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Attribution-NonCommercial-NoDerivs 4.0 (CC BY-NC-ND 4.0)https://creativecommons.org/licenses/by-nc-nd/4.0/
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This dataset was created by greySnow
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Financial overview and grant giving statistics of Southwest Florida Gwi Housing XIV Inc.
Financial overview and grant giving statistics of Southwest Florida Gwi Housing IV Inc.
Financial overview and grant giving statistics of Southwest Florida Gwi Housing XVI Inc.
Subscribers can find out export and import data of 23 countries by HS code or product’s name. This demo is helpful for market analysis.
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This analysis presents a rigorous exploration of financial data, incorporating a diverse range of statistical features. By providing a robust foundation, it facilitates advanced research and innovative modeling techniques within the field of finance.
Historical daily stock prices (open, high, low, close, volume)
Fundamental data (e.g., market capitalization, price to earnings P/E ratio, dividend yield, earnings per share EPS, price to earnings growth, debt-to-equity ratio, price-to-book ratio, current ratio, free cash flow, projected earnings growth, return on equity, dividend payout ratio, price to sales ratio, credit rating)
Technical indicators (e.g., moving averages, RSI, MACD, average directional index, aroon oscillator, stochastic oscillator, on-balance volume, accumulation/distribution A/D line, parabolic SAR indicator, bollinger bands indicators, fibonacci, williams percent range, commodity channel index)
Feature engineering based on financial data and technical indicators
Sentiment analysis data from social media and news articles
Macroeconomic data (e.g., GDP, unemployment rate, interest rates, consumer spending, building permits, consumer confidence, inflation, producer price index, money supply, home sales, retail sales, bond yields)
Stock price prediction
Portfolio optimization
Algorithmic trading
Market sentiment analysis
Risk management
Researchers investigating the effectiveness of machine learning in stock market prediction
Analysts developing quantitative trading Buy/Sell strategies
Individuals interested in building their own stock market prediction models
Students learning about machine learning and financial applications
The dataset may include different levels of granularity (e.g., daily, hourly)
Data cleaning and preprocessing are essential before model training
Regular updates are recommended to maintain the accuracy and relevance of the data
Long term consequences of combined pyridostigmine bromide and permethrin exposure in C57BL6/J mice using a well characterized mouse model of exposure to these Gulf War agents. Expanding on earlier work, we used orthogonal proteomic approaches to identify pathways that are chronically impacted in the mouse CNS due to semi-acute GW agent exposure early in life. These analyses were performed on soluble and membrane-bound protein fractions from brain samples using two orthogonal isotopic labeling LC-MS/MS proteomic approaches – stable isotope dimethyl labeling (SIDL) and isobaric tags for relative and absolute quantitation (iTRAQ). The use of these approaches allowed for greater coverage of proteins than was possible by either one alone and revealed both distinct and overlapping datasets. This combined analysis identified changes in several mitochondrial, as well as immune and inflammatory pathways after GW agent exposure. The work discussed here provides insight into GW-agent exposure dependent mechanisms that adversely affect mitochondrial function and immune and inflammatory regulation at five months post exposure to PB+PER.
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Desalination plants in the U.S. courtesy of Global Water Intelligence (GWI), 2016. For more recent and detailed data, please contact GWI via their website: https://www.globalwaterintel.com/
Transcription (La Ring) Ndai maumwi na gabaw gaw bai nam hpe gwi ni mu yang hparai na grai wau ai ngu ai maumwi re ai. Moi shawng de da bai nam hte gwi nga ai da. Dai moi na prat hta gaw gwi ni mung ga chye shaga ai zawn bai nam ni mung ga chye shaga ga chye shaga ai rai lu ai da i. Dai wa grai nan laklai ai lam langai mi gaw hpabaw rai nga yang dai ten na bai nam ni gaw da nrung ntu ai da. Raitim gwi ni gaw nrung tu ma ai da. Dai wa lani mi gaw da dai nrung tu ai gwi hte bai nam wa shan hkawng dai hku hkrun lam hkawm ma ai da. Re wa lani mi gaw shara mi kaw du re shaloi hka lu ai da. Dai shaloi nrung hte grai nan tsawm taw ai gwi hpe wa bai nam wa manawn ai da. Dai re majaw wa hka lu hkyen ai gwi, gwi hpe wa da bai nam wa kaning nga rai nga yang gaw "E hkau nang hka lu ai rai yang gaw dai nrung rau hpa rau nga yang gaw grai shuk ai le. Na na nrung hpe jahkring mi raw da di hka atsawm lu u le" ngu di tsun ai da. Dai re majaw gwi mung bai myit yu ai da "E re law ndai nrung gaw grai li ai dai re majaw jahkring mi raw da di she hka lu na re" ngu di shi gaw nrung hpe jahkring mi gan raw da na hka bai lu taw ai da. Dai hku rai na jahkring mi hkring la re shaloi bai nam gaw hpabaw bai ngu ai rai nga yang gaw "E hkau na na nrung le grai tsawm ai i, re majaw ngai hpe jahkring mi chyawp shangun u le yaw" ngu di tsun ai da. Dai shaloi gwi wa mung "Mai ai mai ai chyawp yu chyawp yu u" ngu di tsun ai da. Dai hku re di kade nna yang gaw dai bai nam wa gaw kaning bai ngu ai rai nga yang gaw "E hkau gwi na na ndai nrung le grai tsawm ai majaw ngai ndai mare de jahkring mi ndai nrung shachyawp nna wam hkawm yu na yaw" ngu di na tsun ai da. "Bai wa na yaw" ngu di na bai tsun ai da. Dai shaloi shi na nrung, nrung hpe wa arawng mi alu rai na chyawp ya rai na shakawng hkawm na bai nam hpe shi myit na "Ah ndai nrung gaw kadai na rai nga yang gaw gwi na nrung re nga yang gaw gai ngai grai arawng lu ai. Dai re majaw shi hpe chyawp shangun dat na re" ngu myit na she "Mai ai mai ai chyawp u chyawp u raitim bai wa rit yaw" ngu di bai htet dat ai da. Dai rai di dai hku rai re na nrung lu shachyawp, nrung lu shachyawp na rai sana re bai nam wa gaw grai myit pyaw di wa dai nrung shacyawp di ten di swi rai na hku nga. Dai wa galoi ma nwa mat wa ai da. Dai re majaw dai aten kaw na gwi wa nrung hkan tam hkan tam re wa hpang e gaw shi na nrung hpe shamat kau ai da. Dai ten kaw na wa bai nam hpe mu shagu gwi gaw "E ngai na nrung bai jaw ngai na nrung bai jaw" ngu di e hpyi na hku nga. Dai wa anhte ni masha ni bai madat yu yang gaw "Wok wok wok wok" nga mat wa ai le i. Dai hku re ai da. . Language as given: Jinghpaw
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Gulf War Illness (GWI) is a chronic multisymptom illness with a central nervous system component such as memory deficits, neurological, and musculoskeletal problems. There are ample data that demonstrate that exposure to Gulf War (GW) agents, such as pyridostigmine bromide (PB) and pesticides such as permethrin (PER), were key contributors to the etiology of GWI post deployment to the Persian GW. In the current study, we examined the consequences of acute (10 days) exposure to PB and PER in C57BL6 mice. Learning and memory tests were performed at 18 days and at 5 months post-exposure. We investigated the relationship between the cognitive phenotype and neuropathological changes at short and long-term time points post-exposure. No cognitive deficits were observed at the short-term time point, and only minor neuropathological changes were detected. However, cognitive deficits emerged at the later time point and were associated with increased astrogliosis and reduction of synaptophysin staining in the hippocampi and cerebral cortices of exposed mice, 5 months post exposure. In summary, our findings in this mouse model of GW agent exposure are consistent with some GWI symptom manifestations, including delayed onset of symptoms and CNS disturbances observed in GWI veterans.
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Clinical characteristics of cases (GWI+; n = 23) and controls (GWI-; n = 9).
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Gulf War Illness (GWI) is a chronic condition characterized by multisystem symptoms that still affect up to one-third of veterans who engaged in combat in the Gulf War three decades ago. The aetiology of GWI is mainly explained by exposure to multiple toxic agents, vaccines, and medications. As there is a significant overlap in symptoms between GWI and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), the objective of this study was to investigate a biomarker widely reported in Natural Killer (NK) cells from ME/CFS patients, the Transient Receptor Potential Melastatin 3 (TRPM3) ion channel. NK cells from 6 healthy controls (HC) and 6 GWI participants were isolated, and TRPM3 function was assessed through whole-cell patch-clamp. As demonstrated by prior studies, NK cells from HC expressed typical TRPM3 function after pharmacomodulation. In contrast, this pilot investigation demonstrates a dysfunctional TRPM3 in NK cells from GWI participants through application of a TRPM3 agonist and confirmed by a TRPM3 antagonist. There was a significant reduction in TRPM3 function from GWI than results measured in HC. This study provides an unprecedented research field to investigate the involvement of TRP ion channels in the pathomechanism and potential medical interventions to improve GWI quality of life.
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[Keywords] Market include Igel, NComputing, Sun Microsy, GWI, Start
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Participant characteristics and self-reported symptoms for cases with (GWI+) and without (GWI-) Gulf War illness.
Transcription (La Ring) Gwi ni gaw shana myi mu ai da. Moi.. hpan wa ningsang chye wa ningchyang hpan wa ningsang chye wa ningchyang e shinggyim masha ni hpe e nyan hpaji jaw na matu shaga ai da. Shaga yang she shinggyim masha ni gaw aw nat ni hpe mung shaga shalawm ai da. Nat ni hpe mung shaga shalawm rai yang she "Yawng madat la mu" ngu yang she shinggyim masha ni hpe shawng san ai da. "Nanhte e.. masha ni hpe e shana e n hpa hte e nan ai, n hpa hte e masha ni hpe nhpa hte mu ai" ngu yang, "Yawng yawng hpe hpabaw hte mu ai" ngu yang "Myi hte mu ai" ngu ai da. "Myi hte mu ai" nga rai na she gwi ni hpe rai yang gaw "Gara hku mu ai" ngu yang she "Jahkye hku mu ai" ngu ai da. Dai majaw wo ra hpan wa ningsang gaw "E nang gaw shana rai jang e myi hte mu, gwi gaw jahkye hte mu ai nga ai prat tup dai hku nanhte na dai hku nanhte ra ai dai hku rai sai yaw" ngu dat na she wo ra tsa dan wa nnang ai hku rai nga shaloi she tsa dan wa gaw Dai shinggyim masha ni myi hte mu ai nga jang wa e myi nmu na hku na myi shamak kau ya ai majaw shana amyi nmu ai da. Wo gwi ni e gaw jahkye hku mu ai nga na jahkyen hku shamak ya jahkye hku gwi jahkye hku gaw achyang pak re da. Dai majaw gwi ni gaw shinggyim masha ni gaw shana myi nmu mat, gwi ni gaw shana myi mu re ai da. Hpabaw sa wa ai mung nat sa wa mung hkan, sharaw sa wa mung shana myi mu ai da. Gwi gaw dai majaw ya du hkra nam ga hkan rai yang sharaw sa wa mung mu na wau ai le. Dai hku re ai da. Shinggyim masha ni nau nzen mat na shana myi nmu mat shani sha mu lu mat ai. . Language as given: Jinghpaw
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Gulf War illness (GWI) is a chronic and multi-symptomatic disorder with persistent neuroimmune symptomatology. Chemokine receptor 6 (CCR6) has been shown to be involved in several inflammation disorders in humans. However, the causative relationship between CCR6 and neuroinflammation in GWI has not yet been investigated. By using RNA-seq data of prefrontal cortex (PFC) from 31 C57BL/6J X DBA/2J (BXD) recombinant inbred (RI) mouse strains and their parental strains under three chemical treatment groups – saline control (CTL), diisopropylfluorophosphate (DFP), and corticosterone combined with diisopropylfluorophosphate (CORT+DFP), we identified Ccr6 as a candidate gene underlying individual differences in susceptibility to GWI. The Ccr6 gene is cis-regulated and its expression is significantly correlated with CORT+DFP treatment. Its mean transcript abundance in PFC of BXD mice decreased 1.6-fold (p < 0.0001) in the CORT+DFP group. The response of Ccr6 to CORT+DFP is also significantly different (p < 0.0001) between the parental strains, suggesting Ccr6 is affected by both host genetic background and chemical treatments. Pearson product-moment correlation analysis revealed 1473 Ccr6-correlated genes (p < 0.05). Enrichment of these genes was seen in the immune, inflammation, cytokine, and neurological related categories. In addition, we also found five central nervous system-related phenotypes and fecal corticosterone concentration have significant correlation (p < 0.05) with expression of Ccr6 in the PFC. We further established a protein-protein interaction subnetwork for the Ccr6-correlated genes, which provides an insight on the interaction of G protein-coupled receptors, kallikrein-kinin system and neuroactive ligand-receptors. This analysis likely defines the heterogeneity and complexity of GWI. Therefore, our results suggest that Ccr6 is one of promising GWI biomarkers.
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List of stressors and day when applied.
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Approximately 30% of the veterans who fought in the 1991 Gulf War (GW) suffer from a disease called Gulf War Illness (GWI), which encompasses a constellation of symptoms including cognitive deficits. A coalescence of evidence indicates that GWI was caused by low-level exposure to organophosphate pesticides and nerve agents in combination with physical stressors of the battlefield. Until recently, progress on mechanisms and therapy had been limited to rodent-based models. Using peripheral blood mononuclear cells from veterans with or without GWI, we recently developed a bank of human induced pluripotent stem cells that can be differentiated into a variety of cellular fates. With these cells, we have now generated cerebral organoids, which are three-dimensional multicellular structures that resemble the human brain. We established organoid cultures from two GW veterans, one with GWI and one without. Immunohistochemical analyses indicate that these organoids, when treated with a GW toxicant regimen consisting of the organophosphate diisopropyl fluorophosphate (a sarin analog) and cortisol (to mimic battlefield stress), display multiple indicators consistent with cognitive deficits, including increased astrocytic reactivity, enhanced phosphorylation of tau proteins, decreased microtubule stability, and impaired neurogenesis. Interestingly, some of these phenotypes were more pronounced in the organoids derived from the veteran with GWI, potentially reflecting a stronger response to the toxicants in some individuals compared to others. These results suggest that veteran-derived human cerebral organoids not only can be used as an innovative human model to uncover the cellular responses to GW toxicants but can also serve as a platform for developing personalized medicine approaches for the veterans.
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Released under Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)