In the context of global climate change, the impact of ambient temperature change on cardiovascular health has become increasingly significant. Epidemiological studies have shown that both high and low temperature can lead to the occurrence of adverse cardiovascular outcomes. For example, exposure to low temperature and high temperature, and diurnal temperature difference can increase the risk of cardiovascular diseases (CVD) mortality. Exposure to cold and heat, heatwaves and cold spells may induce myocardial infarction. Low temperature, high temperature and variations in temperature can increase the risk of heart failure. There are complex interactions among the effects of temperature and humidity, wind speed, radiation, precipitation and air pollution on adverse cardiovascular outcomes. Valnerable groups such as the elderly, patients with chronic diseases, and outdoor workers are particularly susceptible to temperature-related CVD risks. The mechanisms by which temperature affects adverse cardiovascular outcomes involves hemodynamic changes, autonomic nervous system dysregulation, blood rheology alterations, as well as inflammation and metabolic abnormalities, but many research gaps remain. Future studies should conduct in-depth research on mechanisms, individual differences, climate change impacts, and public health interventions to provide more effective policies and interventions to reduce the burden of CVD.

Objective: To evaluate the efficacy and prognosis of loop cutaneous ureterostomy (LCU) in the treatment of primary obstructive megaureter (POM) with severe hydroureteronephrosis (HUN) in infants under 1 year of age，so as to provide reference for infants unsuitable for stage-Ⅰ ureteral reimplantation. Methods: A retrospective analysis was conducted on 12 infants with POM and severe HUN treated with LCU in our hospital during Jan.2019 and Dec.2023.The clinical characteristics，surgical techniques，indications，postoperative complications，stage-Ⅱ surgical approaches，and follow-up outcomes were summarized. Results: All operations were successful，with an average operation time of (37.08±7.53) min (6 left-sided LCU and 6 right-sided LCU).During the mean follow-up of (10.12±2.70) months，all infants showed clinical improvement，with complete resolution or significant alleviation of hydronephrosis，reduced ureteral diameter，and increased renal cortical thickness.Complications included asymptomatic bacteriuria in 3 cases (25%) and urinary tract infection (UTI) in 1 case，all resolved with oral antibiotics.Four cases developed peristomal rashes，which improved with topical treatment.Eleven infants underwent stage-Ⅱ Cohen ureterovesical reimplantation at a mean age of (15.20±2.07) months.Notably，27.3%(3/11) required ureteral tailoring or plication during reimplantation，which reduced the risk of ischemic necrosis from excessive trimming.During the follow-up of (22.17±13.93) months，hydronephrosis and renal function improved，and no febrile UTI or bladder dysfunction occurred. Conclusion: LCU is a safe and effective method，which can provide adequate urinary drainage，relieve obstruction，stabilize renal function，and allow time for ureteral maturation and renal parenchymal recovery.LCU also facilitates subsequent stage-Ⅱ surgery by reducing ureteral dilation.

Objective:To evaluate the role of microRNA-149-5p (miR-149-5p) in resveratrol-induced reduction of lipopolysaccharide (LPS)-induced cardiomyocyte injury in rats.Methods:Rat cardiomyocyte cell line H9C2 was cultured and then divided into 5 groups ( n=27 each) using a random number method: control group (C group), LPS group, resveratrol group (RSV group), miR149-5p inhibitor negative control group (LRN group), and miR149-5p inhibitor group (LRI group). A cardiomyocyte injury model was prepared by incubating cells with culture medium containing 10 μg/ml LPS for 24 h. RSV group was incubated with resveratrol (final concentration of 10 μmol/L) for 24 h, followed by incubation with culture medium containing 10 μg/ml LPS for another 24 h. LRN group and LRI group were transfected with miR149-5p inhibitor negative control and miR149-5p inhibitor, respectively, and then the other treatments were similar to those previously described in RSV group. The cell viability was measured by CCK-8 assay, the apoptosis rate by flow cytometry, the concentration of lactate dehydrogenase (LDH) and content of glutathione (GSH) in the supernatant by microplate method, the content of malondialdehyde (MDA) by TBA reaction method, the activity of superoxide dismutase (SOD) by WST-1 method, the level of reactive oxygen species (ROS) by DCFH-DA fluorescent probe, the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the supernatant by enzyme-linked immunosorbent assay, and the expression of miR-149-5p by quantitative real-time polymerase chain reaction. Results:Compared with C group, the expression of miR-149-5p was significantly down-regulated, the cell viability was decreased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were increased, and the GSH content and SOD activity were decreased in LPS group ( P<0.05). Compared with LPS group, the expression of miR-149-5p was significantly up-regulated, the cell viability was increased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were decreased, and the GSH content and SOD activity were increased in RSV group ( P<0.05). Compared with RSV group or LRN group, the expression of miR-149-5p was significantly down-regulated, the cell viability was decreased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were increased, and the GSH content and SOD activity were decreased in LRI group ( P<0.05). Conclusions:The mechanism by which resveratrol alleviates LPS-induced cardiomyocyte injury is associated with the up-regulation of miR-149-5p expression and inhibition of cell apoptosis, oxidative stress and inflammatory responses in rats.

Objective:To evaluate the effect of dexmedetomidine on the hippocampal brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrκB) signaling pathway in a rat model of cerebral ischemia-reperfusion (I/R).Methods:Forty-five clean-grade healthy Sprague-Dawley rats, half male and half female, aged 5-6 months, weighing 200-250 g, were divided into 3 groups ( n=15 each) using a random number table method: sham operation group (group S), cerebral I/R group (group I/R), and dexmedetomidine + I/R group (group Dex). A rat model of cerebral I/R injury was established by occluding the middle cerebral artery for 90 min followed by restoring perfusion. In group Dex, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before ischemia, while the equal volume of normal saline was intraperitoneally injected in S and I/R groups. Neurological deficit scores were evaluated at 12 h of reperfusion. The rats were anesthetized and sacrificed, and the hippocampus was isolated for determination of the percentage of cerebral infarct size (by TTC method), expression of BDNF and TrκB (by Western blot), and expression of BDNF mRNA and TrκB mRNA (by real-time polymerase chain reaction) and for microscopic examination of cell apoptosis (by TUNEL method). Results:Compared with group S, the neurological deficit scores and percentage of cerebral infarct size were significantly increased, the number of apoptotic hippocampal neurons was increased, and the expression of BDNF and TrκB protein and mRNA was down-regulated in I/R and Dex groups ( P<0.05). Compared with group I/R, the neurological deficit scores and percentage of cerebral infarct size were significantly decreased, the number of apoptotic hippocampal neurons was reduced, and the expression of BDNF and TrκB protein and mRNA was up-regulated in group Dex ( P<0.05). Conclusions:The mechanism by which dexmedetomidine alleviates cerebral I/R injury may be related to activating hippocampal BDNF/TrκB signaling pathways in rats.

Objective:To explore the relevancy between the uridine diphosphate-glucuronylgly-cosyltransferase 1A1 (UGT1A1) gene mutation and the phenotype of indirect hyperbilirubinemia in children.Methods:Sixteen cases with indirect hyperbilirubinemia who visited the Department of Gastroenterology, Children's Hospital of Nanjing Medical University from July 2013 to November 2019 were retrospectively analyzed and were divided into Gilbert syndrome (GS), Crigler-Najjar syndrome type II (CNS-II), and indirect hyperbilirubinemia groups unexplained by UGT1A1 gene mutations. The differences in gene mutation site information and general clinical data were compared. The association between gene mutation spectrum and bilirubin level was explored by t-test analysis.Results:Ten of the sixteen cases with indirect hyperbilirubinemia had GS, three had CNS-II, and three had indirect hyperbilirubinemia unexplained by UGT1A1 gene mutations. A total of six mutation types were detected, of which c.211G?>?A accounted for 37.5% (6/16), c.1456T?>?G accounted for 62.5% (10/16), and TATA accounted for 37.5% (6/16), respectively. Compared with the GS group, the CNS group had early disease onset incidence, high serum total bilirubin ( t ?=?5.539, P ??0.05) and age of onset ( t ?=?0.3611, P ?>?0.05) between the two groups. There was no significant correlation between the number of UGT1A1 gene mutations and serum bilirubin levels. Children with c.1456T?>?G homozygous mutations had the highest serum bilirubin levels. Conclusion:The common pathogenic variants of the UGT1A1 gene sequence are c.1456T?>?G, c.211G?>?A, and TATA, indicating that these site mutations are related to the occurrence of indirect hyperbilirubinemia and have important guiding significance for the etiological analysis of indirect hyperbilirubinemia in children.

Purpose/Significance To analyze the dynamic changes,influencing factors and weak links of e-health literacy of middle-aged and elderly people,so as to provide references for improving e-health literacy of middle-aged and elderly people.Method/Process A questionnaire survey is conducted among 505 middle-aged and elderly people in Guangzhou,and the results are analyzed by using SPSS 24.0.Result/Conclusion The average score of e-health literacy of middle-aged and elderly people is in the middle level;The weak link of e-health literacy is the lack of health information interaction and evaluation capacity.Individual factors are the primary factors that affect e-health literacy of middle-aged and elderly people.It is suggested to increase policy and financial support,carry out"the younger population helps the aging population"mode,and elderly-oriented transformation of digital health Apps.

Objective To establish and validate a predictive model for acute posterior circulation infarction in patients with vertebral artery dysplasia based on ultrasound and clinical data.Methods A total of 347 patients with an ultrasonic diagnosis of vertebral artery dysplasia who were admitted to our hospital from March 2017 to December 2023 were enrolled as subjects.A multivariate logistic regression analysis was used to identify the risk factors for acute posterior circulation infarction in patients with vertebral artery dysplasia,and R software was used to establish a nomogram predictive model for acute posterior circulation infarction in patients with vertebral artery dysplasia.Then the model was assessed and validated.Results Among the 347 patients with vertebral artery dysplasia,50 patients developed acute posterior circulation infarction,resulting in an incidence rate of 14.4%.The multivariate logical regression analysis showed that the nomogram model based on the predictive factors of hypertension,diabetes,hyperhomocysteinemia,embryonal posterior cerebral artery,and vertebral artery dominance had an area under the ROC curve of 0.772(95%confidence interval:0.700?0.844),with a Brier score of 0.105.Conclusion The nomogram model based on the predictive factors of hypertension,diabetes,hyperhomocysteinemia,embryonal posterior cerebral artery,and vertebral artery dominance has a relatively high value in predicting acute posterior circulation infarction in patients with vertebral artery dysplasia.

AIM:The objective of this study is to examine the expression of profilin 1(PFN1)in mice with di-abetic nephropathy and determine its association with immune cell infiltration.METHODS:This study presents an analy-sis of PFN1 expression and immune cell infiltration in patients with diabetic nephropathy,utilizing transcriptome expres-sion data from kidney tissue microarray.Additionally,the findings were validated in a diabetic nephropathy mouse model.Sixteen C57BL/6 mice were randomly assigned into two groups,namely the normal group and the model group,in an equal manner.The model group underwent the establishment of the diabetic nephropathy model through intraperitoneal injection of streptozotocin.Subsequently,the expression levels of CD11b,F4/80,CC chemokine receptor 4(CCR4),interleukin-1 receptor type I(IL-1R1),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax)and caspase-3 in kidney tissue were assessed upon successful establishment of the diabetic nephropathy model.Furthermore,the overexpression of PFN1 was observed in a cellular model of diabetic nephropathy,and the protein expression levels of monocyte chemotactic pro-tein-1(MCP-1)and caspase-3 were assessed.RESULTS:The expression of PFN1 was found to be significantly in-creased in the GSE30122 dataset of transcriptome expression in kidney tissues affected by diabetic nephropathy(P＜0.01).This increase in PFN1 expression was found to be correlated with the presence of macrophages and T cells.Fur-thermore,the renal tissue of the diabetic nephropathy model group exhibited significant pathological changes.In this mod-el group,the expression levels of PFN1,CD11b,F4/80,CCR4,IL-1R1,Bax,Bcl-2,and caspase-3 were all significant-ly increased(P＜0.01).Overexpression of PFN1 could enhance the expression of MCP-1 and caspase-3 proteins.CON-CLUSION:Macrophages and Th17 cells were identified within the renal tissue of mice with diabetic nephropathy,con-comitant with an up-regulation in the expression of PFN1.This up-regulation was observed to facilitate the induction of apoptosis in the context of diabetic nephropathy.

[Objective]To explore how hyperthyroidism induces ventricular remodeling via activating β-catenin/FoxO1 in rat cardiomyocytes.[Methods]Hyperthyroidism-induced ventricular remodeling rat models were established by intraperitoneal injection of levothyroxine(T4)at 0.1 mg/kg for 30 days.β-catenin inhibitor MSAB(14 mg/kg)was admin-istrated for 30 days.We used western blot to detect the expression of myocardial hypertrophy marker ANP,β-catenin and FoxO1;immunofluorescence to examine the expression and intracellular distribution of β-catenin and FoxO1.Hyperthy-roidism-induced cardiomyocyte hypertrophy rat models were established by treatment of triiodothyronine(T3)into cul-tured primary neonatal rat cardiomyocytes for 24 hours.β-catenin siRNA(30 nmol/L)was used to down-regulate β-catenin expression in cardiomyocytes.Western blot and immunofluorescence were used to analyze the effects of β-catenin inhibition on the hyperthyroidism-induced cardiomyocyte hypertrophy.[Results]Following Wnt/β-catenin activation,β-catenin was found increased nuclear expression,to bind to the nuclear transcriptional factors and regulate the gene ex-pression.β-catenin nuclear expression was significantly increased in the hyperthyroidism-induced ventricular remodeling rats,but no change was found in the expression of typical transcriptional factor TCF7l2.Our results revealed that inhibiting β-catenin by MSAB attenuated the hyperthyroidism-induced rat ventricular remodeling.Further analysis indicated that β-catenin/FoxO1 expression was significantly increased in hyperthyroidism-induced myocardial hypertrophy which could be attenuated by suppressing β-catenin/FoxO1 in cardiomyocytes.[Conclusions]β-catenin/FoxO1 is activated in hyperthy-roidism-induced myocardial hypertrophy and β-catenin/FoxO1 inhibition attenuates hyperthyroidism-induced cardiomyo-cyte hypertrophy.

Sha （痧） is an acute infectious disease characterised by the appearance of rashes on the skin， caused by exposure to epidemic toxin and pestilent qi. Sha Zhang Yu Heng （《痧胀玉衡》） discussed the treatment principles and methods， and listed collateral bloodletting as one of the main treatments. Through organizing the articles and proved cases， we found that the author believes Sha （痧） is caused by epidemic pathogen， belonging to heat toxin with rapid changes， so timely treatment for qi and blood simultaneously could achieve the effect of transforming qi into defensive qi. Sha Zhang Yu Heng focuses on patient's position during treatmet， the material of the needle， the site of treatment， the quantum of stimulation and the operation of the contraindications and other essentials. According to the depth of the disease location， use traditional Chinese herbal medicine， scraping together to identify the root of the disease. In addition， diet suggestions for the prevention of the recrudescence of disease are also described in detail.