Sleep disorders have a high incidence rate in patients with end-stage renal disease(ESRD)and severely affect their quality of life.As the most effective treatment for ESRD,kidney transplantation can significantly improve renal function and prolong survival of patients.However,clinical observations have found that 19.3%to 78.0%of kidney transplant recipients still experience persistent various sleep disorders,such as insomnia,sleep-related breathing disorders and sleep-related movement disorders after surgery.These sleep disorders not only lead to impaired daytime function but are also closely related to adverse outcomes such as cardiovascular complications and increased infection risks.Currently,research on the pathogenesis of sleep disorders in kidney transplant recipients is still insufficient,and clinical diagnosis and treatment face many challenges.This article systematically reviews the epidemiological characteristics,pathophysiological mechanisms,clinical impacts,and new developments in the diagnosis and treatment of sleep disorders in kidney transplant recipients.It aims to provide evidence-based support for clinicians and promote the establishment of more comprehensive early screening and individualized treatment plans to improve the long-term prognosis of recipients.

Sleep disorders have a high incidence rate in patients with end-stage renal disease(ESRD)and severely affect their quality of life.As the most effective treatment for ESRD,kidney transplantation can significantly improve renal function and prolong survival of patients.However,clinical observations have found that 19.3%to 78.0%of kidney transplant recipients still experience persistent various sleep disorders,such as insomnia,sleep-related breathing disorders and sleep-related movement disorders after surgery.These sleep disorders not only lead to impaired daytime function but are also closely related to adverse outcomes such as cardiovascular complications and increased infection risks.Currently,research on the pathogenesis of sleep disorders in kidney transplant recipients is still insufficient,and clinical diagnosis and treatment face many challenges.This article systematically reviews the epidemiological characteristics,pathophysiological mechanisms,clinical impacts,and new developments in the diagnosis and treatment of sleep disorders in kidney transplant recipients.It aims to provide evidence-based support for clinicians and promote the establishment of more comprehensive early screening and individualized treatment plans to improve the long-term prognosis of recipients.

Background Di(2-ethylhexyl) phthalate (DEHP) is the highest consumed and the most widely used phthalic acid ester, their effects on lipid metabolism have attracted the attention of many scholars. However, the associated mechanism is still unclear. Objective To observe the effect of DEHP on lipid metabolism in rats, probe its possible mechanism, and provide a research basis for the effect of DEHP on human lipid metabolism. Methods Forty healthy male SD rats were randomly divided into 4 groups: solvent control (0 mg·kg⁻¹ DEHP), low DEHP (187 mg·kg⁻¹), medium DEHP (375 mg·kg⁻¹), and high DEHP (750 mg·kg⁻¹) groups. DEHP was administered by oral gavage for 6 d per week, consecutively 8 weeks. The rats were weighed once a week during the exposure period. At 24 h after the last exposure, the rats were anesthetized with 20% urethane and sacrificed by apical puncture. Rat livers were harvested and weighed before hematoxylin-eosin (HE) histopathological observation. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA levels of lipid metabolism-related genes Janus kinase 3 (JAK3), signal transducer and activator of transcription 5b (STAT5b), and peroxisome proliferator-activated receptor γ (PPARγ) in liver, and Western blot was used to detect the expression levels of lipid metabolism-related proteins JAK3, STAT5b, and PPARγ in liver. Results Compared with the control group, there was no significant difference in the body weight gain of the rats in each group (P>0.05). The liver organ coefficients of the DEHP exposure groups were higher than that of the control group (P<0.001), and increased with higher DEHP dosages. The level of high-density lipoprotein cholesterol (HDL-C) in serum decreased in all DEHP exposure groups (P<0.05), and the level of low-density lipoprotein cholesterol (LDL-C) in serum increased in the high DEHP group (P<0.05). The results of liver histopathological morphology showed that the hepatocytes of each DEHP group were enlarged and edematous in varying degrees, with loose stroma and irregular arrangement of cells, which were manifested as inflammatory cell infiltration and fatty degeneration of liver cells. Compared to the control group, the mRNA levels of JAK3, STAT5b, and PPARγ in liver tissues of rats in each DEHP group decreased (P<0.001). Compared to the control group, the relative expression levels of JAK3 in each DEHP group decreased (P<0.05), and the relative expression levels of STAT5b and PPARγ in the medium and high DEHP groups decreased (P<0.05). Conclusion DEHP exposure can induce abnormal lipid metabolism in rats, and the mechanism may be related to DEHP inhibiting the activation of JAK3/STAT5b/PPARγ signaling pathway.

Background Di(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) are representative environmental endocrine disruptors of phthalate esters (PAEs). Some studies have shown that PAEs exposure may have an impact on lipid metabolism. Objective To investigate the effects of DEHP and/or DBP on lipid metabolism in rats and their possible mechanisms of action. Methods Thirty-six weaned healthy SD male rats, 3 weeks old, weighing 50-70 g, were divided into four groups, i.e., a corn oil control group, a DEHP (750 mg·kg⁻¹) group, a DBP (500 mg·kg⁻¹) group, and a DEHP+DBP (750 mg·kg⁻¹+500 mg·kg⁻¹) group. The rats were exposed to DEHP and/or DBP by oral gavage for 8 weeks, and weighed once a week. The rats were anesthetized 24 h after the last dose, and blood was taken from the apical part of the heart. Serum high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), and triglyceride (TG) were detected. Liver tissues and perigenital adipose tissues were collected, weighed, and one portion of the tissues was fixed in 10% neutral formalin for pathomorphological observation, and another portion was used for mRNA detection of lipid metabolism-related genes such as Janus kinase 3 (JAK3), signal transducer and activator of transcription 5b (STAT5b), and peroxisome proliferator-activated receptor γ (PPARγ). Results During the DEHP and/or DBP exposure period, the rats in all groups were free to eat and drink without death or injury observed. Compared with the control group: The body weight gain in the DEHP+DBP group was lower at all time points from the 2nd week onwards (P<0.05); the liver organ coefficients of the DEHP and the DEHP+DBP groups were higher (P<0.05); the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). Compared with the DEHP+DBP group: The body weight gains in the DEHP group at the 2nd, 4th, 5th, and 8th weeks were higher (P<0.05), and the body weight gains in the DBP group were higher at all time points except the 1st week (P<0.05); the liver organ coefficients in the DEHP group and the DBP group were lower (P<0.05); the serum TG level in the DEHP group was higher(P<0.05), and the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). The pathomorphological results of liver tissues showed that the hepatocytes in the DEHP, DBP, and DEHP+DBP groups were disordered with loss of cord-like arrangement, swelling (suggesting change of cell proliferation), and presented bilirubin pigmentation. The pathomorphological results of rat perigenital adipose tissues showed had irregular alignment, sizes, and arrangement of adipocyte in the DEHP, DBP, and DEHP+DBP groups. The results of rat liver lipid metabolism-related gene mRNA levels showed that the liver JAK3, STAT5b, and PPARγ mRNA levels in the DEHP, DBP, and DEHP+DBP groups were lower than those in the control group (P<0.05); the rat liver PPARγ mRNA levels in the DEHP and DBP groups were lower than those in the DEHP+DBP group (P<0.05). Conclusion DEHP and/or DBP can inhibit the increase of body weight to varying degrees, induce inflammatory damage to liver tissues, and cause abnormal lipid metabolism in rats, and the associated mechanism may be related to inhibiting the activation of JAK3/STAT5b/PPARγ signaling pathway in rat liver tissues.

Background and purpose:Prostate-speciifc membrane antigen (PSMA), a cell surface protein with high expression in prostate carcinoma (PC) cells, is an attractive target for PC imaging and therapy. Small-molecule radiopharmaceuticals targeting PSMA can detect the location and extent of disease with high sensitivity and speciifcity. The aim of this study was to evaluate the value of technetium-99m-labelled small molecule against PSMA (HYNIC-Glu-Urea-A,99mTc-PSMA) for the detection of primary and metastatic prostate cancers.Methods:Twenty-four prostate cancer patients and 1 patient with benign prostate hyperplasia received whole-body scan followed by abdominopelvic SPECT/CT 2 h after intravenous injection of99mTc-PSMA. Tumor to muscle uptake ratio of99mTc-PSMA was calcu-lated using region of interest (ROI) technology. The sensitivity and specificity of99mTc-PSMA were evaluated. The relationships between positive99mTc-PSMA and prostate speciifc antigen (PSA) level and Gleason Score were analyzed. Results:Based on per patient, the sensitivity and speciifcity of99mTc-PSMA were 72.7% (16/22) and 100% (3/3), re-spectively. The level of PSA in patients with positive99mTc-PSMA imaging was signiifcantly higher than that in patients with negative99mTc-PSMA imaging [(PSA median 17.31 ng/mL, range: 2.26-3 239.0 ng/mL)vs(PSA median 0.49 ng/mL, range: 0.07-9.28 ng/mL)] (Z=-3.51,P<0.001). Among newly diagnosed patients and recurrent patients with PSA more than 2.0 nm/mL, it was apparent that99mTc-PSMA imaging was able to detect lesions with improved sensitivity of 94.1% (16/17). Gleason Scores between positive99mTc-PSMA patients and negative99mTc-PSMA patients were not significantly different (Z=-0.69,P=0.52).Conclusion:With the combination of whole-body scan and tomography, 99mTc-PSMA SPECT/CT can be an excellent and speciifc molecular imaging strategy to detect prostate cancer and its metastases.