10.3969/j.issn.2095-4344.2013.25.014

The acute therapeutic effect of enalapril,an angiotensin converting enzyme inhibitor (ACEI),in reducing blood pressure and urinary albumin excretion rate(UAER) were assessed in 32 NID- DM and 13 essential hypertensive patients.After treatment for three days,24-h blood pressure and UAER in NIDDM patients were reduced significantly.UAER of essential hypertensive patients were reduced while in hypertensive patients UAER were reduced,but blood pressure except night SBP remained unchanged. This study suggests enalapril may have a specific protect effect on kidney which is independent of the de- crease in systemic blood pressure.

OBJECTIVETo study the value of the biochemical markers heart fatty acid binding protein (H-FABP), creatine kinase isoenzyme-MB (CK-MB), myocardial troponin T (cTnT) in early diagnosis of acute myocardial infarction (AMI).

METHODSSerum levels of H-FABP, CK-MB, and cTNT were detected in 95 patients with confirmed AMI at different time points following the onset in comparison with the data from 43 patients without AMI. The sensitivity and specificity of H-FABP in different phases following the onset were compared between those of CK-MB and cTnT.

RESULTSSerum H-FABP activities increased significantly within 3 h after the onset of AMI (P<0.01) and continued to increase at 3-6 h and 6-12 h (P<0.001). Serum level of CK-MB within 6 h and cTnT level within 3 h after AMI onset did not show obvious changes (P<0.05). Both the diagnostic sensitivity and specificity of H-FABP within 3 h and within 3-6 h were higher than those CK-MB and cTnT (P<0.05).

CONCLUSIONH-FABP is superior to CK-MB and cTnT in early diagnosis (within 3 h and 3-6 h following the onset) of AMI.

Acute Disease ; Biomarkers ; blood ; Creatine Kinase, MB Form ; blood ; Early Diagnosis ; Fatty Acid Binding Protein 3 ; Fatty Acid-Binding Proteins ; blood ; Humans ; Myocardial Infarction ; diagnosis ; Sensitivity and Specificity ; Troponin T ; blood

Purpose: Gastric cancer (GC) is a malignant tumor with a high mortality rate. Drug resistance is a major obstacle to GC therapy. This study aimed to investigate the role and mechanism of exosomal circPRRX1 in doxorubicin resistance in GC. Materials and Methods: HGC-27 and AGS cells were exposed to different doses of doxorubicin to construct doxorubicin-resistant cell lines. Levels of circPRRX1, miR-3064-5p, and nonreceptor tyrosine phosphatase 14 (PTPN14) were detected by quantitative real-time PCR or Western blot assay. Then, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, transwell,and Western blot assays were used to explore the function of circPRRX1 in GC cells. Interactions among circPRRX1, miR-3064-5p,and PTPN14 were confirmed by dual-luciferase reporter assay. The in vivo function of circPRRX1 was analyzed in a xenograft tumor model. Results: CircPRRX1 was highly expressed in doxorubicin-resistant GC cell lines. Knockdown of circPRRX1 reversed doxorubicin resistance in doxorubicin-resistant GC cells. Additionally, extracellular circPRRX1 was carried by exosomes to spread doxorubicin resistance. CircPRRX1 silencing reduced doxorubicin resistance by targeting miR-3064-5p or regulating PTPN14. In GC patients,high levels of circPRRX1 in serum exosomes were associated with poor responses to doxorubicin treatment. Moreover, depletion of circPRRX1 reduced doxorubicin resistance in vivo. Conclusion CircPRRX1 strengthened doxorubicin resistance by modulating miR-3064-5p/PTPN14 signaling and might be a therapeutic target for GC patients.

Liver diseases are common in China and the incidence and mortality of primary liver cancer are among the top in the world. As one of the therapeutic methods for hepatocellular carcinoma (HCC), liver transplantation has become an important technique in hepatic surgery. Most of patients with HCC have progressed to stage B or C of Barcelona Clinic Liver Cancer staging when diagnosed. How to reduce the dropout rate of HCC patients due to the progression of tumor when waiting for liver transplantation, develop individualized immunosuppressant plans for HCC patients after liver transplantation, and accurately manage patients with HCC recurrence after liver transplan-tation are the current hotspots of research. The authors review the relevant literature, summarize the treatment experience, and discuss the hot issues in liver transplantation for HCC, in order to provide reference for related treatment.

OBJECTIVE: To analyze the clinical significance of combined newborn hearing and deafness gene screening in Yuncheng area of Shanxi Province. METHODS: Results of audiological examinations, including transient evoked otoacoustic emission and automatic discriminative auditory brainstem evoked potentials, for 6 723 newborns born in Yuncheng area from January 1, 2021 to December 31, 2021, were retrospectively analyzed. Those who failed one of the tests were considered to have failed the examination. A deafness-related gene testing kit was used to detect 15 hot spot variants of common deafness-associated genes in China including GJB2, SLC26A4, GJB3, and mtDNA12S rRNA. Neonates who had passed the audiological examinations and those who had not were compared using a chi-square test. RESULTS: Among the 6 723 neonates, 363 (5.40%) were found to carry variants. These have included 166 cases (2.47%) with GJB2 gene variants, 136 cases (2.03%) with SLC26A4 gene variants, 26 cases (0.39%) with mitochondrial 12S rRNA gene variants, and 33 cases (0.49%) with GJB3 gene variants. Among the 6 723 neonates, 267 had failed initial hearing screening, among which 244 had accepted a re-examination, for which 14 cases (5.73%) had failed again. This has yielded an approximate prevalence of hearing disorder of 0.21% (14/6 723). Among 230 newborns who had passed the re-examination, 10 (4.34%) were found to have carried a variant. By contrast, 4 out of the 14 neonates (28.57%) who had failed the re-examination had carried a variant, and there was a significant difference between the two groups (P < 0.05). CONCLUSION Genetic screening can provide an effective supplement to newborn hearing screening, and the combined screening can provide a best model for the prevention of hearing loss, which can enable early detection of deafness risks, targeted prevention measures, and genetic counseling to provide accurate prognosis for the newborns.
Infant, Newborn ; Humans ; Connexins/genetics* ; Retrospective Studies ; Deafness/genetics* ; Connexin 26/genetics* ; Neonatal Screening/methods* ; Mutation ; Genetic Testing/methods* ; China/epidemiology* ; Hearing ; DNA Mutational Analysis

Pancreatic cancer is one of the fatal malignant tumors, and its dense stroma, which accounts for 90% of the volume of pancreatic tumor, is the main reason for the low survival rate of pancreatic cancer. Cancer-associated fibroblasts (CAFs) are an important group of cells in the tumor stroma of pancreatic cancer, and activated CAFs induce a strong connective tissue interstitial reaction and secretes a variety of soluble molecules to remodel the extracellular matrix, thereby forming a microenvironment that helps with the proliferation, invasion, and metastasis of pancreatic cancer. At present, an increasing number of evidence has shown that CAFs play an important role in the drug resistance of pancreatic cancer, especially in chemotherapy and immunotherapy, and CAFs result in a low response rate of pancreatic cancer treatment by interfering with the metabolism of antitumor drugs, participating in the signaling pathways associated with drug resistance, and forming an immunosuppressive microenvironment. This article elaborates on the specific mechanism of CAFs participating in the drug resistance of pancreatic cancer from the two aspects of chemotherapy and immunotherapy, in order to provide new ideas for identifying new therapeutic targets for pancreatic cancer and improving the response rate of pancreatic cancer treatment.

Objective:To investigate the regulatory effect of miR-26a in radiation-induced heart disease (RIHD) mice.Methods:C57/BL6 mice were used to establish RIHD models. The cardiac function, fibrosis, the expression levels of collagen 1 (COL1) and connective tissue growth factor (CTGF), and miR-26a were detected in RIHD mice. Whether CTGF was the target gene of miR-26a was verified by dual luciferase kit. Moreover, cardiac fibroblasts were transfected with miR-26a up and miR-26a down lentivirus vectors to construct the miR-26a overexpression and underexpression cell models. The expression of CTGF, proliferation, and apoptosis of cardiac fibroblasts were detected.Results:In the RIHD mice, heart function was decreased, myocardial fibrosis was remodeled, the expression levels of COL1 and CTGF were up-regulated, and the expression level of miR-26a was down-regulated. Dual luciferase reporter assay confirmed that CTGF was the target gene regulated by miR-26a. Overexpression of miR-26a could inhibit the expression of CTGF, suppress the proliferation of cardiac fibroblasts, promote cell apoptosis and secrete collagen. Underexpression of miR-26a yielded the opposite results.Conclusion:MiR-26a affects the function of cardiac fibroblasts by targeting CTGF and probably mediates the process of radiation-induced myocardial fibrosis, which may become a new regulatory target of RIHD.

Objective:To investigate the regulatory role of microRNA in radiation-induced heart disease (RIHD) in mice and provide a new strategy for its treatment.Methods:Based on the Gene Expression Omnibus database (GSE147241), which includes normal heart tissue and irradiation heart tissue, we conducted bioinformatics research and analysis to determine the differentially-expressed genes. Then, thirty male C57/BL6 mice were randomly divided into the control group, irradiation group and miR-133a overexpression intervention group. The heart received single dose of X-ray 20 Gy in the irradiation group and miR-133a overexpression intervention group, but not in the control group, and then fed for 16 weeks. Cardiac function was assessed by echocardiography. Myocardial fibrosis was detected by Masson staining. The expression levels of miR-133a, CTGF, COL-1 and COL-3 mRNA were detected by qRT-PCR. The expression levels of CTGF, COL-1 and COL-3 proteins were detected by western blot.Results:miR-133a was the differentially-expressed gene between the irradiation and control groups. Overexpression of miR-133a could mitigate the decrease in cardiac function and increase in myocardial collagen content ( P<0.01). Meantime, overexpression of miR-133a could down-regulate the expression levels of CTGF, COL-1, COL-3 mRNA and protein ( P<0.01). Conclusions:Radiation increases the synthesis of collagen and leads to myocardial fibrosis remodeling. Overexpression of miR-133a can alleviate the radiation-induced myocardial fibrosis.