Objective To explore the predictive value of fibrinogen (FIB)/albumin (ALB) ratio (FAR), neutrophil (NEU)/lymphocyte (LYM) ratio (NLR) and platelet (PLT)/lymphocyte (LYM) ratio (PLR) to acute exacerbation of chronic obstructive pulmonary disease (COPD). Methods Acute exacerbation COPD (AECOPD) patients hospitalized in the Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Chengde Medical College from September 2019 to July 2021 were selected as AECOPD group (n=96), and patients with stable chronic obstructive pulmonary disease (SCOPD) and without acute exacerbation in the outpatient clinic for nearly three months in the same period were selected as SCOPD group (n=103), and healthy people who had physical examination in the same period were randomly selected as control group (n=80). According to the severity classification, AECOPD patients were divided into grade Ⅰ (n=20), grade Ⅱ (n=33) and grade Ⅲ (n=43). The general data and clinical data of each group were recorded, and the serum C-reactive protein (CRP), procalcitonin (PCT), white blood cells (WBC),NEU, LYM, PLT, FIB, ALB were detected. In AECOPD patients, carbon dioxide partial pressure (PaCO₂) and arterial oxygen partial pressure (PaO₂) were also detected, the FAR, NLR, PLR and oxygenation index (PaO₂/FiO₂) were calculated. The differences of the above indicators in each group were compared, and their correlation was analyzed. The risk factors of AECOPD were analyzed by multivariate logistic regression, and the receiver operating characteristics (ROC) curves were developed to analyze the significance of each indicator in the prediction of AECOPD. Results The levels of CRP, PCT, WBC, NEU, NLR, PLR and FAR decreased gradually (P<0.05) in control group, SCOPD group and AECOPD group; with the increase of AECOPD severity, the improvement time of patients, the levels of CRP, PCT, WBC, NEU as ell as NLR, PLR, FAR and PaCO₂ increased gradually, and PaO₂/FiO₂ decreased gradually (P<0.05). Pearson or Spearman correlation analysis showed that FAR, NLR and PLR were positively correlated with the severity of AECOPD, improvement time, CRP, PCT, WBC and PaCO₂, but negatively correlated with PaO₂/FiO₂ (P<0.01).Multivariate logistic regression analyses showed that FAR, NLR and PLR were the independent risk factors for AECOPD (P<0.05).ROC curve analysis showed that the AUC value was greater than 0.7 for predicting AECOPD with FAR, NLR and PLR alone or in combined usage, and the sensitivity was 0.990, 0.698, 0.563 and 0.958 respectively, and the specificity was 0.641, 0.883, 0.932 and 0.961. Conclusion FAR, NLR, PLR have certain correlation with the inflammatory level, severity and respiratory function of AECOPD, and joint use of the three indicators for detection may have higher predictive value for its occurrence.

Oddi sphincter is an important valve controlling the biliopancreatic duct passage, and its injury can cause enterobiliary reflux, resulting in a series of long-term complications such as reflux cholangitis, cholecystitis, recurrence of calculi, and even cholangiocarcinoma. As one of the most common diseases of digestive system, choledocholithiasis is increasing year by year in recent years. Endoscopic retrograde cholangiopancreatography (ERCP) is the preferred minimally invasive method for the treatment of choledocholithiasis and has been widely used in clinical practice. But different ERCP procedures may damage Oddi sphincter. This article reviews the effects of ERCPs (endoscopic sphincterotomy, endoscopic papillary balloon dilation, endoscopic sphincterotomy plus balloon dilation, endoscopic endoclip papilloplasty) on Oddi sphincter and their respective advantages and disadvantages and application prospect.

Long non-coding RNA (lncRNA) is a kind of non-protein coding RNA with a sequence length of more than 200 bp. It regulates the epigenetic characters of organisms by regulating pre-transcription, transcription, and post-translation modification. Atherosclerosis is a kind of vascular disease that gradually narrowed and blocked due to the atherosclerotic lesions in the large and middle arteries. The mechanisms of initiation and progression of atherosclerosis can be summarized as "Injury-Response" doctrine, which involves lipid deposition, intimal inflammation, cell proliferation and apoptosis. It is reported that lncRNA can regulate the "Injury-Response" process by regulating different gene and molecular expression. Here, we provide a mechanistic review of how lncRNA regulate the "Injury-Response", which will provide reference for the future basic research and clinical diagnosis and treatment.

Portal hypertensive enteropathy (PHE) is the appearance of intestinal mucosal capillary stasis and expansion,ultrastructural changes in mucosal epithelial cells, and ectopic varicose veins in patients with portal hypertension (PH), and its scope is limited to intestinal lesions characterized by vascular changes. PHE, including portal hypertensive small bowel disease and portal hypertensive colonopathy (PHC), is one of the important causes of PH complicated by gastrointestinal bleeding. The pathogenesis of PHE is not fully understood, the lack of specificity of histopathological findings, atypical clinical symptoms, and the uniqueness of anatomical location makes its diagnosis difficult. Abdominal CT, multi-slice spiral CT perfusion imaging, ^99mTc-RBC and single photon emission CT (SPECT)/CT can provide certain diagnostic information and help guide follow-up treatment. This article summarizes the research progress of PHE from the aspects of pathogenesis, histopathological findings, clinical manifestations,examination and diagnosis and treatment methods, in order to deepen clinicians' understanding of this disease.

Functional metabolomics is an extension of metabolomics, through detecting changes in endogenous metabolites that are stimulated and disturbed by a particular organism, after obtaining the biomarker, experiments were conducted to verify the functions of the biomarker and the associated enzymes, genes and proteins. The molecular mechanism of pathophysiology can be revealed systematically from the perspective of "metabolite-enzyme-gene-protein", solving the upstream and downstream biological mechanisms of metabolite association. This article reviews and analyzes the current common methods and research strategies of functional metabolomics, the exploration of disease targets and pathogenesis, and the analysis of drug action mechanisms in the field of biomedicine. At the same time, the extended research on the combination of functional metabolomics with network pharmacology and reprogramming metabolomics is summarized, and finally the application prospects of functional metabolomics are analyzed and prospected in the field of biomedicine.

Objective To investigate the role of autophagy in acute lung injury in rats with exertional heat stroke (EHS). Methods A total of 60 male Wistar rats were randomly divided into four groups: control group, EHS group, EHS+bafilomycin A1 (Baf A1) group, and EHS+rapamycin (RAPA) group, with 15 rats in each group. The EHS+Baf A1 group (Baf A1, 1 mg/kg)and EHS+RAPA group (RAPA, 1 mg/kg) were injected intraperitoneally for 4 consecutive days before modeling the rats. After establishing the EHS model, we observed for 5 hours, followed by anesthesia for these rats to collect tissues. We observed and compared the morphological changes in lung tissue, performed arterial blood gas analysis, and measured the lung coefficient and Evans blue (EB) leakage. We also examined the lung tissue pathological changes using HE staining, evaluated lung tissue apoptosis through the TdT-mediated dUTP Nick-end labeling (TUNEL) method, and detected microtubule-associated protein Ⅰ light chain 3(LC3)-Ⅱ/LC3-Ⅰ ratio in lung tissue and p62 protein level through Western blotting. Results Compared with control group,the lung tissue of the EHS group was obviously swollen and more fluid exuded; the arterial blood oxygen partial pressure (PaO₂)decreased, while the arterial blood carbon dioxide partial pressure (PaCO₂) increased; the lung coefficient and EB leakage were significantly increased; HE staining and apoptosis staining showed uneven thickening of alveolar septum and alveolar wall, alveolar exudation increased and the number of apoptotic cells increased, the difference was statistically significant (P<0.05); Compared with EHS group, the EHS+Baf A1 group had more severe lung tissue swelling, lung coefficient and EB leakage were increased; PaO₂ further decreased, while PaCO₂ further increased; HE staining and apoptosis staining showed that lung tissue lesions and damage were significantly worsened, and the number of apoptotic cells increased significantly (P<0.05). Compared with EHS group, the EHS+RAPA group had a significant decrease in various pulmonary edema indicators; PaO₂ increased, PaCO₂ is close to the normal range; HE staining and apoptosis staining showed lung tissue lesions and the degree of damage was significantly reduced, and the number of apoptotic cells was reduced, and the difference was statistically significant (P<0.05); Western blotting results showed that compared with control group, the ratio of LC3-Ⅱ/LC3-Ⅰ in the lung tissue of rats in the EHS group was significantly reduced(0.3±0.1 vs. 1.0±0.1, P<0.05), the expression of p62 increased (1.4±0.2 vs. 0.8±0.1, P<0.05). Compared with EHS group, the ratio of LC3-Ⅱ/LC3-Ⅰ in the lung tissue of the EHS+Baf A1 group was reduced (0.10±0.04), and the expression of p62 was further increased (1.7±0.1), while the ratio of LC3-Ⅱ/LC3-Ⅰ in the lung tissues of rats in the EHS+RAPA group was significantly increased (0.5±0.1), and the expression of p62 was significantly decreased (1.1±0.1), the differences were statistically significant(P<0.05). Conclusion The reduction of autophagy levels is one of the mechanisms of EHS leading to lung injury. Up-regulation of autophagy can reduce the acute lung injury of EHS.

Objective To explore the effect and mechanism of phosphatase and tensin homolog (PTEN) on renal interstitial fibrosis in diabetic nephropathy. Methods We culture NRK52E cells in vitro, cells were randomly assigned to three groups: normal glucose group (NG), high glucose group (HG) and mannitol group (MA), Western blotting was used to detect the protein levels of PTEN, LC3, P62, collagen-Ⅰ and Ⅲ in vitro. To detect the effect of PTEN on autophagy and collagen, the NRK52E were randomly assigned to three groups: NG group, HG group and HG+pPTEN group, the autophagy changes were observed by laser confocal microscopy, and the changes of collagen were observed by fluorescence microscopy. Results Western blotting in vivo showed that, compared with NG group, the expression levels of PTEN and LC3 were decreased, but of P62, collagen-Ⅰ and Ⅲ obviously increased in HG group (P<0.01), while no obvious change of the expression of PTEN and LC3, P62, collagen-Ⅰ and Ⅲ in MA group. The confocal microscope showed that, the number of red spots and yellow spots were decreased and significant autophagy inhibition in HG group, there were no significant autophagy inhibition in other two groups. The cellular immunofluorescence staining showed that, the red fluorescence of PTEN and protein expression were decreased, the collagen fluorescence staining and protein expression were increased in HG group, there were no significant change in other two groups. Conclusions In NRK52E cells under high glucose, PTEN expression reduced significantly,autophagy was inhibited, and then aggravate renal fibrosis. Overexpression of PTEN can restore autophagy and alleviate the progression of renal interstitial fibrosis.

Objective To investigate the effect of activated protein kinase C receptor 1 (RACK1) on the proliferation and apoptosis of human cervical cancer cells and its potential mechanism. Methods The cervical cancer tissues of 24 patients diagnosed as cervical squamous cell carcinoma (CSCC), admitted in the First Affiliated Hospital of Xinjiang Medical University from Dec. 2020 to Dec. 2021, were collected as the experimental group (CSCC group), and 24 normal cervical (NC) tissues were collected as the control group (NC group). The expression levels of RACK1 mRNA in CSCC tissues and NC tissues and in proliferation and apoptosis related genes c-myc, caspase-3, caspase-9, Bax and Bcl-2 in CSCC tissue samples were detected by qRT-PCR, and the correlation between RACK1 mRNA expression and apoptosis-related genes was analyzed by Spearman rank correlation. qRT-PCR and Western blotting were used to detect the expression of RACK1 in cervical cancer cells C33a and SiHa and normal cervical epithelial cells H8. C33a and SiHa cells were transfected with lentivirus to silence the expression of RACK1. According to different treatments, they were divided into: normal control (NC) group, sh-NON (RACK1 silent expression no-load group), shRACK1-1(RACK1 silent expression group 1), shRACK1-2 (RACK1 silent expression group 2), and the transfection efficiency was verified.MTT assay and plate cloning assay were used to detect cell proliferation, and flow cytometry was performed to detect cell apoptosis.After RACK1 was silenced, qRT-PCR was used to detect the expression levels of c-myc, caspase-3, caspase-9, Bax and Bcl-2. Western blotting was used to detect the expression levels of c-myc, caspase-3, caspase-9, Bax, Bcl-2, phosphorylated Janus kinase 2 (p-JAK2),JAK2, phosphorylated cell signal transduction and transcription activating factor 3 (p-STAT3) and STAT3. Results The expression level of RACK1 mRNA was significantly higher in CSCC tissue than that in NC tissue (P<0.001). Spearman rank correlation analysis showed that the expression level of RACK1 mRNA in cervical cancer tissues was significantly negative correlated with caspase-3(r=–0.679, P<0.001), caspase-9 (r=–0.735, P<0.001), Bax (r=–0.691, P<0.001) mRNA expression, but positively correlated with c-myc (r=0.713, P<0.001) and Bcl-2 (r=0.846, P<0.001) mRNA expression. qRT-PCR and Western blotting showed that compared with H8 cells, RACK1 mRNA and protein were highly expressed in C33a and SiHa cells (P<0.001). After RACK1 silence, the expression levels of RACK1 mRNA and protein declined obviously, the proliferation and colony formation ability also decreased,while the apoptosis level was significantly increased (P<0.001) in shRACK1-1 and shRACK1-2 groups than those in sh-NON group (P<0.001). In addition, compared with sh-NON group, the expression of caspase-3, caspase-9, Bax, p-JAK2 and p-STAT3 were significantly increased in shRACK1-1 and shRACK1-2 groups, but of c-myc and Bcl-2 decreased significantly (P<0.001 or P<0.01). Conclusion RACK1 is highly expressed in cervical cancer tissues and cells. Targeted silencing RACK1 gene can effectively reduce the expression of proliferation related protein c-myc and anti-apoptotic protein Bcl-2, but significantly increase the expression of apoptosis related protein caspase-3, caspase-9 and Bax in cervical cancer cells, which may be related to the activation of JAK2/STAT3 signaling pathway.

Objective To explore the mechanism of nodakenin (NDK) affecting the invasion and migration of cervical cancer cells by regulating epithelial-mesenchymal transformation (EMT), and analyze its effect on microRNA (miR)-324-3P/WNT3a axis. Methods Human cervical cancer HeLa cells in logarithmic growth phase were divided into four groups: blank group(cultivated in a 37 ℃, 5% CO₂-saturated humidity incubator), NDK group (20 mmol/L NDK was added to culture), miR-324-3P inhibitor group (hsa-miR-324-3p inhibitor transfection), and miR-324-3P inhibitor+NDK group (after transfection of miR-324-3P inhibitor, 20 mmol/L NDK was added to culture) all were treated for 48 h. Transwell test was used to detect the invasion ability of cells in each group. Cell scratch test was performed to detect cell migration ability of each group. qRT-PCR to detect the mRNA level of miR-324-3P and WNT3a in each group of cells. Western blotting was carried out to detect the expression of EMT-related marker proteins E-cadherin, vimentin, Neural cadherin (N-cadherin), WNT3a, and β-catenin protein in each group of cells. Dual luciferase reporter gene was used to detect the targeting relationship between miR-324-3P and WNT3a gene. Results Compared with the blank group, the number of transmembrane HeLa cells increased in miR-324-3P inhibitor group, the scratch healing rate increased, the mRNA expression level of miR-324-3P decreased, and of WNT3a increased; the relative expression of E-cadherin protein decreased, while the relative expressions of vimentin, N-cadherin, WNT3a and β-catenin increased (P<0.05). While for NDK group and miR-324-3P inhibitor+NDK group, the number of transmembrane HeLa cells decreased, the scar healing rate was also decreased, the mRNA expression level of miR-324-3P increased, the expression level of WNT3a mRNA decreased, the relative expression of E-cadherin protein increased, and the relative expression of vimentin, N-cadherin, WNT3a and β-catenin protein decreased (P<0.05); All the indexes mentioned above were lower in NDK group than those in miR-324-3P inhibitor+NDK group.The dual luciferase reporter gene results showed that miR-324-3P mimic could reduce WNT3a WT luciferase activity (P<0.05), but did not affect WNT3a mut luciferase activity (P>0.05). Conclusion NDK can inhibit the invasion and migration of cervical cancer cells by regulating EMT, and the mechanism of such action may be related to the regulation of miR-324-3P/WNT3a axis.

Objective To establish an improved method for estimating the mean blood glucose by glycosylated hemoglobin(HbA_1c) in diabetic patients with renal insufficiency. Methods The clinical data were retrospectively analyzed of 329 patients with type 2 diabetes mellitus who were hospitalized in the Department of Hypertension and Endocrinology of Daping Hospital of Army Medical Center of PLA from January 2018 to December 2021. All patients were divided into control group [estimated glomerular fraction rate, eGFR≥60 ml/(min.1.73 m²), n=165] and renal insufficiency group [eGFR<60 ml/(min.1.73 m²), n=164]based on their eGFR levels. The basic demographic data, oral glucose tolerance test (OGTT) 2 hours post plasma glucose, and other laboratory test results of the patients were collected. The HbA_1c and OGTT models were adopted separately to estimate the 24-hour average blood glucose of the enrolled patients, and the gap glucose level of the two methods was calculated. The influencing factors of estimating blood glucose deviation with HbA_1c in patients with renal insufficiency were analyzed, and a correction model of estimating average blood glucose with HbA_1c was established. A total of 29 patients with type 2 diabetes mellitus and renal insufficiency hospitalized in the Department of Hypertension and Endocrinology of Daping Hospital of Army Medical Center of PLA from January to March 2022 were collected for external verification. Results Compared with control group, diabetic patients with renal insufficiency were relatively older (P=0.001), with longer course of diabetes (P<0.001), and had lower HbA_1c (P=0.034),eGFR (P<0.001), Hb (P<0.001), and ALB (P<0.001) levels. The mean blood glucose of the two groups was estimated by HbA_1c. The gap of estimated blood glucose was significantly higher in renal insufficiency group than in control group [(0.88±1.64) mmol/L vs.(–0.09±2.10) mmol/L, P<0.001], and was negatively correlated with the Hb level (r=–0.377, P<0.001), while with no relation with ALB level (P=0.551). A linear regression model was used to include HbA_1c, Hb, age, diabetes course, eGFR and ALB into the analysis,and to establish an estimation model for estimating the daily mean blood glucose of diabetic patients with renal insufficiency: mean blood glucose (mmol/L) =4.539+0.95×HbA_1c-0.016×Hb (adjusted R²=0.829, P<0.001). Using this model, the gap glucose level between the estimated mean blood glucose and the detected blood glucose were remarkably reduced in renal insufficiency group [(0.02±1.05) mmol/L vs. (0.88±1.64) mmol/L, P<0.001]. The goodness-of-fit index RNL=0.830 was obtained by external validation of 29 patients, indicating that the model obtained is highly feasible. Conclusions A correction model of estimating mean blood glucose by HbA_1c for diabetic patients with renal insufficiency has been successfully established. It is of great significance to further develop individualized HbA_1c control and improve the prognosis of diabetes patients.