Marcusmarcus2284

OBJECTIVES To evaluate the renal function after adrenalectomy in patients with Cushing's syndrome in comparison with that in patients with primary aldosteronism. METHODS This retrospective study included 35 patients with Cushing's syndrome and 51 patients with primary aldosteronism who underwent unilateral adrenalectomy and were followed up for >6 months. The renal function was analyzed before and after adrenalectomy using the estimated glomerular filtration rate. Postoperative renal impairment was defined as a >25% reduction in the estimated glomerular filtration rate from baseline at 1 month after adrenalectomy. Multivariate logistic regression analyses were carried out to examine whether the differences between Cushing's syndrome and primary aldosteronism increased the risk of postoperative renal impairment. Longitudinal changes were calculated starting 1 month after adrenalectomy using the linear mixed model. RESULTS The mean estimated glomerular filtration rate in both groups significantly decreased at 1 month after adrenalectomy from baseline. Postoperative renal impairment was observed in four (11%) and 12 (24%) patients in the Cushing's syndrome and primary aldosteronism groups, respectively. Multivariate analysis showed that preoperative systolic blood pressure was independently associated with postoperative renal impairment, but not with the type of the disease. There was no significant increase or decrease in postoperative estimated glomerular filtration rate observed after the initial decrease after adrenalectomy in either group. CONCLUSIONS Patients with Cushing's syndrome show the same persistent renal impairment after adrenalectomy as that reported in patients with primary aldosteronism. Attention should be given to possible masked renal damage in clinical practice for the management of Cushing's syndrome. © 2020 The Japanese Urological Association.Urolithiasis is highly prevalent in dogs and cats, with struvite and calcium oxalate being most commonly diagnosed. Some commercial diets aimed at reducing the risk of urolithiasis are based on inclusion of sodium chloride (NaCl) in an attempt to dilute the urine and the risk of crystallization, but more information on the effect of differing levels of sodium inclusion is needed. The objective of this study was to compare the short-term effect of four diets differing only in NaCl content (base diet with 0.3% sodium and diets with added NaCl to achieve 0.7, 1.0 and 1.3% sodium as fed) on urinary ion concentrations and relative supersaturation (RSS) of struvite and calcium oxalate in dogs and cats. In both species, there was a significant increase in water intake and urine volume as dietary NaCl increased. Urine sodium concentration increased with increasing dietary NaCl. The highest sodium diet increased urinary calcium excretion in dogs only, while decreasing urinary calcium concentration. Calcium oxalate RSS and struvite RSS both significantly decreased, with the lowest RSS values reported on the highest sodium diet in both dogs and cats (p  less then  .001). These results suggest that an increase in dietary NaCl decreases RSS values in both dogs and cats. Despite an increase in urinary calcium excretion in dogs, urinary calcium concentration and calcium oxalate RSS were lower on high sodium diets due to urine dilution. Long-term studies are needed to confirm the relationship between RSS and stone occurrence and recurrence. © 2020 The Royal Canin. Journal of Animal Physiology and Animal Nutrition published by Blackwell Verlag GmbH.OBJECTIVES Oestrogen is known to inhibit osteoclastogenesis, and numerous studies have identified it as an autophagic activator. To date, the role of oestrogen in the autophagy of osteoclast precursors (OCPs) during osteoclastogenesis remains unclear. This study aimed to determine the effect of autophagy regulated by the biologically active form of oestrogen (17β-estradiol) on osteoclastogenesis. MATERIALS AND METHODS After treatment with 17β-estradiol in OCPs (from bone marrow-derived macrophages, BMMs) and ovariectomy (OVX) mice, we measured the effect of 17β-estradiol on the autophagy of OCPs in vitro and in vivo. In addition, we studied the role of autophagy in the OCP proliferation, osteoclast differentiation and bone loss regulated by 17β-estradiol using autophagic inhibitor or knock-down of autophagic genes. RESULTS The results showed that direct administration of 17β-estradiol enhanced the autophagic response of OCPs. Interestingly, 17β-estradiol inhibited the stimulatory effect of receptor activator of nuclear factor-κB ligand (RANKL) on the autophagy and osteoclastogenesis of OCPs. Moreover, 17β-estradiol inhibited the downstream signalling of RANKL. Autophagic suppression by pharmacological inhibitors or gene silencing enhanced the inhibitory effect of 17β-estradiol on osteoclastogenesis. In vivo assays showed that the autophagic inhibitor 3-MA not only inhibited the autophagic activity of the OCPs in the trabecular bone of OVX mice but also enhanced the ability of 17β-estradiol to ameliorate bone loss. CONCLUSIONS In conclusion, our study showed that oestrogen directly enhanced the autophagy of OCPs, which inhibited its anti-osteoclastogenic effect. Drugs based on autophagic inhibition may enhance the efficacy of oestrogen on osteoporosis. © 2020 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.Curcumin is a naturally occurring nutraceutical compound with a number of therapeutic and biological activities such as antioxidant, anti-inflammatory, anti-diabetic, antitumor, and cardioprotective. This plant-derived chemical has demonstrated great potential in targeting various signaling pathways to exert its protective effects. Signal transducers and activator of transcription (STAT) is one of the molecular pathways involved in a variety of biological processes such as cell proliferation and cell apoptosis. Accumulating data demonstrates that the STAT pathway is an important target in treatment of a number of disorders, particularly cancer. Curcumin is capable of affecting STAT signaling pathway in induction of its therapeutic impacts. Curcumin is able to enhance the level of anti-inflammatory cytokines and improve inflammatory disorders such as colitis by targeting STAT signaling pathway. Furthermore, studies show that inhibition of JAK/STAT pathway by curcumin is involved in reduced migration and invasion of cancer cells. Curcumin normalizes the expression of JAK/STAT signaling pathway to exert anti-diabetic, renoprotective, and neuroprotective impacts. At the present review, we provide a comprehensive discussion about the effect of curcumin on JAK/STAT signaling pathway to direct further studies in this field. © 2020 John Wiley & Sons, Ltd.BACKGROUND CircRNA plays an important role in the development of tumors, but its mechanism of action in ovarian cancer is still unclear. METHODS The expression level of hsa_circ_0013958 in 45 pairs of ovarian cancer tissues and cells was quantified by qRT-PCR, further revealing whether it is related to clinicopathological features and diagnostic value. Next, the effects of hsa_circ_0013958 on the proliferation, migration, invasion, and apoptosis of A2780 and OVCAR-3 cells were detected by CCK-8 assay, Transwell assay, and flow cytometry, respectively. Last, the expression levels of epithelial-mesenchymal transition-related proteins (E-cadherin and Vimentin) and apoptosis-related proteins (Bcl-2 and Bax) were detected by Western blotting. RESULTS Hsa_circ_0013958 was highly expressed in ovarian cancer tissues and cells, and its expression was closely related to patient FIGO stage and lymph node metastasis. Further, in vitro studies showed that knockdown of hsa_circ_0013958 suppressed proliferation, migration, and invasion of ovarian cancer cells but elevated the cell apoptotic rate. The expression levels of both epithelial-mesenchymal transition-related proteins and apoptosis-related proteins were also changed. CONCLUSIONS Hsa_circ_0013958 may contribute to the development of ovarian cancer by affecting epithelial-mesenchymal transition and apoptotic signaling pathways. © 2020 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.Small cerebral vascular disease (SCeVD) demonstrated by white matter hyperintensity (WMH) on MRI contributes to the development of dementia in Alzheimer's disease (AD), but it has not been possible to correlate onset, severity, or protein components of SCeVD with characteristics of WMH in living patients. Plasma endothelial-derived exosomes (EDEs) were enriched by two-step immunoabsorption from four groups of participants with no clinical evidence of cerebrovascular disease cognitively normal (CN) without WMH (CN without SCeVD, n = 20), CN with SCeVD (n = 22), preclinical AD (pAD) + mild cognitive impairment (MCI) without SCeVD (pAD/MCI without SCeVD, n = 22), and pAD/MCI with SCeVD (n = 16) for ELISA quantification of cargo proteins. Exosome marker CD81-normalized EDE levels of the cerebrovascular-selective biomarkers large neutral amino acid transporter 1 (LAT-1), glucose transporter type 1 (Glut-1), and permeability-glycoprotein (p-GP, ABCB1) were similarly significantly higher in the CN with SCeVD and pAD/MCI with SCeVD groups than their corresponding control groups without SCeVD. CD81-normalized EDE levels of Aβ40 and Aβ42 were significantly higher in the pAD/MCI with SCeVD group but not in the CN with SCeVD group relative to controls without SCeVD. Levels of normal cellular prion protein (PrPc), a receptor for amyloid peptides, and phospho-181T-tau were higher in both CN and pAD/MCI with SCeVD groups than in the corresponding controls. High EDE levels of Aβ40, Aβ42, and phospho-181T-tau in patients with WMH suggesting SCeVD appear at the pre-clinical or MCI stage of AD and therapeutic lowering of neurotoxic peptide levels may delay progression of AD angiopathy. © 2020 Federation of American Societies for Experimental Biology.OBJECTIVE Lumbar disk herniation (LDH) is a complex condition based on lumbar disk degeneration (LDD). Previous studies have shown that genetic factors are highly associated with the severity and risk for LDH. This case-control study was aimed to evaluate the association between the matrix metalloproteinase (MMP)-3 gene rs591058 C/T polymorphism and LDH risk in a southern Chinese population. METHODS A total of 231 LDH patients and 312 healthy controls were recruited in this study. Genotyping was analyzed using a standard polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). RESULTS It was observed that TT genotype or T allele carriers of the MMP-3 gene rs591058 C/T polymorphism was more likely associated with an increased risk for LDH. Subgroup analyses showed the following characteristics increased the risk for LDH female sex; cigarette smoking; and alcohol consumption. Furthermore, individuals with high whole body vibration, bending/twisting, and lifting were associated with an increased risk for LDH. CONCLUSION Taken together, these data indicated that the MMP-3 gene rs591058 C/T polymorphism was associated with an increased risk for LDH. The MMP-3 gene rs591058 C/T polymorphism might serve as a clinical indicator and marker for LDH risk in the Chinese population. © 2020 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.