Atmospheric River Tracking Method Intercomparison Project (ARTMIP) Tier 2 Paleoclimate source data and developer catalogues. Each ARTMIP method/algorithm (named by the developer) submits a catalogue comprised of 0's (no AR exists) or 1's (yes AR exists) for each time slice, for each grid point, using output from CESM2 paleoclimate simulations for PreIndustrial, orbital forcing comparable to the Holocene at 10ka, and greenhouse forcing comparable to 21ka. LGM (Last Glacial Maximum). Each simulation has 30 years of data. Derived quantities required for algorithms, such as IVT or IWV, were computed by the ARTMIP project so that all methods use the same data.

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Background/Aim: The impacts of health insurance status on survival outcomes in multiple myeloma (MM) have not been addressed in depth. The present study was conducted to identify definite relationships of cancer-specific survival (CSS) and overall survival (OS) with health insurance status in MM patients. Methods: MM patients aged 18–64 years and with complete insurance records between January 1, 2007, and December 31, 2016, were identified from 18 Surveillance, Epidemiology, and End Results (SEER) Database registries. Health insurance condition was categorized as uninsured, any Medicaid, insured, and insured (no specifics). Relationships of health insurance condition with OS/CSS were identified through Kaplan-Meier, and uni-/multivariate Cox regressions using the hazard ratio and 95% confidence interval. Potential baseline confounding was adjusted using multiple propensity score (mPS). Results: Totally 17,981 patients were included, including 68.3% with private insurance and only 4.9% with uninsurance. Log-rank test uncovered significant difference between health insurance status and OS/CSS among MM patients. Patients with non-insurance or Medicaid coverage in comparison with private insurance tended to present poorer OS/CSS both in multivariate Cox regression and in mPS-adjusted model (non-insurance vs. private insurance [OS/CSS]: 1.33 [1.20–1.48]/1.13 [1.00–1.28] and 1.45 [1.25–1.69]/1.18 [1.04–1.33], respectively; Medicaid coverage vs. private insurance [OS/CSS]: 1.67 [1.56–1.78]/1.25 [1.16–1.36] and 1.76 [1.62–1.90]/1.23 [1.13–1.35], respectively). Conclusions: Our observational study of exposure-outcome associations suggests that insufficient or no insurance is moderately linked with OS among MM patients aged 18–64 years. Wide insurance coverage and health-care availability may strengthen some disparate outcomes. In the future, prospective cohort research is needed to further clarify concrete risks with insurance type, owing to the lack of definite division of insurance data in SEER.

Background/Aim: The impacts of health insurance status on survival outcomes in multiple myeloma (MM) have not been addressed in depth. The present study was conducted to identify definite relationships of cancer-specific survival (CSS) and overall survival (OS) with health insurance status in MM patients. Methods: MM patients aged 18–64 years and with complete insurance records between January 1, 2007, and December 31, 2016, were identified from 18 Surveillance, Epidemiology, and End Results (SEER) Database registries. Health insurance condition was categorized as uninsured, any Medicaid, insured, and insured (no specifics). Relationships of health insurance condition with OS/CSS were identified through Kaplan-Meier, and uni-/multivariate Cox regressions using the hazard ratio and 95% confidence interval. Potential baseline confounding was adjusted using multiple propensity score (mPS). Results: Totally 17,981 patients were included, including 68.3% with private insurance and only 4.9% with uninsurance. Log-rank test uncovered significant difference between health insurance status and OS/CSS among MM patients. Patients with non-insurance or Medicaid coverage in comparison with private insurance tended to present poorer OS/CSS both in multivariate Cox regression and in mPS-adjusted model (non-insurance vs. private insurance [OS/CSS]: 1.33 [1.20–1.48]/1.13 [1.00–1.28] and 1.45 [1.25–1.69]/1.18 [1.04–1.33], respectively; Medicaid coverage vs. private insurance [OS/CSS]: 1.67 [1.56–1.78]/1.25 [1.16–1.36] and 1.76 [1.62–1.90]/1.23 [1.13–1.35], respectively). Conclusions: Our observational study of exposure-outcome associations suggests that insufficient or no insurance is moderately linked with OS among MM patients aged 18–64 years. Wide insurance coverage and health-care availability may strengthen some disparate outcomes. In the future, prospective cohort research is needed to further clarify concrete risks with insurance type, owing to the lack of definite division of insurance data in SEER.

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Background: The protective effects of taurine supplementation on diabetic kidney disease (DKD) have been defined, but the mechanisms are not quite clear yet. TRPC6 has been shown to function in the homeostasis of podocytes, but whether TRPC6-modulated mitochondrial dysfunctions participating in taurine-induced renal protection during diabetes are unclear. Methods: A DKD model was constructed using streptozocin (STZ), and an immortalized mouse podocytes cell line MPC-5 was used. Renal histology and western blot were used to analyze the expression levels of certain proteins. Cell proliferation assays, apoptosis assays, calcium influx, and mitochondrial functions were evaluated. Results: In this study, taurine intervention improved STZ-induced DKD injuries, while it decreased both 24-h urinary protein and podocytes apoptosis. In detail, this study showed that taurine treatment decreased mitochondrial ROS productions by suppressing calcium overload and improving mitochondrial respiratory functions. Furthermore, the upregulation of TRPC6 is partially responsible for the calcium overload during high glucose treatment, whereas taurine treatment inhibited TRPC6 expression and partially attenuated high glucose-induced podocytes injuries. In addition, we demonstrated that taurine could upregulate CSE expression and inhibits TRPC6 expression via promoting the synthesis of H₂S. Conclusion: Our study reveals that taurine intervention could partially attenuate the lesions of DKD by modulating the CSE/TRPC6 axis.

Background: The protective effects of taurine supplementation on diabetic kidney disease (DKD) have been defined, but the mechanisms are not quite clear yet. TRPC6 has been shown to function in the homeostasis of podocytes, but whether TRPC6-modulated mitochondrial dysfunctions participating in taurine-induced renal protection during diabetes are unclear. Methods: A DKD model was constructed using streptozocin (STZ), and an immortalized mouse podocytes cell line MPC-5 was used. Renal histology and western blot were used to analyze the expression levels of certain proteins. Cell proliferation assays, apoptosis assays, calcium influx, and mitochondrial functions were evaluated. Results: In this study, taurine intervention improved STZ-induced DKD injuries, while it decreased both 24-h urinary protein and podocytes apoptosis. In detail, this study showed that taurine treatment decreased mitochondrial ROS productions by suppressing calcium overload and improving mitochondrial respiratory functions. Furthermore, the upregulation of TRPC6 is partially responsible for the calcium overload during high glucose treatment, whereas taurine treatment inhibited TRPC6 expression and partially attenuated high glucose-induced podocytes injuries. In addition, we demonstrated that taurine could upregulate CSE expression and inhibits TRPC6 expression via promoting the synthesis of H₂S. Conclusion: Our study reveals that taurine intervention could partially attenuate the lesions of DKD by modulating the CSE/TRPC6 axis.