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05). 3-Methyladenine ic50 Changes of systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate fluctuations in group B were lower than those in group A (P less then 0.05). At 24 h after surgery, VAS scores of group B were lower than those of group A (P less then 0.05); levels of IL-6 and TNF-α were lower than those of group A (P less then 0.05); CD3+ cells, CD4+ cells, CD8+ cells, and CD4/CD8 ratio were higher than those of group A (P less then 0.05), and MMSE score was higher than that of group A (P less then 0.05). The incidence of gastrointestinal reactions and postoperative cognitive dysfunction (POCD) in group B was lower than that in group A (P less then 0.05). In conclusion, administration of dexmedetomidine can effectively shorten the recovery time of patients, stabilize intraoperative hemodynamics of patients, protect immune function, and reduce postoperative pain and POCD occurrence during anesthesia of hip replacement.Diabetic cardiomyopathy (DCM) is a worldwide public health concern that continues to display rapid growth trends. This study investigated the function of sirtuin 3 (SIRT3), a primary mitochondrial deacetylase with important roles in antioxidant defense and oxidative metabolism, during high glucose-induced cardiomyocyte (AC16 cell) injury. Peroxisome proliferator-activated receptor-α (PPAR-α) is directly related to the occurrence of DCM. Hence, we further examined the relationship between SIRT3 and PPAR-α. AC16 cells were treated with various concentrations of glucose. Relative mRNA expression and protein levels were detected by RT-qPCR and western blot analysis, respectively. Cell proliferation and apoptosis were assessed using CCK8 and Annexin V-FITC apoptosis detection kits, respectively. DCFH-DA assay was used to measure reactive oxygen species (ROS) accumulation. The results indicated that high glucose treatment reduced the expression of mRNA and protein of SIRT3 and PPAR-α in AC16 cells. Moreover, high glucose inhibited cell proliferation, as well as induced apoptosis, intracellular hydrogen peroxide production, and JNK1/2 phosphorylation. These effects were antagonized by SIRT3 overexpression or treatment with the PPAR-α agonist, Wy14643. Conversely, inhibition of SIRT3 via 3-TYP led to similar phenomena as those induced by high glucose treatment in AC16 cells, which were blocked by Wy14643. Lastly, chromatin immunoprecipitation (ChIP) and luciferase assays demonstrated SIRT3 as a direct target of PPAR-α. Taken together, the results provide evidence for an important role of SIRT3 in high glucose-induced cardiomyocyte injury and regulation of JNK1/2 signaling. Further, SIRT3 is a direct downstream target of PPAR-α.The present study aimed to investigate the clinical characteristics of von Hippel-Lindau (VHL) disease and the clinical significance of VHL gene detection. The clinical materials of patients with VHL disease were collected from 3 different families between May 1985 and October 2017. A systematic pedigree study and VHL gene detection at the germline level were performed together with a literature review. Of the 22 patients from 3 VHL pedigrees, 10 exhibited VHL gene mutations (3 genotypes) at the germline level. The genotypes of pedigree were VHL-p.R161Q (c.482G>A), VHL-p.N78S (c.233A>G), and VHL-p.R167Q (c.500G>A). During the follow-up period, the symptoms were stable in 10 patients, including 2 cases of central nervous system hemangioblastomas (CNS-HB), 3 cases of bilateral multiple renal cell carcinoma (RCC) and 5 cases of adrenal pheochromocytoma without local recurrence or distant metastasis. Patients with p.R161Q and p.N78S were not associated with CNS-HB, which was different from the clinical phenotype of previously reported families. RCC were Fuhrman II grade, which was consistent with the previous study. The results of the present study indicated that the standardization of early diagnosis and the improvement of long-term efficacy may be achieved by combining clinical screening and VHL gene detection.The adrenal gland serve important roles in the modulation of the immune response, the adjustment of blood pressure, the stress reaction via glucocorticoids and the hydroelectrolytic balance via mineralocorticoids. Primary adrenal insufficiency, known as Addison disease, is characterized by a decrease in glucocorticoid secretion (cortisol) and, more rarely, by a hyposecretion of mineralocorticoids (aldosterone). The production of cortisol, which is a hormone that helps the body respond to stress, is regulated in the brain, the hypothalamus and the pituitary gland. The hypothalamus stimulates the pituitary gland to produce adrenocorticotropic hormone, which stimulates cortisol production from the adrenal gland. If left untreated, Addison disease has a high mortality rate. Corticotherapy used in the treatment of Addison disease is associated with a certain cardiovascular risk. The proatherogenic effect of corticoids is based on the chronic inflammatory response of the vascular wall to a series of events. The aim of the current case report was to review the pathophysiological mechanisms and interactions that may lead to the onset of acute coronary syndrome with ST elevation in a patient with Addison disease.Na+/H+ exchangers (NHEs) are a family of membrane proteins that contribute to exchanging one intracellular proton for one extracellular sodium. The family of NHEs consists of nine known members, NHE1-9. Each isoform represents a different gene product that has unique tissue expression, membrane localization, physiological effects, pathological regulation and sensitivity to drug inhibitors. NHE1 was the first to be discovered and is often referred to as the 'housekeeping' isoform of the NHE family. NHEs are not only involved in a variety of physiological processes, including the control of transepithelial Na+ absorption, intracellular pH, cell volume, cell proliferation, migration and apoptosis, but also modulate complex pathological events. Currently, the vast majority of review articles have focused on the role of members of the NHE family in inflammatory bowel disease, intestinal infectious diarrhea and digestive system tumorigenesis, but only a few reviews have discussed the role of NHEs in liver disease. Therefore, the present review described the basic biology of NHEs and highlighted their physiological and pathological effects in the liver.