Automatic Biochemical Analyzer Research Articles

Combined electronic medical records and gene polymorphism characteristics to establish an anti-tuberculosis drug-induced hepatic injury (ATDH) prediction model and evaluate the prediction value.

Anti-tuberculosis drug-induced hepatic injury (ATDH) lacks specific diagnostic markers. The characteristics of gene polymorphisms have been preliminarily used for the risk classification of ATDH, and the activation of Pregnane X receptor/aminole-vulinic synthase-1/forkhead box O1 (PXR/ALAS1/FOXO1) axis is closely related to ATDH. Therefore, we consider combining general clinical features of the electronic medical record, laboratory indications, and genetic features of key genes in this axis for predictive model construction to help early clinical diagnosis and treatment. The general characteristics derived from the Hospital Information System (HIS) medical record system, the biochemical tests and hematology tests were detected by Roche automatic biochemical immunoassay analyzer cobas8000 and Sysmex automatic hemocytometer XE2100. The single nucleotide polymorphisms (SNPs) genotyping work was conducted with a custom-designed 48-plex SNP scan® TM Kit. A total of 746 cases were included which were divided into training set and validation set according to the ratio of 3:2 randomly. Taking the occurrence of confirmed ATDH as the outcome variable, lasso regression and logistic regression were used to identify the predictors preliminarily. alanine aminotransferase, aspartate aminotransferase, monocyte, uric acid, albumin, fever, the polymorphisms of rs4435111 (FOXO1) and rs3814055 (PXR) were chosen from all variables to combine the predictive model. The goodness of fit, predictive efficacy, discrimination, and consistency, and clinical decision curve analysis was used to assess the clinical applicability of the models. The best model had a discriminant efficacy C-index of 0.8164, a sensitivity of 34.25%, specificity of 97.99%, a positive predictive value of 78.13% and negative predictive value of 87.69%, the two-tailed value of Spiegelhalter Z test of consistency test S:P =0.896, maximum absolute difference Emax =0.147, and average absolute difference Eave =0.017. In the validation set, performance was close. The clinical decision curve showed the clinical applicability of the prediction model when the prediction risk threshold was between 0.1 and 0.8. The ATDH prediction model was constructed using a machine learning approach, combining general characteristics of the study population, laboratory indications, and SNP features of PXR and FOXO1 genes with good fit and certain predictive value, and has potential and value for clinical application.

Effect of Transcatheter Arterial Chemoembolization Combined with Radiofrequency Ablation on Liver Function and Immune Function in Patients with Hepatocellular Carcinoma.

Objectives To investigate the effects of transcatheter arterial chemoembolization (TACE) combined with radiofrequency ablation (RFA) on liver function and immune function in patients with hepatocellular carcinoma (HCC). Methods From December 2016 to January 2019, patients with primary liver cancer who could not be operated on were selected as the study subjects. 170 patients were randomly divided into two groups. The control group was treated with transcatheter arterial chemoembolization (n = 85). The patients in the observation group were treated with transcatheter arterial chemoembolization combined with radiofrequency ablation (n = 85). The clinical effects of the two groups were analyzed. The changes of liver function and immune function were detected by automatic biochemical analyzer before and after treatment. The changes of hypoxia inducible factor-1 (HIF1) alpha and vascular endothelial growth factor (VEGF) levels before and after treatment were analyzed by enzyme-linked immunosorbent assay (ELISA). Results The total effective rate in the observation group was significantly higher than that in the control group (P < 0.05). After treatment, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), CD8+, HIF1 alpha, and VEGF decreased significantly (P < 0.05), while levels of total bilirubin, direct bilirubin, indirect bilirubin, CD3+, CD4+, and CD4+/CD8+ increased significantly (P < 0.05). The changes of the above indexes in the observation group were more significant than those in the control group (P < 0.05). Conclusion Hepatic arterial chemoembolization combined with radiofrequency ablation has a significant effect on liver function and immune function in patients with liver cancer, which may be related to the abnormal levels of HIF1α and vascular endothelial growth factor.

Intercellular mitochondrial transfer as a means of revitalizing injured glomerular endothelial cells.

BACKGROUNDRecent studies have demonstrated that mesenchymal stem cells (MSCs) can rescue injured target cells via mitochondrial transfer. However, it has not been fully understood how bone marrow-derived MSCs repair glomeruli in diabetic kidney disease (DKD).AIMTo explore the mitochondrial transfer involved in the rescue of injured glomerular endothelial cells (GECs) by MSCs, both in vitro and in vivo.METHODS In vitro experiments were performed to investigate the effect of co-culture with MSCs on high glucose-induced GECs. The transfer of mitochondria was visua lized using fluorescent microscopy. GECs were freshly sorted and ultimately tested for apoptosis, viability, mRNA expression by real-time reverse transcri ptase-polymerase chain reaction, protein expression by western blot, and mitochondrial function. Moreover, streptozotocin-induced DKD rats were infused with MSCs, and renal function and oxidative stress were detected with an automatic biochemical analyzer and related-detection kits after 2 wk. Kidney histology was analyzed by hematoxylin and eosin, periodic acid-Schiff, and immunohistochemical staining.RESULTSFluorescence imaging confirmed that MSCs transferred mitochondria to injured GECs when co-cultured in vitro. We found that the apoptosis, proliferation, and mitochondrial function of injured GECs were improved following co-culture. Additionally, MSCs decreased pro-inflammatory cytokines [interleukin (IL)-6, IL-1β, and tumor necrosis factor-α] and pro-apoptotic factors (caspase 3 and Bax). Mitochondrial transfer also enhanced the expression of superoxide dismutase 2, B cell lymphoma-2, glutathione peroxidase (GPx) 3, and mitofusin 2 and inhibited reactive oxygen species (ROS) and dynamin-related protein 1 expression. Furthermore, MSCs significantly ameliorated functional parameters (blood urea nitrogen and serum creatinine) and decreased the production of malondialdehyde, advanced glycation end products, and ROS, whereas they increased the levels of GPx and superoxide dismutase in vivo. In addition, significant reductions in the glomerular basement membrane and renal interstitial fibrosis were observed following MSC treatment.CONCLUSIONMSCs can rejuvenate damaged GECs via mitochondrial transfer. Additionally, the improvement of renal function and pathological changes in DKD by MSCs may be related to the mechanism of mitochondrial transfer.

Protective effect and mechanism of electroacupuncture of "Biao-Ben" acupoints combination for mitochondrial dysfunction in diabetic nephropathy rats

To study the protective effect of electroacupuncture (EA) at "Biao"-acupoints, "Fenglong"(ST40) and "Zhongwan"(CV12), used for treating symptoms of the disease, and "Ben"-acupoints, "Zusanli"(ST36) and "Guanyuan"(CV4), for treating the root cause of the disease on oxidative stress injury of renal mitochondria through SIRT1/PGC-1α signal pathway in rats with diabetic nephropathy (DN). A total of 33 male Wistar rats were randomized into normal (n=10), model (n=12) and EA (n=11) groups.The DN model was established by feeding the rats with high-sugar and high-fat diet for 6 weeks combined with streptozotocin (STZ, 35 mg/kg, i.p.). EA (4 Hz/60 Hz, 1 mA)was applied to ST36-ST40 and CV4-CV12 for 15 min, once every other day for 8 weeks. The rats' body weight was recorded, urine in 24 hours (24-h UP) was collected to measure the urine protein level, and the fasting blood glucose (FBG) level detected by using a glucometer. The levels of serum glycosylated hemoglobin (HbA1c), creatinine (Scr) and urea nitrogen (BUN) were assayed using immunoturbidi-metry, picric acid method and urease method, respectively, and those of serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) detected using an automatic biochemical analyzer. The kidney tissue was collected for assaying the activity of superoxide dismutase (SOD) with xanthine oxidase method, glutathione (GSH) activity with dithio-dinitrobenzoic acid method, catalase （CAT） activity with ammonium molybdate spectrometric method, and malondialdehyde (MDA) content with thiobarbituric acid method. Histopathological changes of the kidney tissue were observed by microscope after hematoxylin-eosin staining (HE), periodate Schiff staining (PAS) and Masson staining, separately, and its subcellular structure was observed under transmission electron microscopy. The expression levels of renal SIRT1 and PGC-1α mRNAs and proteins were detected by quantitative real-time PCR and Western blot, and the immunoactivity of renal α-smooth muscle actin (α-SMA), and immunofluorescence density of renal collagen Ⅰ (Col Ⅰ), collagen Ⅳ(Col Ⅳ) and fibronec-tin (FN) detected by immunohistochemistry and immunofluorescence assay, respectively. Compared with the normal group, the levels of FBG, HbA1c, BUN, Scr, 24-h UP, TG, TC, LDL-C, MDA, α-SMA, Col Ⅰ, Col Ⅳ and FN proteins were significantly increased (P<0.01), and the levels of body weight, HDL-C, SOD, GSH, CAT, SIRT1 and PGC-1α mRNAs and proteins were decreased in the model group (P<0.01, P<0.05). In comparison with the model group, the levels of FBG, HbA1c, BUN, Scr, 24-h UP, TG, TC, LDL-C and MDA, and the expressions of α-SMA, Col Ⅰ, Col Ⅳ and FN proteins were markedly down-regulated (P<0.05, P<0.01), and those of body weight, HDL-C, SOD, GSH, CAT, and the expressions of SIRT1 and PGC-1α mRNAs and proteins significantly up-regulated (P<0.01, P<0.05) in the EA group. HE staining showed mesangial dilatation, glomerular hypertrophy and mesangial matrix accumulation; PAS staining showed an increase of the glomerular extracellular matrix deposition; and Masson staining displayed an enhancement of glomerular fibrosis and interstitial space expansion; and electron microscope revealed foot process fusion, basement membrane thickening and organelle injury in the rat's kidney of the model group, which were relatively milder in the EA group. EA of ST36-ST40 and CV4-CV12, "Biao-Ben" acupoints combination, can alleviate oxidative stress and mitochondrial dysfunction in DN rats, which may be associated with its functions in up-regulating SIRT1/PGC-1α signaling, and decreasing renal fibrosis.

Relationship Between Markers of Chronic Inflammation and Copper Nutritional Status in Obese Women.

Adipose tissue dysfunction causes the development of metabolic complications, such as low-grade chronic inflammation, which may to alter copper homeostasis in obese individuals. Thus, the objective of this study is to analyze the relationship between markers of chronic inflammation and copper nutritional status in obese women. Cross-sectional study involved women aged 20-50years, divided into two groups: case (BMI > 35kg/m2) and control (18.5 > BMI > 24.9kg/m2). Plasma and erythrocyte copper concentrations were determined by inductively coupled plasma optical emission spectrometry (ICP-OES) method. Activity of superoxide dismutase (SOD) enzyme in the erythrocytes was determined with an automatic biochemical analyzer. Serum concentrations of interleukin (IL)-6, IL-8, IL-12, IL-10, and IL-1β and tumor necrosis factor-alpha (TNF-α) were determined by using flow cytometer. Serum IL-6 concentrations were 105% higher in the case group compared to eutrophic women. Plasma copper concentrations were 20.5% higher, and erythrocyte copper concentrations were 23.5% lower in patients with obesity. In addition, erythrocyte SOD activity was 20% lower in obese participants when compared to eutrophic women. Our study identified significant negative correlation between the cytokines TNF-α and IL-10 and the SOD activity in the case group, suggesting a possible influence of chronic inflammation on copper distribution in obese individuals.

Circulating levels of DDIT4 and mTOR, and contributions of BMI, inflammation and insulin sensitivity in hyperlipidemia.

Evidence shows a high incidence of insulin resistance, inflammation and excess body mass index (BMI) in adults with hyperlipidemia. The present study aimed to determine the circulating levels of DNA damage inducible transcript 4 (DDIT4) and mTOR and assess the contributions of lipids, inflammatory markers, insulin sensitivity and BMI in hyperlipidemia. The study subjects were divided into a hyperlipidemia group and a normal control group (n=55 per group). Sex, age, blood pressure, waist circumference (WC), height, weight and BMI were recorded. Fasting venous blood samples were collected and an automatic biochemical analyzer was used to detect fasting blood glucose (FBG), fasting insulin (FINS), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C). Quantitative ELISA kits were used to determine the levels of DDIT4, mTOR and inflammatory markers and calculate the homeostatic model assessment of insulin resistance (HOMA-IR). Compared with the normal control group, the hyperlipidemia group had significantly increased blood pressure, WC, weight, BMI, FBG, FINS, HOMA-IR, mTOR and inflammatory markers, but significantly reduced DDIT4. A concurrent correlation analysis showed that insulin resistance was positively correlated with blood pressure, BMI, lipid profiles (TG, TC, LDL-C), mTOR and inflammatory markers, but negatively correlated with HDL-C and DDIT4. Lipid profiles were positively correlated with BMI, mTOR and inflammatory markers, but negatively correlated with DDIT4. A factor analysis identified four domains in hyperlipidemia (inflammation-lipid 1 domain, 44.429%; overweight domain, 21.695%; insulin sensitivity domain, 11.782%; lipid 2 domain, 6.723%). In conclusion, people with hyperlipidemia have elevated mTOR and reduced DDIT4 and are accompanied by abnormal indicators such as insulin sensitivity, BMI and inflammatory factors. The identified domains may be applied to predict the outcomes of cardiovascular diseases and metabolic diseases in the future.

The Predicting Role of Serum TSGF and sIL-2R for the Lymph Node Metastasis of Papillary Thyroid Carcinoma.

Objective To explore the clinical utility of tumor-specific growth factor (TSGF) and the soluble interleukin-2 (IL-2) receptor (sIL-2R) as immune-related factors for predicting lymph node metastases (LNM) of papillary thyroid carcinoma (PTC). Methods A total of 206 patients with PTC subjected to curative surgery were enrolled. All patients had complete medical records. Serum levels of TSGF were detected using Automatic Biochemistry Analyzer and the serum sIL-2R concentration was detected by enzyme-linked immunosorbent assay (ELISA). Furthermore, we analyzed the relationship between the two indicators and the clinicopathological characteristics and assessed their effect on lymphatic metastasis in patients with PTC by logistic regression analysis. Results Receiver operating characteristic (ROC) analysis revealed that the determined cut-off value of serum TSGF and sIL-2R was 63.35 U/mL and 507 U/mL, respectively. Serum TSGF was associated with focality (χ2 = 4.97, P = 0.026) and lymphatic metastasis (χ2 = 4.154, P = 0.042), while serum sIL-2R was remarkably related to gender (χ2 = 4.464, P = 0.035). Univariate logistic regression analysis indicated that age, tumor size, serum TSGF level, capsule invasion, and nodular goiter were the lymphatic metastasis-related factor of PTC. Multivariate regression analysis revealed that age > 45 years was a protective factor (OR: 0.4, 95% CI: 0.206-0.777, P = 0.007). Conversely, larger tumor size (OR: 4.594, 95% CI: 2.127-9.921, P = 0.000), higher serum TSGF levels (OR: 1.888, 95% CI: 1.009-3.533, P = 0.047), and capsule invasion (OR: 1.939, 95% CI: 1.009-3.726, P = 0.047) were associated with an increased risk of LNM. Conclusion Serum TSGF levels were identified as an independent factor for LNM in patients with PTC.

The Xiaogu San Attenuates Pain and Cartilage Damage in Rats with Monosodium Iodoacetate Induced Osteoarthritis.

Osteoarthritis (OA) is a degenerative joint disease with an increasing incidence associated with increased life expectancy. The application of traditional Chinese medicine in the treatment of OA has become a research hotspot. This study investigated the effects of XGS externally applied to osteoarthritic joints and analyze its effect on pain in monosodium iodoacetate (MIA)-induced OA rats. This study also evaluates potential mechanisms behind the anti-osteoarthritic effects of XGS. A total of 24 Sprague Dawley rats were evenly and randomly divided into three separate groups, including the normal control (NC), OA and XGS groups. MIA (50 μL, 10 mg/mL) was injected into the left knee joints of the rats to induce OA. After 7 days, The rats of XGS group were given XGS (0.45 g) that was externally applied to the left knee joint, were fixed with gauze, and continuously administered XGS for 28 days. Morphological changes in tissues and organs were examined using H&E staining. Biochemical indicators were measured using an automatic biochemical analyzer. Inflammatory cytokines were detected using ELISA kits and immunohistochemistry. RNA-based high-throughput sequencing (RNA-seq) was performed to detect differential expression of mRNAs in normal and MIA-induced OA rats. Stride of the left leg was extended in rats, matrix increased on cartilage tissue surfaces, and inflammatory cytokines were reduced when treated with XGS. RNA-seq results revealed that the PI3K-Akt signaling pathway is activated in the OA model. The qRT-PCR showed that the expression levels of Tnn, Col6a6, Igf1 and Lamb1 were up-regulated by XGS. Altogether, this work demonstrated the potential therapeutic effects of XGS in rats with OA induced by MIA. The XGS may be considered an alternative therapy to manage OA.

Amorphous selenium nanodots alleviate non-alcoholic fatty liver disease via activating VEGF receptor 1 to further inhibit phosphorylation of JNK/p38 MAPK pathways

In clinic, there is still no unified standard for the treatment of non-alcoholic fatty liver disease (NAFLD), and the development of effective novel drugs to alleviate NAFLD remains a challenge. This study aimed to explore the effect and mechanism of amorphous selenium nanodots (A SeNDs) in alleviating NAFLD. Model rats with NAFLD were induced by the high-fat diet (HFD). Histomorphology was used to observe liver tissue, automatic biochemical analyzer was used to analyze liver function indicators, and ELISA kit was used to detect the effect of A SeNDs on oxidative stress and inflammatory factors in NAFLD rats. The results exhibited that A SeNDs could reduce hepatocyte steatosis, liver index, blood lipid level, and transaminase level in NAFLD rats. Furthermore, A SeNDs could relieve the oxidative stress and inflammatory reaction and maintain liver tissue structure in NAFLD rats. Mechanistically, A SeNDs (0.3 mg/kg/day) inhibit the phosphorylation of JNK/p38 MAPK pathways after activating vascular endothelial growth factor receptor 1 (VEGFR1) in the liver of rats with NAFLD to allay oxidative stress and inflammatory response and improves hepatic structure and liver function. Therefore, it should be an important method to mitigate NAFLD by supplementing A SeNDs to normalize hepatic structure and liver function.

Fuzi-Lizhong Decoction Alleviates Nonalcoholic Fatty Liver Disease by Blocking TLR4/MyD88/TRAF6 Signaling.

Background Fuzi-Lizhong decoction (FLD) derives from the ancient Chinese Pharmacopoeia and has been clinically used for years. The present study aimed to investigate the activities and underlying mechanisms of FLD against nonalcoholic fatty liver disease (NAFLD). Methods In vivo studies were conducted by inducing NAFLD in rats with a high-fat diet, and in vitro studies were performed on HL-7702 cells treated with oleic and linoleic acids. Total cholesterol (TC), triglyceride (TG), and blood glucose (Glu) levels were detected using an automatic biochemical analyzer. The expression of IL-2, IL-6, and TNF-α in sera and cell culture supernatants was measured by ELISA. The mRNA and protein levels of TLR4, MyD88, and TRAF6 were measured in liver tissue and HL-7702 cells using reverse transcription-quantitative polymerase chain reaction and western blot. Results FLD significantly reduced the TC, TG, Glu, FFA, IL-2, IL-6, and TNF-α levels in NAFLD rats and HL-7702 cells. Analysis of liver lipid content by Oil Red O staining revealed a significant increase in hepatic lipid accumulation in rats with NAFLD, but this lipid accumulation was reversed by FLD treatment. In addition, the mRNA expression levels of TLR4, MyD88, TRAF6, and NF-κB p65 as well as the protein levels of TLR4, MyD88, TRAF6, and NF-κB p65 were decreased after FLD treatment. FLD significantly reduced inflammation and improved collagen accumulation in vivo and in vitro by inhibiting the activation of the TLR4/MyD88/TRAF6 signaling pathway. Conclusions FLD exerted potent protective effects against NAFLD via TLR4/MyD88/TRAF6 signaling. These findings provide novel insights into the mechanisms whereby this compound acts as an anti-inflammatory agent and highlight the potential application of FLD in the treatment of acute liver failure (ALF).

1,2,3,4,6‑penta‑O‑galloyl‑β‑D‑glucose alleviates inflammation and oxidative stress in diabetic nephropathy rats through MAPK/NF‑κB and ERK/Nrf2/HO‑1 signaling pathways.

Diabetic nephropathy (DN) is one of the main causes of chronic renal failure, which is also the final cause of mortality in ~30% of diabetic patients. 1, 2, 3, 4, 6-penta-O-galloyl-β-D-glucose (PGG) from Galla rhois has anti-inflammation, anti-oxidation and angiogenesis effects. The present study aimed to explore the protective effects on diabetic nephropathy rats by alleviating inflammation and oxidative stress and the underlying mechanism. High-fat diet/STZ induced rats and high glucose (HG) induced podocytes (MPC5) were used to simulate the DN in vivo and in vitro. The blood glucose level was measured using a blood glucose meter and renal function was determined by an automatic biochemical analyzer. The pathological changes and renal fibrosis were observed through hematoxylin and eosin, periodic acid-Schiff and Masson staining. The expression of nephrin in tissues, fibrosis-related proteins in tissues, MAPK/NF-κB and ERK/nuclear factor erythroid-derived 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway related proteins in tissues and apoptosis related proteins in tissues and podocytes was detected by western blotting. The inflammatory response and oxidative stress in tissues and podocytes were determined by respective commercial kits and apoptosis in tissues and podocytes was detected by TUNEL assay. The viability of podocytes treated with PGG with or without HG was analyzed by CCK-8 assay. As a result, the blood glucose level, urinary albumin/creatinine ratio, blood urea nitrogen and serum creatinine in blood were all increased and nephrin expression was decreased. The pathological changes and renal fibrosis were aggravated and the inflammation, oxidative stress and apoptosis in renal tissues were enhanced. The above effects were reversed by PGG treatment dose-dependently. MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways were activated in DN rats and were suppressed by PGG treatment. The reduced viability and increased apoptosis, inflammation and oxidative stress in MPC5 cells were shown in HG induction, which was reversed by PGG treatment. However, P79350 (p38 agonist) and LM22B-10 (ERK1/2 agonist) weakened the effect of PGG. In conclusion, PGG protects against DN kidney injury by alleviating inflammation and oxidative stress by suppressing the MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways.

Hsp72-Based Effect and Mechanism of Microwave Radiation-Induced Cardiac Injury in Rats.

The purpose of this study was to determine the role of heat shock protein 72 (Hsp72) changes in cardiac injury caused by microwave radiation, aimed at providing novel insights into the mechanism of this damage. A digital thermometer was used to measure the rectal temperature of the rats' pre- and post-radiation. On the 1st, 7th, 14th, and 28th days post-radiation, the changes in electrocardiogram (ECG) were analyzed by a multi-channel physiological recorder. The myocardial enzyme activities and ion concentrations were detected by an automatic biochemical analyzer. Additionally, the levels of myocardial injury markers were established by the enzyme-linked immunosorbent assay (ELISA), and those of hormones were measured by radioimmunoassay. The structure and ultrastructure of the myocardial tissue were observed using an optical microscope and transmission electron microscopy (TEM). The expression of Hsp72 was measured by Western blot and immunofluorescence analyses. Post-exposure, the rectal temperature in the R-group increased significantly, ECG was disordered, and the concentrations of ions were decreased. Furthermore, the activities of myocardial enzymes were changed, and the contents of myocardial injury markers and hormones were increased. We observed damage to the structure and ultrastructure and significantly increased expression of Hsp72. As a whole, the results indicated that S-wave microwave radiation at 30 mW/cm2 for 35 min resulted in damage to the cardiac functionality organigram, caused by a combination of the thermal and nonthermal effects.

Role of signal transducer, and activator of the transcription 4 (STAT4) gene polymorphism as predictive marker for type-1 autoimmune hepatitis

Introduction: Autoimmune hepatitis (AIH) is one of autoimmune disorder with complex pathophysiology. Many genes involved in lethal autoimmune hepatitis disorder including STAT4 gene. The aim of this study is to determine STAT4 gene polymorphisms and relation of SNPs with disease severity among AIH patients. Method: One hundred AIH patient which diagnosed by clinically, ANA and ASMA and 100 control age matched healthy children were enrolled in this study. Patients' blood samples (5mL) were taken and split into two tubes, one tube used for immunological and clinical parameters and the second containing EDTA for PCR analysis. The first tubes were then left at room temperature for 10 minutes before being centrifuged (3500 rpm). After that, the serum was isolated the both tubes stored at -70°C until analysis, biochemical parameters were measured in full automated biochemistry analyzer while, IgG, ANA and ASMA was investigated using the enzyme-linked immunosorbent assay (ELISA) commercially available kits (Bioneer, Korea), while the STAT4 (rs7574865, rs7582694) gene was investigated using RFLP PCR How, and the commercially available kits (Bioneer, Korea).

Lower ATG7 Levels are Associated with a Higher Risk of Gestational Diabetes Mellitus: A Cross-Sectional Study.

ObjectiveThis study aimed to investigate ATG7 levels in pregnant women with and without gestational diabetes mellitus (GDM) and explore the potential associations between ATG7 levels and GDM.MethodsThis was a cross-sectional study conducted in a large tertiary hospital in Chengdu, China. The ATG7 levels in pregnant women at between 24 and 28 weeks of gestation with (n=84) and without GDM (n=649) were measured by using an ELISA kit. Glucose, HbA1c, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were measured by an automatic biochemistry analyser. The homeostasis model assessment of insulin resistance (HOMA-IR) and insulin secretion (HOMA-β) were calculated according to published formulas. The associations of ATG7 levels with laboratory parameters, GDM, and insulin resistance were evaluated using correlation analysis or a regression model.ResultsThe ATG7 levels were significantly lower in pregnant women with GDM than in those without GDM. The correlation analyses found that ATG7 levels correlated positively with HOMA-β but correlated negatively with HOMA-IR, oral glucose tolerance test (OGTT) glucose levels, TGs, and LDL-C. There were no significant correlations between ATG7 levels and HbA1c, HDL-C, or TC. After adjusting for potential confounders, lower ATG7 levels were shown to be associated with a higher risk of GDM. Furthermore, multiple linear regression analyses showed that ATG7 levels were negatively associated with insulin resistance.ConclusionATG7 levels are significantly lower in pregnant women with GDM than in those without GDM, and lower ATG7 levels are associated with a higher risk of GDM. ATG7 levels were negatively associated with insulin resistance. Autophagy deficiency, which is caused by lower ATG7 levels, may be the underlying mechanism that mediates insulin resistance in the development of GDM.

Correlação entre traços produtivos e interiores de bois de diferentes genótipos

ABSTRACT The objective was to study the productive and biological traits of young cattle of the Kalmyk breed and its crosses. The experiment was conducted on 4 groups of steers, 10 heads each, at OAO Shurupovskoe, Frolovsky District, Volgograd Region. The experimental steers were kept in rooms separately in groups on a deep bed of straw and had free access to walking yards with mounds. The hemoglobin content and the numbers of erythrocytes and leukocytes were determined on a Medonic CA 530 hematological analyzer. The total protein in blood serum and protein fractions were found on an automatic biochemical analyzer Stat Faks 1904. The digital experimental data were processed by the variation statistics method in terms of the significance of the compared parameters using the Student's test accepted in biology and animal science. The study evidenced that the contents of morphological elements and proteins in blood reflected the metabolism and potential for crossbred steers to gain muscle mass.

Asiatic acid improves high-fat-diet-induced osteoporosis in mice via regulating SIRT1/FOXO1 signaling and inhibiting oxidative stress.

Asiatic acid can attenuate osteoporosis through suppressing adipogenic differentiation and osteoclastic differentiation. Oxidative stress enhances osteoclastic differentiation but represses osteogenic differentiation to promote osteoporosis. However, the role and mechanism of asiatic acid in osteoporosis have not been reported. Firstly, mice were fed with high-fat-diet (HFD) with or without asiatic acid for 16 weeks. Data from an automatic biochemical analyzer showed that HFD induced down-regulation of high-density lipoprotein (HDL) and an increase of serum levels of triglyceride (TG), total cholesterol (TC) and low-density lipoprotein (LDL). However, asiatic acid administration attenuated the decrease of HDL and increase of serum TG, TC and LDL in osteoporotic mice. Secondly, HFD induced high levels of malondialdehyde (MDA) and reactive oxygen species (ROS), low levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in osteoporotic mice. However, the levels of MDA, ROS, SOD and GSH-Px in osteoporotic mice were reversed by asiatic acid administration. (this section is unclear and requires revision) Asiatic acid administration reduced expression of c-telopeptide of type 1 collagen (CTX-1), enhanced alkaline phosphatase (ALP) and procollagen type 1 N-terminal propeptide (P1NP) in HFD-induced osteoporotic mice. (this section is unclear and requires revision) Thirdly, asiatic acid promoted calcium deposition in bone marrow cells and osteogenic differentiation in osteoporotic mice, but decreased ALP in bone marrow cells. Lastly, asiatic acid enhanced SIRT1 and nuclear FOXO1 (Nu-FOXO1) expression, while it reduced Acetyl FOXO1 (Ac-FOXO1) in osteoporotic mice. In conclusion, asiatic acid might inhibit oxidative stress and promote osteogenic differentiation through activating SIRT1/FOXO1 to attenuate HFD-induced osteoporosis in mice.

Antioxidant Status of Serum Bilirubin, Uric Acid and Albumin in Pemphigus Vulgaris

Objective: To determine antioxidant status of serum bilirubin, uric acid and albumin in pemphigus vulgaris. Study Design: Cross sectional study Place of Study and Duration: This study was done at Department of Dermatology Mayo Hospital Lahore from July 11, 2019 to January 11, 2020. Methodology: All 60 cases meeting inclusion criteria was enrolled after taking informed consent, from outdoor Department of Dermatology Mayo Hospital Lahore. A total of 200 cases meeting inclusion criteria was taken after getting approval from CPSP. A brief demographic information and contact detail was taken. Venous blood was collected from each subject for the evaluation of Serum Bilirubin, Uric Acid and Albumin. Total bilirubin, direct bilirubin, indirect bilirubin, UA and albumin levels was determined using an automatic biochemical analyzer (Model 7600‐120; Hitachi High Technologies, Tokyo, Japan). All the values was recorded as per operational definition. Results: The mean age of patients was 40.08±12.89 years with minimum and maximum age as 18 and 60 years. There were 22(36.7%) male and 38(63.3%) female cases with higher female to male ratio. The mean BMI was 29.08±2.70 with minimum and maximum BMI as 24 and 33.90. The mean serum bilirubin level was 8.51±1.64µmol/L with minimum and maximum serum bilirubin was 5.80µmol/L and 11µmol/L. The mean uric acid levels in this study was 234.37±33.46µmol/L with minimum and maximum value as 160.00µmol/L and 280.00µmol/L. The mean Albumin level in this study was 34.20 ±3.69g/l with minimum and maximum albumin level as 29.00g/l and 41g/l. Conclusion: It is concluded that oxidative stress and antioxidant status are important in the pathogenic mechanism of PV. Hence by keeping these profile in mind that it can be of benefit to administer bilirubin, UA and albumin or their precursors as a replacement therapy to patients with PV who have low antioxidant status. Key Words: Antioxidant status, serum bilirubin, uric acid, albumin, pemphigus vulgaris.

Correlation between Smoking and Dyslipidemia in Elderly Males: An Analytical Cross-Sectional Study

Aim: To investigate the association between smoking and dyslipidemia in elderly males while accounting for age, BMI, and alcohol use. Study design: Analytical cross-sectional study Place and Duration: This study was conducted at Bhitai Dental and Medical College Mirpurkhas from march 2021 to march 2022 Methodology: The research comprised 2,160 participants who were divided into 3 different groups: current smokers, non-smokers, &amp; past smokers. The research excluded those who smoked just sometimes (one cigarette per day). This study separated smokers into four categories: light (26.7 pack-years), medium (426.7-90.5 pack-years), heavy (440.5-75.5 pack-years), and extremely heavy (455.5-165.5 pack-years).On the same day, a survey, physical examination, and laboratory study of blood samples were used to evaluate the study population. The person was assessed while wearing light clothes and no shoes, and anthropometric measures comprised height and body weight. Weight was divided by height squared (kg/m2) to get the BMI. Using established protocols in the clinical laboratory, an automated biochemistry analyzer measured the blood levels of total cholesterol, triglycerides, high-density lipid cholesterol, low- density lipid cholesterol, Apo protein B, and Lipoprotein. Result: When compared to present smokers, the levels of triglycerides and high-density lipid cholesterol among non-smokers and former smokers were statistically significantly different (P=0.001). Other variables, such as Age, body mass index, use of liquor, systolic and diastolic blood pressure, did not significantly differ between non-, past, and present smokers. In comparison to light smokers, moderate, heavy, and very heavy smokers more commonly displayed abnormal levels of TGs, Apo-B, and TC, while very heavy smokers less frequently displayed abnormal levels of low-density lipid cholesterol. It was unexpected to find that among very heavy smokers, aberrant Apo-B levels were seen more frequently than low-density lipid cholesterol levels. The prevalence of abnormal HDL-C and lipoprotein (a) was higher among light smokers. After accounting for alcohol, BMI, and age, smoking remained a significant independent threat fact for dyslipidemia (P = 0.032). Conclusion:The study revealed that smoking caused TGs and apoB levels to rise in elderly males, and HDL-C levels to decrease, making it an independent risk factor for dyslipidemia. Keywords: smoking, dyslipidemia, elderly, males

Dimethyl fumarate improves cognitive impairment by enhancing hippocampal brain-derived neurotrophic factor levels in hypothyroid rats

BackgroundDimethyl fumarate (DMF) is an effective drug for multiple sclerosis and can improve the cognitive dysfunction caused by streptozotocin, but the effect on cognitive dysfunction caused by hypothyroidism is unclear.MethodsAfter the hypothyroidism rat model induced by propylthiouracil, we gave rats 25 mg/kg DMF by gavage. The body weight during model building and administration was recorded. The levels of T4 and T3 in serum were detected by an automatic biochemical analyzer. Morris water maze test was used to detect the effect of DMF on cognitive learning ability. The effect of DMF on Nissl bodies in the brain tissue was evaluated by Nissl staining. The mRNA and protein levels of BDNF in brain tissue were detected by quantitative reverse transcription-polymerase chain reaction and Western blot. The degrees of p-AKT/AKT and p-CREB/CREB in brain tissue were detected by Western blot.ResultsAfter DMF treatment, the body weight of hypothyroid rats recovered, and the levels of T3 and T4 in the serum were ameliorated. DMF also reduced the escape latency and distance traveled, and increased the swim speed. The number of Nissl bodies and expression of BDNF, p-AKT/AKT, and p-CREB/CREB in the brain tissue were increased after DMF treatment.ConclusionDMF improved the cognitive dysfunction of hypothyroid rats by increasing the level of BDNF in the brain tissue of hypothyroid rats.

Effects of lactoferrin on intestinal flora of metabolic disorder mice

To study the mechanism of lactoferrin (LF) regulating metabolic disorders in nutritionally obese mice through intestinal microflora. Twenty-one male C57BL/6 mice were randomly divided into 3 groups: control group, model group and LF treatment group. The mice in control group were fed with maintenance diet and drank freely. The mice in model group were fed with high fat diet and drank freely. The mice in LF treatment group were fed with high fat diet and drinking water containing 2% LF freely. Body weight was recorded every week. Visceral fat ratio was measured at week 12. Blood glucose and serum lipid level were detected by automatic biochemical analyzer. The gut microbiota of mice was examined using 16 s rRNA sequencing method. LF treatment significantly reduced the levels of visceral adipose ratio, blood glucose, triglyceride, total cholesterol and low-density lipoprotein cholesterol (LDL-C) in high-fat diet mice (p < 0.05). It can be seen that drinking water with 2% LF had a significant impact on metabolic disorders. At the same time, the Firmicutes/Bacteroidetes ratio(F/B) of LF treated mice was decreased. The abundance of Deferribacteres, Oscillibacter, Butyricicoccus, Acinetobacter and Mucispirillum in LF treatment group were significantly decreased, and the abundance of Dubosiella was significantly increased (p < 0.05). In the LF-treated group, the expression levels of glucose metabolism genes in gut microbiota were increased, and the expression levels of pyruvate metabolism genes were decreased. It can be seen that metabolic disorders were related to intestinal flora. In conclusion, LF regulates metabolic disorders by regulating intestinal flora.