Objective:To investigate the value of serum vascular endothelial growth factors (VEGF), pepsinogen ratio (PGR) combined with magnifying chromoendoscopy in the diagnosis of Epstein-Barr virus associated gastric carcinoma (EBVaGC).Methods:A retrospective case control study was conducted. The clinical data of 314 patients with gastric cancer who were confirmed by pathological examination in Baoji Central Hospital from January 2018 to January 2023 were retrospectively collected. All patients were divided into EBVaGC group (34 cases) and EB virus negative gastric cancer (EBVnGC) group (280 cases) according to the result of EB virus quantitative real time polymerase chain reaction in serum before treatment, while 50 healthy volunteers who underwent the physical examination in the same period were selected as the control group. The level of VEGF was detected by using enzyme-linked immunosorbent assay (ELISA), and serum levels of pepsinogen (PG) Ⅰ and PGⅡ were detected by using fluorescence immunochromatography. PGR was calculated by PGⅠ-to-PGⅡ ratio. Electronic magnification gastroscopy was performed, suspicious lesions were stained and the pathological state of gastric tissues was observed. Taking the pathological results of living tissues as the gold standard, the diagnostic efficacy of each index alone and the combination detection for EBVaGC was calculated. Multivariate logistic regression model was used to analyze the independent risk factors of the incidence of EBVaGC.Results:The age of patients in EBVaGC group, EBVnGC group and the healthy control group was (61±10) years, (63±12) years and (61±12) years, respectively; and there were 28 males (82.4%), 228 males (81.4%) and 41 males (82.0%), respectively. There were no statistically significant differences in age and gender among the 3 groups (all P>0.05). The serum VEGF level and the proportion of positive patients detected by endochromatography in EBVaGC group were higher than those in the EBVnGC group and the healthy control group [VEGF: (253±48) pg/ml vs. (183±38) pg/ml, (92±25) pg/ml; positive proportion: 94.1% (32/34) vs. 77.9% (218/280), 2.0% (1/50)], and the PGR in EBVaGC group was lower than that in EBVnGC group and the healthy control group (2.1±1.0 vs. 3.1±1.1, 14.1±1.9), and the differences were statistically significant (all P<0.05). The sensitivity of serum VEGF in the diagnosis of EBVaGC was higher than that of PGR [73.5% (25/34) vs. 66.9% (22/34)]. The diagnostic specificity of PGR [78.2% (219/280) vs. 69.3% (194/280)] and accuracy [76.8% (241/314) vs. 69.8% (219/314)] were higher than those of VEGF. The sensitivity [85.3% (29/34)], specificity [82.9% (232/280)] and accuracy [83.1% (261/314)] of magnifying chromoendoscopy in the diagnosis of EBVaGC were higher than those of VEGF and PGR. The sensitivity [94.1% (32/34)], specificity [95.7% (268/280)] and accuracy [95.5% (300/314)] of the 3 combined detection were higher than those of single and pairwise detection. Multivariate logistic regression analysis showed that the independent risk factors for the incidence of EBVaGC included alcoholism ( OR = 2.310, 95% CI: 1.243-3.581, P = 0.007), spicy food preference ( OR = 1.516, 95% CI: 1.084-2.142, P = 0.026), irregular diet ( OR = 1.448, 95% CI: 1.013-2.104, P = 0.043), family history of gastric cancer ( OR = 2.732, 95% CI: 1.312-4.894, P = 0.001). Conclusions:Serum VEGF and PGR combined with magnifying chromoendoscopy can improve the diagnostic efficiency of EBVaGC, and developing good eating will be helpful to prevent or slow down the progression of stomach diseases.

Single-cell multi-Omics(SCM-Omics)and spatial multi-Omics(SM-Omics)technologies provide state-of-the-art methods for exploring the composition and function of cell types in tissues/organs.Since its emergence in 2009,single-cell RNA sequencing(scRNA-seq)has yielded many groundbreaking new discoveries.The combination of this method with the emergence and development of SM-Omics tech-niques has been a pioneering strategy in neuroscience,developmental biology,and cancer research,especially for assessing tumor heterogeneity and T-cell infiltration.In recent years,the application of these methods in the study of metabolic diseases has also increased.The emerging SCM-Omics and SM-Omics approaches allow the molecular and spatial analysis of cells to explore regulatory states and determine cell fate,and thus provide promising tools for unraveling heterogeneous metabolic processes and making them amenable to intervention.Here,we review the evolution of SCM-Omics and SM-Omics technologies,and describe the progress in the application of SCM-Omics and SM-Omics in metabolism-related diseases,including obesity,diabetes,nonalcoholic fatty liver disease(NAFLD)and cardiovascular disease(CVD).We also conclude that the application of SCM-Omics and SM-Omics approaches can help resolve the molecular mechanisms underlying the pathogenesis of metabolic diseases in the body and facilitate therapeutic measures for metabolism-related diseases.This review concludes with an overview of the current status of this emerging field and the outlook for its future.

Objective:To analyze the correlation between 21-gene recurrence score (RS) and clinicopathological characteristics of patients with Lumina type breast cancer, and to explore its significance in individualized treatment.Methods:The clinicopathological data of 59 patients with surgical resection and pathological diagnosis of Lumina type breast cancer in Shanxi Provincial Cancer Hospital from May 2018 to May 2019 were retrospectively analyzed. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of 21 gene and RS was calculated. According to the 21-gene RS, the patients were divided into low recurrence risk group (RS < 18 points), intermediate recurrence risk group (RS 18-31 points) and high recurrence risk group (RS > 31 points). Univariate and multivariate logistic regression analyses were made to evaluate the correlations between different recurrence risk and clinicopathological characteristics of patients and their influence on the choice of adjuvant chemotherapy.Results:Based on the 21-gene RS, 29 patients were in low recurrence risk group, 22 cases were in intermediate recurrence risk group, and 8 cases were in high recurrence risk group. Single-factor analysis showed that age ( P = 0.012), maximum mass diameter ( P = 0.031), histological grade ( P = 0.036), progesterone receptor (PR) level ( P = 0.015), Ki-67 positive index ( P = 0.049) and molecular typing ( P = 0.010) were influencing factors of 21-gene RS recurrence risk. Multivariate logistic regression analysis showed that the age and Ki-67 positive index were negatively correlated with 21-gene RS recurrence risk (both P < 0.05). After grouping according to the 21-gene RS, 17 patients in the intermediate recurrence risk group (according to the traditional postoperative recurrence risk grouping method for breast cancer) were classified as low recurrence risk group, and 4 patients in the low recurrence risk group were classified as intermediate recurrence risk group ( χ2 = 4.535, P = 0.033). After grouping based on 21-gene RS, the number of patients who needed chemotherapy in individualized treatment decreased. Of the 17 cases, 11 cases did not undergo postoperative chemotherapy, and the remaining patients received chemotherapy. The postoperative follow-up period was 11-22 months. As of March 2020, there was no recurrence or disease progress. Conclusion:The 21-gene RS can provide objective basis for the individualized precise treatment and prognosis prediction for patients with early-stage Lumina type breast cancer.

Objective To detect the expression of miR-26a/b in the aorta and serum of mice so as to explore the role of miR-26a/b in vascular remodeling of hypertension.Methods C576L/BJ male mice were randomly divided into AngⅡ group and control group.Mini-osmotic pump was implanted subcutaneously into the back of mice, and the model of blood vessel remodeling in mice was established by continuous infusion of AngⅡ(2.0mg/kg·d).The mice in control group were injected with saline.Blood pressure was taken before the intervention and at 3, 5, 7, 10 and 14 days after the intervention.After 2 weeks, the mice were killed, the serum and aorta tissues were collected, and the expression of miR-26a/b was determined by RT-PCR.HE staining, Masson staining and immunohistochemistry were performed to observe changes in vascular morphology, fibrosis and protein expression.Results After the intervention, systolic blood pressure and diastolic blood pressure were significantly higher in AngⅡ group than in control group (P<0.05).HE staining showed that the vessel wall of AngⅡ group was thicker than that of control group.Masson staining showed more blue collagen deposition in the middle of aorta in AngⅡ group but no obvious collagen deposition in control group.RT-PCR showed that the expression of miRNA-26a/b in the serum and aorta of AngⅡ group was significantly lower than in control group (P<0.05).Immunohistochemistry indicated that the expressions of CTGF, collagen Ⅰ and collagen Ⅲ all increased after AngⅡ infusion (P<0.05).Conclusion MiR-26a/b, CTGF, collagen Ⅰ and collagen Ⅲ may be involved in AngⅡ-induced vascular remodeling in hypertension.MiR-26a/b may be a new therapeutic target of vascular remodeling in hypertension.

Objective To study the effect of dexmedetomidine in the functional endoscopic sinus surgery (FESS) on the recovery period of general anesthesia. Methods Fifteen min before the end of surgery, 40 FESS patients were treated with intravenous infusion of dexmedetomidine at 0.6μg/kg. The occurrence of cough response, degree of pain and agitation in patients were observed. Result The response score of choking cough of the patients with intravenous infusion of dexmedetomiindine was (1.2 ± 0.5), the score of VSA was (1.9 ± 0.5), and the degree of agitation was (1.2 ± 0.4). Conclusion For those undergoing FESS, postoperative use of dexmedetomidine 15 min before the end of surgery, can not only have an effective effect for reducing the incidence of choking cough and agitation and but also decrease the pain degree so that the patients can live through the general anesthesia recovery period.

1 1 patients with moderate or severe crowding in the anterior arch were treated with 4 premolar extraction.After canine distaliza-tion first approach,the teeth were aligned and leveled.The results of the study suggest that,with strict implementation of indication,this method may be a viable treatment for the moderate or severe crowding anterior.

Heart Failure ; genetics ; Humans ; Hypertrophy ; genetics ; MicroRNAs ; genetics

Objective To investigate the effects of telmisartan on the expression of angiotensin converting enzyme2 (ACE2) mRNA in monocyte-derived macrophages of hypertensive patients companied with diabetes.Methods 62 essential hypertensive patients companied with diabetes were randomly divided into two groups:regular treatment group,and telmisartan group.Then the content of ACE and ACE2 in serum was detected by ELISA,and the expression of ACE mRNA and ACE2 mRNA in monocyte-derived macrophages of patients was detected by RT-PCR before and after having been treated.Results (1) After having been treated for 4 weeks and 12 weeks,the blood pressure of the patients in two groups were decreased significantly,Comparing with regular group,telmisartan group seemed to have more obvious therapeutic effect (P ＜ 0.05) ; (2) After having been treated for 12 weeks,glycosylated hemoglobin diseased in both group,but there was no significant difference between the two group (P ＞ 0.05) ; (3) In telmisartan group,the content of ACE2 in serum was increased after having been treated for 12 weeks than that in regular treatment group,[(23.9 ± 8.2) U/L vs (16.3 ± 8.9) U/L,P ＜ 0.05] ; and the expression of ACE2 mRNA in monocyte-derived macrophages in telmisartan group was obviously increased after 12 weeks comparing with regular treatment group (0.73 ±0.06 vs 0.51 ±0.04,P ＜0.01).Conclusion The role of telmisartan in decreasing blood pressure and it's advantage to the metabolism of glucose are partly related with the up-regulation of ACE2 mRNA.

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA3867 (mtDNA3867) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3 (TCID50=108), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA3867 deletion rate was significantly higher in experimental group than in control group (P＜0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P＞0.05). At day 11 after injection, the mtDNA3867 deletion rate of both cells in experimental group was increased to the peak level (P＜0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P＞0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P＜0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P＜0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocardifis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA(3867) (mtDNA(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3(TCID50=10(8)), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA(3867) deletion rate was significantly higher in experimental group than in control group (P<0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P>0.05). At day 11 after injection, the mtDNA(3867) deletion rate of both cells in experimental group was increased to the peak level (P<0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P>0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P<0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P<0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.