Intensive care unit (ICU) is important in the rehabilitation of critically ill patients. In the past decades, many patients who received aggressive treatment in ICU developed sclerosing cholangitis in multiple centers. Sclerosing cholangitis in critically ill patients (SC-CIP) is a relatively new issue. To investigate the causes, clinical manifestation, treatment, and prognosis of SC-CIP, we searched for published cases in the databases of PubMed, Highwire, and Elsevier from 2001 to 2012. Data were extracted using a standard form and retrospectively analyzed. Twelve eligible studies covering 88 patients, with 64 men and 24 women, were enrolled in this analysis. The mean age was 49.8 years. All of the patients recovered from critical illnesses, such as trauma, infection, burn, and major surgeries. High pressure positive end-expiratory pressure (PEEP, peak level at 12.8 cm H₂O) was utilized for all patients, with the average duration of 36.3 d. In addition, vasopressor agents were administered in approximately 60%of SC-CIP. A rapid increase in cholestasis and irregular strictures in the intrahepatic bile ducts was observed in the following months. With an average follow-up period of 17.9 months, poor outcomes were observed in 54 patients, including 34 deaths. In conclusion, ischemic injury of the biliary tree, which may be affected by PEEP and/or vasopressor administration, affects cholangiopathic procedure. As a newly discovered type of secondary sclerosing cholangitis, SC-CIP is a severe progressive complication of patients in ICU and should be carefully monitored by clinicians.

Elevated ALP and GGT levels were risk predictors in HCC patients. Our prognostic model might vary the outcomes of patients from different risk groups.

The role of melatonin in promoting the yield of Cashmere goat wool has been demonstrated for decades though there remains a lack of knowledge regarding melatonin mediated hair follicle growth. Recent studies have demonstrated that long non-coding RNAs (lncRNAs) are widely transcribed in the genome and play ubiquitous roles in regulating biological processes. However, the role of lncRNAs in regulating melatonin mediated hair follicle growth remains unclear. In this study, we established an in vitro Cashmere goat secondary hair follicle culture system, and demonstrated that 500 ng/L melatonin exposure promoted hair follicle fiber growth. Based on long intergenic RNA sequencing, we demonstrated that melatonin promoted hair follicle elongation via regulating genes involved in focal adhesion and extracellular matrix receptor pathways and further cis predicting of lncRNAs targeted genes indicated that melatonin mediated lncRNAs mainly targeted vascular smooth muscle contraction and signaling pathways regulating the pluripotency of stem cells. We proposed that melatonin exposure not only perturbed key signals secreted from hair follicle stem cells to regulate hair follicle development, but also mediated lncRNAs mainly targeted to pathways involved in the microvascular system and extracellular matrix, which constitute the highly orchestrated microenvironment for hair follicle stem cell. Taken together, our findings here provide a profound view of lncRNAs in regulating Cashmere goat hair follicle circadian rhythms and broaden our knowledge on melatonin mediated hair follicle morphological changes.

The change of blood oxygen in renal cortex and medulla could be detected with BOLD-MRI, so as to evaluate the renal function and anoxic injury of CKD.

Recent advances indicate that cancer‑associated fibroblasts (CAFs) play a key role in cancer progression by contributing to invasion, metastasis and angiogenesis. Solid tumors often experience low oxygen tension environments, which induce gene expression changes and biological features leading to poor outcomes. The G-protein estrogen receptor (GPER) exhibits a stimulatory role in diverse types of cancer cells and in CAFs under hypoxic conditions. We investigated the role of CAFs and hypoxia in breast cancer aggressiveness, and examined the effect of GPER in CAFs on hypoxia-driven breast cancer progression. The results showed that hypoxia upregulated HIF-1α, GPER and α-SMA expression in CAFs, and induced the secretion of Interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF) in CAFs. However, GPER silencing abrogated the above hypoxia-driven cytokine expression in CAFs. Moreover, knockdown of GPER in CAFs suppressed breast cancer cell invasion induced by CAF conditioned media (CM). Furthermore, GPER silencing in CAFs inhibited hypoxia-increased CTGF expression in CAFs and breast cancer cells cultured with CM from CAFs under hypoxic conditions. In addition, CTGF is responsible for the observed effects of GPER on CAFs activation and breast cancer invasion. Our findings further extend the molecular mechanisms through which the tumor microenvironment may contribute to cancer progression.