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BACKGROUND HMex-3A, an RNA-binding protein, was found to be associated with tumorigenesis. However, the roles of hMex-3A in hepatocellular carcinoma (HCC) progression remained unclear. METHODS The different expression of hMex-3A between HCC tissues and non-tumor tissues were evaluated using The Cancer Genome Atlas database. Thereafter, the hMex-3A expression was evaluated in HCC tissues using Western blotting and qRT-PCR. Immunohistochemistry was performed to investigate the association between hMex-3A level and clinicopathological features including prognosis in HCC patients. In addition, we used si-hMex-3A to knockdown hMex-3A in HCC cells to test Cell Counting Kit-8, colony formation, cell migration and invasion. RESULTS The hMex-3A expression was significantly elevated in HCC tissues. Analysis of the clinicopathological parameters suggested that hMex-3A expression was significantly associated with pathological grade (P = 0.019) and TNM stage (P = 0.001) in HCC. Moreover, univariate and multivariate Cox-regression analyses revealed that high hMex-3A expression (HR=1.491, 95% CI 1.107-2.007; P = 0.009) was an independent risk factor for overall survival in HCC patients. Finally, we confirmed that si-hMex-3A could significantly inhibit HCC cell proliferation, migration, and invasion in vitro. CONCLUSIONS HMex-3A may contribute to the progression of HCC and might be used as a novel therapeutic target and prognostic marker in HCC. V.Cytology-based cervical screening had unequivocal success in reducing the incidence and mortality of cervical cancer in the last century. The recognition of the role of human papillomavirus (HPV) as a necessary cause of cervical cancer led to the development of HPV testing. Gradually, there has been a shift from reflex HPV testing for mild cytological abnormalities, to co-testing with cytology and HPV, and lately to primary HPV screening, based on evidence from well-designed large randomized controlled trials and meta-analyses. Advantages of primary HPV screening include higher sensitivity to detect pre-neoplastic lesions, better re-assurance with a negative test, and safe prolongation of screening intervals. However, clinicians and policy makers must ensure the availability of clinically validated HPV assays and triage protocols of screen positive cases prior to implementation of primary HPV screening. This is likely to reduce potential harm from over-treatment as well as extra burden on the health care system. The large-scale initiatives to address the global unmet needs for family planning (FP) have gathered and compelled scientists, providers, program managers, and other stakeholders (including users) to re-examine the various methods of modern contraception, focusing on those that are proven to be more effective (long-acting reversible contraceptives and permanent methods), historically more widely used (oral contraceptives, condoms), and in development (male hormonal contraception). Implementing FP programs requires an understanding of the human rights principles underpinning the delivery of contraceptive services, the various indicators related to demand, need, and use (demand satisfied, unmet need, and contraceptive prevalence), and its effectiveness (perfect or correct use and typical use), which will be presented in this article. Tools and guidance documents developed using the best available evidence have also been listed in this review article. This issue will also look at new initiatives about providing care (self-care), and key population groups (post-pregnancy and adolescence). NVP-BGT226 in vitro The clinical use of the methods should go hand in hand with the programmatic initiatives to ensure that women, men, or couple take up the appropriate method of choice and continue using these based on their reproductive health goals. BACKGROUND Postoperative acute pancreatitis (POAP) can be a possible cause of postoperative pancreatic fistula (POPF). The present study aimed to evaluate the role of clinically-relevant POAP (CR-POAP), defined according to different cut-offs of postoperative amylase (AMS) values and C-reactive protein (CRP), in the development of clinically relevant POPF (CR-POPF) after pancreaticoduodenectomy (PD). METHODS Data from 610 patients who underwent PD (2015-2018) were analyzed. Patients were divided according to the upper limit (100 U/l) and 3-fold the upper limit (300 U/l) of serum POD1 AMS. Univariate and multivariable analysis of possible predictors of CR-POPF were performed. RESULTS Overall, 360 patients (59%) had POD1 serum AMS ≤100 U/l, 142 patients (23%) had POD1 serum AMS >100 U/l and ≤300 U/l, and 108 patients (18%) had POD1 serum AMS >300 U/l. Patients with POD1 serum AMS >300 had a higher frequency of soft pancreatic texture, complications, main pancreatic duct diameter ≤3 mm, and CR-POPF. POD1 serum AMS >100 U/l associated to POD2 CRP ≥180 mg/l (OR 4.3, p 100 U/l and POD2 CRP ≥ 180 mg/l, is associated with an increased risk of CR-POPF. Cardiomyocyte necrosis has been reported to be a major component in pathogenesis of cardiac diseases. We noticed that baicalein, a kind of principal components in the roots of Scutellaria baicalensis Georgi, exerts cardioprotective effects by inhibiting oxidative stress and apoptosis of Cardiomyocytes. However, it is rarely reported whether baicalein exerts myocardial protection by inhibiting necrosis. In addition, the death receptor-dependent necrotic cell death is mediated by receptor interacting serine/threonine kinase 1/3(RIPK1/RIPK3). Thus, targeting RIPK1/RIPK3 may represent potential preventive and therapeutic opportunities of necrosis-related cardiac diseases. Carboxyl terminus of Hsc70-interacting protein (CHIP) has been reported to play a significant role on cardiac protection through its E3 ubiquitin ligase activity, but it is not clear whether CHIP regulates RIP1K/RIPK3 in cardiomyocytes necrosis. In our study, we firstly found that baicalein attenuated myocardial necrosis in vitro and in vivo, and it significantly suppressed myocardial necrosis induced by oxidative stress through disturbing RIPK1/RIPK3 necrososme formation in vitro. Besides, we verified that CHIP suppressed myocardial necrosis through ubiquitylation-dependent degradation of RIPK3. And then we firstly speculated that baicalein may promote stability of CHIP to exert cardioprotective effects, and we also found that baicalein promoted the E3 ubiquitin ligase activity of CHIP to negatively regulate RIPK3. Taken together, our results for the first time reveal a pivotal role of baicalein in stabilizing CHIP activity to promote RIPK1/RIPK3 ubiquination and degradation in order to attenuate Cardiomyocyte necrosis.

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