says that these types of purchases are bad or irrational. Far from it!
The issue at hand is that all spending — extravagant spending included — should be consciously compared with what the money could alternatively be spent on. If your current financial plan already includes extravagances, feel free to spend bonus money on it! If not, the fact that you have received "a bonus" does not change the other, less exciting things you know are factually more deserving of that money.
Investors are, as a group, highly prone to the "money you can afford to lose" variant of mental accounting. Under this notion, investors view some arbitrary amount of their investment capital as "play money" which they feel comfortable squandering on speculative and uncertain things. At first glance, this has the makings of sensible decision-making. It seems prudent to clearly delineate between money that matters and money that doesn't.
The problem, of course, is that "money you can afford to lose" is a purely mental creation. An economist would say that true financial rationality dictates never putting money somewhere that it was likely to be lost, and that no amount of mental maneuvering would make this an acceptable fate for any amount of money in your possession.
Earlier, we discussed how some people treat differently the money they have designated as "money I can afford to lose." This is also known as "play money" or "risk money." The other side of that coin is, as Investopedia calls it, "safety capital." True to the mental accounting fallacy, this is the money people regard as "money they need." Consequently, these funds are handled with the prudence and care befitting of money one expects to pay a mortgage, fund retirement accounts, or other serious financial purposes.
In reality, as you now know, this is the way that all of a person's money should be treated. There is no dividing line between money that matters (safety capital) and money you can afford to lose (risk capital). Any dividing line you honor is nothing more than a misleading mental illusion.
Indeed, countless lottery winners have managed to go bankrupt after spending their millions on dubious purchases that "seemed" to be justified by the unexpected prize they had won. Had these fallen winners spent even slightly more in line with how they spent their job income prior to winning, they would likely still be rich today.
A man buys an expensive membership in a tennis club. Right after he puts down the money, which is nonrefundable, he hurts his ankle. He grits his teeth and continues to play through the pain — even though not playing would mean much less agony. Mental accounting is behind the problem. Playing is the only way to ensure that the tennis club membership remains in the man's mental category of money well spent. To not play would be to write off the membership cost as a loss, which is more painful to the man than the agony of hobbling through games on an injured ankle.
Had the man in this fictional example not bound himself to honoring a self-created, illusory, mental category, he would have spared himself considerable pain!
Imagine you just arrived at a theater and as you reach into your pocket to pull out the $10 ticket you purchased in advance, you discover that it's missing. Would you fork over another $10 to see the movie?
They discovered that only 46% of the study participants in scenario one said they would spend another $10 to buy another movie ticket. However, a whopping 88% of the subjects in scenario two said they would still spend $10 to buy a theater ticket.
So, how can you avoid these mental accounting traps? It's not easy, but there are some strategies you can employ to help yourself avoid the pitfalls.
First, you need to get organized financially. This means using a tool like Personal Capital (which is free and we love) to keep track of all your income and expenses. Knowing what comes in and what goes out can help you avoid several of these traps.
Second, stop keeping everything in your mind and write it down. This can be by creating a budget or using a tool like The Personal Finance Planner, or even just doing something as simple as writing down your goals for the year. The goal here is to translate your mental accounting notes into something physical and tangible.
Finally, get an accountability buddy to help you. One of the biggest "problems" we have when it comes to money is we treat it like taboo – don't talk about it, don't ask others about it, never share anything. That's a bad mentality because it can compound these mental accounting traps. If you need help overcoming a roadblock, share your goal or your budget with a friend. Let them know what you want to do, and allow them to remind you of it in the future.
Have you ever fallen into these mental accounting traps?


We are often asked how to plan for the occurrence of a disabling event or accident and how to make sure loved ones receive the degree of health care they desire. A popular tool for communicating to your doctors and family upon the occurrence of a disabling event is a health care directive.
What It Is: Also known as a living will or health care power of attorney, a Georgia Advance Directive for Health Care (ADHC) allows you to: 1) select a health care agent; 2) communicate with your doctors and loved ones if you have a terminal condition or are permanently unconscious; and 3) choose an agent to act on your behalf if a court determines you need a guardian. Guardians are appointed in the event you become unable to make everyday decisions for yourself.
How to Create One: Creating a health care directive in Georgia can be a time consuming process. A health care directive is an extensive legal document detailing who and how will help you if you are unable to do so. The process involves selecting a health care agent and guardian, outlining the types and extent of treatment you want, and defining the amount of power or authority health care agent will have over your treatment.
At A. Bishop Law, our Georgia Probate attorney welcomes anyone with any Georgia Will, Estate or Probate questions to Call or Email us today. Please remember that all initial consultations are free of charge. For more information on our Georgia estate planning packages, including a simple will, and health care directive and Georgia power of attorney, please contact our office today at 770-783-5296.
A Health Care Power of Attorney or Health Care Directive helps a loved one make decisions if you are unable.
About the attorney: Anne Bishop is a North Georgia Lawyer with A. Bishop Law and handles matters regarding Wills, Estate Planning and Georgia Probate and can assist clients throughout Georgia including: Hall County (Gainesville, Oakwood, Flowery Branch), White County (Cleveland), Dawson County (Dawsonville), Habersham County (Demorest, Cornelia), and all of Northeast Georgia.


I stumbled across this awesome video, which seems to have been original uploaded to YouTube on 11th November 2018, from my Twitter steam last week.
DHH is a truly outspoken guy who has some extremely strong opinions on a number of things in our industry. In this video he highlights the simplicity of an extremely important topic that many get lost in.


Author(s): Lokendra K. Sharma, Jianxin Lu, Yidong Bai. Department of Cellular and Structural Biology, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229, USA.
Mitochondria are ubiquitous organelles in eukaryotic cells whose primary function is to generate energy supplies in the form of ATP through oxidative phosphorylation. As the entry point for most electrons into the respiratory chain, NADH:ubiquinone oxidoreductase, or complex I, is the largest and least understood component of the mitochondrial oxidative phosphorylation system. Substantial progress has been made in recent years in understanding its subunit composition, its assembly, the interaction among complex I and other respiratory components, and its role in oxidative stress and apoptosis. This review provides an updated overview of the structure of complex I, as well as its cellular functions, and discusses the implication of complex I dysfunction in various human diseases.
Affiliation:Department of Cellular and Structural Biology, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229, USA.
Abstract: Mitochondria are ubiquitous organelles in eukaryotic cells whose primary function is to generate energy supplies in the form of ATP through oxidative phosphorylation. As the entry point for most electrons into the respiratory chain, NADH:ubiquinone oxidoreductase, or complex I, is the largest and least understood component of the mitochondrial oxidative phosphorylation system. Substantial progress has been made in recent years in understanding its subunit composition, its assembly, the interaction among complex I and other respiratory components, and its role in oxidative stress and apoptosis. This review provides an updated overview of the structure of complex I, as well as its cellular functions, and discusses the implication of complex I dysfunction in various human diseases.


text:
SYNONYM

#### According to
The Catalogue of Life, 3rd January 2011

#### Published in
Mycena 1(1): 91 (2001)

#### Original name
Polyporus portoricensis Fr., 1828

### Remarks
null

redpajama_set_name: RedPajamaGithub


text:
Creating a programming language: Larry Wall and Perl
Home/Technical/Perl/Creating a programming language: Larry Wall and Perl
Programming is beyond the grasp of most people, it doesn't matter if we're talking about Perl or another language. Most individuals will look at it as more than a foreign language, as something beyond comprehension, something that takes a special kind of thinking. There is some truth to this, as in not everybody can become a developer, it does take a special little something, a certain mindset beyond hardwork and dedication. But in the end most programmers just work with a language, be it Perl or another, the true masters are the builders of those languages.
Creating a programming language is truly extraordinaire, it's more than just creating a language, it's building an entire world that doesn't just have to make sense to other people, but also has to have a practical attribution. Think about it like this, driving a car seems hard before you take a few lessons on it. After you gain some experience it's the most natural thing in the world. But building a car, that's another story, there are so many intricacies, so many things that have to work, that lessons and experience just don't cut it.
That's sort of how we look at people who create programming languages, they are extraordinary individuals, programming is a part of their inner self, not just a second language, but a way of thinking. Their background vary from case to case, but each one of them bring their own backstory into their creation. One of these amazing people is Larry Wall, the creator of the Perl programming language.
So how does one go about creating a programming language?
Is there a class, a school you go to for something like this? Well, no. The word genius had been thrown around so much these days that it's lost part of its meaning, but I would dare say that it takes a spark of genius to get to create a programming language. Larry Wall majored in chemistry at Seattle Pacific University, but changed to pre-med before taking a few years off to work in the university's computing center. He finally graduating with a bachelor's degree in Natural and Artificial Languages, only suiting for someone who had and who has a great interest in languages. Creating Perl wasn't a conclusion of a plan, it was just a solution to a problem coupled with an inner desire to contribute. But let's get back to the how.
The how is more than a reason, I'm sure a lot of people think about the background that one needs to be able to do such a thing. You don't just stumble and fall into a programming language. In Larry Wall's own words, his "decent set of brain construction genes", rich heritage of ideas, his love for communication and of understanding the world, changing the world, a desire to build things and a certainty that "true wealth is measured not by what you accumulate, but by what you pass onto others." had its own part. This was more or less, the "baggage" he had. The creation of Perl came, like most things, as a solution to a problem he couldn't solve as easily as he would like to.
" I could have solved my problem with awk and shell eventually, but I possess a fortuitous surplus of the three chief virtues of a programmer: Laziness, Impatience and Hubris. I was too lazy to do it in awk because it would have been hard to get awk to jump through the hoops I was wanting it to jump through. I was too impatient to wait for awk to finish because it was so slow. And finally, I had the hubris to think I could do better."
These are the three virtues that every great programmer should have, and they still stand today:
Laziness: The quality that makes you go to great effort to reduce overall energy expenditure. It makes you write labor-saving programs that other people will find useful and document what you wrote so you don't have to answer so many questions about it.
Impatience: The anger you feel when the computer is being lazy. This makes you write programs that don't just react to your needs, but actually anticipate them. Or at least pretend to.
Hubris: The quality that makes you write (and maintain) programs that other people won't want to say bad things about.
It didn't happen overnight in a dark basement, it happened through a lot of hard work in 1987, while Larry was working for System Development Corporation. Of course, he didn't build an entire language just for one problem, but it wasn't just his problem, it was something that could be improved for other people as well. That's the thing in programming, there's always a community around, you're never helping just yourself.
There are plenty of things to say about how Perl evolved and dominated the 90's but that's another story. People don't suddenly decide that they want to build their own language, it's something that happens organically when the right situation occurs. It's not by chance, it's more by intent coupled with the right time and place. In the 1980s computer programming was still in its infant stage and there was plenty of room to grow, but people invent language even today, so there will always be room for more, room to grow.
Perl had a huge impact in computer programming not just through itself, but also through others. Just like it was influenced by C, Lisp, Python, C++, Unix shell, BASIC and other it also influenced other languages like: Ruby, PHP, Python, JavaScript, ECMAScript, Windows PowerShell, Dao Language, Groovy, Frink, LPC, Perl 6, BeanShell, Sleep programming language, Judoscript, Aikido Programming Language, MIVA Script, Falcon, Haskell, CoffeeScript.
In the plenitude of programming languages that exist today, Perl keeps its head high, 28 years later it's a cherished and valued programming language. Perl code exists in millions of websites today, countless projects have been written in Perl and a large and very tight community supports and develops it today. That's the thing with any programming language, an individual may bring it to life, but a community develops it and spreads it beyond its origin point.
We're proud to have started as a Perl company and more than 10 years later to have a large and skilled team of Perl programmers working on various projects. From all the technologies we cover, Perl is different, not just because it was one of the first technologies we covered, but because of the way the community of developers works together. We carry on spreading Perl, one line of code at a time, for us and our clients.
Samuel Andras
admin2019-03-29T15:11:58+03:00December 6th, 2016|Categories: Perl, Technical|Tags: Aikido Programming Language, BeanShell, Cluj, CoffeeScript, Dao Language, ECMAScript, Evozon, Falcon, Frink, Groovy, Haskell, javascript, Judoscript, larry wall, LPC, MIVA Script, Perl, Perl 6, php, Python, Ruby, Sleep programming language, Windows PowerShell|


text:
package org.apache.hadoop.fs;

import com.google.common.annotations.VisibleForTesting;
import com.google.common.base.Preconditions;
import org.apache.hadoop.classification.InterfaceAudience;
import org.apache.hadoop.classification.InterfaceStability;
import org.apache.hadoop.conf.Configuration;
import org.apache.hadoop.fs.Options.ChecksumOpt;
import org.apache.hadoop.fs.permission.FsPermission;
import org.apache.hadoop.util.Progressable;

import javax.annotation.Nonnull;
import java.io.IOException;
import java.util.Collections;
import java.util.EnumSet;
import java.util.HashSet;
import java.util.Set;

import static org.apache.hadoop.fs.CommonConfigurationKeysPublic.IO_FILE_BUFFER_SIZE_DEFAULT;
import static org.apache.hadoop.fs.CommonConfigurationKeysPublic.IO_FILE_BUFFER_SIZE_KEY;

/**
 * Builder for {@link FSDataOutputStream} and its subclasses.
 *
 * It is used to create {@link FSDataOutputStream} when creating a new file or
 * appending an existing file on {@link FileSystem}.
 *
 * By default, it does not create parent directory that do not exist.
 * {@link FileSystem#createNonRecursive(Path, boolean, int, short, long,
 * Progressable)}.
 *
 * To create missing parent directory, use {@link #recursive()}.
 *
 * To be more generic, {@link #opt(String, int)} and {@link #must(String, int)}
 * variants provide implementation-agnostic way to customize the builder.
 * Each FS-specific builder implementation can interpret the FS-specific
 * options accordingly, for example:
 *
 * <code>
 *
 * // Don't
 * if (fs instanceof FooFileSystem) {
 *   FooFileSystem fs = (FooFileSystem) fs;
 *   OutputStream out = dfs.createFile(path)
 *     .optionA()
 *     .optionB("value")
 *     .cache()
 *   .build()
 * } else if (fs instanceof BarFileSystem) {
 *   ...
 * }
 *
 * // Do
 * OutputStream out = fs.createFile(path)
 *   .permission(perm)
 *   .bufferSize(bufSize)
 *   .opt("foofs:option.a", true)
 *   .opt("foofs:option.b", "value")
 *   .opt("barfs:cache", true)
 *   .must("foofs:cache", true)
 *   .must("barfs:cache-size", 256 * 1024 * 1024)
 *   .build();
 * </code>
 *
 * If the option is not related to the file system, the option will be ignored.
 * If the option is must, but not supported by the file system, a
 * {@link IllegalArgumentException} will be thrown.
 *
 */
@InterfaceAudience.Public
@InterfaceStability.Evolving
public abstract class FSDataOutputStreamBuilder
    <S extends FSDataOutputStream, B extends FSDataOutputStreamBuilder<S, B>> {
  private final FileSystem fs;
  private final Path path;
  private FsPermission permission = null;
  private int bufferSize;
  private short replication;
  private long blockSize;
  /** set to true to create missing directory. */
  private boolean recursive = false;
  private final EnumSet<CreateFlag> flags = EnumSet.noneOf(CreateFlag.class);
  private Progressable progress = null;
  private ChecksumOpt checksumOpt = null;

  /**
   * Contains optional and mandatory parameters.
   *
   * It does not load default configurations from default files.
   */
  private final Configuration options = new Configuration(false);

  /** Keep track of the keys for mandatory options. */
  private final Set<String> mandatoryKeys = new HashSet<>();

  /**
   * Return the concrete implementation of the builder instance.
   */
  protected abstract B getThisBuilder();

  /**
   * Constructor.
   */
  protected FSDataOutputStreamBuilder(@Nonnull FileSystem fileSystem,
      @Nonnull Path p) {
    Preconditions.checkNotNull(fileSystem);
    Preconditions.checkNotNull(p);
    fs = fileSystem;
    path = p;
    bufferSize = fs.getConf().getInt(IO_FILE_BUFFER_SIZE_KEY,
        IO_FILE_BUFFER_SIZE_DEFAULT);
    replication = fs.getDefaultReplication(path);
    blockSize = fs.getDefaultBlockSize(p);
  }

  protected FileSystem getFS() {
    return fs;
  }

  protected Path getPath() {
    return path;
  }

  protected FsPermission getPermission() {
    if (permission == null) {
      permission = FsPermission.getFileDefault();
    }
    return permission;
  }

  /**
   * Set permission for the file.
   */
  public B permission(@Nonnull final FsPermission perm) {
    Preconditions.checkNotNull(perm);
    permission = perm;
    return getThisBuilder();
  }

  protected int getBufferSize() {
    return bufferSize;
  }

  /**
   * Set the size of the buffer to be used.
   */
  public B bufferSize(int bufSize) {
    bufferSize = bufSize;
    return getThisBuilder();
  }

  protected short getReplication() {
    return replication;
  }

  /**
   * Set replication factor.
   */
  public B replication(short replica) {
    replication = replica;
    return getThisBuilder();
  }

  protected long getBlockSize() {
    return blockSize;
  }

  /**
   * Set block size.
   */
  public B blockSize(long blkSize) {
    blockSize = blkSize;
    return getThisBuilder();
  }

  /**
   * Return true to create the parent directories if they do not exist.
   */
  protected boolean isRecursive() {
    return recursive;
  }

  /**
   * Create the parent directory if they do not exist.
   */
  public B recursive() {
    recursive = true;
    return getThisBuilder();
  }

  protected Progressable getProgress() {
    return progress;
  }

  /**
   * Set the facility of reporting progress.
   */
  public B progress(@Nonnull final Progressable prog) {
    Preconditions.checkNotNull(prog);
    progress = prog;
    return getThisBuilder();
  }

  protected EnumSet<CreateFlag> getFlags() {
    return flags;
  }

  /**
   * Create an FSDataOutputStream at the specified path.
   */
  public B create() {
    flags.add(CreateFlag.CREATE);
    return getThisBuilder();
  }

  /**
   * Set to true to overwrite the existing file.
   * Set it to false, an exception will be thrown when calling {@link #build()}
   * if the file exists.
   */
  public B overwrite(boolean overwrite) {
    if (overwrite) {
      flags.add(CreateFlag.OVERWRITE);
    } else {
      flags.remove(CreateFlag.OVERWRITE);
    }
    return getThisBuilder();
  }

  /**
   * Append to an existing file (optional operation).
   */
  public B append() {
    flags.add(CreateFlag.APPEND);
    return getThisBuilder();
  }

  protected ChecksumOpt getChecksumOpt() {
    return checksumOpt;
  }

  /**
   * Set checksum opt.
   */
  public B checksumOpt(@Nonnull final ChecksumOpt chksumOpt) {
    Preconditions.checkNotNull(chksumOpt);
    checksumOpt = chksumOpt;
    return getThisBuilder();
  }

  /**
   * Set optional Builder parameter.
   */
  public B opt(@Nonnull final String key, @Nonnull final String value) {
    mandatoryKeys.remove(key);
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   * @see #opt(String, String)
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  /**
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   * If the option is not supported or unavailable on the {@link FileSystem},
   * the client should expect {@link #build()} throws IllegalArgumentException.
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  /**
   * Set mandatory boolean option.
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   * @see #must(String, String)
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  /**
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  /**
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text:
Liste der Monuments historiques in Chilly steht für:

 Liste der Monuments historiques in Chilly-Mazarin
 Liste der Monuments historiques in Chilly (Ardennes)

redpajama_set_name: RedPajamaWikipedia


text:
GreatPoint Ventures Invests In Leading Gene Therapy Delivery Platform
ATLANTA - March 1, 2019 - PrZen -- GreatPoint Ventures, a leading San Francisco based venture capital firm, announced the closing of an investment in Guide Therapeutics, Inc. (GuideRx), a developer of lipid nanoparticles (LNPs) for delivery of therapeutics for gene therapy. GuideRx was organized around the work of Professor James E. Dahlman, formerly of the labs of pioneers in gene therapy including Robert Langer of MIT and Feng Zhang of the Broad Institute. Professor Dahlman is faculty in the Department of Biomedical Engineering at Georgia Institute of Technology and Emory School of Medicine. Dr. Dahlman was recently recognized by MIT Technology Review as one of the Top 35 Scientists under 35 for this work. Based upon the work of Dr. Dahlman, GuideRx is able to screen more than 30,000 LNPs in vivo per year to develop LNPs with high affinity for non-liver cell types and low affinity for non-target tissues employing its unique patented platform technology. GuideRx's technology has identified nanoparticles that have shown functional delivery to non-liver cell types, greatly extending the potential for treating genetic disease.
Tom Saylor, CEO of GuideRx said, "The investment by GreatPoint Ventures provides GuideRx with an opportunity to accelerate its development of therapeutic candidates for treatment of genetic diseases. The ability to deliver to non-liver tissue has become a key bottleneck in the wider application of gene therapies. In partnership with GreatPoint Ventures, GuideRx not only expects to shorten drug development timescales by side-stepping in vitro reseach but to offer safer ways to treat genetic disease."
Andrew Perlman, Managing Partner at GreatPoint Ventures stated, "GreatPoint has been fortunate to seal a partnership with GuideRx, which promises to be a major player in the next generation of gene therapy utilizing its proprietary ability to develop drugs that can selectively target non-liver cell types. We are confident that Guide will be one of the top players in the rapidly emerging field of gene therapy."
Tom Saylor
Guide Therapeutics, Inc.
***@guiderx.com
Source: Guide Therapeutics, Inc.
Filed Under: Investment, Health, Technology, Science, Biotech


text:
Bio-Rad introduces StarBright UltraViolet 400 Dye for flow cytometry
StarBright UltraViolet 400 Dye offers maximal brightness and narrow excitation and emission profiles for precise resolution.
HERCULES, Calif.– November 16, 2021–Bio-Rad Laboratories, Inc. (NYSE: BIO and BIOb), a global leader of life science research and clinical diagnostic products, today announced the launch of StarBrightTM UltraViolet 400 Dye, the first in its range of unique fluorescent nanoparticles designed for use with a UV laser in flow cytometry applications.
StarBright UltraViolet 400 Dye offers exceptional brightness with narrow excitation and emission profiles, making it suitable for use in multicolor flow cytometry panels. Bio-Rad's range of StarBright Dyes are conjugated to highly validated flow antibodies and are compatible with most flow cytometers and experimental protocols.
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Key Benefits of StarBright Dyes
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Ensure no loss of signal in fixation
Offer narrow excitation and emission profiles for improved resolution in new and existing multicolor flow cytometry experiments.
For more information about Bio-Rad's StarBright UltraViolet 400 Dye, please visit:
https://www.bio-rad-antibodies.com/flow-cytometry-starbright-ultraviolet-dyes.html
Zyme Communications provides PR and marketing services for the life science sector. We support companies to raise their profile, build corporate value and generate interest from commercial leads, investors and partners.
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Zyme Communications directory information


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text:
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Board index Writing Novel in a Day
Jaysen's 150 word story?
pigfender
Platform: Mac, Win + iOS
Location: I share a head with a great many personalities
Contact pigfender
Mon Apr 03, 2017 6:10 pm Post
If you're familiar with Novel-in-a-Day and Three-Word-Story, you may be aware that Jaysen has been trying to persuade me to let him produce a crowd-sourced chapter within that collaborative novel for a little while. He brought the suggestion up again in the Feature Request thread, and I challenged him to prove that it's a good idea; you can work on a chapter together in a style that will not jar the resulting experience for readers of the finished books.
Anyway, to give him fair opportunity to prove that it works, here is a sample chapter for a "150 word story". Like the "Three-word-story" format, you take it in turns to write sections that follow on from the previous section. Unlike three word story, you're not forced to write just three words. You can write between 100 and 150 words. (NO MORE AND NO LESS PLEASE!). You must follow from the previous sections, and you must work towards the overall chapter outline (shown below).
If you get to the "Ends With" in a sensible time, and you're having fun, I'll put up an outline for the next chapter... and then the next... and then the next.
MARCH 2017, in WILMINGTON NORTH CAROLINA
JOHN THOMAS TAYLOR is a 32 year old man, in a failing marriage. He's a slightly overweight and relatively average if unspectacular guy who works as office manager for a cape tour company (that he doesn't own). John has a small scar on his left temple from a being knocked off his bike by a car when he was 7.
His wife of 10 years, LUCY FIONA TAYLOR (nee WILLIAMS, age 32) works part time for the local news station as a researcher. Lucy is having an affair with a work colleauge, but John doesn't know that.
John and Lucy have a single child, an 8 year old daughter called ALICE ELIZABETH TAYLOR. They all live together in a 3 bedroom, 2 storey house in downtown Wilmingon, about 5 blocks from the waterfront.
Things that have happened previously
KELLY MARIE MARTIN came over to the Taylor's house for lunch who John has known since he was young, and who was at Lucy's class at the University of North Carolina where John also studied (Nicola introduced Lucy to John). John made something for Lucy and Kelly to eat before he took Alice out to soccer. Lucy and Kelly were gossiping as he left.
It is SATURDAY MID AFTERNOON. Alice has just finished a soccer practice and John is going to drive her home.
Chapter details
John drives Alice home
When he gets back to the house, Lucy and Kelly are still there, but the atmosphere is a bit awkward - Kelly is treating John a bit oddly.
Something happens that cause Lucy and John to have an argument in front of Kelly and Alice.
Lucy snaps telling John about the affair.
John storms out and gets in his car.
Pulling out of his drive, John's car is in the side by a school bus. [End at the point of impact]
gr wrote: For the conduct of the experimental spirit, I am imagining the following procedure: The chapter gets composed serially right here in this thread, but to avoid duplication of efforts, at each joint, someone must "dibs" the next segment and then come back within x amount of time to post his or her block of text. Each post should include a running total of the word count of the whole chapter, b/c things have to wind up sometime. I suppose that, but for the occasional flying saucer, common purpose and general good will will hold the reigns on the flippant and genre-busting impulses to which we are all prone.*
* Though I have to say I was almost sure the spat between Lucy and John had something to do with the mechanical dolphin that just went in down at the pub.
OK -- we'll work like that in this thread. I suggest we have 45 minutes reservations on writing the next bit, but flag in your section if you'll need a slightly different amount of time. NOTE: at Jaysen's suggestion, there should be at least four other people between any individual's contribtutions.
I'll kick things off, since it's probably easier to follow than start. If we've not got a sensible number of replies by the end of this week, I'll call off and close the thread.
"Some dice only have sixes." nom, 19 Oct 2013
"Piggy, I'm beginning to wonder if you are the best person to take advice from." Jaysen, 26 Sept 2014
http://www.pigfender.com | http://www.novelinaday.com
Mon Apr 10, 2017 12:03 pm Post
'Did you see me, Dad?'
John squatted down as Alice bounded over towards him. He gave her a quick hug and stood up again. 'I did, love. Ready to go?'
'Yes, Dad.'
'You don't need do any team stuff? Talk about the match?' he asked, already walking towards the car.
'No, we do all that at school.'
'Ok.'
Alice beamed a full-beam smile and grabbed John's hand as they walked. 'I scored a goal!'
'No, you didn't, hon.'
'I did, Dad.'
They didn't break stride.
'Alice, you had a great game, but you didn't score a goal.'
Alice let go of her dad's hand. 'Did!'
'Honey, I watched the game.'
'It was before you arrived.' Her arms folded tightly in a familiar pre-tantrum gesture.
John sighed. 'I saw the whole game, sweetie. I didn't arrive late. I even drove you here.'
'Hmmph!'
'Story-tellers don't get ice-cream.'
Jaysen
Platform: Mac + Windows
Location: East-Be-Jesus-Nowhere SC, USA
John opened the door for Alice.
"Climb in and let's get headed home."
"I want chocolate with sprinkles."
Sighing to himself John started the car. "What is is with me and women? Lucy seems to be … gone, and now Alice is starting to lie to me. Is it me? Is it something I'm doing?"
"Alice, you know that telling the truth is important. I saw the game. When did you score a goal?"
The ice cream shop was just ahead. John really wanted to stop and have a treat with Alice. That would give Lucy and Kelly, John and Lucy's college friend, time to chat.
"I did score a goal. i really did. I swear."
"When did you score the goal?"
"Before you got there. When the other team was still getting to the field."
John chuckled. "Well, that was before I got there. Chocolate with sprinkles it is."
I have a wife and 2 kids that I can only attribute to a wiggle, a giggle, and the realization that she was out of my league so I might as well be happy with her as a friend. 26 years marriage later, I can't imagine life without her. -Me 10/7/09
vic-k
Location: Protesting in the nude, outside ex Red Lion TESCO Store
As he closed the front door, John called out, "Honeys. We're home", including their guest, Kelly, in the greeting. John found the unexpected silence, eerily foreboding. Hiding his unease from Alice, he smiled at her and said, "They've probably slipped out for a bit of female retail therapy." Alice replied with a quizzical look. John tutted and explained, "They've gone shopping for clothes."
Too young and of the wrong sex to appreciate her Dad's sexist banter, Alice handed him her holdall of footballing tackle to sort out, as she turned and ran into the kitchen.
It wasn't the shock of hearing Lucy and Kelly greeting Alice as she entered the kitchen, but the lack of bonhomie contained within their greetings, that stirred the butterflies in John's stomach. "What the f?"
John dropped the holdall by the kitchen door, and leant against the doorframe. "Hi". Their replies were two icy stares.
As a professional, you, are your one and only asset. Without integrity you are worthless, but with it, you are priceless.
Tue Apr 11, 2017 8:54 pm Post
"You never told me about Kelly."
"Luce... what do you mean?
"Alice, to your room."
"But mom— "
"Upstairs. Now."
A deep silence as eight-year-old shoes shuffle to top of the stairs.
"Okay. I'll bite. What the fuck did I not tell you about Kelly?"
"That the two of you slept together through most of your junior and senior years."
"We what?"
"Don't play innocent. You're lousy at it."
"Kelly, what is going on here. Did you tell Lucy...?"
"I told her we... that we were together. And we were."
"Enough. You two old flames can sit here and smoulder together."
Another pair of shoes, older ones, stomp to the top of the stairs.
"Kelly, what the hell is this? You and I never— "
"Jesus Christ, man, I tried to give you some street cred."
"Cred?"
"A back story to make you look good in a bad light, dummy."
You can't conquer stupid — or cure it — with more stupid.
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Forum - Novel in a Day
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In my hunt for pictures, which was limited to my desktop at work, my external hard drive, and my cell phone (I don't have the cord to connect my camera to my computer), I found these. They are all from my cell phone, so I apologize for the quality and randomness of them.
In honor of Towel Day, May 25, I baked a rhubarb pie that reads "Don't Panic!" and has a towel next to it. Yes, I am a dork. But I am a dork that can make pie crust from scratch!
One of the Ikea options for a buffet-like storage system for the kitchen. It's probably not going to work out.
This is a print I saw in Target that I think is cute and that I could totally reproduce myself (using the fancy GT library printers) without paying $20.
The backyard! I loooooooove the hammock that Chris' dad got me for my birthday last year. We grill, we play with the puppy, and in the background you can see where Chris burns stuff (like trees that he cuts down - I have a video somewhere of the chainsaw in action) and you can also see his teeter for mountain biking and dog trick training.
At the Dogwood Festival, I got four little dogwood saplings for $10. It supports the Friends of Piedmont Park, and we need trees anyway. One has died, but one has lots of fresh little leaves, and the other two are still green and growing leaf buds. I hope they'll survive! They're all in their own planters, too, until we can put them in the ground.
Hula is a typical cat. "Clean laundry? Now it's hairy laundry. You're welcome."
I took this after the guys did the first coat of stain. Omigosh it's so pretty!
Again, I apologize for the quality of the pictures, and I promise that we'll round up some more this weekend.


text:
Junshirō Kobayashi (jap. , Kobayashi Junshirō; * 11. Juni 1991 in Hachimantai, Präfektur Iwate) ist ein japanischer Skispringer und ehemaliger Nordischer Kombinierer. Sein bisher größter Erfolg ist der Gewinn der Bronzemedaille im Mannschaftswettbewerb bei den Skiweltmeisterschaften 2019 in Seefeld in Tirol.

Werdegang
Junshirō Kobayashi war zunächst Nordischer Kombinierer. Am 14. Dezember 2007 gab er in Høydalsmo sein Debüt und belegte den 77. Platz. Am 15. Januar 2008 gewann er in Iiyama als 18. erstmals Punkte im B-Weltcup der Nordischen Kombination. Am 10. Januar 2009 gab er im Val di Fiemme sein Weltcup-Debüt und belegte den 52. Platz. Am nächsten Tag wurde er 45. Wenig später ging Kobayashi bei der Junioren-WM 2009 in Štrbské Pleso an den Start und wurde 21. im Einzel und Achter im Team. Ein Jahr später war er erneut bei der Junioren-WM am Start, hier allerdings nur im Einzel, wo er die Goldmedaille gewann. Die Junioren-WM war in Hinterzarten. Nach der Saison 2009/10 beendete er seine Karriere als Nordischer Kombinierer und wechselte zum Skispringen.

Erstmals war er hier bei der Junioren-WM 2011 in Otepää im Einzel am Start und belegte den 18. Platz. Am Ende der Saison startete Kobayashi erstmals im FIS-Cup in Zaō und gewann beide Springen. Als Kombinierer war er bereits seit 2008 bei mehreren FIS-Rennen in Japan dabei gewesen. Am 2. Juli 2011 sprang Kobayashi in Kranj erstmals im Continental Cup und konnte mit Platz 14 seine ersten Punkte sammeln. Nachdem er eine Woche später auf der Brunnentalschanze in Stams mit Platz drei und vier gleich zwei hervorragende Platzierungen nachlegen konnte, wechselte er in den höherklassigen Sommer-Grand-Prix. Bereits bei seinem zweiten Springen am 20. Juli 2011 im polnischen Szczyrk belegte er den zehnten Rang. Nach weiteren Top-Ten-Platzierungen erreichte er in der Gesamtwertung des Grand Prix den 23. Rang. Kobayashi gab sein Weltcup-Debüt am 27. November 2011 beim Teamspringen auf der Rukatunturi-Schanze im finnischen Kuusamo, als er mit der japanischen Mannschaft Platz zwei belegte. Am selben Tag debütierte er auch im Einzelwettbewerb, in dem er auf Anhieb als 24. seine ersten Weltcuppunkte erzielen konnte. Seine beste Einzel-Platzierung im Weltcup in dieser Saison war Platz 16 in Bischofshofen. Er beendete seine erste Weltcup-Saison als 52. der Gesamtwertung mit 40 Punkten. Nachdem er in der Saison 2012/13 erneut 17 Weltcuppunkte holen konnte, ging er in der Saison 2013/14 nur als Teil der nationalen Gruppe in Sapporo im Weltcup an den Start, wo er zweimal die Punkteränge verpasste. Bei der Winter-Universiade 2013 im italienischen Predazzo belegte er auf der Normalschanze den vierten Rang. Im Mixed-Teamwettbewerb wurde er Fünfter und im Mannschaftswettbewerb Vierter. Im Einzelwettbewerb auf von der Großschanze holte er die Bronzemedaille hinter Krzysztof Biegun und Sami Niemi.

Im Sommer 2014 erzielte Kobayashi mehrere Top-Ten-Platzierungen im Grand Prix und belegte damit Platz sechs in der Gesamtwertung. Ab der Saison 2014/15 sprang er wieder regelmäßig im Weltcup. Am 12. März 2015 erzielte er sein bis dahin bestes Ergebnis im Weltcup als 13. im norwegischen Trondheim. Im Gesamtweltcup erreichte er mit Platz 44 ebenfalls sein bis dahin bestes Karriere-Ergebnis. Bei der Winter-Universiade 2015 im slowakischen Štrbské Pleso belegte er den fünften Rang im Einzelwettbewerb auf der Normalschanze. Mit seiner Schwester Yuka Kobayashi gewann er den Mixed-Teamwettbewerb und mit seinen Landsleuten Kanta Takanashi und Minato Mabuchi holte er die Silbermedaille hinter Russland im Mannschaftsspringen der Herren von der Normalschanze. Bei den Nordischen Skiweltmeisterschaften 2015 in Falun belegte er in den beiden Einzelwettbewerben den 25. Platz auf der Normalschanze und den 13. Platz auf der Großschanze. Mit der japanischen Mannschaft wurde er Vierter.

Am 13. September 2015 konnte er auf der Gorney Gigant im kasachischen Almaty sein erstes Sommer-Grand-Prix-Springen gewinnen. In den Saisons 2015/16 und 2016/17 erreichte er jeweils nur wenige Male die Punkteränge im Weltcup und kam in diesen beiden Jahren nicht über Rang 17 in Sapporo hinaus.

Am 26. und 27. August 2017 gewann er beide Grand-Prix-Springen in Hakuba. Den zweiten Wettbewerb gewann er vor seinem Bruder Ryōyū. Er beendete den Sommer-Grand-Prix 2017 als Dritter der Gesamtwertung und damit mit dem bis dahin besten Ergebnis seiner Karriere. Am 19. November 2017 holte Kobayashi beim Auftaktspringen der Saison 2017/18 in Wisła überraschend seinen ersten Weltcupsieg, nachdem zuvor lediglich ein 13. Platz sein bestes Weltcupresultat war. Er beendete die Vierschanzentournee 2017/18 als Vierter der Gesamtwertung, nachdem er bei allen vier Springen unter den besten zehn sprang (Plätze 6, 4, 6 und 7). Im Januar 2018 nahm er in Oberstdorf erstmals an der Skiflug-Weltmeisterschaft teil, wobei er im Einzelwettbewerb den 29. Rang belegte. Bei den Olympischen Winterspielen 2018 in Pyeongchang nahm er an zwei von drei Wettbewerben teil. Im Einzelwettbewerb auf der Normalschanze belegte er den 31. Platz und im Einzelwettbewerb auf der Großschanze wurde er 24. Im Mannschaftsspringen auf der Großschanze kam er nicht zum Einsatz. Neben seinem Sieg zum Auftakt erzielte er einige weitere Top-Ten-Platzierung im Weltcup und absolvierte seine mit Abstand beste Weltcup-Saison. Er belegte mit 568 Punkten den elften Rang im Gesamtweltcup. Bei den Weltmeisterschaften 2019 in Seefeld in Tirol gewann er mit seinen Mannschaftskameraden Daiki Itō, Yukiya Satō und Ryōyū Kobayashi die Bronzemedaille im Mannschaftsspringen. In den Einzelwettbewerben belegte er sowohl von der Groß- als auch von der Normalschanze jeweils den 17. Platz. Zwei Jahre später wurde er bei den Weltmeisterschaften 2021 in Oberstdorf  von der Normalschanze 29. und von der Großschanze 32.

Bei den Olympischen Spielen 2022 in Peking wurde er in den Einzelspringen von der Normalschanze 27. und von der Großschanze 24., während er mit der japanischen Mannschaft Fünfter wurde. Bei der Skiflug-Weltmeisterschaft 2022 belegte er im Einzelwettbewerb den 33. Rang und wurde mit der japanischen Mannschaft im Team-Wettbewerb Sechster.

Erfolge

Weltcupsiege im Einzel

Grand-Prix-Siege im Einzel

Grand-Prix-Siege im Team

Statistik

Weltcup-Platzierungen

Grand-Prix-Platzierungen

Privates
Junshirō Kobayashi ist der Bruder der Skispringerin Yuka Kobayashi und des Skispringers Ryōyū Kobayashi.

Weblinks

  – Nordische Kombination
  – Skispringen

Einzelnachweise

Skispringer (Japan)
Nordischer Kombinierer (Japan)
Universiadesieger (Skispringen)
Japanischer Meister (Skispringen)
Olympiateilnehmer (Japan)
Teilnehmer der Olympischen Winterspiele 2018
Teilnehmer der Olympischen Winterspiele 2022
Teilnehmer der Winter-Universiade 2013
Teilnehmer der Winter-Universiade 2015
Japaner
Geboren 1991
Mann
Universiadeteilnehmer (Japan)