Objective To investigate the effects of valsartan on insulin resistance of type 2 diabetes in patients with Ⅰ hypertension.Methods Newly diagnosed 152 patients of type 2 diabetes with Ⅰ hypertension were randomly divided into treatment group and control group.The treatment group and control group undergone lifestyle changes( diet and adequate exercise) for two weeks.After that,the control group were given Diltiazem,while the treatment group were given valsartan,an angiotensin receptor blocker(ARB) drugs.Both groups were treated for 8 weeks.Fasting plasma glucose (FPG) and fasting plasma insulin (FINS) before and after treatment in both groups were determined.Homeostasis model assessment evaluation of insulin resistance index(HOMA-IR) and insulin sensitivity index (IAI) were carried out and compared between the two groups.Results After 8 weeks of treatment,HOMA-IR in the treatment group was significantly decreased compared with the control group ( P ＜ 0.01 ),while IAI was significantly increased( P ＜ 0.01 ).Conclusion Application of valsartan in type 2 diabetes mellitus with Ⅰ hypertension can significantly improve the level of insulin resistance.

Objective:To investigate the expression of long non-coding RNA growth retard-specific transcript 5 (LncRNA GAS5) and micrornas (miR) 23a-3p in patients with sepsis complicated with acute kidney injury (AKI) and their clinical significance.Methods:A total of 206 patients with sepsis admitted to the Department of Emergency Medicine, Fuyang First Hospital Affiliated to Binjiang College of Zhejiang University of Traditional Chinese Medicine from May 2020 to February 2023 were prospectively selected and divided into AKI group (95 cases) and control group (111 cases) according to whether they had concurrent AKI. Serum LncRNA GAS5 and miR-23a-3p expressions were detected. logistic regression analysis was used to screen the influencing factors of patients with sepsis complicated with AKI, and receiver operating characteristic (ROC) curve was used to analyze the value of LncRNA GAS5 and miR-23a-3p in predicting sepsis complicated with AKI.Results:Mechanical ventilation, blood transfusion treatment ratio, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score, Sequential Organ Failure Assessment (SOFA) score, white blood cell count (WBC), serum C-reactive protein (CRP), procalcitonin (PCT), blood urea nitrogen (BUN), Scr, blood lactic acid level of the AKI group were higher than those of the control group (all P<0.05); mean arterial pressure (MAP), urine volume, estimate glomerular filtration rate (eGFR) at admission were lower than those of the control group (all P<0.05). Serum LncRNA GAS5 expression (5.12±1.69 vs 2.30±0.42) in AKI group was higher than that in the control group ( P<0.05), and miR-23a-3p expression (1.05±0.13 vs 3.04±0.67) was lower than that in the control group ( P<0.05). Logistic regression analysis showed that high APACHE Ⅱ score, high SOFA score and high expression of LncRNA GAS5 were risk factors for AKI in sepsis patients (all P<0.05). High eGFR and high expression of miR-23a-3p were protective factors (all P<0.05). The area under the curve (AUC) predicted by LncRNA GAS5 and miR-23a-3p for patients with sepsis complicated with AKI was 0.808 and 0.759, and the AUC of combined prediction was 0.882, which was higher than that predicted by single indicator. Conclusions:The expression of LncRNA GAS5 is up-regulated and the expression of miR-23a-3p is down-regulated in serum of patients with sepsis complicated with AKI. The combined detection of LncRNA GAS5 and miR-23a-3p is of high value in predicting the risk of AKI in patients with sepsis.

Cancer toxin is a specific pathogenesis leading to the heterogeneity of breast cancer.The nature and virulence of the cancer toxin determine the differences in the heterogeneity of breast cancer,which can dynamically evolve over time and space,resulting in varying invasion abilities and characteristics of the tumor.Cancer cells in the primary lesion possess"toxicity"that targets specific organs for metastasis,and cancer toxins can influence the metastatic propensity of different types of breast cancer.Therefore,breast cancer treatment strategies based on the theory of cancer toxins emphasize the continuous eradication of the cancer toxin,focusing on differentiating its strength and nature,protecting unaffected areas first,identifying the state based on symptoms,and targeting accordingly to combat resistance arising from tumor heterogeneity.This article aims to provide a new theoretical basis for the treatment strategies of different types of breast cancer.

Objective To conduct a detailed clinical phenotypic analysis and gene mutation detection on an au-tosomal dominant Van der Hoeve syndrome family,and to identify the pathogenic gene mutation sites of the family and the impact of the mutation on gene coding.Methods Clinical data including medical history,physical examina-tion and auxiliary examination were collected and peripheral blood samples were collected from the Van der Hoeve syndrome families.Exome sequencing and Sanger sequencing were performed on 22 family members.The data were analyzed using bioinformatics software.Results The family had a total of 5 generations,with each generation expe-riencing consecutive illnesses.Each generation of men and women could suffer from the disease,which conformed to the characteristics of autosomal dominant inheritance.The 12 patients in this family were all born with blue sclera and short stature.8 patients had a history of fractures and could heal normally.3 patients were considering hearing loss caused by Van der Hoeve syndrome.12 patients had a base deletion(c.1128delT)in exon 17 of the COL1A1 gene,causing a change in the amino acid coding after position 376 and ending the amino acid coding prematurely at position 539.10 asymptomatic individuals in this family didn't had this mutation.Conclusion The patient of this family was identified as Van der Hoeve syndrome caused by c.1128 delT mutation.

Integrating evidence from animal experiments is a critical component of biomedical research, providing essential prior information for in-depth investigations of disease mechanisms and new drug development. Animal models have played an irreplaceable role in simulating human diseases. However, the integration of evidence from animal experiments has faced numerous challenges, including insufficient emphasis, significant heterogeneity in study designs, high publication bias, and discrepancies with clinical research practices. This paper first identifies existing issues in the original research evidence from animal experiments, such as the selection and applicability of animal models, considerations in the design of experimental studies, and factors influencing the translation of animal experimental evidence. It then discusses various methods for integrating this evidence, including systematic review and meta-analysis, overview of systematic review/umbrella review, scoping review, and evidence mapping, while highlighting recent advancements in their application. Finally, the paper addresses the main challenges currently encountered in the integration of evidence from animal experiments and proposes targeted improvement strategies aimed at enhancing the efficiency of translating research outcomes into clinical practice and promoting the advancement of evidence-based medicine. By continuously optimizing original experimental research protocols and evidence integration practices, this work aims to establish a more efficient and scientific environment for the synthesis of evidence from animal experiments, ultimately contributing to clinical trials and human health.