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Objective To verify whether miR-498 can inhibit A549 cell migration and invasion by down-regulating FOXM1. Methods miR-498 mimic and miR-NC were transfected into A549 cells. Wound healing and Transwell method were employed to test the migratory ability and invasion ability of A549 cells; Western blot was used to detect the expressions of COL1A1, COL1A5 and FOXM1 in A549 cells. Luciferase assay was used to confirm whether FOXM1 is the target gene of miR-498. Results Compared with those in the control group, the expressions of COL1A1, COL1A5 and FOXM1 were decreased, and the migration and invasion abilities of A549 cells were decreased in the miR-498 group (both P<0.01). The luciferase activity of the FOXM1-3′-UTR plasmid was significantly suppressed by miR-498 (P<0.05); over-expression of FOXM1 could reverse the effect of miR-498 on A549 cells. Conclusion miR-498 inhibits A549 cell migration and invasion by down-regulating FOXM1. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the role of clinical pharmacists in the infection treatment for one patient with severe maxillofacial space infection,so as to provide reference for the rational drug application in clinic. METHODS: The clinical pharmacists participated into the treatment process of one patient with severe maxillofacial space infection,and provided pharmaceutical care from the aspect of drug selection, treatment regimen adjustment and deescalation therapy. RESULTS: According to patients' conditions, the clinical pharmacists assisted the clinicians to formulate and optimize the treatment regimen, and the patient's disease had been effectively controlled and discharged smoothly. CONCLUSIONS: Based on pharmaceutical professional knowledge, the clinical pharmacists participate the clinical drug treatment, assist the clinicians adjust the treatment regimen, which is helpful to improve the level of clinical medication and can promote the rational drug application in clinic. [ABSTRACT FROM AUTHOR]

Objective To investigate the therapeutic effect of Qingjie Huagong decoction (QJHGD) on a mouse model of severe acute pancreatitis (SAP) and the mechanism of action of QJHGD against inflammatory response. Methods A total of 36 male C57BL/6J mice were randomly divided into blank group, model group, Western medicine group (ulinastatin), and low-, middle-, and high-dose QJHGD groups, with 6 mice in each group. All mice except those in the blank group were given 5% sodium taurocholate by retrograde pancreaticobiliary injection to establish a model of SAP. After modeling, the mice in the low-, middle-, and high-dose groups were given QJHGD (1，2, and 4 g/kg, respectively) by gavage, and those in the Western medicine group were given intraperitoneal injection of ulinastatin (5×104 U/kg), for 7 days in total. HE staining was used to observe the histopathological changes of the pancreas； ELISA was used to measure the levels of α-amylase, lipase, interleukin-1β（IL-1β), interleukin-6（IL-6), interleukin-8（IL-8), interleukin-18（IL-18), and tumor necrosis factor-α（TNF-α) in mice； RT-qPCR was used to measure the mRNA expression levels of NOD-like receptor protein3 (NLRP3), Toll-like receptor 4（TLR4), and nuclear factor-kappa B (NF-κB) in pancreatic tissue； immunohistochemistry was used to measure the positive expression rates of NLRP3, TLR4, and NF-κB in pancreatic tissue； Western blot was used to measure the protein expression levels of NLRP3, TLR4, NF-κB, IL-1β, and IL-6. An analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results Compared with the blank group, the model group had diffuse destruction of pancreatic tissue structure, focal dilatation of pancreatic lobular septum, pancreatic acinar atrophy, and massive inflammatory cell infiltration, as well as significant increases in the content of α-amylase, lipase, IL-1β, IL-6, IL-8, IL-18, and TNF-α（all P<0.05), the mRNA expression levels and positive expression rates of NLRP3, TLR4, and NF-κB (all P< 0.05), and the protein expression levels of NLRP3, TLR4, NF-κB, IL-1β, and IL-6（all P<0.05) . Compared with the model group, the low-, middle-, and high-dose QJHGD groups and the Western medicine group had slightly tighter and more intact structure of pancreatic tissue, ordered arrangement of pancreatic acinar cells, a small amount of inflammatory cell infiltration, and hemorrhagic foci of pancreatic lobules, as well as significant reductions in the content of α-amylase, lipase, IL-1β, IL-6, IL-8, IL-18, and TNF-α（all P<0.05), the mRNA expression levels and positive expression rates of NLRP3, TLR4, and NF-κB (all P<0.05), and the protein expression levels of NLRP3, TLR4, NF-κB, IL-1β, and IL-6（all P<0.05) . Conclusion QJHGD may exert a protective effect on the pancreatic tissue of SAP mice by inhibiting the activation of NLRP3/TLR4/NF-κB signaling pathway-related proteins, reducing the release of inflammatory mediators, and preventing the enhancement of inflammatory cascade response. [ABSTRACT FROM AUTHOR]

Background and purpose: Chemotherapy-induced nausea and vomiting (CINV) can cause severe damage to body functions and even lead to death. The prevention of CINV is critically important in patients receiving emetogenic chemotherapy regimen. This study aimed to investigate the prevalence and treatment of CINV in Grade-A tertiary hospitals in Shanghai and explore risk factors of CINV to improve its management. Methods: The clinical data of 376 cancer patients in Grade-A tertiary hospitals in Shanghai from October 2022 to December 2022 were collected retrospectively. The questionnaire was used to conduct a crosssectional study. The univariate and multivariable logistic regression models were used to evaluate the influencing factors of CINV. Results: The management and coincidence of the guideline in 2022 significantly improved compared to five years ago. For patients receiving high-emetic-risk chemotherapy regimen, the coincidence of the guideline increased from 21.6% to 67.0%. For patients receiving moderate-emetic-risk chemotherapy regimen, the neurokinin-1 (NK-1) receptor antagonist was not significantly associated with CINV. Multivariable analysis showed that the chemotherapy regimen was the only risk factor for CINV during the whole period (P＜0.05). Conclusion: The chemotherapy regimen is the main risk factor for CINV. To control CINV better, clinical practitioners should focus on the intrinsic risk of chemotherapy regimens preferentially, estimate the risk and adhere better to guidelines. [ABSTRACT FROM AUTHOR]

Objective　To investigate the expression and clinical significance of matrix metalloproteinase 7 (MMP7) and heparan sulfate proteoglycan 2 (HSPG2) in patients with pancreatic cancer. Methods　Pancreatic cancer tissue samples, normal adjacent tissue samples, and serum samples were collected from 30 patients who were admitted to Guangxi Medical University Cancer Hospital from January 2018 to December 2020, and serum samples were collected from 30 healthy volunteers as controls. Immunohistochemistry was used to measure the protein expression levels of MMP7 and HSPG2 in pancreatic cancer tissue samples and normal adjacent tissue samples; ELISA was used to measure the expression levels of MMP7 and HSPG2 in the serum samples of the pancreatic cancer patients and the healthy controls; related clinical data were collected to analyze the association of the expression of MMP7 and HSPG2 with clinicopathological features, survival, and prognosis. The independent－samples t test was used for comparison of continuous data between two groups, and the chi－square test or the Fisher’s exact test was used for comparison of categorical data between two groups; the Spearman correlation analysis was used to investigate the correlation between MMP7 and HSPG2; the Kaplan－Meier method was used to plot survival curves, and the Log－rank test was used for survival analysis. Results　Immunohistochemistry showed that the protein expression levels of MMP7 and HSPG2 in pancreatic cancer tissue were significantly higher than those in adjacent tissue (χ²=31.093 and 35.623, both P<0.05) . The patients with pancreatic cancer had significantly higher serum levels of MMP7 and HSPG2 than the healthy controls ( t=20.174 and 32.600, both P<0.05) . The expression of MMP7 and HSPG2 was associated with tumor diameter and TNM stage (both P<0.05) . The Spearman correlation analysis showed a positive correlation between HSPG2 and MMP7 (r=0.539, P=0.002) . The patients with positive protein expression of MMP7 and HSPG2 had a significantly lower overall survival rate than those with negative expression (χ²= 4.084 and 12.554, both P<0.05) . Conclusion　MMP7 and HSPG2 are highly expressed in pancreatic cancer tissue and serum and are associated with tumor diameter and TNM stage. They may also be associated with the development and progression of pancreatic cancer, and therefore, they are expected to become potential markers for the diagnosis and prognostic evaluation of pancreatic cancer. [ABSTRACT FROM AUTHOR]

Background and purpose: Colorectal cancer is one of the most common malignant tumors of digestive system. The incidence of colorectal cancer has increased significantly in China in recent years. Various clinical and pathological indicators are helpful for the diagnosis, clinical staging and prognostic evaluation of colorectal cancer. This study aimed to observe the correlation between the expression of mismatch repair protein and serum tumor markers and Ki-67 proliferation index in colorectal cancer, and to analyze the prognostic value of mismatch repair protein, serum tumor markers and Ki-67 proliferation index. Methods: Data of 234 patients with colorectal cancer were collected after surgery in Huadong Hospital Affiliated to Fudan University from July 2014 to June 2018, and the preoperative serum levels of tumor markers (CEA, CA19-9, CA72-4, CA12-5), Ki-67 proliferation index and mismatch repair protein expression rate in surgical specimens were analyzed, in order to find the relationship between these clinicopathological features and prognosis of colorectal cancer. Results: Among 234 postoperative specimens of colorectal cancer patients, a total of 29 cases (12.4%) had defective expression of mismatch repair protein (dMMR), and 205 cases (87.6%) had normal expression of mismatch repair protein (pMMR). In the correlation analysis of clinicopathological features, there were statistically significant differences in tumor primary site, differentiation type, stage, T stage and lymph node metastasis between dMMR group and pMMR group (P<0.05). In the correlation analysis of the observed indicators, the differences in Ki-67 proliferation index, preoperative CEA and CA72-4 levels between dMMR group and pMMR group were statistically significant (P<0.05). Among the univariate prognostic analyses, the overall survival rate was significantly lower in the lymph node metastasis group and the advanced stage group (P<0.001). There was significant difference in overall survival rate between dMMR group (100%) and pMMR group (83%) (P<0.05). In the prognostic analysis of the preoperative tumor markers, CEA and CA72-4 levels had prognostic value in survival analysis (P<0.05). Multivariate COX regression analysis of 5 variables showed no significant correlation between expression of mismatch repair protein and lymph node metastasis in prognostic analysis, while significant correlation between staging and preoperative CA72-4 level was found in prognostic analysis (P<0.05). It was suggested that staging and preoperative CA72-4 level were the most important risk factors affecting the prognosis of colorectal cancer patients. Conclusion: dMMR was more common in right-sided colon cancer and in poorly differentiated adenocarcinoma and mucinous adenocarcinoma with poor type. T stage was late, while general pathological stage was early. Lymph node metastasis was rare. In dMMR group, Ki-67 proliferation index was mostly below the mean level (<70% expression), most patients had normal preoperative CEA level and elevated preoperative CA72-4 level. The dMMR group had a higher survival rate compared with the pMMR group, and later stage and increased preoperative CA72-4 level were risk factors affecting prognosis of patients. The expression deficiency of mismatch repair protein has certain prognostic value in patients with colorectal cancer. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of all-trans-retinoic acid (ATRA) on signaling pathway and regulations of neural stem cells (NSCs) in adult mice and the effects on the family of cytochrome P450 (CYP450). Methods NSCs were isolated from the sub-ventricular zone ( SVZ) of brain in adult mice and then were cultured. The cells were divided into the ATRA group and blank control group. The ATRA group was added with 10-6 mol/L ATRA. Flow cytometry (FCM) was used to detect the cell surface markers in the two groups, and we calculated the percentage of neurons, astrocytes ,oligodendrocytes and the percentage of NSCs accounting for total cells. The real-time PCR was used to detect the related gene expression of CYP450 family, and we screened statistically significant gene. ELISA was applied to detect the activity of cytochrome P450 reductase (CPR). The expression levels of P38 and p-P38 were detected by using Western blotting. Results In the ATRA group, NSCs mainly differentiated into neurons, and some differentiated into astrocytes, with less differentiation of oligodendrocytes. Compared with the blank control group, the expression of CYP26A1 , CYP26B1 and CYP26C1 in the P450 family genes of the ATRA group was up-regulated (all P<0.05). The activity of CPR and the expression of p-P38 protein in the ATRA group were higher than those in the blank control group (both P<0. 05). Conclusion ATRA promotes the differentiation of mouse NSCs into neurons, and it may play a regulatory role by up-regulating the CYP26 family genes in CYP450 and increasing CPR activity and the P38 MAPK pathway. [ABSTRACT FROM AUTHOR]