An effective method has been developed for laboratory scale production of IgG. Hybridomas were cultured in serum-free media with 2% IgG-free ascites. Cell density of up to 3.55 × 10 6cells/ml and antibody concentration of 135μ g/ml after purification were abtained, which is four time more than total production of that of IgG concentration in serum-free media. This in vitro method allows great improvement in antibodies production in batch tissue culture. The method reported here is easy to handle and is economical and universally adaptable.

Objective: To compare the biotype and genetic similarity between groups of commensal and pathogenic strains of candida species. Methods:Random amplified polymorphic DNA (RAPD) was used to analyse the type of Candida albicans. Results: 12 pathogenic isolates of Candida albicans, 3 commensal isolates of Candida abicans and 3 isolates of pathogenic non-albicans were obtained. The similarity coefficient of albicans with non-albicans was 51.7% by RAPD. Intra-candida similarity coefficient was more than 70%. Both the commensal and pathogenic isolates showed the genetically similar to C. albicans. Intro-isolate DNA polymorphism was observed by RAPD. Conclusion: Both the commensal and pathogenic groups contain a major cluster of genetically similar C. albicans isolates.

OBJECTIVETo test whether folic acid offers protection of the brain tissue against acute cerebral infarction in rats.

METHODSSprague-Dawley rats were divided into control (n=8), pre-treatment (n=12) and treatment (n=16) groups, all having routine feed for 7 days. The rats in the control and treatment groups were given normal saline daily, and those in the pre-treatment group received folic acid suspension daily. All the rats were then subject to middle cerebral artery occlusion (MCAO) for 24 h followed by reperfusion. On and after the operation day, the rats in the control group were given normal saline and those in the other two groups were given folic acid suspension daily. Neural function deficiency was evaluated on a daily basis after the operation, and on day 6 after the operation, brain biopsy was performed for examination with TTC staining. Monocyte chemokine -1 (MCP-1) in both normal and infarct tissues was measured by ELISA.

RESULTSOn day 6 after the operation, the neural function deficiency scores of the control, pre-treatment and treatment groups were 4.56∓3.63, 2.94∓2.94 and 1.00∓1.00, and the percentages of the infarct area (to the whole brain area) were (44.23∓10.06)%, (20.64∓6.78)% and (14.61∓13.51)%, respectively. The contents of MCP-1 in the infarct area of the brain tissues were 168.58∓107.21 ng/L, 152.91∓64.78 ng/L, and 97.74∓46.19 ng/L in the 3 groups, respectively.

CONCLUSIONFolic acid can protect brain tissue against acute cerebral infarction in rats.

Animals ; Cerebral Infarction ; drug therapy ; Female ; Folic Acid ; therapeutic use ; Infarction, Middle Cerebral Artery ; drug therapy ; Neuroprotective Agents ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Thrombolytic Therapy

Objective To test whether folic acid offers protection of the brain tissue against acute cerebral infarction in rats. Methods Sprague-Dawley rats were divided into control (n=8), pre-treatment (n=12) and treatment (n=16) groups, all having routine feed for 7 days. The rats in the control and treatment groups were given normal saline daily, and those in the pre-treatment group received folic acid suspension daily. All the rats were then subject to middle cerebral artery occlusion (MCAO) for 24 h followed by reperfusion. On and after the operation day, the rats in the control group were given normal saline and those in the other two groups were given folic acid suspension daily. Neural function deficiency was evaluated on a daily basis after the operation, and on day 6 after the operation, brain biopsy was performed for examination with TTC staining. Monocyte chemokine-1 (MCP-1) in both normal and infarct tissues was measured by ELISA. Results On day 6 after the operation, the neural function deficiency scores of the control, pre-treatment and treatment groups were 4.56 ± 3.63, 2.94 ± 2.94 and 1.00 ± 1.00, and the percentages of the infarct area (to the whole brain area) were (44.23 ± 10.06)%, (20.64 ± 6.78)%and (14.61 ± 13.51)%, respectively. The contents of MCP-1 in the infarct area of the brain tissues were 168.58 ± 107.21 ng/L, 152.91 ± 64.78 ng/L, and 97.74 ± 46.19 ng/L in the 3 groups, respectively. Conclusion Folic acid can protect brain tissue against acute cerebral infarction in rats.

Objective: To analyze the associations among body mass index (BMI), learning screen/gaming screen exposure and executive function in preschool children in Anhui Province, so as to provide a basis for promoting the development of executive function in preschool children. Methods: In June 2022, a stratified cluster sampling and convenience sampling methods were used to survey 3 534 mothers of preschool children in Wuhu City, Luan City, and Fuyang City, Anhui Province. The Behavior Rating Inventory of Executive Function-Preschool Version (BRIEF-P) was used to assess the preschool childrens executive function abnormalities. Binary Logistic regression was conducted to examine the relationships among BMI, learning screen/gaming screen exposure, and their combined effects on executive function abnormalities. Results: The detection rate of abnormal executive function in preschool children was 9.65%. Logistic regression analysis showed that after adjusting for the confounding factors such as pregnancyinduced hypertension, primary caregivers, family per capita monthly income and family structure, the risk of abnormal executive function of children in overweight/obesity group and high learning screen/gaming screen exposure group increased significantly (overweight/obesity:OR=1.78, 95%CI=1.31-2.42, learning screen exposure:OR=1.48, 95%CI=1.18-1.86, gaming screen exposure:OR=1.50, 95%CI=1.18-1.91,P<0.05). Compared with children with normal BMI and low learning screen/gaming screen screen exposure, those with both overweight/obesity and high learning screen/gaming screen exposure had a significantly greater risk of executive function abnormalities (OR=2.07, 95%CI=1.29-3.31; OR=2.42, 95%CI=1.59-3.68,P<0.05). Conclusions Overweight/obesity and high learning screen/gaming screen exposure are important risk factors for executive function abnormalities in preschool children. Therefore, actively guiding preschool children to develop healthy life habits to promote the normal development of their executive functions is essential.

Background/Aims: The occurrence and development of hepatitis B virus-associated acute-onchronic liver failure (HBV-ACLF) is closely related to the immune pathway. We explored the heterogeneity of peripheral blood T cell subsets and the characteristics of exhausted T lymphocytes, in an attempt to identify potential therapeutic target molecules for immune dysfunction in ACLF patients. Methods: A total of 83,577 T cells from HBV-ACLF patients and healthy controls were screened for heterogeneity by single-cell RNA sequencing. In addition, exhausted T-lymphocyte subsets were screened to analyze their gene expression profiles, and their developmental trajectories were investigated. Subsequently, the expression of exhausted T cells and their capacity in secreting cytokines (interleukin 2, interferon γ, and tumor necrosis factor α) were validated by flow cytometry. Results: A total of eight stable clusters were identified, among which CD4 + TIGIT + subset and CD8 + LAG-3 + subset, with high expression of exhaust genes, were significantly higher in the HBV-ACLF patients than in normal controls. As shown by pseudotime analysis, T cells experienced a transition from naïve T cells to effector T cells and then exhausted T cells. Flow cytometry confirmed that the CD4 + TIGIT + subset and CD8 + LAG-3 + subset in the peripheral blood of the ACLF patients were significantly higher than those in the healthy controls. Moreover, in vitro cultured CD8 + LAG-3 + T cells were significantly fewer capable of secreting cytokines than CD8 + LAG-3- subset. Conclusions Peripheral blood T cells are heterogeneous in HBV-ACLF. The exhausted T cells markedly increase during the pathogenesis of ACLF, suggesting that T-cell exhaustion is involved in the immune dysfunction of HBV-ACLF patients.

Objective To test whether folic acid offers protection of the brain tissue against acute cerebral infarction in rats. Methods Sprague-Dawley rats were divided into control (n=8), pre-treatment (n=12) and treatment (n=16) groups, all having routine feed for 7 days. The rats in the control and treatment groups were given normal saline daily, and those in the pre-treatment group received folic acid suspension daily. All the rats were then subject to middle cerebral artery occlusion (MCAO) for 24 h followed by reperfusion. On and after the operation day, the rats in the control group were given normal saline and those in the other two groups were given folic acid suspension daily. Neural function deficiency was evaluated on a daily basis after the operation, and on day 6 after the operation, brain biopsy was performed for examination with TTC staining. Monocyte chemokine-1 (MCP-1) in both normal and infarct tissues was measured by ELISA. Results On day 6 after the operation, the neural function deficiency scores of the control, pre-treatment and treatment groups were 4.56 ± 3.63, 2.94 ± 2.94 and 1.00 ± 1.00, and the percentages of the infarct area (to the whole brain area) were (44.23 ± 10.06)%, (20.64 ± 6.78)%and (14.61 ± 13.51)%, respectively. The contents of MCP-1 in the infarct area of the brain tissues were 168.58 ± 107.21 ng/L, 152.91 ± 64.78 ng/L, and 97.74 ± 46.19 ng/L in the 3 groups, respectively. Conclusion Folic acid can protect brain tissue against acute cerebral infarction in rats.

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease that is difficult to diagnose clinically, and finding appropriate biomarkers to assist in the diagnosis and prognosis monitoring of IPF can improve the proportion of early diagnosis and timely treatment of these patients and improve the quality of life of patients

Objective:The combined diagnosis models was constructed with the test indicators and its application value in the clinical evaluation of patients with interstitial lung disease was evaluated.Methods:Methodology development and validation. A total of 101 patients with idiopathic pulmonary fibrosis (IPF) and 107 patients with non-IPF interstitial lung disease admitted to China-Japan Friendship Hospital from 2022 to 2023 were collected, and 98 healthy people were collected during the same period. The population in each group was divided into modeling group (180 cases) and validation group (126 cases) by complete randomization. Serum samples and clinical test results were collected. The test indicators included white blood cell count, lymphocyte count, monocyte count, hemoglobin concentration, highly sensitive C-reactive protein, Krebs von den Lungen 6, total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, adenosine deaminase, neuron-specific enolase, alpha-fetoprotein, carcinoembryonic antigen, cytokeratin 19 fragment, carbohydrate antigen 15-3, gastrin releasing peptide precursor, squamous cell carcinoma antigen and interleukin 1 (IL-1), IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, tumor necrosis factor-α, interferon-α, interferon-γ. Multiple collinearity test, univariate and multivariate logistic regression were performed for the included test indicators in each group, and nomograms were established and validated by receiver operating characteristic (ROC) curves, calibration curves and clinical decision curves.Results:By comparing interstitial lung disease to healthy people, carbohydrate antigen 15-3 ( OR=1.285, 95% CI 1.178-1.402), IL-6 ( OR=1.128, 95% CI 1.011-1.258), adenosine deaminase ( OR=1.465, 95% CI 1.261-1.702), and Krebs von den Lungen-6 ( OR=1.013, 95% CI 1.008-1.017) were independent risk factors for interstitial lung disease. Based on these four indexes, the nomogram model was constructed. The AUCs of the combined diagnosis model in the modeling group and validation group were 0.967(95%CI 0.941-0.993)and 0.948(95% CI 0.911-0.984), respectively.Decision curve analysis showed that the net benefit of the combined diagnosis model in diagnosing IPF was higher than that of a single indicator within the threshold range of 0.01-1. In the comparison of IPF and non-IPF interstitial lung disease, alpha-fetoprotein ( OR=1.403, 95% CI 0.975-2.019) and squamous cell carcinoma antigen ( OR=0.531, 95% CI 0.321-0.878) were independent risk factors for IPF. The AUCs of the combined diagnosis model in the modeling group and validation group were 0.703 (95% CI 0.597-0.81) and 0.642 (95% CI 0.528-0.757), respectively. Through calibration curve and clinical decision curve verification, it was found that it had a certain value in the differential diagnosis of IPF. Conclusions:Carbohydrate antigen 15-3, IL-6, adenosine deaminase and Krebs von den Lungen 6 are risk factors of interstitial lung disease, which can be used to construct a combined diagnostic model for the diagnosis of interstitial lung disease. Alpha-fetoprotein and squamous cell carcinoma antigen are risk factors of IPF, which can be used to construct a combined diagnostic model to distinguish IPF from non-IPF interstitial lung disease and assist clinical diagnosis of IPF.

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease that occurs mostly in the middle-aged and eldly people, with a short median survival and cannot be cured, and the etiology is still unclear. Currently, it is believed that the pathogenesis is related to cellular aging, and abnormal cellular aging leads to the failure of damaged alveolar epithelial cells that cannot be repaired normally, which promotes the occurrence of pulmonary fibrosis. Senescence-associated secretory phenotype (SASP), SASP affects pulmonary fibrosis through different signaling pathways in IPF patients, and this article reviews the expression level and mechanism of existing SASP in IPF patients.