Objective To observe the activation of pancreatic stellate cells (PSC) during the formation of pancreatic fibrosis induced by the pancreatic injection of trinitrobenzene sulfonic acid (TNBS). Meanwhile, the effects of PSC-related factors, such as transforming growth factor ? 1 (TGF-? 1), collagen Ⅰ and MMP-2 on the pathogenesis of pancreatic fibrosis in rats were also evaluated. Methods Pancreatic fibrosis model in rats was induced by the injection of 2% TNBS in ethanolate-phosphate buffer solution into the pancreatic duct. The rats were sacrificed and the pancreata were removed at the 72nd hour, 3rd week, 4th week, 5th week, 6th week and 7th week after the operation respectively. Expressions of ?-smooth muscle actin (?-SMA), transforming growth factor ? 1 (TGF-? 1), collagen Ⅰ and MMP-2 were determined by either immunohistochemistry or RT-PCR, or Western blot respectively. The ultrastructure of pancreas was studied by electron microscope at different time points. Results The inflammation, swelling and necrosis were the major pathological changes of the pancreas at the early stage after the injection of 2% TNBS. Subsequently, the fibrotic manifestations such as proliferation of the fibrosis, atrophy of vesicles, deposition of collagen because prominent at the 3rd week after the operation, which peaked at 4th week. The expression of TGF-? 1 was increased significantly at the 3rd week after the operation and reached maximum at the 4th week. The expression of ?-SMA, which indicated the activation of PSC, could be detected at the 3rd week and also reached the peak value at the 4th week. After wards, it was decreased gradually. During the first 72 hours, the expression of MMP-2 mRNA was increased significantly and then was fluctuated but still higher than that in normal rats. The deposition of type Ⅰ collagen was increased in the areas of fibrotic tissues. Conclusions PSC might involve in the courses of the development and progression of TNBS induced pancreatic fibrosis in rats. This action was achieved via the activation of PSC by TGF-? 1, the production of those extracellular matrix metabolic associated enzymes such as the synthesis of collagen Ⅰ and the secretion of MMP-2.

AIM To investigate the effects and possible mechanism s of Glycyrrhizin on rat pancreatic fibrosis induced by TNBS (trinitrobenzenesulfonic acid, TNBS ). METHODS Chronic pancreatitis model was induced in male Sprague -Dawley rats by injection of 2% TNBS into bile duct. All the rats were randomly divided into two groups. The rats in Glycyrrhizin intervention group were treat ed with Glycyrrhizin 8 mg?kg -1 by injection into tail vein from day 3 to day 28, while the rats in control group were administrated with same volume of saline vehicle. Ten rats in the Glycyrrhizin intervention group and eight rats in the control group wer e sacrificed on day 29, the blood was collected to determine amylase and hyaluro nic acid by enzyme dynamic and RIA method. The histological change of pancreatic tissue was evaluated by H&E stain and modified Van-Gieson stain. Mast cell in pancreas was stained by thionine blue. Expression of TGF-? 1,Collagen Ⅰ and ?-SMA in pancreas were assessed by immunohistochemistry and western blot. RESULTS In the Glycyrrhizin intervention group, the mast cell number and the percentage of degranulation decreased significantly, and the expression of ?-SMA protein also decreased compared to the control group, but there was no difference in amylase or hyaluronic acid between the treatment group and the control group. In the Glycyrrhizin intervention group, inflammation and fibrosis were ameliorated and expression of collageⅠ and TGF-? 1 was also decreased significantly compared to the control group. CONCLUSION Glycyrrhizin inhibits pancreatic fibrosis in chronic pancreatitis rats induced by TNBS. This action might be related to protecting pancreatic acinus cells from being destructed by mast cell activation and inhibiting extracellular matrix synthesis stimulated by pancreatic stellate cell.

Adoptive immune cells can regulate and strengthen immune function of cancer patients,thus effectively inhibit tumor escaping.Cytokine induced killer cells (CIK),natural killer cells (NK),tumor infiltrating lymphocytes (TIL),dendritic cells (DC),T cell receptor-modified T cells (TCR-T) and chimeric antigen receptor-modified T cells (CAR-T) eliminate tumor by killing tumor cells directly or stimulating the immune response against tumor cells through different mechanisms.

AIM: To determine the effects of NF-?B on the development of rat pancreatic fibrosis mediated by angiotensin II. METHODS: Spraque-Dawley rats (200-300g) were randomly divided into normal group, control group and losartan-treatment group. Pancreatic fibrosis was induced by injection of 2% TNBS into biliopancreatic duct. Rats in losartan-treatment group and control group were respectively treated with losartan (10 mg?kg~(-1)?d~(-1)) by gavage and the same volume of saline vehicle. The expression, distribution, and activation of NF-?B were studied by Western blot, immunohistochemistry and TransAM~(TM). Toluidine blue staining and transmission electron microscopy were also used to observe the number, distribution and degranulation of mast cells. In addition, RT-PCR was performed to detect the intrapancreatic ICAM-1 mRNA expression. RESULTS: The expression and activity of intrapancreatic NF-?B p65 protein were significantly increased on day 3 after operation, reaching peak on day 7 [(0.406?0.086) mg/g total protein]. Mast cell activation was observed and ICAM-1 mRNA levels on day 3 and 7 were up-regulated in control group. Losartan treatment inhibited NF-?B expression and activation, reduced mast cell infiltration and degranulation and decreased ICAM-1 mRNA expression compared with control rats. CONCLUSION: It might be associated with the expression and activation of NF-?B that angiotensin II mediates inflammation and fibrosis in the early stage of pancreatic fibrosis. [

AIM: To examine the effects of PPAR? activation on the growth of human pancreatic carcinoma in vitro and to explore the role of NF-?B and activator protein-1 (AP-1) in this process. METHODS: SW-1990 pancreatic cancer cells were treated with ligand of RXR?, 9-cis-RA, ligand of PPAR?, 15d-PGJ_2, and both. Antiproliferative effect was evaluated by using MTT assay; the expression of NF-?B p65 active protein was assayed by using TransAM~TM technique. Expression of c-jun and c-fos by SW1990 cells, which were treated with 15d-PGJ_2, 9-cis-RA and both at varying concentrations, were detected by RT-PCR. RESULTS: MTT assay demonstrated that 15d-PGJ_2, 9-cis-RA and the combination of both had a potent inhibitory effect on the growth of SW1990 cells in a dose-dependent manner. 9-cis-RA had a synergic action with 15d-PGJ_2 on the growth inhibition of pancreatic carcinoma. TransAM~TM showed a down-regulation trend of P65 active protein in SW1990 cells treated with 15d-PGJ_2, 9-cis-RA and both. RT-PCR demonstrated that the expression of c-jun mRNA in 15d-PGJ_2, 9-cis-RA and the combination of both-treated cells were firstly increased and then decreased, the expression of c-fos was decreased in 15d-PGJ_2 or 9-cis-RA treated SW1990 cells, but increased in cells treated with both 15d-PGJ_2 and 9-cis-RA. CONCLUSION: Activation of PPAR? exerts a negative regulatory effect on the growth of pancreatic carcinoma in vitro. Activation of RXR? has a synergic action with PPAR? agonist. The mechanism is probably associated with down-regulating the expression of NF-?B and AP-1. [

By Analyzing the significance and objective,practicing the organizing and management of the clinical application teaching in department of gynecology,the author explored the new teaching methods in current social condition.

Objective To investigate the status of life quality in the elderly in Shanxi Province Changzhi City, and to analyze its influencing factors. Methods The quality of life, activities of daily living and status of community services were measured simultaneously by 36-Item Short Form Health Survey (SF-36). Activities of Daily Living Scale, Community Healthy Needs Scale and survey results were used and analyzed using t-test, correlation and stepwise regression analysis. Results According to the criterion of life quality in the elderly which were proposed by Zhang Lei, the quality of life in the elderly scored 72. 1-117.0, reached 98.5%. The quality of life in the elderly was impacted by the ability of caring oneself, marital status, degree of culture, economic situation and so on. The demand rate for health guidance and periodic physical examination was higher. Conclusions The quality of life in the elderly is at a medium level. There is a wide gap between the demand of community healthy services and the utilization of community healthy services.

Objective To investigate the quality of life of elderly caregivers and its factors. Methods Elderly caregivers living in Changzhi City were enrolled in this study. 36-item short-form (SF-36) health survey and Activity of Daily Living Scale ( ADL) were used as study tools. The data was analyzed by statistical description,t test or multiple regression. Results Those with score of quality of life reaching 72. 1 to 117. 0 accounted for 98. 8%. The total score and score of eight dimensions of SF-36 showed statistically significant difference between different daily living activity groups ( P < 0.05) . The state of health and self-care ability of the elderly imposed a major impact on eight dimensions of SF-36. Age, sex, level of education, marital status and wage had different impact on each dimension of SF-36. Conclusion The quality of life of elderly caregivers is at a medium level. The main factors of quality of live of elderly caregiver are their state of health and self-care ability of the elderly.

ObjectiveOptimize the latex perfusion technique and apply it to the construction of a murine craniofacial venous vascular model.Methods A total of nine 8-week-old male C57BL/6 mice weighing (25.0±1.3) g were randomly divided into three groups: 60% latex physiological saline group, 60% latex heparin group, and 30% latex heparin group. After completion of the perfusion, the specimens were immersed in 4 °C formalin fixative for 24 h, followed by dissection, observation, and measurement of the extracranial blood vessel diameters. Results After 200 μL latex perfusion solution was injected into the external jugular vein, the supraorbital vein, infraorbital vein, temporal vein, retrofacial vein, masseter vein and external jugular vein were perfused in each group.After comparing the perfusion degree of the distal branches of blood vessels, sublingual vein and tip venule, it was found that the 30% latex heparin group had the best perfusion effect, followed by the 60% latex heparin group, and the 60% latex saline group had the worst perfusion effect.ConclusionThe optimized latex perfusion technique can effectively infuse the veins in the head and face of mice, and this technique can provide a good reference for the study of the direction and morphology of facial veins in mice.

Objective The aim is to utilize CRISPR/Cas9 gene editing technology to construct Dmd gene mutant mice with a point mutation in exon 23 of the Dmd gene. Subsequently, the phenotypic changes of the mice in muscles and immune systems are analyzed and verified, providing an evaluation model for Duchenne muscular dystrophy and other related diseases.MethodsBased on the sequence characteristics of exon 23 of the Dmd gene, small guide RNA (sgRNA) was designed and synthesized. Cas9 mRNA, sgRNA fragments, and oligo donor DNA were microinjected into fertilized eggs of C57BL/6J mice. After transferring the fertilized eggs to surrogate mice, F0 generation mice were born. After mating with F0 generation mice, offspring mice were obtained, and Dmd gene positive mutant (Dmd^Mu/+) mice were obtained after genotype identification. Male hemizygous Dmd^Mu/+(Dmd^Mu/Y) mice were selected for phenotype validation. The body weight of live 3- and 9-month-old mice were recorded. Muscle tension was evaluated through the grid test. Hearts and semitendinosus muscles were collected, and the histopathological changes were observed using HE staining. Further, the expression of Dmd protein in muscle tissue of 9-month-old mice was analyzed by Western blotting.An acute inflammation model was established in Dmd^Mu/Y mice using lipopolysaccharide induction. Peripheral blood from the submandibular vein was collected, and the changes in the proportion of neutrophils and monocytes were detected by flow cytometry.Results The results of genome sequencing and Western blotting confirmed the successful construction of Dmd gene point mutant mice (Dmd^Mu/+ mice). Dmd protein expression was not detected in skeletal muscle and myocardium of Dmd^Mu/+ mice, and it was significantly reduced compared to wild-type C57BL/6J mice (P<0.05). Compared with wild-type mice of the same background, Dmd^Mu/Y mice at 3 and 9 months of age showed significant weight loss (P<0.01) and decreased muscle tension (P<0.05). 9-month-old Dmd^Mu/Y mice exhibited significant pathological changes in skeletal muscle and myocardium, including widening of intermuscular space. Under normal condition, compared with wild-type mice, the proportion of neutrophils and monocytes in the peripheral blood of 3-month-old Dmd^Mu/Y mice was significantly lower than that of wild-type mice (P<0.01). After lipopolysaccharide stimulation, the proportion of neutrophils in peripheral blood of 3-month-old Dmd^Mu/Y mice remained significantly lower compared to that of wild-type mice (P<0.01). The proportion of neutrophils in peripheral blood of 9-month-old Dmd^Mu/Y mice significantly decreased after lipopolysaccharide induction (P<0.01), with a trend of change observed in monocytes between groups.Conclusion The successful construction of the Dmd gene mutant mouse model has confirmed the vital function of Dmd gene in maintaining normal muscle tissue morphology and muscle tone. It preliminarily indicated that Dmd gene deletion could significantly reduce the proportion of neutrophils in peripheral blood, offering a new perspective for the study of immune system alterations in Duchenne muscular dystrophy patients.