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Enteric Glia Regulate Lymphocyte Activation via Autophagy-Mediated MHC-II Phrase.
001) in the volunteers, irrespective of the solution administered (remifentanil or normal saline). At NRS 5, the SPI showed similar values, irrespective of remifentanil administration, while the ANI showed significantly lower values on remifentanil administration (P = 0.028). The SPI and ANI values at NRS 5 and NRS 7 did not differ significantly in the parturients (P = 0.101 for SPI, P = 0.687 for ANI). Thus, the SPI and ANI were effective indices for detecting pain in healthy volunteers and parturients.
To investigate the effects of Bushen Huatan Granules (BHG) and Kunling Wan (KW), the two Chinese medicines, on the regulation of polycystic ovary syndrome (PCOS) and their underlying mechanisms.

PCOS rat model was established by subcutaneous injection of dehydroepiandrosterone (DHEA) (6 mg/100 g/day) for 20 days, followed by treatment with BHG (0.75, 1.49, and 2.99 g/kg) or KW (0.46, 0.91, and 1.82 g/kg) by gavage for 4 weeks. Estrous cycle was detected by vaginal smears. Follicles development was assessed by histology. Levels of testosterone and insulin in serum were tested by ELISA. Apoptosis of Granulosa cells (GCs) was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining. Pathways associated with apoptosis were detected with western blot. Pregnancy outcome was also assessed. GCs were pre-treated with 10
M testosterone
for 24 h, then incubated with serum from rats receiving BHG (1.49 g/kg) or KW (1.82 g/kg). The parameters concerning apoptosis, mitochowere mediated by different pathway with the effect of BHG being correlated with the regulation of mitochondria, while the effect of KW being attributable to protection of endoplasmic reticulum stress.
This study demonstrated BHG or KW as a potential strategy for treatment of PCOS induced by DHEA, and suggested that the beneficial role of the two medicines were mediated by different pathway with the effect of BHG being correlated with the regulation of mitochondria, while the effect of KW being attributable to protection of endoplasmic reticulum stress.Background Antipsychotics modulate expression of inflammatory cytokines and inducible inflammatory enzymes. Elopiprazole (a phenylpiperazine antipsychotic drug in phase 1) has been characterized as a therapeutic drug to treat SARS-CoV-2 infection in a repurposing study. We aim to investigate the potential effects of aripiprazole (an FDA approved phenylpiperazine) on COVID-19-related immunological parameters. Methods Differential gene expression profiles of non-COVID-19 vs. COVID-19 RNA-Seq samples (CRA002390 project in GSA database) and drug-naïve patients with non-affective psychosis at baseline and after three months of aripiprazole treatment were identified. An integrative transcriptomic analyses of aripiprazole effects on differentially expressed genes in COVID-19 patients was performed. Findings 82 out the 377 genes (21.7%) with expression significantly altered by aripiprazole have also their expression altered in COVID-19 patients and in 93.9% of these genes their expression is reverted by aripiprazole.le medications could be of use in countering SARS-CoV-2 infection, but require further studies and trials.Background ABCG2 and ABCB1 are genes related to the pharmacokinetics of sunitinib and have been associated with its toxicity and efficacy. However, the results have been controversial. This study aimed to evaluate the associations of ABCG2 and ABCB1 polymorphisms with sunitinib-induced toxicity and efficacy in renal cell carcinoma (RCC) by meta-analysis. Methods PubMed, EMBASE, Cochrane Library, and Web of Science were systematically searched for studies investigating the associations of the ABCG2 rs2231142 polymorphism with sunitinib-induced toxicity and the associations of the ABCB1 rs1128503 and ABCB1 rs2032582 polymorphisms with sunitinib-induced toxicity and clinical outcomes. The associations were evaluated by effect size (ES) with 95% confidence intervals (CIs). Results Eight and five studies were included in the toxicity and efficacy analysis, respectively, including a total of 1081 RCC patients. The ABCG2 rs2231142 A allele was associated with an increased risk of sunitinib-induced thrombocytopenia a = 0.326; ES = 1.02, 95% CI = 0.65-1.62, p = 0.919; ES = 1.32, 95% CI = 0.85-2.05, p = 0.215). Conclusion The results indicate that the ABCG2 rs2231142 polymorphism may serve as a predictor of sunitinib-induced thrombocytopenia and HFS in Asians, while the ABCB1 rs1128503 polymorphism may serve as a predictor of sunitinib-induced hypertension, and both the ABCB1 rs1128503 and rs2032582 polymorphisms may serve as predictors of PFS in RCC. These results suggest a possible application of individualized use of sunitinib according to the genetic background of patients.In this work, we reviewed the progress in the phytochemical and biological investigations of bioactive components derived from medicinally valuable Lobelia species. In the last 60 years, Lobelia has garnered significant attention from the phytochemist from around the world, majorly due to the discovery of bioactive piperidine alkaloids (e.g., lobinaline and lobeline) in the early 1950s. Later, lobeline underwent clinical trials for several indications including the treatment of attention deficit hyperactivity disorder and a multicenter phase three trial for smoking cessation. Subsequently, several other alkaloids derived from different species of Lobelia were also investigated for their pharmacological characteristics. However, in the last few years, the research focus has started shifting to the characterization of the other novel chemical classes. The major shift has been noticed due to the structurally similar alkaloid components, which essentially share similar pharmacological, physicochemical, and toxicological profiles. In this review, we present an up-to-date overview of their progress with special attention to understanding the molecular mechanisms of the novel bioactive components.Urinary tract infections (UTIs) are very common disorders that affect adult women. Indeed, 50% of all women suffer from UTIs at least one time in their lifetime; 20-40% of them experience recurrent episodes. The majority of UTIs seems to be due to uropathogenic Escherichia coli that invades urothelial cells and forms quiescent bacterial reservoirs. Recurrences of UTIs are often treated with non-prescribed antibiotics by the patients, with increased issues connected to antibiotics resistance. D-mannose, a monosaccharide that is absorbed but not metabolized by the human body, has been proposed as an alternative approach for managing UTIs since it can inhibit the bacterial adhesion to the urothelium. This manuscript discusses the mechanisms through which D-mannose acts to highlight the regulatory aspects relevant for determining the administrative category of healthcare products placed on the market. The existing literature permits to conclude that the anti-adhesive effect of D-mannose cannot be considered as a pharmacological effect and, therefore, D-mannose-based products should be classified as medical devices composed of substances.Insufficient transport of therapeutic cargo into tumor bed is a bottleneck in cancer nanomedicine. Block copolymers are promising carriers with smaller particle size by ratio modification. Here, we constructed cisplatin nanoparticles with sizes ranging from 8 to 40 nm to study the permeability and therapy of Lewis lung carcinoma. We synthesized methoxypoly(ethylene glycol)2000-block poly(L-glutamic acid sodium salt)1979 loading cisplatin through complexation reaction. The cisplatin nanomedicine has high drug loading and encapsulation efficiency. In vitro data demonstrated that cisplatin nanoparticles had equivalent growth-inhibiting effects on Lewis lung carcinoma cells compared to free cisplatin. In vivo evidences showed cisplatin nanoparticles had superior antitumor effects on the Lewis lung carcinoma mouse model with no obvious side effects. All results indicated that optimizing the ratio of block copolymers to obtain smaller sized nanomedicine could act as a promising strategy for overcoming the inadequate accumulation in poorly vascularized tumors.COVID-19 pandemic has spread worldwide at an exponential rate affecting millions of people instantaneously. Currently, various drugs are under investigation to treat an enormously increasing number of COVID-19 patients. This dreadful situation clearly demands an efficient strategy to quickly identify drugs for the successful treatment of COVID-19. Hence, drug repurposing is an effective approach for the rapid discovery of frontline arsenals to fight against COVID-19. Successful application of this approach has resulted in the repurposing of some clinically approved drugs as potential anti-SARS-CoV-2 candidates. Several of these drugs are either antimalarials, antivirals, antibiotics or corticosteroids and they have been repurposed based on their potential to negate virus or reduce lung inflammation. Large numbers of clinical trials have been registered to evaluate the effectiveness and clinical safety of these drugs. Till date, a few clinical studies are complete and the results are primary. WHO also conductendings, therapeutic regimens, pharmacokinetics, and drug-drug interactions.Background Development of resistance to doxorubicin-based chemotherapy limits its curative effect in osteosarcoma. In the current study, we focused on investigating the mechanisms underlying the development of doxorubicin resistance in osteosarcoma. Methods The human osteosarcoma cell line MG-63 and doxorubicin-resistant MG-63/Dox cells were used in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of the long non-coding RNA LINC01116 in the two cell lines. Then, the specific shRNA for LINC01116 was employed to suppress LINC01116 expression in MG-63/Dox cells. Cell viability was assessed by the CCK-8 and colony formation assays. Cell migration and invasion were evaluated by the transwell assay. Moreover, the epithelial-mesenchymal transition (EMT)-related proteins, E-cadherin, vimentin, and N-cadherin were evaluated by Western blotting. The regulation of LINC01116 on miR-424-5p expression was examined using methylation-specific PCR, RNA immunoprecipitation, and Western blotting assay. The potential targeting of HMGA2 by miR-424-5p was predicted using the bioinformatics databases TargetScan and miRanda and verified by a dual-luciferase reporter assay. Results LINC01116 was more highly expressed in MG-63/Dox cells than in MG-63 cells. Inhibition of LINC01116 suppressed cell viability, migration, and invasion, along with upregulating the expression of E-cadherin, downregulating vimentin, and attenuating doxorubicin resistance in MG-63/Dox cells. Further mechanism-related investigations indicated that LINC01116 regulated HMGA2 expression via the EZH2-associated silencing of miR-424-5p. Conclusion LINC01116 exerts regulatory effects on doxorubicin resistance through the miR-424-5p axis, providing a potential approach to overcoming chemoresistance in osteosarcoma.Background Vancomycin-associated acute kidney injury (VA-AKI) is a recognizable condition with known risk factors. However, the use of vancomycin in clinical practices in China is distinct from other countries. We conducted this longitudinal study to show the characteristics of VA-AKI and how to manage it in clinical practice. Patients and Methods We included patients admitted to hospital, who received vancomycin therapy between January 1, 2016 and June 2019. VA-AKI was defined as a patient having developed AKI during vancomycin therapy or within 48 h following the withdrawal of vancomycin therapy. Results A total of 3719 patients from 7058 possible participants were included in the study. Sodiumhydroxide 998 patients were excluded because of lacking of serum creatinine measurement. The incidence of VA-AKI was 14.3%. Only 32.3% (963/2990) of recommended patients performed therapeutic drug monitoring of vancomycin. Patients with VA-AKI were more likely to concomitant administration of cephalosporin (OR 1.55, 95% CI 1.08-2.21, p = 0.
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