Biomass fuels related-PM promotes lung fibroblast-myofibroblast transition through PI3K/AKT/TRPC1 pathway.

Emerging evidence has suggested that exposure to PM is a significant contributing factor to the development of chronic obstructive pulmonary disease (COPD). However, the underlying biological effects and mechanisms of PM in COPD pathology remain elusive. In this study, we aimed to investigate the implication and regulatory effect of biomass fuels related-PM (BRPM) concerning the pathological process of fibroblast-to-myofibroblast transition (FMT) in the context of COPD.

Successful treatment of new-onset diabetes mellitus and IgA nephropathy after COVID-19 vaccination: a case report.

De novo glomerular injuries or relapse of nephropathy following COVID-19 vaccine has been reported. Here we present the first case of successful treatment of new-onset diabetes mellitus and biopsy-proven IgA nephropathy after COVID-19 vaccination. A 56-year-old man with no known medical history of renal dysfunction or diabetes mellitus developed both within 3 months after receiving a third dose of inactivated COVID-19 vaccine (Vero cells).

Alcoholic Setdb1 suppression promotes hepatosteatosis in mice by strengthening Plin2.

Background And Aims: Hepatosteatosis is one of the early features of alcoholic liver disease (ALD) and pharmaceutical or genetic interfering of the development of hepatosteatosis will efficiently alleviate the progression of ALD. Currently, the role of histone methyltransferase Setdb1 in ALD is not yet well understood.

Method: Lieber-De Carli diet mice model and NIAAA mice model were constructed to confirm the expression of Setdb1.

Super Enhancer-Associated Circular RNA-CircKrt4 Regulates Hypoxic Pulmonary Artery Endothelial Cell Dysfunction in Mice.

Background: Circular RNAs (circRNAs) have been implicated in pulmonary hypertension progression through largely unknown mechanisms. Pulmonary artery endothelial cell (PAEC) dysfunction is a hallmark in the pathogenesis of pulmonary hypertension. However, the specific role of circular RNAs in PAEC injury caused by hypoxia remains unclear.

Elevated Urinary IL-6 Predicts the Progression of IgA Nephropathy.

Introduction: Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis worldwide. However, biomarkers for predicting the progression or regression of IgAN remain a clinical challenge. In the present study, we aim to identify promising prognostic markers of IgAN.

Alpha1B-adreneroceptor is involved in norepinephrine-induced pulmonary artery smooth muscle cell proliferation via p38 signaling.

The higher norepinephrine (NE) concentration induced by sympathetic nerve hyperactivation participated in pulmonary artery smooth muscle cells (PASMCs) over-proliferation and led to pulmonary vascular remodeling (PVR), which played an important role in pulmonary artery hypertension (PAH). However, the underlying mechanism by which NE induced PASMCs proliferation had not been fully elucidated. In the present study, we found that prazosin, the inhibitor of α-AR, reversed hypoxia-induced changes in pulmonary circulatory function which were analyzed by echocardiography to measure pulmonary artery acceleration time (PAT) and pulmonary arterial velocity time integral (PAVTI) and right heart catheterization to test right ventricular systolic pressure (RVSP), respectively.

Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation.

Background: Excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) is the main cause of hypoxic pulmonary hypertension (PH), and mitochondrial homeostasis plays a crucial role. However, the specific molecular regulatory mechanism of mitochondrial function in PASMCs remains unclear.

Methods: In this study, using the CCK8 assay, EdU incorporation, flow cytometry, Western blotting, co-IP, mass spectrometry, electron microscopy, immunofluorescence, Seahorse extracellular flux analysis and echocardiography, we investigated the specific involvement of apoptosis-inducing factor (AIF), a mitochondrial oxidoreductase in regulating mitochondrial energy metabolism and mitophagy in PASMCs.

circRNA CDR1as Promotes Pulmonary Artery Smooth Muscle Cell Calcification by Upregulating CAMK2D and CNN3 via Sponging miR-7-5p.

Emerging evidence has suggested that circular RNAs (circRNAs) are involved in multiple physiological processes and participate in a variety of human diseases. However, the underlying biological function of circRNAs in pulmonary hypertension (PH) is still ambiguous. Herein, we investigated the implication and regulatory effect of a typical circRNA, CDR1as, in the pathological process of vascular calcification in PH.

Impact of parathyroidectomy on left ventricular function in end stage renal disease patients.

Background: Secondary hyperparathyroidism (SHPT) is a common complication in end-stage renal disease (ESRD) patients, and parathyroidectomy (PTX) is an effective treatment intervention of SHPT. However, the curative impact of PTX on left ventricular function still remains incompletely understood. To evaluate the impact of parathyroidectomy on left ventricular function in ESRD patients, we conducted this retrospective study.

Correction: Tacrolimus dose requirement based on the CYP3A5 genotype in renal transplant patients.

[This corrects the article DOI: 10.18632/oncotarget.18150.

Plasma metabolite biomarkers related to secondary hyperparathyroidism and parathyroid hormone.

Background: Hyperphosphatemia, hypocalcemia, and elevation of parathyroid hormone (PTH) are typical abnormalities of uremic patients with Secondary hyperparathyroidism (SHPT). However, metabolic imbalance associated with SHPT is not well understood.

Methods: A total of 15 SHPT patients with an intact parathyroid hormone (iPTH) level > 600 pg/mL were set as preoperative (PR) group, 15 age- and gender-matched controls who had undergone parathyroidectomy plus forearm transplantation because of hyperparathyroidism and achieved an iPTH level <150 pg/mL were set as postoperative (PO) group.

The Mitochondria-Targeted Metabolic Tubular Injury in Diabetic Kidney Disease.

Background/aims: Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease (ESRD) worldwide, and the importance of tubular injury has been highlighted in recent years. However, the underlying mechanisms and effective therapeutic targets are still unclear. In this study, we investigated mtDNA, mitochondrial dynamics, function and metabolic pathways to determine if mitochondrial damage plays a critical role in the development of tubular injury in DKD patients.

Dacomitinib, a new pan-EGFR inhibitor, is effective in attenuating pulmonary vascular remodeling and pulmonary hypertension.

Accumulating evidence suggests that epidermal growth factor receptor (EGFR) plays a role in the progression of pulmonary arterial hypertension (PAH). Clinically-approved epidermal growth factor inhibitors such as gefitinib, erlotinib, and lapatinib have been explored for PAH. However, None of them were able to attenuate PAH.

alpha1A-adrenoceptor is involved in norepinephrine-induced proliferation of pulmonary artery smooth muscle cells via CaMKII signaling.

Pulmonary arterial hypertension (PAH) is a progressive disease of the pulmonary vasculature characterized by excessive proliferation of pulmonary artery smooth muscle cells (PASMCs). Some studies have demonstrated the sympathetic nervous system is activated in PAH and norepinephrine (NE) released is closely linked with its activation. However, the subtypes of adrenoreceptor (AR) and the downstream molecular cascades which are involved in the proliferation of PASMCs are still unclear.

Whole-Genome Analysis of an Extensive Drug-Resistant Acinetobacter Baumannii ST195 Isolate from a Recipient After DCD Renal Transplantation in China.

Background/aims: Infection with Acinetobacter baumannii was emerging as one of the leading causes of mortality after donation after cardiac death transpalantion.

Methods: We reported a case of a recipient who underwent DCD renal transplantation and later got infected by A.baumannii.

Tacrolimus dose requirement based on the CYP3A5 genotype in renal transplant patients.

Tacrolimus (FK506) and cyclosporine A (CsA) are widely used to protect graft function after renal transplantation. The aim of the present study is to determine whether the single nucleotide polymorphism of CYP3A5 is a predictive index of FK506 dose requirement, and also the selection yardstick of FK506 or CsA treatment.We tested archival peripheral blood of 218 kidney recipients for CYP3A5 genotyping with PCR-SSP.

Evolution of Drug-resistant Acinetobacter baumannii After DCD Renal Transplantation.

Infection after renal transplantation remains a major cause of morbidity and death, especially infection from the extensively drug-resistant bacteria, A. baumannii. A total of fourteen A.

Norepinephrine stimulation of alpha1D-adrenoceptor promotes proliferation of pulmonary artery smooth muscle cells via ERK-1/2 signaling.

It has been shown that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH). Norepinephrine (NE) levels are increased by chemoreflex-dependent sympathetic overactivation and involved in pulmonary vascular remodeling. However, the underlying mechanisms of the remodeling induced by NE are poorly understood.

The Neuroprotective Effects of Carvacrol on Ethanol-Induced Hippocampal Neurons Impairment via the Antioxidative and Antiapoptotic Pathways.

Chronic alcohol consumption causes hippocampal neuronal impairment, which is associated with oxidative stress and apoptosis. Carvacrol is a major monoterpenic phenol found in essential oils from the family Labiatae and has antioxidative stress and antiapoptosis actions. However, the protective effects of carvacrol in ethanol-induced hippocampal neuronal impairment have not been fully understood.

Clinical Significance of the Sympathetic Nervous System in the Development and Progression of Pulmonary Arterial Hypertension.

Background: Pulmonary arterial hypertension (PAH) is defined as a complex disease of clinically characterized by elevated pulmonary pressure eventually resulting in right heart failure and premature death. To date, PAH still remains a life-threatening disease. Published evidence suggests that patients with PAH present profound sympathetic nervous system abnormalities and sympathetic activity has been shown to be increased.

Effect of uric acid-lowering therapy on blood pressure: systematic review and meta-analysis.

Background: The purpose of this meta-analysis was to determine if uric acid-lowering therapy is associated with a decrease in blood pressure (BP) and serum creatinine levels.

Materials And Methods: Medline, Cochrane, EMBASE, and Google Scholar databases were searched until 29 June 2016, with keywords: uric-acid-lowering therapy, allopurinol, febuxostat, uricosuric, and BP. Only randomized controlled trials were included.

Baicalin alleviates ischemia-induced memory impairment by inhibiting the phosphorylation of CaMKII in hippocampus.

Baicalin has a significant neuroprotective effect in stroke. However, the mechanism remains unclear. This study was to reveal the mechanisms by which baicalin protected hippocampal neurons and improved learning and memory impairment after global cerebral ischemia/reperfusion in gerbil.

Inward Rectifier K+ Currents Are Regulated by CaMKII in Endothelial Cells of Primarily Cultured Bovine Pulmonary Arteries.

Endothelium lines the interior surface of vascular walls and regulates vascular tones. The endothelial cells sense and respond to chemical and mechanical stimuli in the circulation, and couple the stimulus signals to vascular smooth muscles, in which inward rectifier K+ currents (Kir) play an important role. Here we applied several complementary strategies to determine the Kir subunit in primarily cultured pulmonary arterial endothelial cells (PAECs) that was regulated by the Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII).

Nociceptin/orphanin FQ-induced inhibition of delayed rectifier potassium currents by calcium/calmodulin-dependent protein kinase type II.

The neuropeptide nociceptin/orphanin FQ (N/OFQ) has been shown to inhibit delayed rectifier potassium current (IK) in acutely dissociated rat parietal cortical neurons. However, the detailed mechanism of N/OFQ-induced inhibition on IK is not clear. This study is the first to explore an involvement of calcium/calmodulin (CaM)-dependent protein kinase type II (CaMKII) in mediating N/OFQ-induced responses.

Depolarization-induced depression of inhibitory transmission in cerebellar Purkinje cells.

Several forms of depolarization-induced plasticity in inhibitory transmission have been reported to occur in cerebellar Purkinje cells (PCs), namely depolarization-induced suppression of inhibition (DSI), depolarization-induced potentiation of inhibition (DPI), and rebound potentiation (RP). Here, we describe another form of synaptic plasticity for gamma-amino butyric acid (GABA)ergic transmission in PCs. Immediately following depolarization trains in a PC, evoked inhibitory postsynaptic currents (eIPSCs) changed their direction from outward to inward currents under a recording condition in which eIPSCs were elicited as an outward current.