Unraveling the relationship between ACTH and cortisol levels in COVID-19 infections: A meta-analysis.

Objective: In December 2019, a novel pneumonia associated with the 2019 coronavirus emerged unexpectedly. However, limited data exist on the effects of COVID-19 on ACTH and cortisol levels. To address this gap in knowledge, we conducted a meta-analysis of published studies on the relationship between COVID-19 patients and their ACTH and cortisol levels.

Cathelicidin promotes liver repair after acetaminophen-induced liver injury in mice.

Background & Aims: Acetaminophen (APAP)-induced acute liver injury (AILI) is a leading cause of acute liver failure (ALF). -acetylcysteine (NAC) is only effective within 24 h after APAP intoxication, raising an urgent need for alternative approaches to treat this disease. This study aimed to test whether cathelicidin (), which is a protective factor in chronic liver diseases, protects mice against APAP-induced liver injury and ALF.

Impact of obstructive sleep apnea on aortic disease occurrence: A meta-analysis.

Objective: Aortic diseases, mainly including aortic dilatation, aortic aneurysm (AA) and aortic dissection (AD), have high morbidity and mortality. Many studies have suggested that obstructive sleep apnea (OSA) acts as a candidate risk factor for aortic diseases. Thus, we performed a meta-analysis to explore comprehensively the effect of OSA on the risk of aortic disease occurrence.

miR-182-5p promotes hepatocyte-stellate cell crosstalk to facilitate liver regeneration.

A unique feature of the liver is its high regenerative capacity, which is essential to maintain liver homeostasis. However, key regulators of liver regeneration (LR) remain ill-defined. Here, we identify hepatic miR-182-5p as a key regulator of LR.

GRB10 regulates β-cell mass by inhibiting β-cell proliferation and stimulating β-cell dedifferentiation.

Decreased functional β-cell mass is the hallmark of diabetes, but the cause of this metabolic defect remains elusive. Here, we show that the levels of the growth factor receptor-bound protein 10 (GRB10), a negative regulator of insulin and mTORC1 signaling, are markedly induced in islets of diabetic mice and high glucose-treated insulinoma cell line INS-1 cells. β-cell-specific knockout of Grb10 in mice increased β-cell mass and improved β-cell function.

Sex difference in lipid levels in first-diagnosed drug-naïve depression patients: A case-control and 12-weeks follow-up study.

Aim: Patients with depression have a high prevalence of developing dyslipidemia. In this study, we aim to investigate the difference of serum lipids, including total cholesterol (TCH), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), between the depressed patients and healthy controls. Sex differences in lipids and their psychological correlations were also included.

The miR-182-5p/FGF21/acetylcholine axis mediates the crosstalk between adipocytes and macrophages to promote beige fat thermogenesis.

A dynamically regulated microenvironment, which is mediated by crosstalk between adipocytes and neighboring cells, is critical for adipose tissue homeostasis and function. However, information on key molecules and/or signaling pathways regulating the crosstalk remains limited. In this study, we identify adipocyte miRNA-182-5p (miR-182-5p) as a crucial antiobesity molecule that stimulated beige fat thermogenesis by promoting the crosstalk between adipocytes and macrophages.

Adiponectin restrains ILC2 activation by AMPK-mediated feedback inhibition of IL-33 signaling.

ILC2s are present in adipose tissue and play a critical role in regulating adipose thermogenesis. However, the mechanisms underlying the activation of adipose-resident ILC2s remain poorly defined. Here, we show that IL-33, a potent ILC2 activator, stimulates phosphorylation of AMPK at Thr172 via TAK1 in primary ILC2s, which provides a feedback mechanism to inhibit IL-33-induced NF-κB activation and IL-13 production.

Rheb promotes brown fat thermogenesis by Notch-dependent activation of the PKA signaling pathway.

Increasing brown and beige fat thermogenesis have an anti-obesity effect and thus great metabolic benefits. However, the molecular mechanisms regulating brown and beige fat thermogenesis remain to be further elucidated. We recently found that fat-specific knockout of Rheb promoted beige fat thermogenesis.

De-silencing contributes to acute ER stress-induced steatosis in mouse liver.

The growth factor receptor bound protein GRB10 is an imprinted gene product and a key negative regulator of the insulin, IGF1 and mTORC1 signaling pathways. GRB10 is highly expressed in mouse fetal liver but almost completely silenced in adult mice, suggesting a potential detrimental role of this protein in adult liver function. Here we show that the gene could be reactivated in adult mouse liver by acute endoplasmic reticulum stress (ER stress) such as tunicamycin or a short-term high-fat diet (HFD) challenge, concurrently with increased unfolded protein response (UPR) and hepatosteatosis.

Myeloid adrenergic signaling via CaMKII forms a feedforward loop of catecholamine biosynthesis.

Type 2 immune response has been shown to facilitate cold-induced thermogenesis and browning of white fat. However, whether alternatively activated macrophages produce catecholamine and substantially promote adaptive thermogenesis in adipose tissue remains controversial. Here, we show that tyrosine hydroxylase (TyrH), a rate-limiting enzyme of catecholamine biosynthesis, was expressed and phosphorylated in adipose-resident macrophages.

Hepatic DsbA-L protects mice from diet-induced hepatosteatosis and insulin resistance.

Hepatic insulin resistance and hepatosteatosis in diet-induced obesity are associated with various metabolic diseases, yet the underlying mechanisms remain to be fully elucidated. Here we show that the expression levels of the disulfide-bond A oxidoreductase-like protein (DsbA-L) are significantly reduced in the liver of obese mice and humans. Liver-specific knockout or adenovirus-mediated overexpression of DsbA-L exacerbates or alleviates, respectively, high-fat diet-induced mitochondrial dysfunction, hepatosteatosis, and insulin resistance in mice.

Identification of miR-106b-93 as a negative regulator of brown adipocyte differentiation.

microRNAs (miRNAs) have been reported to play an essential role in the regulation of brown adipocyte adipogenesis. In the present study, we investigated the role of the miR-106b-93 cluster in the differentiation of brown adipocytes. We found that knockdown of miR-106b and miR-93 significantly induced the expression of brown fat-specific genes and promoted the accumulation of lipid-droplet in differentiating brown adipocytes.

[Compositions of organic acids in PM10 emission sources in Xiamen urban atmosphere].

The possible organic acid emission sources in PM10 in Xiamen urban atmosphere such as cooking, biomass burning, vehicle exhaust and soil/dust were obtained using a re-suspension test chamber. A total of 15 organic acids including dicarboxylic acids, fatty acids and aromatic acids were determined using GC/MS after derivatization with BF3/n-butanol. The results showed that the highest total concentration of 15 organic acids (53%) was found in cooking emission and the average concentration of the sum of linoleic acid and oleic acid was 24% +/- 14%.

[1α, 25(OH)(2) D(3) protects pancreatic β-cell line from cytokine-induced apoptosis and impaired insulin secretion].

Objective: To explore the protective effects and potential mechanisms of 1α, 25(OH)(2) D(3) (VitD(3)) on pancreatic β-cells.

Methods: The apoptosis of NIT-1 cells was induced by interleukin-1β (IL-1β) and interferon-γ (IFN-γ) in vitro. Then the apoptotic rate of NIT-1 cells was determined by Hoechest33342 staining and Annexin V-FITC/PI flow cytometry.

[Characteristics of PCBs in a capacitor storage site and an industrial brownfield].

The levels and congener patterns of 28 PCBs compounds were investigated in soil and dust fallout collected in a capacitor storage site and an industrial brownfield, respectively in Sichuan Ziyang Locomotive Factory. The highest concentration of the total PCBs(sigma PCBs =227 502 ng x g(-1)) was found in soil collected from the front gate (unsealed) of the capacitor storage tunnel. Very high levels of sigma PCBs, exceed 10 microg x g(-1), were also found in the dust collected from the window sill of an iron foundry.

[Uncertainty analysis of gas/particle partitioning of atmospheric polycyclic aromatic hydrocarbons].

During the period from August 10, 2010 through August 14, 2010, particle and gas phase PAHs were collected and analyzed using double filters plus PUFs (Poly Urethane Foam) sampling system, and the uncertainties of gas/particle partitioning coefficients of PAHs were investigated using the propagation of errors formulas. The results showed that low-molecular weight PAHs such as naphthalene, acenaphthylene, acenaphthene and fluorene possessed the strong breakthrough capacity with the breakthrough rates close to 50% in double PUF cartridges. The corrected K(p) values based on the sorption of PAHs to the primary filter were more than an order of magnitude higher than those without sorption correction for naphthalene, acenaphthylene and acenaphthene.

Thiazolidinediones protect mouse pancreatic β-cells directly from cytokine-induced cytotoxicity through PPARγ-dependent mechanisms.

Since most of the current studies of thiazolidinediones (TZDs) are only focused on improving glycemic control, increasing insulin sensitivity, and regulating inflammatory states in Type 2 Diabetes, it is still controversial whether TZDs have direct, protective effects on pancreatic β-cells in autoimmune diabetes. Here, we show the protective effects of TZDs on mouse pancreatic β-cell line cells (NIT-1) impaired by exposure to inflammatory cytokines (IL-1β and IFN-γ) and explore the potential mechanisms for this. The apoptosis rate and caspase-3 activity were remarkably increased, and insulin secretion response to glucose was impaired severely by exposure to IL-1β/IFN-γ for 48 h compared to control cells, whereas apoptosis rate and caspase-3 activity were significantly decreased in cells with treatment of rosiglitazone (RGZ) or pioglitazone (PIG), and the capacity for insulin secretion response to glucose was recovered.

[Glitazones protects beta cell function from cytotoxic cytokines through PPAR gamma-dependent mechanisms].

Objective: To investigate the protective effects of glitazones on islet beta cells and PPAR gamma dependence of such effects.

Methods: IL-1beta and IFN-gamma were used to treat NIT-1 cells, a beta cell line, to induce beta cell damage. The cells were pretreated with rosiglitazone and pioglitazone at different concentrations to study the protective effects of these drugs.

[The effect and mechanism of transient continuous subcutaneous insulin infusion therapy on beta cell function, insulin resistance and vascular endothelial injury in newly diagnosed type 2 diabetes].

Objectives: To explore the effect of transient continuous subcutaneous insulin infusion (CSII) on ß cell function, insulin resistance and vascular endothelial injury in newly diagnosed type 2 diabetic patients and its potential mechanism.

Methods: Ten patients with newly diagnosed type 2 diabetes mellitus (T2DM) accepted CSII for two weeks. Intravenous glucose tolerance test (IVGTT) and hyperinsulinemia euglycemia clamp test were performed before and after CSII.

[Inhibitory effects of thiazolidinedione upon cytokine-induced apoptosis in pancreatic beta-cell line].

Objective: To investigate the protective effects and potential mechanisms of TZD upon pancreatic beta-cells.

Methods: Apoptosis was induced in vitro by interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma). After treatment with rosiglitazone (RSG)/pioglitazone (PIG) at the final concentrations of 1 micromol/L, 10 micromol/L, 20 micromol/L respectively, the apoptotic rate of NIT-1 cells was determined by Hoechest33342 staining and Annexin V-FITC/PI flow cytometry respectively.