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text:
Inflammatory Blockade Restores Adult Hippocampal Neurogenesis
Michelle L. Monje,
Hiroki Toda,
Theo D. Palmer*
Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, 1201 Welch Road, Stanford, CA 94305–5487, USA.
↵* To whom correspondence should be addressed. E-mail: tpalmer{at}stanford.edu
Science 05 Dec 2003:
Vol. 302, Issue 5651, pp. 1760-1765
Michelle L. Monje
Hiroki Toda
Theo D. Palmer
Cranial radiation therapy causes a progressive decline in cognitive function that is linked to impaired neurogenesis. Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes may contribute to neural stem cell dysfunction. Here, we show that neuroinflammation alone inhibits neurogenesis and that inflammatory blockade with indomethacin, a common nonsteroidal anti-inflammatory drug, restores neurogenesis after endotoxin-induced inflammation and augments neurogenesis after cranial irradiation.
The birth of new neurons within the hippocampal region of the central nervous system continues throughout life, and the amount of neurogenesis correlates closely with the hippocampal functions of learning and memory (1, 2). The generation of new neurons within the hippocampus is mediated by proliferating neural stem or progenitor cells (NPC) (3–5) that are widespread within the adult brain but instructed by local signaling to produce neurons only in discrete areas (6, 7). Alterations in the microenvironment of the stem cell may allow ectopic neurogenesis to occur (8, 9) or even block essential neurogenesis, leading to deficits in learning and memory (10–12) such as that observed in patients who receive therapeutic cranial radiation therapy (13). In animal models, cranial irradiation ablates hippocampal neurogenesis, in part by damaging the neurogenic microenvironment, leading to a blockade of endogenous neurogenesis (12, 13). Injury induces pro-inflammatory cytokine expression both peripherally and within the central nervous system and induces stress hormones, such as glucocorticoids, that inhibit hippocampal neurogenesis (10). The extensive microglial inflammation and release of proinflammatory cytokines that accompanies this irradiation-induced failure suggests that inflammatory processes may influence neural progenitor cell activity (12, 14, 15).
To determine the effects of inflammation on adult hippocampal neurogenesis, we injected bacterial lipopolysaccharide (LPS) into adult female rats to induce systemic inflammation (16–19). The intraperitoneal (i.p.) administration of LPS causes a peripheral inflammatory cascade that is transduced to the brain via interleukin 1β (IL-1β) from the cerebral vasculature (16) and causes a strong up-regulation of central pro-inflammatory cytokine production (16, 19). After LPS exposure, rats were treated systemically with bromo-deoxyuridine (BrdU) for 6 days to label proliferating cells within the hippocampus. Animals were then killed on day 7. The fate of the BrdU-labeled, proliferative cells was analyzed with immunofluorescent staining and confocal microscopy.
Using confocal analysis, we found that peripheral LPS exposure resulted in a 240% increase in the density of activated microglia (CD68+/ED1+) in the dentate gyrus (Fig. 1, A to C, and F). In normal animals, few ED1+ cells are found. The neuroinflammation achieved in the LPS paradigm was accompanied by a failure to recruit proliferation within the perivascular space, as indicated by an increase in the average distance between dividing cells (Fig. 1, B, C, and H) as well as a 35% decrease in hippocampal neurogenesis (Fig. 1, D, E, and G), as determined by the proportion of nonmicroglial BrdU+ proliferative cells that co-express the early neuronal marker doublecortin (Dcx).
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Inflammation inhibits hippocampal neurogenesis. LPS (1 mg/kg, i.p.) was given to induce a systemic inflammatory response, followed by daily injections of BrdU for 6 days to label proliferating cells. Some rats were given the anti-inflammatory drug indomethacin twice each day (2.5 mg/kg, i.p.) starting concurrently with LPS and continuing for the 1-week paradigm. (A) Schematic depicting the anatomic location of the dentate gyrus of the hippocampus within the rodent brain. The neurogenic region of the hippocampus, the granule cell layer, is highlighted in red. To the right, a confocal photomicrograph shows detail of the dentate gyrus stained for the immature neuronal marker Dcx (red) and BrdU for proliferative cells (green). Immature neurons line the subgranule zone at the junction between the granule cell layer and the hilus of the hippocampal dentate gyrus. Bar, 100 μm. (B and C) Confocal micrographs of vasculature (tomato lectin, blue), BrdU-labeled cells (green), and activated microglia (ED-1, red). Proliferative cells are clustered in large groups proximal to the vasculature in naïve animals (B), but clustering and proximity to the vasculature is decreased in concert with striking activation of microglia after LPS treatment (C). Bar, 30 μm. (D and E) BrdU-labeled newborn neurons (BrdU, green; Dcx, red) are abundant in naïve animals (D) but are significantly reduced after systemic LPS exposure (E). (F) Density of activated microglia (ED1+) in the granule cell layer and subgranule zone. Data are expressed as ED-1 positive cells per mm2 in a 40-μm section. Systemic LPS exposure significantly increases the density of activated microglia (P < 0.05; n = 3); treatment with indomethacin decreases this inflammatory response. (G) Neuroinflammation induced by systemic LPS inhibits neurogenesis (P < 0.05; n = 3), as determined by phenotype-specific immunohistochemistry and confocal analysis. Anti-inflammatory therapy with indomethacin restores neurogenesis after LPS exposure (P < 0.05; n = 3). Data are expressed as the percent of nonmicroglial proliferating cells (BrdU+/ED-1–) that co-express Dcx at the end of a 1-week BrdU labeling paradigm. (H) Inflammation causes dissociation of the normal relation between proliferating cells and the microvascualture. The average distance from the middle of a BrdU+ nucleus to it nearest tomato lectin–stained vessel was significantly increased in the context of inflammation (P < 0.05; n = 6); indomethacin restores the vascular association (P < 0.05; n = 3). Distance measurements were performed on 40-μm sections as measured in the x and y plane. Proliferating microglia (BrdU+/ED-1+) were excluded from the distance measurements.
Inflammation in the central nervous system is effectively managed using steroidal anti-inflammatory drugs, yet it is clearly demonstrated in rodents that corticosteroids are potent inhibitors of neurogenesis and their use in the context of augmenting neurogenesis would be strongly contraindicated. To determine whether inflammatory effects could be countered pharmacologically, animals were treated concurrently with a single dose of intraperitoneal LPS and daily doses of the nonsteroidal anti-inflammatory drug (NSAID) indomethacin [2.5 mg/kg, i.p., twice each day]. The effect of peripheral LPS exposure on neurogenesis was completely blocked by systemic treatment with indomethacin, whereas indomethacin alone had no effect on neurogenesis in control animals (Fig. 1, G and H).
Neuroinflammation could inhibit neurogenesis by a variety of mechanisms, including stimulation of the hypothalamic-pituitary-adrenal (HPA) axis with subsequent elevation of glucocorticoids, alterations in the relations between progenitor cells and cells of the neuro-vasculature, or direct effects of activated microglia on the precursor cells. To determine the extent to which microglial activation might directly affect neural stem or progenitor cells, microglia were stimulated in vitro with LPS. LPS is a potent activator of microglia and up-regulates the elaboration of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor–α (TNF-α). LPS-stimulated or resting microglia were then co-cultured with normal neural stem cells from the hippocampus under conditions that typically stimulate the differentiation of 30 to 40% of the progenitor cells into immature Dcx-expressing neurons (normalized to a value of 1 in Fig. 2A, control). Neurogenesis in the presence of microglia was assessed as the increase or decrease in Dcx-expressing cells relative to control. Co-culture with activated but not resting microglia decreased in vitro neurogenesis to approximately half of control levels (Fig. 2A). LPS added directly to precursor cells had no effect on neurogenesis (20).
Activated microglia inhibit neurogenesis via soluble factors that include IL-6. (A) Co-culture with microglia (MG), conditioned media (CM) or exposure to recombinant IL-6 decreases neuronal differentiation in vitro. GFP+ neural progenitor cells (NPCs) were induced to differentiate for 60 hours in the presence or absence of MG that were cultured under nonstimulated conditions (–) or stimulated with LPS for 24 hours before co-culture (+). NPCs were also treated with CM from these same microglial cultures, CM from activated MG pre-mixed with a blocking antibody to IL-6 (αIL6), or recombinant IL-6 in the presence or absence of blocking antibody. Data were collected as the fraction of GFP-expressing cells (NPCs) that co-express the early neuronal marker doublecortin. Co-culture with unstimulated microglia (–MG) had no effect on neuronal differentiation (Student's t test, P = 0.53). Co-culture with LPS-stimulated microglia decreased neurogenesis (P < 0.05, relative to control or microglial co-culture) as did CM from activated but not resting microglia (Student's t test, P < 0.05). A blocking antibody to IL-6 abrogates the CM effects and IL-6 alone (50 ng/ml) reproduced effects of activated microglial CM in reducing neurogenesis (P < 0.05; n = 3). Data are expressed as the fraction Dcx+ cells relative to untreated control cultures. (B to D) Confocal micrographs of representative NPC cultures stained for GFP (green) and Dcx (red). (B) Naïve cells. (C) Cells exposed to conditioned media from activated microglia. (D) Cells exposed to IL-6 (50 ng/ml). Bar, 15 μm. (E) Cell fate profile after IL-6 exposure. NPCs were induced to differentiate for 60 hours in the presence of IL-6 (50 ng/ml), and the percentage of cells expressing lineage-specific markers for neurons (type III β-tubulin, βTubulin), astroctyes (GFAP), and immature oligodendrocytes (NG2) was analyzed. Data are expressed as the fraction of cells positive for a given marker normalized to untreated controls. IL-6 caused a significant decrease in the proportion of cells adopting a neuronal fate (P < 0.05; n = 3), whereas astrogliogenesis and oligogliogenesis were unaffected. (F) TUNEL staining in Dcx+ cells. As in (A), cultures were treated with conditioned medium from LPS-stimulated microglia or treated directly with recombinant IL-6 (50 ng/ml). TUNEL was then scored in the total population, as well as within the subset of cells that had adopted a neuronal phenotype (F). Apoptosis increased significantly overall but not to a larger extent in neurons relative to nonneuronal cells.
To determine whether this effect was due to soluble factors or due to cell-cell contact, hippocampal precursor cells were differentiated in the presence of media preconditioned by resting or activated microglia. A similar decrease in neurogenesis was found when precursor cells were exposed to the conditioned medium (CM) from activated microglia (Fig. 2, A and C), indicating that activated microglia produce soluble antineurogenic factors.
Activated microglia produce the potent pro-inflammatory cytokines IL-1β, TNF-α, interferon-γ (INF-γ), and IL-6. Progenitor cells were allowed to differentiate in the presence of each cytokine, and the relative expression of Dcx was scored after 60 hours. Exposure to recombinant IL-6 (50 ng/ml) (Fig. 2, A, D, and E) or to TNF-α (20 ng/ml) (20) decreased in vitro neurogenesis by approximately 50%, whereas the effects of IL-1β or INF-γ were not significant (20). Addition of neutralizing anti–IL-6 antibody to CM from activated microglia was able to fully restore in vitro neurogenesis (Fig. 2A). This implicated IL-6 as a key inhibitor of neurogenesis in microglial CM. Although recombinant TNF-α also suppressed neurogenesis, IL-6 blockade alone appeared sufficient to restore neurogenesis in the presence of microglial CM. In contrast to neurogenesis, gliogenesis was unaffected by IL-6 exposure, as indicated by the lack of change in the number of cells expressing the astrocyte [glial fibrillary acidic protein (GFAP)] or early oligodendrocyte (NG2) markers relative to control cultures (Fig. 2E). The hippocampal precursors used here do express the IL-6 receptor, as confirmed by reverse transcriptase–polymerase chain reaction (RT-PCR) (fig. S1).
TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling) was used to determine the potential effects of microglial CM or IL-6 on cell death. Microglial CM and IL-6 significantly increased the fraction of TUNEL-positive apoptotic cells in each differentiating culture (control, 0.013 ± 0.007; CM, 0.092 ± 0.023; IL-6, 0.068 ± 0.005; mean ± SEM; n ≥3). Although this increase was substantial, there was no increase in the relative apoptotic index within Dcx+ versus Dcx–cells, indicating that cell death was unlikely to select specifically against newborn neurons in vitro (Fig. 2F). The fraction of TUNEL-positive cells that co-labeled with Dcx was 0.92 ± 0.11 for controls (almost all TUNEL-positive profiles are also immunoreactive for Dcx), 0.89 ± 0.07 of TUNEL profiles were Dcx+ in cultures treated with microglial CM, and 0.83 ± 0.02 (mean ± SEM) in cultures treated with IL-6 (fig. S1).
Mitotic index (fraction of cells labeled with BrdU in 24 hours) in stem cell cultures was unaffected either by CM from stimulated microglia or by IL-6 (92 ± 2.8% in controls versus 95 ± 0.7% in CM or 95 ± 1.7% in IL-6 treated cultures). When the subset of spontaneously forming immature neurons was independently evaluated, there was a subtle but nonsignificant trend to reduced BrdU labeling within the neuronal progeny (88 ± 7.6% in controls versus 82 ± 1.6% in IL-6 treated cultures). Thus, the effect of IL-6 on in vitro neurogenesis appears to induce both a nonspecific decrease in cell survival as well as decreased accumulation of neurons, most likely due to reduced neuronal differentiation rather than selective changes in the proliferation or death of neuroblasts or immature neurons. These findings, taken together with the effect of IL-6 overexpression in transgenic mice (15), implicate IL-6 as a potential regulator of hippocampal neurogenesis in neuroinflammation.
Signaling via gp130, the co-receptor of the IL-6 receptor, stimulates the Notch1 pathway (21–24), resulting in an increase in expression of the mammalian homolog of hairyenhancer-of-split (Hes 1) transcription factor (25, 26) and antagonism of pro-neural basic helix-loop-helix (bHLH) genes and hippocampal neurogenesis during development (27, 28). To determine whether IL-6 treatment of adult stem cells leads to an increase in Hes 1 consistent with the reduction in neuronal cell fate, we performed "real-time" quantitative RT-PCR on total RNA extracted from neural precursors exposed for 60 hours to activated microglial CM or IL-6. Both CM and IL-6 caused a dramatic increase in Hes1 mRNA expression (3.2- and 7.7-fold increase respectively, relative to control).
Next, we used the irradiation model to determine the relative role of inflammation in this irradiation-induced deficit. Adult rats were treated with indomethacin beginning 2 days before 10 Gray (Gy) cranial irradiation with x-rays (x-irradiation) and continuing daily for 2 months thereafter. Because rats are more radio-resistant than humans, 10 Gy approximates a clinically relevant dose and is below the threshold to cause demyelination or overt vasculopathy in rats (29–32). This dose of x-irradiation spares roughly 30% of the NPC proliferative activity but completely ablates the production of neurons (12). X-irradiation was limited to a 1.5-cm cylinder centered over the cranium (remaining body parts were shielded). One month later, BrdU was administered systemically and, at 2 months after irradiation, brain tissues were analyzed for hippocampal neurogenesis.
As previously reported, (12) irradiation caused a striking inflammatory response characterized by the persistence of activated microglia (Fig. 3, A to C) relative to the minimal levels in normal control animals. Unbiased stereologic quantification of CD68+/ED1+ activated microglia in irradiated animals revealed that indomethacin treatment caused a 35% decrease in activated microglia per dentate gyrus (Fig. 3A). Many of these microglia were proliferative, and a large fraction of all dividing cells within the dentate gyrus were labeled for the monocyte or microglia marker CD11b, which labels both activated and resting microglia (Fig. 3D). A subpopulation of CD11b+ microglia co-expressed the marker NG2 (Fig. 3, C and D; fig. S2), which represents peripheral blood monocytes or microglia that contribute to chronic neuroinflammatory lesions within the brain (33, 34). Indomethacin was particularly effective at decreasing this CD11b+/NG2+ subpopulation of infiltrating, proliferating peripheral monocytes after irradiation (Fig. 3D), suggesting an indomethacin-induced change in chemokine and/or integrin signaling that recruits transendothelial migration of immune cells after injury.
Indomethacin decreases microglial inflammation after irradiation. Microglial proliferation and activation in nonirradiated (NIR) and irradiated (IR) hippocampi. Indomethacin (IND, ± 2.5 mg/kg) administered orally every 12 hours beginning the day before and for 2 months after irradiation. All groups received BrdU once a day for 6 days starting 4 weeks after irradiation. Animals were killed 2 months after irradiation. (A) Unbiased stereologic quantification of ED1-positive activated microglia per dentate gyrus demonstrates that indomethacin reduces the total number of activated (ED1-positive) microglia per dentate gyrus by roughly 35% (n = 4 animals per group; Student's t test, P < 0.05). (B and C) Examples of BrdU-labeled (red) microglia (CD11b, green) that are either negative (B) or positive (C) for NG2 (blue). The NG2 epitope is known to be expressed by peripheral monocytes that are recruited into the brain during inflammation (33, 34). Bar, 25 μm. (D) Quantification of microglia and invading peripheral monocytes in IR or NIR animals concurrently treated with indomethacin (±). Irradiation caused a dramatic increase in proliferating microglia (CD11b+/BrdU+ cells) in the granule cell layer and subgranule zone of irradiated animals relative to nonirradiated controls (n = 4 animals per group; Student's t test, P < 0.000001). Indomethacin had little effect on the relative fraction of BrdU-labeled cells that were microglia after irradiation but significantly reduced the activation state (A) and the relative number of cells that were recruited from the periphery (NG2+/CD11b+ monocytes, P < 0.05, Student's t test; n = 4).
If inflammation were the primary cause of the lack of neurogenic signaling within the dentate subgranule zone (SGZ), then inflammatory blockade would be expected to restore neurogenesis. Confocal microscopy was used to analyze the proportion of proliferative (BrdU+) cells that co-express markers (Fig. 4A) for mature neurons (NeuN) (Fig. 4B), immature neurons (type III beta tubulin) (Fig. 4C), astrocytes (GFAP) (Fig. 4D), and immature oligodendrocytes (NG2+/CD11b–) (Fig. 4E). Indomethacin treatment in nonirradiated rats had no effect on cell fate relative to untreated, nonirradiated controls. As previously reported (12), irradiation decreased the proportion of proliferative cells adopting a neuronal fate (Fig. 4A). Indomethacin treatment during and after radiation exposure partially restored the relative proportion of proliferative cells adopting a neuronal fate relative to untreated, irradiated animals (37% versus 15%, respectively) (Fig. 4, A to C).
Anti-inflammatory therapy restores neurogenesis after irradiation. Effect of indomethacin on newborn cells within the SGZ and GCL. NIR, white bars; IR, black bars. Indomethacin (±2.5 mg/kg) was administered orally every 12 hours beginning the day before and for 2 months after irradiation. (A) Relative proportion of proliferative cells adopting a recognized cell fate (NeuN, mature neurons; Tuj1, immature neurons; GFAP, astrocytes; NG2+/CD11b–, immature oligodendrocytes). Data are expressed as means ± SEM; n = 4 animals per group. Anti-inflammatory therapy with indomethacin increased the relative proportion of the proliferative cells adopting a neuronal phenotype by 2.5-fold (Student's t test, P < 0.01). (B to E) Representative confocal micrographs of BrdU-labeled (B) mature neurons (NeuN, green; GFAP, blue; BrdU, red), (C) immature neurons (type III β tubulin, blue; NG2, green; BrdU, red); (D) astrocytes (GFAP, green; NeuN, blue); and (E) oligodendrocytes (NG2, green, CD11b, blue; BrdU, red). Bars, 10 μm. (F) Increase in total number of newborn neurons per GCL plus SGZ in irradiated animals treated with indomethacin. Unbiased stereologic quantification of BrdU+ cells adjusted for fraction of BrdU+ cells adopting a neuronal phenotype (NeuN+ plus Tuj1+). IR, irradiated; IR+Indo, irradiated, indomethacin treated. Anti-inflammatory therapy substantially increases the absolute number of newborn neurons per hippocampus (Student's t test, P < 0.01). (G) Inflammation negatively correlates with the accumulation of new neurons. The fraction of dividing cells adopting a neuronal phenotype is inversely proportional to total number of activated microglia per dentate gyrus. Each data point represents one irradiated animal. Control irradiated animals, black diamonds; indomethacin-treated irradiated animals, gray squares.
Unbiased stereological quantification of total BrdU+ proliferative cells per neurogenic region [granule cell layer (GCL) plus subgranule zone (SGZ)] of the dentate gyrus revealed no significant difference in overall proliferation between indomethacin-treated and untreated irradiated animals (958 ± 136 proliferative cells versus 828 ± 135 proliferative cells, respectively; control animals exhibited 1938 ± 429 proliferative cells per neurogenic region). Correcting the fraction of proliferative cells adopting a neuronal fate for the total number of proliferative cells yields a significant increase in total newborn hippocampal neurons in indomethacin-treated, irradiated animals compared with untreated, irradiated animals (360 ± 68 newborn neurons versus 125 ± 25 newborn neurons, respectively) (Fig. 4F). This is a substantial increase in neurogenesis but still is only 20% to 25% of the neurogenesis observed in naïve animals (∼1600 newborn neurons).
To describe further the relation between microglial inflammation and neurogenesis, we plotted neurogenesis against activated microglial load for each irradiated animal (Fig. 4G). Neurogenesis and inflammation show a striking negative correlation (R= – 0.93 for activated microglial loads above 1000 per dentate gyrus; activated microglial load was ∼500 in controls), suggesting that the extent of inflammation has a direct titrating role on neurogenesis within the adult dentate gyrus.
Our data indicate that inflammation itself can suppress neurogenesis and that chronic inflammation after radiation treatment contributes to the neural stem cell dysfunction that is linked to a progressive postirradiation decline in learning and memory. Chronic microglial activation and peripheral monocyte recruitment with the accompanying increase in local pro-inflammatory cytokine production, including IL-6, emerge as potent antineurogenic components of brain injury. Both IL-6 and the IL-6 receptor-gp130 complex are expressed in the postnatal hippocampus (19, 35), overexpression of IL-6 in the hippocampus suppresses neurogenesis (15), and hippocampal expression of the IL-6 receptor increases after systemic challenge with LPS (19). IL-6 promotes both astrogliogenesis (36) and oligodendrogliogenesis (37) and may divert stem cells into a glial program at the expense of neurogenesis after radiation. We find that gliogenesis is relatively well preserved in the irradiated microenvironment (Fig. 4A), and the in vitro data suggests that IL-6 inhibition of neurogenesis is primarily due to a blockade in neuronal differentiation rather than selective influences on cell death or proliferative activity.
Inflammatory blockade with indomethacin decreased microglial activation, accounting for part of the restorative effect of this treatment on neurogenesis after irradiation. However, inflammatory blockade is accompanied by a broad spectrum of effects that could influence neurogenesis in several ways (fig. S3). Restoration of neurogenesis with inflammatory blockade may reduce newborn cell death (38) and/or attenuate HPA axis activation (39, 40). The subsequent decrease in pro-inflammatory cytokines and serum glucocorticoid levels may contribute to restored neurogenesis (41, 42). In addition, the microvasculature of the hippocampus is a critical element of the neurogenic microenvironment (43–45) and both endotoxin and irradiation-induced inflammation disrupts the association of proliferating progenitor cells with microvessels (12). The recruitment of circulating inflammatory cells is highly dependent on the endothelial status and elaboration of chemokines. One of the most robust effects of indomethacin in the present paradigm is the reduction in peripheral monocyte recruitment, suggesting that the inflammatory status of endothelial cells [e.g., expression of chemokines and/or ICAM (intercellular adhesion molecule)] may be normalized by indomethacin. Indeed, one known attribute of indomethacin treatment is the normalization of vascular permeability (46), which likely affects the neurogenic vascular microenvironment.
Neuroinflammation and microglial pathology are associated with many diseases of cognition in which memory loss features prominently, such as Alzheimer's Disease, Lewy Body Dementia, and AIDS Dementia Complex (47–49). Further, serum IL-6 levels in humans correlate with poor cognitive performance and predict risk of dementia (50). Clinical treatment with indomethacin and other NSAIDs ameliorates the risk and/or progression of memory loss (51, 52). Our findings may shed some light on the potential contribution of inflammation-induced neurogenic blockade to memory pathology and on the mechanism of the beneficial effects of NSAID treatment in certain dementias.
Supporting Online Material
www.sciencemag.org/cgi/content/full/1088417/DC1
Figs. S1 to S3
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T. D. Palmer, A. R. Willhoite, F. H. Gage, J. Comp. Neurol. 425, 479 (2000).
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I. R. Mackenzie, Neurology 55, 132 (2000).
B. J. Brew, Neurol. Clin. 17, 861 (1999).
J. D. Weaver et al., Neurology 59, 371 (2002).
J. Rogers et al., Neurology 43, 1609 (1993).
B. A. in t' Veld et al., N. Engl. J. Med. 345, 1515 (2001).
We thank T. Wyss-Coray for his gift of BV-2 microglial cells; B. E. Hoyte for help with manuscript graphics; R. Malenka for use of the Pritzker Foundation confocal microscope; B. D. Hoehn and S. P. K. Samagh for technical assistance; and S. K. McConnell, W. C. Mobley, M. Tessier-Lavigne D. Schall, O. Mitrasinovic and P. G. Fisher for valuable insights. We would also like to thank C. Ekdahl, Z. Kokaia, and O. Lindvall and colleagues for their helpful discussion of parallel findings in models of epilepsy. Supported by grants MH20016-05 from the National Institutes of Mental Health, F30 NS04696701 from the National Institutes of Neurological Disorders and Stroke, and Palmer Lab Start up funds from the Department of Neurosurgery, Stanford University.
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Back to that Time top 100 list, we decided to go head to head and compare our high school educations. Monica edged me out at 16 to 12. But there's a link on the side to the top ten graphic novels. There we're both at 80% (or I will be, once I finish off Bone — I just don't want it to end).
Been up to all sorts of comic-related stuff that doesn't actually involve working on this comic. Last weekend, we joined some fellow 7000 BC members in running a comic workshop at a teen center at the town north of here. We went straight from there to an opening at Feral Gallery where the group had a table and conducted a respectable amount of business and met a bunch of interested folks. Monday found more of us back at IAIA for the second part of a workshop for an English comp class there. And now we're gearing up for an event next weekend at Sol Arts in Albuquerque.
Matt was kind enough to mail a couple of issues of Wonka Vision, the Philly-based indy music magazine. Their latest (not on their Web site) features art and design, and has a nice one-page article (with photos) on the DC Conspiracy. Available at Tower Records and Newbury Comics and the like.
I was tipped off to this major comics exhibit a while back by my inside source at the Hammer, and been waiting ever since. Looks to be a thorough look at the a century of the medium. Hope to get out there early next year.
As noted on Icarus, Time has compiled a list of the 100 greatest English novels (since the founding of the magazine), and Watchmen was on it. A solid choice, pretty bold sticking a comic in there — and good, as it greatly helped me improve my total. Recently pulled out V for Vendetta for a re-read, and was impressed with how well it held up. What little I've read about the movie has me expecting the worst, but the trailer is pretty seductive.


KUALA LUMPUR: AirAsia 's online reservation services will be unavailable at certain times over the weekend as the airline will be upgrading its system.
In a statement today, AirAsia said it will be upgrading its Navitaire New Skies reservation system as part of its ongoing effort to improve its guest online experience.
"Flight booking will be unavailable during this period from 2.00pm (GMT +8) on Saturday, 16 February 2019 to 3.00am on Sunday, 17 February 2019 on airasia.com, AirAsia mobile app, AirAsia sales offices, counters and call centres," it said.
"Guests will also not be able to perform self-check in via the web, mobile app and airport kiosks or manage their bookings until the upgrade is completed."
The airline advised all guests flying during this period to check-in online ahead of the upgrade period and to print out their boarding passes or use the E-Boarding pass where available.
"Web and mobile check-in are available from 14 days prior to departure for all AirAsia and AirAsia X flights," it said.
"Guests are also encouraged to be at the airport at least 3 hours before their flight to avoid any travel inconvenience."


text:
Q: When do you use the plural form for nouns that are generally considered uncountable? When should the plural form of the nouns combustible, material and liquid be used?

A: The plural form is used when the speaker wishes to emphasize a reference to different types of the mass noun in question.
At least in Am. E., "combustible" most often plural when it is used as a noun ("Put the combustibles in that closet") unless you are really singling out one category ("Is gasoline a combustible?", and even that sounds a little odd).
Since it is used more and is a more general term, "material" sometimes can refer to more than one type, where it is just referring to general stuff ("We'll need more material to build a house") but could just as easily be plural if you want to emphasize that it's not just one type ("We'll need more materials to build a house"). Liquid is similar, "Liquids go under the sink" implies a grouping of different liquids, but if it is all of one type, or the type is not important, then singular: "The host of You Can't Do That On Television was covered in liquid".

A: There is a very common construction in English that pluralizes mass nouns.
Of course, mass nouns don't take plurals normally, but that's the point -- if an unused
construction is floating around, it's very likely to be appropriated for special purposes.
There is no grammatical difference; mass nouns form plurals just like count nouns.
So countification of a mass noun X normally takes one of these semantic shapes:

*

*Vast extenses of X: the seas, the deserts, the slops, the shits

*Several different kinds of X: seven liquids, three combustibles, eighteen materials
(This is the second kind.)

There is also massification of a count noun Y, relating to some property of Y:

*

*more leg, not so much airbrush, dinner all over the wall

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Great question that pops up on the coin and paper side often.
Even greater responses! Thanks to you all.
It's hard not to pull the trigger too quick and learn, learn, learn. If I miss something, oh well, something else will come along.
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back to top The Long Range Identification and Tracking (LRIT) system is a designated International Maritime Organization (IMO) system designed to collect and disseminate vessel position information received from IMO member States ships that are subject to the International Convention for the Safety of Life at Sea (SOLAS).
As with all major modern day industrial networks, there is a shift happening in Maritime Industry towards implementing modern fiber / Ethernet networks. In previous years, the industry typically viewed cruise or ship Ethernet networks as "IT infrastructure" and saw this primarily as a cost center. However, today rugged and heavy duty VoIP telephones represent a highly cost effective way for rig & ship owners to future-proof their fiber network for expansion using open standards whilst improving their offshore communications.
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back to top Information provided by AIS equipment, such as unique identification, position, course, and speed, can be displayed on a screen or an ECDIS. AIS is intended to assist a vessel's watchstanding officers and allow maritime authorities to track and monitor vessel movements.
back to top Gyro Compass a type of non-magnetic compass which is based on a fast-spinning disc and rotation of the Earth to automatically find geographical direction. These are widely used for navigation onships, because they have two significant advantages over magnetic compasses.
Voyage data recorder, or VDR, is a data recording system designed for all vessels required to comply with the IMO's International Convention SOLAS Requirements in order to collect data from various sensors on board the vessel. It then digitizes, compresses and stores this information in an externally mounted protective storage unit. The protective storage unit is a tamper-proof unit designed to withstand the extreme shock, impact, pressure and heat, which could be associated with a marine incident (fire, explosion, collision, sinking, etc.).
back to top Emergency Position Indicating Radio beacons (EPIRB) distress radio is one of the best mechanisms operative to help adventure enthusiasts and explorers keep in touch with the world. Ships could keep in touch with the mainland without the fear of getting lost in the oceans.
back to top The use for CCTV aboard ship is fast becoming an important aid to the safety and security of the crew, passengers and the vessel itself. Whether your aboard a Trawler or other fishing vessel, a private Yacht or even a luxury cruise liner CCTV has an important part to play.
3mushrooms Marine is a branch of a successful growth of 3mushrooms Group, founded back in 2007 to meet the demands of the growing marine Industry. 3mushrooms Marine is the next generation of providing innovative, reliable and cost effective broadband solutions that can travel with you worldwide. We have developed and fine-tuned successful solutions that; not only are functional, but also provide the proper grounds for future expansion. Adaptability, quality of work paired with the software development expertise are some of the factors that make us a future leader and a role model for our competitors.


I am creating this profile on behalf of my sister. She is currently working in the private sector as an administrative professional, after having completed her bachelor's degree. We come from an upper middle class family with moderate family values. We belong to joint family currently living in Bangalore.
I have completed my Bachelor's degree. I am currently not working and I live in Pune. I come from a rich, nuclear family background with moderate values.
Smart, well traveled, well read, working in an MNC in Bangalore. I am an extrovert with varied interests and believe in trying things once. Seeking someone to have interesting conversations with and a companion to discover the as yet unexplored.
My daughter is self-employed with a Bachelor's degree currently living in Bangalore. We come from a Middle class, Nuclear family background with Moderate values.
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My brother is a businessperson with a Bachelor's degree currently living in Bangalore. We belong to a middle class, nuclear family with moderate values.
I am a self-made man that has been through a lot of challenges in life and quote "If life throws lemons at you make lemonade" pretty much sums up my life so far! Born and raised in a joint Gujju family in Mumbai; completed Diploma in Instrumentation Engg from New Mumbai and continued to pursue graduation by joining AMIE; its currently stalled on last semester primarily due to job. But have attained Technology certifications and attempting few more to ensure brightest and best opportunities are there for me. Currently working with one of the software cloud based MNC in Bangalore and have enjoyed working in the same company for last 12 years . I don't believe in entering a rat race to acquire material comforts and would rather pay attention to building closer relationships with family and friends. But at the same time i stay focused on my career ambitions. I am a health conscious person and like to hit the gym but its on and off. Reading is not my forte but to ensure i am not missing everything i try to get it through media library/YouTube. Not at all a good cook but can do a bit with eggs most of the times to keep the hunger away. Try to keep myself updated on the economy and social issues. Like to watch movies play/watch Cricket like travelling places do a bit of ppl photography love spending weekends with family /friends- socialize a bit.


A multi-award winner, Manchester holds several wins and nominations in both national and international festivals. His debut feature film drama, The Things We've Seen, is available for purchase on Amazon Prime, iTunes, and GooglePlay.
Based out of Chicago, IL.
Copyright © 2018 Tré Manchester. All rights reserved.


text:
Boston filmmakers Steffen and Christian Pierce will be at HFA
Harvard's Faculty of Arts and Sciences votes to change the name Division of Engineering and Applied Sciences to School of Engineering and Applied Sciences
Boston filmmaking brothers Steffen and Christian Pierce will screen their second and latest movie, "Marrakech Inshallah," at 7 p.m. Saturday (Dec. 16) at the Harvard Film Archive, 24 Quincy St., and answer questions afterward. ($8 general public, $6 students and senior citizens.)
Shot in Arabic and Berber using local actors, the 90-minute film is about two young brothers who hitchhike from their mountain village across a stunning desert landscape to Marrakech, only to end up on the streets. "The viewer becomes drawn into the poverty, the magic, and the struggles of their everyday lives," said Steffen Pierce in an interview with NewEnglandFilm.com. Their lives, he said, "are torn between the traditions of the past and encroaching Western consumer values." (Steffen is assistant curator at the Harvard Film Archive.)
The Inshallah of the title is "God willing" in Arabic, a frequently used expression in the Muslim world. It represents a sense of fate that is largely absent in the West, with its cultural imperative that people be individualistic and have their lives in their own hands.
"Marrakech Inshallah," which may be the last feature movie shot on Super 8, was filmed over three months in the Moroccan cities of Marrakech, Rich, and Essouaira.
Morocco was also the setting of the first film by the Pierce brothers, a documentary titled "The Bride Market of Imilchil" (1987). Returning to the United States after filming, they discovered their subjects had all been arrested for questioning by Moroccan authorities.
Because of that experience, "Marrakech Inshallah" evolved into a meditation not only on Morocco, but on the responsibilities documentary filmmakers have to their subjects.
– Corydon Ireland


text:
Why the roaring 20s are coming to Austin sooner than you think
By On Feb 24, 2021
I am sure that, like me, you have seen and heard the numerous comparisons between Spanish flu and COVID-19. You've probably also read one of the many pieces that discuss the likelihood of being prepared for a repeat of the 20s that followed the eradication of this pandemic some 100 years ago and a new era of artistic expression, consumer culture , initiated, manufacturing, technological innovation and urban living.
To be honest, if the recent winter storm is a sign of it, we really don't know what we're getting into. And with fewer than 15 percent of Americans having received a vaccine (and even fewer in Western European countries), the pessimistic view is that we still have a long way to go before we see the promised euphoria of this decade. But listen to me: given that the pandemic has already caused much agony to families around the world – I just lost my grandmother to the virus myself – I want to offer you the much-needed dose of optimism on this matter.
To imagine what our own Roaring '20s would look like here in Austin, you first need to inventory the similarities between that era and our current circumstances. For starters, the 1920s saw an influx of people transitioning from the rural and agricultural lifestyle to a more modern city life, in close proximity to job opportunities. We can relate to this: Austin has been the fastest growing subway area in the country for more than a decade. This phenomenon is fueled by people flocking here from smaller Texas cities and major US cities in hopes of joining our growing technology-minded workforce.
There was also a media switch in the 1920s as sound became an important part of movies and more or less put silent filmmaking out of business. With that in mind, Netflix and its streaming peers may not be closing the doors of our beloved Alamo Drafthouse (thanks to a unique business model that focuses on pre-show content and delicious food), but national chain theaters like AMC and Cinemark are undoubtedly feeling probably the pain. When we look at 2030, it's easy to imagine a vastly different movie industry – one that has networked TV shows like Queer Eye, 911: Lone Star, and a restart of Walker, Texas Ranger all filming here The capital should be a blessing.
Of course, more weighty parallels also play a role here. In 1928, the city of Austin implemented a new "master plan" that triggered changes that affected local governance and shaped the city's dynamism for decades. The decision that separated all black and Latin American Austinites east of I-35 resulted in devastating cultural and financial results, including redlining and lack of urban investment that left the East Side vulnerable to rampant gentrification. Today, as Austin continues to grapple with race and justice issues, it also faces unprecedented challenges, ranging from homelessness to endless traffic – things that are being fueled by upcoming election initiatives in May to a possible camping ban and efforts to bring more civic responsibility into the world Laying hands could be influenced by local elected officials.
You understand: if ever there was a city best suited for its own Roaring 20s moment, it is Austin. But to seize this moment and make this the best decade this city has ever seen, we must also learn from the mistakes and painful damage that also occurred in the 1920s. After all, the roaring 20s weren't just jazz parties and great American novels. Rather, its economic and social policies also led to the misfortune of the Great Depression, to racially motivated lynchings and murders of black families throughout the South, and to national trauma that tainted America long after World War II.
With that in mind, I have one clear thought – more of a request – how best to approach our own 20s here in Austin as a plan (and hope) for a future of uninterrupted growth. If we want to roar in the 2020s, let's roar about something useful.
Let's have a Roaring '20s that overwhelms our "Buy Local" consumer culture. Let us experience a roaring 1920s that brings us a new creative and cultural renaissance, as experienced by Ernest Hemingway, F. Scott Fitzgerald and Pablo Picasso in Paris or Duke Ellington, Zora Neale Hurston and Langston Hughes in Harlem. Let's have a Roaring '20s considering the possibility that the next Coco Chanel or Walt Disney will be a Spanish woman or a black man. Let's roar the 20s making life in a modern city something we envision rather than something that turns our city limits into suburban sanctuaries. Let's have a Roaring '20s that promotes affordability and equity as well as technological innovation. And let's roar the 20s to make the government work better for the masses than for the powerful and the well-connected.
I think we are ready for this moment. With our influx of new residents and jobs, our penchant for fitness, our passion for supporting local people, and our renewed emphasis on creating and nurturing (rather than simply extracting) creativity from musicians, artists, tech entrepreneurs and restaurateurs we're ready to ride the wave of the roaring 20s. After all, we're Austin, Texas, damn it.
But let's not let things get out of hand. Let's do this thoughtfully, with compassion and empathy, and most importantly, with one another. Because if last week's winter storm showed us something, we will be stronger, better, and able to overcome anything if we do it together. The 1920s, while famous and decadent, couldn't bring our country closer together. Therefore, here in Austin, the cultural and political history of the 1920s should be learned, not repeated.
With that in mind, we have the opportunity to create a new and improved version of the Roaring '20s that will not leave us depressed for ourselves and economically, but more uniform and refreshed as we move forward into the future.
That's the kind of roar I want to hear.
Joah Spearman is the founder and CEO of Localeur and a board member of the ZACH Theater. Follow him at @joahspearman on Twitter and Instagram.
New affordable shared apartments for housing development in Central El Paso
The former leader of Fort Hood, Scott Efflandt, moves to San Antonio


text:
The Kroger Co. named Monroe, Ohio, as the site of the first automated warehouse to be built under its alliance with U.K. online grocer Ocado.
News>Online Retail
Disruptors 2019: Automation and Robotics
Russell Redman 1 | Jan 22, 2019
This is part of Supermarket News' 2019 Disruptors package. See the entire lineup here.
Brick-and-mortar retailers are following up their push to put up an online grocery front end with investment in the back end.
Chains of all sizes are piloting and deploying automation and robotics solutions to build smart, efficient operations and infrastructure geared for e-commerce. Industry observers expect these efforts to mount over the next year as grocery stores hone their omnichannel capabilities to close the gap with tech-savvy Amazon as it integrates more closely with Whole Foods Markets.
"I think automated fulfillment from the store level, particularly when it comes to center-of-store items, is going to be meaningfully important on a go-forward basis in order to cover all of your fixed and operating costs for the four walls," Jefferies analyst Christopher Mandeville said at a Supermarket News roundtable discussion.
Leading the charge are big players like The Kroger Co., which in November named Monroe, Ohio, as the site of the first automated warehouse to be built under its alliance with U.K. online grocer Ocado. Plans call for Kroger to have ordered three of these "sheds," which feature digital and robotic capabilities, by the end of 2018 and to deploy 20 of the facilities during the first three years of the agreement. For online grocery delivery, Kroger also is piloting self-driving vehicles from robotics and artificial intelligence (AI) specialist Nuro in Scottsdale, Ariz.
A few weeks before Kroger's announcement, Albertsons Cos. unveiled a partnership with e-grocery automation startup Takeoff Technologies to test a hyperlocal micro-fulfillment center at one of its stores. Takeoff's AI-enabled robots can collect items for online grocery orders in minutes.
Also working with Takeoff are Miami-area grocer Sedano's Supermarkets, which is piloting an automated fulfillment center with 14 of its stores, and Ahold Delhaize USA, which is using Takeoff's technology for mini robotic warehouses serving its Peapod online grocery arm and chains such as Stop & Shop.
Ahold Delhaize's ability to invest in technology and roll out omnichannel improvements gives it an advantage in its East Coast U.S. market, according to President and CEO Frans Muller. "Not every player can afford these investments," he said. "There will be more consolidation in the industry for smaller and midsize companies."
Not to be outdone is Walmart. The retail giant is engaged in a range of automation and robotics initiatives. In October, Walmart said it plans to build its "first high-tech distribution center for fresh and frozen groceries" in Shafter, Calif. Using robotics from Witron, the facility will process 40% more products than a traditional DC and is due to open in the fall of 2020. Walmart also has teamed with Alert Innovation in a test of its Alphabot robot to help fill online grocery orders faster at its Salem, N.H., supercenter. Another pilot in Chandler, Ariz., is using autonomous vehicles from Waymo (formerly Google's self-driving car project) to pick up customers at their homes and take them to the store to collect their online grocery orders.
Robots are being put to work in-store as well. St. Louis-based Schnuck Markets has deployed shelf-scanning robots at around 15 stores. The Tally robots from Simbe Robotics roam the aisles to scan over 1.5 million products daily, giving Schnucks deeper insight into product flow and store operations.
"As a result of working with Simbe, we've experienced a phenomenon we call 'the Tally effect,' an immediate improvement in in-store operations and increased teammate productivity," said Dave Steck, vice president of IT infrastructure and application development at Schnucks.
Less than half of shoppers buy most groceries in-store: report
Online grocery sales projected to grow 11.7% over five years
Tops transitions to in-house shoppers for pickup orders
Instacart settles benefits lawsuit for $5.25M


text:
Q: gnuplot multiplot images in column I'm trying to use multiplot to stack two image plots on top of one another, in a column. When I try to test this with x11 terminal, the images are produced separately, only one visible at a time. When I use the epslatex terminal, which is what I want, then the text is drawn correctly within the LaTeX document, but the EPS portion of the plot is produced as two separate pages, resulting in a figure that is missing a lower half.
Here's the multiplot section of my script:
set multiplot 2,1

set cbrange [-0.4:0.4]
set cbtics -0.4,0.2,0.4
unset xlabel
set tmargin at screen 0.95
set bmargin at screen 0.60
plot data u 1:2:3 with image notitle

set cbrange [-0.1:0.1]
set cbtics -0.1,0.05,0.1
set xlabel "$x$"
set tmargin at screen 0.50
set bmargin at screen 0.15
plot data u 1:2:3 with image notitle

unset multiplot
unset output

What results in the document is this:

I have tried enlarging the vertical size of the plotting area(per this question), but what this does is increase size of each page in the EPS file. To be clear, the product of plotting with epslatex is an EPS file containing two pages, the first with the first plot at the position that I want (near the top), and the second with the second plot at the position that I want (near the bottom).

A: This normally happens when you are not in multiplot mode. For me, set multiplot 2,1 gives an error message "only valid in the context of an auto-layout command". The command set multiplot layout 2,1 works with Gnuplot 5.0 and 4.6.
As a side note: This behavior can be used to produce animated gifs with set terminal gif animate, each plot command creates a new frame.


Posted on 12, April 2016 by EuropaWire PR Editors | This entry was posted in Banks, France, Management and tagged Credit Agricole, Eric Baudson, Pascal Célérier. Bookmark the permalink.
Montrouge, France, 12-Apr-2016 — /EuropaWire/ — Eric Baudson has been appointed Group Information Systems Officer, reporting to Pascal Célérier, Deputy Managing Director of Crédit Agricole S.A., in charge of Operations and Transformation. This appointment will take effect from 9 May 2016. He will join Crédit Agricole S.A.'s Extended Executive Committee.
Since January 2013, Eric Baudson has been head of the IT & Digital practice at Boston Consulting Group's Paris office.
Currently 48 years old, Eric Baudson holds a degree in agricultural engineering (Montpellier – 1989) and a specialised master's degree in financial techniques from ESSEC (1990).


Retail Leader recently identified the women it believes are most instrumental to advancing the retail landscape. The editors selected 27 women who display leadership that optimizes shareholder wealth, impacts industry dynamics and transforms business results.
SmartCommerce is proud to announce our own CEO, Jennifer Silverberg, is included on this distinguished roster of women leaders for "winning the online CPG war." The international success of the executives on this list is remarkable and the companies they represent have the admiration of business leaders and consumers throughout the world. Walmart, Target, Amazon, Home Depot, Procter & Gamble, NCR, Lord & Taylor, Salesforce and Apple are among the organizations honored.
Click here to read the article in Retail Leader and see the full list of honorees.
Contact SmartCommerce today to learn more about our Click2Cart technology and how it can help your company drive online sales.


text:
Q: How to calculate bearings between two points (in decimal degrees) using Excel Having problems formulating the bearing from two points in decimal degrees in excel.  I'm using the following formula:
=MOD(ATAN2(SIN(LonB-LonA)*COS(LatB),COS(LatA*SIN(LatB)-SIN(LatA)*COS(LonB-LonA))),6.30318)

Example data

*

*Lat A (38.6318909290283)

*Lon A (-90.2828979492187)

*Lat B (38.5352759115441)

*Lon B(-89.8448181152343)

The answer I get is 5.024 degrees it should be 105.619 degrees

A: Looks like you mistyped the formula when entering into excel.
Also, you need to convert degrees to radians, because excel takes input for trigonometric functions as radians. At the end, need to convert the result of ATAN2 back to degrees.
Solution:
=DEGREES(ATAN2(COS(RADIANS(latA))*SIN(RADIANS(latB))-SIN(RADIANS(latA))*COS(RADIANS(latB))*COS(RADIANS(lonB-lonA)),SIN(RADIANS(lonB-lonA))*COS(RADIANS(latB))))

Source for formula: http://www.movable-type.co.uk/scripts/latlong.html

A: Calculating Azimuth referenced to North (0 degrees) between two x,y locations using UTM Easting and Northing coordinates in metres, I use the following formula:
Azimuth=
=IF(AND(x>=0,y>=0),90-MOD(360+DEGREES(ATAN2(x,y)),360),450-MOD(360+DEGREES(ATAN2(x,y)),360))
Cell name 'x' = distance (difference) between eastings in metres (target minus source)
Cell name 'y' = distance (difference) between northings in metres (target minus source)


text:
Taraji P. Henson missed Met Gala to attend her friend John Singleton's funeral
Kia Morgan-Smith
LOS ANGELES, CA - SEPTEMBER 17: Actor Taraji P. Henson attends the 70th Annual Primetime Emmy Awards at Microsoft Theater on September 17, 2018 in Los Angeles, California. (Photo by Rich Polk/Getty Images for IMDb)
On Monday, Taraji P. Henson didn't attend the Met Gala like her famous friends. Instead, the Empire star took time out to say her final goodbyes to director John Singleton at his private funeral in Los Angeles.
—John Singleton's death certificate reveals he died a day earlier—
When famed fashion designer Vera Wang sent well wishes to Henson because of her absence from the fashion affair, the actress explained that Singleton's funeral was first on her agenda.
"Y'all I was supposed to be @verawang date tonight for the #metgala but as some of you may know I had to bury my dear sweet friend #JohnSingleton today in LA. I had to back out of the #Met because My head would NOT have been in the game. @verawang is such a classy Lady she sent flowers and totally understood my position. I LOVE YOU FOREVER @verawang NEXT YEAR WILL BE THE CHARM FOR US!!! GOOD LUCK TONIGHT!!!"
Y'all I was supposed to be @verawang date tonight for the #metgala but as some of you may know I had to bury my dear sweet friend #JohnSingleton today in LA. I had to back out of the #Met because My head would NOT have been in the game. @verawang is such a classy Lady she sent flowers and totally understood my position. I LOVE YOU FOREVER @verawang NEXT YEAR WILL BE THE CHARM FOR US!!! GOOD LUCK TONIGHT!!! ?????
A post shared by taraji p henson (@tarajiphenson) on May 6, 2019 at 2:50pm PDT
Henson and Singleton had developed a bond over the years, with the actress crediting him for giving her a start that helped her rise to fame.
Singleton directed Henson in Baby Boy (2001) and Four Brothers (2005) and he served as a producer for the 2005 movie Hustle & Flow.
When Henson got wind of Singleton's death, she took to social media to praise the acclaimed Boyz n the Hood writer/director for being a positive force in her life.
"My heart is broken!!! I am at a loss for words. Can't stop crying. I WILL MISS YOU MY DEAR FRIEND JOHN SINGLETON!!! You gave me my first big break in #BabyBoy and again in #HustleandFlow you believed in me when Hollywood did not get me at all!!!Throughout my career when I needed advice it was YOU I called and you answered EACH AND EVERY TIME with sound advice. YOU NOTICED MY FUNNY AND COMEDIC TIMING LOOOONG BEFORE HOLLYWOOD CAUGHT ON and you named me Lucy (after Lucille Ball)!!! MY GOD!!! Up next for us was the Emmett Till story……………..I am just broken!!! God bless your mom and your beautiful babies and family. Praying for ALL of our strength as we try and move on without you. MY GOD MY GOD!!! #RIHJohnSingleton."
My heart is broken!!! I am at a loss for words. Can't stop crying. I WILL MISS YOU MY DEAR FRIEND JOHN SINGLETON!!! You gave me my first big break in #BabyBoy and again in #HustleandFlow you believed in me when Hollywood did not get me at all!!!Throughout my career when I needed advice it was YOU I called and you answered EACH AND EVERY TIME with sound advice. YOU NOTICED MY FUNNY AND COMEDIC TIMING LOOOONG BEFORE HOLLYWOOD CAUGHT ON and you named me Lucy (after Lucille Ball)!!! MY GOD!!! Up next for us was the Emmett Till story……………..I am just broken!!! God bless your mom and your beautiful babies and family. Praying for ALL of our strength as we try and move on without you. MY GOD MY GOD!!! #RIHJohnSingleton ??????
A post shared by taraji p henson (@tarajiphenson) on Apr 29, 2019 at 6:24pm PDT
The ceremony which was planned for Singleton's loved ones was described as a "very small, intimate goodbye for family and very close friends," Deadline reports. The initial goodbye service didn't have any fanfare and was closed to cameras, the public and the media.
—Private funeral for director John Singleton set for Monday; larger memorial planned later—
Singleton's untimely death on April 29 brought great sadness to his industry friends who hailed him as a man who became an iconic filmmaker beginning with 1991's Boyz N the Hood. That film earned him Oscar nominations for Best Director and Best Screenplay.


text:
Global Newspapers
Macarthur Chronicle Camden Macarthur, Sydney - Australia
Tuesday - January 23rd 2018
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Honouring our legacy RESIDENTS across the Macarthur region are invited to the annual Anzac Day memorial service at Leppingtons Forest Lawn Memorial Park on Friday. Community leaders and visitors will honour the courage of Australian servicemen and women at the service,... Page 2
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Molecular Formula: C2286H3500N578O666S9 (light chain) C4422H6863N1151O1329S23 (heavy chain).
Preservative-free 0.9% sodium chloride injection.
If the patient receives an overdose of incobotulinumtoxinA or the drug is injected into the wrong muscle (i.e., misinjection), contact the local or state health department to process a request for botulism antitoxin through the CDC Drug Service.403 If a response is not received within 30 minutes, contact the CDC Emergency Operations Center directly at 770-488-7100.403 Information about the antitoxin is available at [Web].
1. Allergan. Botox (onabotulinumtoxinA) for injection prescribing information. Irvine, CA; 2017 Apr.
2. Solstice Neurosciences. Myobloc (rimabotulinumtoxinB) injection prescribing information. South San Francisco, CA; 2010 May.
5. Allergan. Botox Cosmetic (onabotulinumtoxinA) for injection prescribing information. Irvine, CA; 2017 Oct.
38. Cobb DB, Watson WA, Fernandez MC. Botulism-like syndrome after injections of botulinum toxin. Vet Hum Toxicol. 2000 Jun; 42:163.
384. Ipsen Biopharmaceuticals, Inc. Dysport for injection (abobotulinumtoxinA) prescribing information. Basking Ridge, NJ; 2017 Sep.
387. Costa J, Espirito-Santo CC, Borges AA et al. Botulinum toxin type A therapy for cervical dystonia (review). Cochrane Database of Systematic Reviews. 2005, Issue 1. Article No: CD003633. DOI: 10.1002/14651858.CD003633.pub2.
403. Merz Pharmaceuticals. Xeomin incobotulinumtoxinA for injection, for intramuscular use prescribing information. Raleigh, NC; 2015 Dec.
404. Merz Pharmaceuticals. Xeomin (incobotulinumtoxinA) for injection, intramuscular medication guide. Raleigh, NC; 2015 Dec.
415. Simpson DM, Gracies JM, Graham K et al. Assessment: botulinum neurotoxin for the treatment of spasticity (an evidence-based review). Neurology. 2009; 73:736-7; author reply 737-8.


text:
Пистолет ČZ vz. 27 () — чехословацкий самозарядный пистолет времён Второй мировой войны производства компании «Чешска зброёвка». Состоял на вооружении чехословацкой армии и полиции, а позднее — у немецких полицейских формирований в Чехословакии.

История
Конструктором пистолета является немецкий инженер Йозеф Никл. Пистолет производился с 1927 по 1955 годы.

После оккупации Чехословакии производство было продолжено для полицейских формирований и вермахта. После окончания Второй мировой войны производство пистолетов продолжилось (изготовленные на экспорт пистолеты послевоенного производства имели надпись "Made in Czechoslovakia" на английском языке).

Всего было произведено от 620 до 650 тысяч пистолетов (из них 452 500 во время немецкой оккупации).

Конструкция
Автоматика пистолета работает по принципу отдачи свободного затвора. Крепление ствола осуществляется сухарным способом. Ударно-спусковой механизм — куркового типа, одинарного действия. Запирание канала ствола осуществляется массой кожуха-затвора и возвратной пружиной.

Пистолет оснащен ручным предохранителем, рычаг включения которого расположен за спусковым крючком, с левой стороны рамы, а под рычагом размещается кнопка выключения предохранителя. Для включения необходимо перевести рычаг предохранителя в нижнее положение, в котором он фиксируется. Выключается предохранитель нажатием кнопки. При этом рычаг освобождается и под действием пружины возвращается в исходное положение.

Защелка магазина расположена в основании рукоятки, позади магазина. Прицельные приспособления состоят из нерегулируемой мушки и закрепленного в пазе типа «ласточкин хвост» целика, с возможностью внесения боковых поправок. Однорядный магазин вмещает 8 патронов.

Страны-эксплуатанты
  — до настоящего времени на вооружении армии, полиции и органов государственной безопасности
  — первые пистолеты оказались в распоряжении после оккупации Судетской области в 1938 году и оккупации Чехословакии в марте 1939 года, всего до конца войны в вооружённые формирования поступило около 475 000 единиц пистолетов CZ vzor 27, которые были приняты на вооружение под наименованием P.27(t) и поступали на вооружение полицейских формирований в Чехословакии и некоторых подразделений вермахта
  — в 1973 году закуплено 5 500 единиц
  — в 1948 году закуплено 5 000 единиц
  — около 3 500 единиц

  - после оккупации 1 октября 1938 года Тешинской области польскими войсками в их распоряжении оказалось оружие государственных структур Чехословакии
  - после окончания второй мировой войны некоторое количество пистолетов было ввезено из стран Европы и продавалось на внутреннем рынке в качестве гражданского оружия

Примечания

Литература

 J. B. Wood, The Gun Digest Book of Automatic Pistols, 2007. ISBN 0-89689-473-8

Ссылки
 Пистолет CZ 27 / Vz.27 / Pistole 27(t). История, конструкция и особенности на сайте armoury-online.ru
 М. Р. Попенкер. Самозарядный пистолет CZ 27 / P.27(t) (Чехословакия)
 CZ 27 / Internet Movie Firearms Database (использование в кинофильмах)

27
Пистолеты Второй мировой войны
Стрелковое оружие Германии периода Второй мировой войны
Самозарядные пистолеты Чехословакии
Самозарядные пистолеты по алфавиту
Пистолеты со свободным затвором
Появились в 1927 году
Оружие под патрон .32 ACP

redpajama_set_name: RedPajamaWikipedia


The L'Oreal Group retained DMA United to manage and implement the U.S. launch of its premier styling brand, Kerastase Nutri-Sculpt.
In order to cut through the very cluttered marketplace, DMA United developed a multi-tiered marketing strategy for Kerastase, including backstage fashion show integration, an interactive educational video for professionals, and original content created for digital purposes. Imagery from each fashion show was integrated into Kerastase's national direct-to-salon marketing campaign, further establishing alignment between the brand and industry professionals.


Crazy fishing trip to Vänern with a 13,5kg monster pike!
Crazy fishing trip to Vänern with a 13,5kg fish!
Sean and Jesper are back from yet another crazy fishing trip to Vänern in Dalsland, Sweden. Conditions where rough on lake Vänern, to say the least. Frost, rain, heavy wind, even snowstorms! But they made the best out of the situation and it paid off! More than 150 fish with over 60 pike crossing the 90cm mark and 23 100cm or bigger! Top fish 119cm / 13,5kg and a 116cm / 11,5kg!
As the week progressed temperatures kept rising and thus pike migrated back into the bays. We tried to do best of both worlds, focussing on the bays whenever conditions where good enough. Jerkbaits and softbaits did the trick. We didn't try any trolling since the casting / spin fishing was so productive (like last year). We tend to choose the technique that appears to be the most productive in our point of view, but hooking monster pike like these casting / spin fishing beats getting them trolling.
Next stop: Sean and Frans will do a trolling trip end of June. Meanwhile Sean has been guiding on Vänern with some assistance from Jesper as a 2nd guide for bigger groups. More on that in another update!
Spring Fishing Madness Volume 2 is in the making (with some awesome drone footage!) and will be up as soon as possible! Stay tuned on our website or YouTube channel so you don't miss out anything!
Next year we will participate once again in the Swedish Predatortour, hoping we will improve our 4th place in the 2017 edition. Lets hope it will be yet another crazy fishing trip to Vänern :P Make sure to check out the video about our experience at the Swedish Predatortour on lake Vänern.
Massive 119cm / 13,5kg Vänern pike!
Massive 116cm / 11,5kg fish for Jesper on Day 1!
The new Marcraft 535 Commander performed superb!


text:
← Genetic Genealogy: it's all in the Hill (DNA) – Part 2, "Operation Spit and Swab"
My County Mayo Family and the National Library of Ireland Catholic Parish Registers Website →
Removal Orders and Child-Stealing Chimney Sweeps: How Newspapers Demolished a Brick Wall – Part 1
In my post about Bigamy in Batley I introduced my 4x great grandparents Robert Burnett and Ann Jackson. Due to Robert's job as a tinner/brazier, the Burnett family moved frequently in the early days of their marriage. They finally settled in Drighlington in the early 1800s, presumably once Robert had earned sufficient money to establish his own business. Their first children were born in the Halifax area (1794 and 1798) and Flockton (1796). But for a while the origins of the couple remained a puzzle to me.
Robert died before the 1841 census[1]. Ann's entry in that census indicated Yorkshire roots. She died in 1848, so there were no further clues. From death certificates it appears Robert was born in around 1771 and Ann in 1772. I suspected Ann's maiden name was Jackson. This theory was based on the fact that two of her sons, John and James, had children named Jackson Burnett and Ann Jackson Burnett. Their wives had no apparent link to this surname. The only likely marriage I could find between a Robert Burnett and Ann Jackson took place on 7 January 1793 at Kendal, Westmorland[2].
After that I drew a blank. There the mystery lay for quite some time, until FindMyPast began rolling out their British Newspaper collection. Playing about with names I was trying to find out any information about their son, Stephen Burnett, and his wife's possible bigamous marriage. A search for him fetched the following extract from the West Riding Easter Sessions as reported in the Leeds Intelligencer of 29 April 1830:
"….She proved that when about 22 years of age, she lived some time in a slate of concubinage a man named Stephen Burnett, who was a chimney sweeper at Stockton…."
By this time Stephen, Robert and Ann's son, had died. Neither was Durham associated with my family history research. But the name piqued my interest.
The article turned out to be a newspaper report of a case heard in Pontefract in which All Saints Parish, Newcastle upon Tyne was appealing against an order for the removal of a pauper Jane Burnett, widow of John Burnett, and her four children from Drighlington to All Saints. John Burnett, who was one of Robert and Ann's sons, died in June 1829.
Under the complex Poor Law rules of settlement everyone "belonged" to a parish and this parish and its ratepayers were responsible for supporting them if the need arose. In larger parishes of the north the financial burden was the responsibility of the smaller township unit. This issue of settlement was a complex and contentious one, the number of inter-parish disputes and court cases a testimony to this. Generally your settlement parish was that of your father but this could be superseded by a number of other factors. For example a woman took the settlement parish of her husband on marriage. If illegitimate your settlement was the place you were born, but this changed from 1743/4 when you took the settlement parish of your mother regardless of your birthplace. There were other permutations too including being a parish ratepayer, renting a property in the parish assessed at £10 pa or more, serving an apprenticeship, or being hired to work in the parish for 12 months; but all in all the rules were a veritable minefield.
In the case of Jane Burnett and her children the Officials responsible for the Poor Law in Drighlington township were trying to prove their rightful settlement for this family was Newcastle All Saints. They were seeking to ship them off to an area of the country the family in all probability had never visited, in order to save Drighlington poor rate payers the expense of providing parish relief for them. And All Saints Newcastle similarly did not want the burden of costs falling to their ratepayers, possibly for many years to come as the children were all under ten years of age.
All Saints Church Newcastle upon Tyne, Blue Plaque
In the course of the case Mr Maude, acting for Drighlington, called forward Ann Burnett, wife of Robert. She affirmed that her maiden settlement was Newcastle All Saints where members of her family had received frequent parish relief. Ann had also given birth to an illegitimate child in the workhouse there.
So this appeared to be the very thin grounds for the wish to send the family to this Parish: the fact that Newcastle All Saints was the Parish of John's mother. However from Parish Registers John was born in wedlock so to my mind should, in the absence of other superseding reasons, have taken the settlement of his father Robert.
All Saints Church, Newcastle upon Tyne
In turn Mr Blackburn, acting for All Saints, called Charlotte Burnett the 82 year-old grandmother of the deceased. The report contains no mention of Charlotte Burnett's maiden name, unless that too was Burnett, or her origins. She now lived in Carlisle with her daughter, Mrs McGregor.
In her testimony she stated that when she was around 22 years old she had lived for some time in a state of "concubinage" with a man named Stephen Burnett, a Stockton chimney sweep. Going one day with his apprentices to sweep chimneys in Darlington, she went into labour and gave birth to Robert[3], the father of the deceased, at a place called Long Newton. Darlington is just over 11 miles from Stockton-on-Tees, with Long Newton a shade over four miles into the journey, so a fair trek in circa 1771 for a heavily pregnant woman. And I am baffled as to why she was making the journey in the first place; she could hardly be sweeping chimneys!
It was therefore claimed that, being born illegitimate, Robert's place of settlement was Long Newton. And because his son John had gained no other settlement elsewhere the decision was made that he too belonged to Long Newton, as did his widow and children. The court therefore decided that Jane and her children should be removed forthwith to that Parish.
There is some doubt about whether the order was ever carried out. If it was, it only lasted for a short period. Jane Burnett remarried on 27 September 1832 at Leeds Parish Church. The Parish Register entry states that she lived in Armley Parish. The 1841 census shows she was living once more in Drighlington with her children by John, new husband Jeremiah Newell and their children.
So even though I have been unable to trace records of the case in West Yorkshire Archives, due to the contentious nature of the operation of the Poor Law in that period and the newspaper report of the ensuing court case I have a wealth of information, including names and locations, which I am in the process of following up.
From initial searches on FreeReg and a visit to Tyne and Wear Archives it appears that John Jackson, mariner, married Elizabeth Hay at All Saints on 20 April 1772. Ann was baptised on 22 August 1773; daughters Amelia and Jane were baptised on 4 November 1787 at the ages of six and two respectively. Various Jacksons feature frequently in the return of clothes given to the poor. Sadly the poor house admission/discharge register does not cover the period for the birth Ann Jackson's illegitimate child. However the bastardy bonds include an entry on 27 May 1788 for an Ann Jackson. Jas Atkinson, Shoemaker, appears to be the putative father and house carpenters Gilbert Dodds and Wm [Reid?] are named as those charged with paying bonds of indemnity. However further research is needed so another visit to Tyne and Wear Archives beckons.
That is not the end though. Newspaper searches have produced some further articles which potentially relate to my 5x great grandfather Stephen Burnett, father of Robert. I will return to these in Part 2.
Ancestry.co.uk – West Yorkshire Parish Register collection: http://home.ancestry.co.uk/
British Newspaper Archive: http://www.britishnewspaperarchive.co.uk/
Family Search: https://familysearch.org/
FindMyPast British Newspaper Collection and Census information: http://www.findmypast.co.uk/
FreeReg and FreeReg2: http://www.freereg.org.uk/ and http://freereg2.freereg.org.uk/
GRO Death Certificates for Robert and Ann Burnett
Mark Herber – "Ancestral Trails"
Tyne and Wear Archives – Poor Law Records: http://www.twmuseums.org.uk/userfiles/UG22.pdf
The Workhouse Website: http://www.workhouses.org.uk
Photos – Jane Roberts
[1] GRO Death Certificate date 31 July 1837
[2] "England Marriages, 1538–1973 ," database, FamilySearch (https://familysearch.org/ark:/61903/1:1:NJV1-NYQ : accessed 5 July 2015), Robert Burnett and Ann Jackson, 07 Jan 1793; citing Kendal, Westmoreland, England, reference yrs 1700-1795; FHL microfilm 97,376.
[3] Giving an estimated birth year for Robert of around 1770-1771
This entry was posted in Ancestry, Chimney Sweep, Drighlington, Durham, Family History, Genealogy, Newcastle upon Tyne, Poor Law, Tyne and Wear, Yorkshire and tagged Ancestry, Chimney Sweeps, Drighlington, Durham, family history, genealogy, Newcastle upon Tyne, Northumberland, Poor Law, Tyne and Wear, Yorkshire. Bookmark the permalink.
5 responses to "Removal Orders and Child-Stealing Chimney Sweeps: How Newspapers Demolished a Brick Wall – Part 1"
pasttopresentgenealogy | October 28, 2015 at 9:26 pm | Reply
Many thanks for reading this post. Hope it is of interest. I'm thrilled it is receiving an exceptional volume of traffic from Facebook today (28 October 2015). I'm intrigued as to which Facebook page this link is on. Would love to know.
Pingback: Elation and Frustration: The Reality of Family History Research | PastToPresentGenealogy
Pollie Scott | February 21, 2018 at 8:10 pm | Reply
Hi My name is Pollie Scott, I am related to Jane (Muffit) Burnett and Jeremiah Newell. They are my 3x great grandparents! I'm descended through their son Joseph b. 1842 and his wife Phoebe Newell. I am astonished to find this info, and so pleased to find the connection to Newcastle! Thanks very much for writing this article, I would love to be in touch. I run a facebook page for Spen Valley family and local history, with over 1000 members, I've been researching about 18 years. I hope you don't mind if I add the research from this to my tree? I have Jane's first husband John in my tree, but not his parents, or grandmother Charlotte.I found your article by searching for another chap, Mark Newell of Drighlington (not a relative I think). I'm overjoyed at this 🙂
pasttopresentgenealogy | February 21, 2018 at 10:44 pm | Reply
Hi Pollie
Glad you liked the story. It's one of my family history highlights. I'm thrilled with my Newcastle links, as up to this discovery I was almost exclusively Yorkshire or County Mayo with my family tree. And isn't it a small world? All these family trees and links to the local area today! Feel free to add the research.
I just realised, your are Jane Roberts who is a member of my page, and we are related! 🙂