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The anthropology of wellness systems: A brief history and evaluation.
Our findings concretize a further and relevant milestone on how the diet may prevent/mitigate disease risk.The aim of this study was to investigate the association of body mass index (BMI), alcohol consumption, and smoking status with the occurrence of Bell's palsy. The Korean National Health Insurance Service-Health Screening Cohort of a ≥ 40-year-old population from 2000-2003 was used. A total of 5,632 Bell's palsy participants were matched with 22,528 control participants in terms of age, sex, income, region of residence, and past medical histories of hypertension, diabetes, and dyslipidemia. Bell's palsy was classified by a history of ≥2 diagnoses with ICD-10 code (G510) and steroid treatment. BMI (kg/m2) was classified as less then 18.5 (underweight), ≥18.5 to less then 23 (normal), ≥23 to less then 25 (overweight), ≥25 to less then 30 (obese I), and ≥30 (obese II). Alcohol consumption was divided into non-drinkers and those who drank 2-3 times a month, 1-2 times a week, and ≥3 times a week. Smoking status was categorized as current smokers, past smokers, and non-smokers. The odds of obesity, alcohol consumption, and smoking with Bell's palsy were analyzed using logistic regression analysis. BMI showed proportionally positive associations with Bell's palsy (adjusted OR [95% CI] = 0.61 [0.47-0.79] for underweight, 1.16 [1.08-1.26] for normal, 1.24 [1.15-1.33] for obese I, and 1.61 [1.38-1.88] for obese II, P  less then  0.001). The odds of alcohol consumption with Bell's palsy were 0.90 (95% confidence interval [CI] = 0.82-0.99) for 2-3 times a month, 0.77 (95% CI = 0.69-0.85) for 1-2 times a week, and 0.79 (95% CI = 0.71-0.88) for ≥3 times a week compared to nondrinkers (P  less then  0.001). Smoking did not show a relationship with the occurrence of Bell's palsy. Obesity was related to the risk of Bell's palsy in the population over 40 years old. On the other hand, alcohol consumption was negatively associated with the occurrence of Bell's palsy.In the Trinity Test, the energy was released not only from the fission of Pu-239 core but also from the fast neutron fission of tamper surrounding it. The high energy photons produced from the fissioning core can also induce fission in U-238 tamper. In this work, an effort has been made, for the first time, to develop an approach to investigate the possibility of photon-induced fission in U-238 tamper used in Trinity Test nuclear weapon. GEF nuclear reaction code, version 2018/1.1 is used to calculate the prompt γ-spectrum from the fast fission of Pu-239 core of the device. It is estimated that 14.5 ton (t) of TNT of the total 21 kT yield of the Trinity nuclear device is contributed by the photo-fission of U-238 tamper.Ocean deoxygenation driven by global warming and eutrophication is a primary concern for marine life. Resistant animals may be present in dead zone sediments, however there is lack of information on their diversity and metabolism. Here we combined geochemistry, microscopy, and RNA-seq for estimating taxonomy and functionality of micrometazoans along an oxygen gradient in the largest dead zone in the world. Nematodes are metabolically active at oxygen concentrations below 1.8 µmol L-1, and their diversity and community structure are different between low oxygen areas. This is likely due to toxic hydrogen sulfide and its potential to be oxidized by oxygen or nitrate. Zooplankton resting stages dominate the metazoan community, and these populations possibly use cytochrome c oxidase as an oxygen sensor to exit dormancy. Our study sheds light on mechanisms of animal adaptation to extreme environments. These biological resources can be essential for recolonization of dead zones when oxygen conditions improve.Cancer cells are defective in DNA repair, so they experience increased DNA strand breaks, genome instability, gene mutagenesis, and tumorigenicity; however, multiple classic DNA repair genes and pathways are strongly activated in malignant tumor cells to compensate for the DNA repair deficiency and gain an apoptosis resistance. The mechanisms underlying this phenomenon in cancer are unclear. We speculate that a key DNA repair gene or signaling pathway in cancer has not yet been recognized. Here, we show that the lipogenic liver X receptor (LXR)-sterol response element binding factor-1 (SREBF1) axis controls the transcription of a key DNA repair gene polynucleotide kinase/phosphatase (PNKP), thereby governing cancer cell DNA repair and apoptosis. Notably, the PNKP levels were significantly reduced in 95% of human pancreatic cancer (PC) patients, particularly deep reduction for sixfold in all of the advanced-stage PC cases. PNKP is also deficient in three other types of cancer that we examined. In addition, the expression of LXRs and SREBF1 was significantly reduced in the tumor tissues from human PC patients compared with the adjacent normal tissues. The newly identified LXR-SREBF1-PNKP signaling pathway is deficient in PC, and the defect in the pathway contributes to the DNA repair deficiency in the cancer. Strikingly, further diminution of the vulnerable LXR-SREBF1-PNKP signaling pathway using a small molecule triptonide, a new LXR antagonist identified in this investigation, at a concentration of 8 nM robustly activated tumor-suppressor p53 and readily elevated cancer cell DNA strand breaks over an apoptotic threshold, and selectively induced PC cell apoptosis, resulting in almost complete elimination of tumors in xenograft mice without obvious complications. Our findings provide new insight into DNA repair and apoptosis in cancer, and offer a new platform for developing novel anticancer therapeutics.Alveolar rhabdomyosarcoma (aRMS) is a highly malicious childhood malignancy characterized by specific chromosomal translocations mostly encoding the oncogenic transcription factor PAX3-FOXO1 and therefore also referred to as fusion-positive RMS (FP-RMS). BAY 2666605 clinical trial Previously, we have identified fenretinide (retinoic acid p-hydroxyanilide) to affect PAX3-FOXO1 expression levels as well as FP-RMS cell viability. Here, we characterize the mode of action of fenretinide in more detail. First, we demonstrate that fenretinide-induced generation of reactive oxygen species (ROS) depends on complex II of the mitochondrial respiratory chain, since ROS scavenging as well as complexing of iron completely abolished cell death. Second, we co-treated cells with a range of pharmacological inhibitors of specific cell death pathways including z-vad (apoptosis), necrostatin-1 (necroptosis), 3-methyladenine (3-MA) (autophagy), and ferrostatin-1 (ferroptosis) together with fenretinide. Surprisingly, none of these inhibitors was able to prevent cell death.
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