Investigation of the relationships among respiratory syncytial virus infection, T cell immune response and intestinal flora.

The aim of this work was to evaluate the relationships among respiratory syncytial virus infection, T cell immune response and intestinal flora. Peer-reviewed papers published in English were collected through extensive searches performed in PubMed, Web of Science, Google Scholar, and China National Knowledge Infrastructure databases. The articles were reviewed to extract relevant information on the immune responses of Th1/Th2 and Treg/Th17 to respiratory syncytial virus infection in the body. RSV (Respiratory syncytial virus, RSV) infection leads to imbalance between Th1/Th2 and Treg/Th17 immune cells, resulting in Th2 or Th17 dominant immune responses, which can generate immune disorder and aggravate clinical symptoms. Intestinal micro-organisms play very important roles in maintaining stable immune environment, stimulating immune system maturation and balancing Th1/Th2 and Treg/Th17 immune systems in children. In our review of various papers from around the world, we speculated that the steady state of intestinal bacteria was disturbed after children got infected with RSV, resulting in intestinal flora disorder. Then, the imbalance between Th1/Th2 and Treg/Th17 immune cells was increased. Both intestinal flora disorder and RSV infection could cause cellular immunity imbalance of Th1/Th2 or Treg/Th17, eventually leading to disease deterioration and even a vicious cycle. Normal intestinal flora can maintain immune system stability, regulate the dynamic balance of Th1/Th2 and Treg/Th17 and prevent or mitigate adverse consequences of RSV infection. Because probiotics can improve intestinal barrier function and regulate immune response, they can effectively be used to treat children with recurrent respiratory tract infections. Using conventional antiviral therapy strategy supplemented with probiotics in the treatment of clinical RSV infection may be better for the body.

[Clinical characteristics of immune checkpoint inhibitor-related type 1 diabetes mellitus].

The clinical data of ten patients with immune checkpoint inhibitor-related type 1 diabetes mellitus were enrolled in the Second Xiangya Hospital of Central South University from January 2020 to October 2022 including 9 males and 1 female, with an average age of (57±8) years. There were 7 cases of fulminant type 1 diabetes and 3 cases of acute type 1 diabetes. Among the 10 patients, there were 5 cases of lung cancer, 2 cases of esophageal cancer, 1 case of gastric carcinom, 1 case of renal cell carcinoma, and 1 case of nasopharyngeal cancer. The drugs used in 10 patients were all programmed cell death receptor 1 (PD-1) inhibitors, including 5 cases of pembrolizumab, 3 cases of sintilimab, 1 case of tanezumab, and 1 case of toripalimab. Among them, 8 patients had diabetic ketoacidosis (DKA), 1 patient had ketosis, and 1 case had no ketosis at onset; 9 patients were negative for diabetes-related antibodies, and 1 patient was positive. All the 10 patients were successfully treated and depended on insulin therapy. Immune checkpoint inhibitors can cause type 1 diabetes, including fulminant type 1 diabetes, which mostly begins with DKA, requiring early identification and aggressive insulin therapy.

Propofol suppresses migration, invasion, and epithelial-mesenchymal transition in papillary thyroid carcinoma cells by regulating miR-122 expression.

OBJECTIVE: Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer and PTC patients with invasion and metastases features have a poor prognosis. Propofol is an intravenous anesthetic which has been reported to be involved in cancer progression. However, the roles of propofol and the exact molecular mechanisms in PTC remain largely unknown. MATERIALS AND METHODS: Cells viability was detected using the CCK-8 (Cell Counting Kit-8) assay. The expressions of microRNA-122 (miR-122) were measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cells migration and invasion abilities were investigated by transwell. Western blot was used to demonstrate the expression of metastasis-and EMT-related proteins. RESULTS: We found a significant inhibition of cells viability in TPC-1 and IHH-4 cells compared to Nthy-ori 3-1 cell line after exposed to propofol. The functional experiment showed propofol could suppress cells migration, invasion, and EMT in PTC. Subsequently, a decreased expression of miR-122 was detected in TPC-1 and IHH-4 cells, while a promotion of propofol on miR-122 expression was identified. Furthermore, we found miR-122 could inhibit cells migration, invasion, and EMT in PTC. Next, the rescue study indicated that miR-122 inhibitor transfection could attenuate propofol-induced suppression on TPC-1 and IHH-4 cells metastasis. CONCLUSIONS: Propofol suppresses migration, invasion, and EMT in papillary thyroid carcinoma cells by regulating miR-122 expression. The findings may indicate significant clinical implications for anesthetic agents to prevent metastasis and improve outcomes in papillary thyroid carcinoma.

Organic trace minerals improve eggshell quality by improving the eggshell ultrastructure of laying hens during the late laying period.

The objective of this study was to investigate the effects of low inclusion levels of organic trace minerals (iron, copper, manganese, and zinc) on performance, eggshell quality, serum hormone levels, and enzyme activities of laying hens during the late laying period. A total of 405 healthy hens (HY-Line White, 50-week-old) were randomly divided into 3 treatments, with 9 replications per treatment and 15 birds per replication. The dietary treatments included a basal diet supplemented with inorganic trace minerals at commercial levels (CON), a basal diet supplemented with inorganic trace minerals at 1/3 commercial levels (ITM), and a basal diet supplemented with proteinated trace minerals at 1/3 commercial levels (TRT). The trial lasted 56 D (8 wk). Compared with the CON group, the ITM group showed decrease in (P < 0.05) egg production, eggshell strength, eggshell palisade layer, palisade layer ratio, serum estrogen, luteinizing hormone, glycosaminoglycan concentration, and carbonic anhydrase activity and increase in (P < 0.05) egg loss and mammillary layer ratio. However, the TRT group almost kept all the indices close to the CON group (P > 0.05). Furthermore, hens fed with low inclusion levels of organic trace minerals had smaller mammillary knobs (P < 0.05) than those in the CON and ITM groups. In conclusion, hens fed with low inclusion levels of proteinated trace minerals had better performance and eggshell strength than those fed with identical levels of inorganic compounds; organic trace minerals improved eggshell quality by improving the eggshell ultrastructure of laying hens during the late laying period.

Sevoflurane inhibits the progression of PTC by downregulating miR-155.

OBJECTIVE: Surgery resection is the primary treatment for papillary thyroid carcinoma (PTC) patients with the risk of tumor cell invasion and distant metastasis. Sevoflurane is a volatile anesthetic agent widely used in clinical applications. However, the effect of sevoflurane on PTC cells and its precise mechanism remain largely unknown. MATERIALS AND METHODS: Cell viability was assessed by MTT assay. The migrative and invasive abilities of the cells were measured by transwell assay. The protein expression level of Bax, Bcl-2, MMP 9, and MMP 2 were detected by Western blot. Cell apoptosis was analyzed by flow cytometry. The qRT-PCR analysis was used to determine miR-155 expressions. RESULTS: Sevoflurane greatly decreased the viability of PTC cells in a dose-dependent manner. Moreover, sevoflurane significantly inhibited migration and invasion, but increased the apoptosis in PTC cells, which could be reversed by the addition of miR-155. Besides, sevoflurane evidently increased the Bax protein level and inhibited the protein level of Bcl-2, MMP9, and MPP2 in PTC cells. In addition, miR-155 was upregulated in PTC cells; however, the amount of miR-155 would be decreased in PTC cells treated with sevoflurane. Furthermore, abrogation of miR-155 promoted cell apoptosis and inhibited cell migration and invasion in PTC cells. CONCLUSIONS: Sevoflurane inhibited migration and invasion, while enhanced cell apoptosis by downregulating miR-155 in PTC cells, suggesting important clinical implications for anesthetic agents to prevent the metastasis in PTC.

Aspartate aminotransferase-to-platelet ratio predicts response to transarterial chemoembolisation and prognosis in hepatocellular carcinoma patients.

AIM: To evaluate the value of the aspartate aminotransferase-to-platelet ratio index (APRI) for hepatocellular carcinoma (HCC) patients who underwent transarterial chemoembolisation (TACE). MATERIALS AND METHODS: A total of 315 patients were enrolled, who were randomly divided into the training cohort (n=158) and the validation cohort (n=157). The optimal cut-off value of the APRI was determined using the X-tile software in the training cohort, and was validated in the validation cohort. Several serum-based markers, neutrophil-to-lymphocyte (N/L) and aspartate aminotransferase-to-alanine aminotransferase (AST/ALT) ratios were included to compare with the APRI. To predict individual survival rate, independent predictors were included to build a nomogram. RESULTS: Using the X-tile, a cut-off value of the APRI as 0.40 was yielded to distinguish patients with distinct outcomes in the training cohort, but failed for the N/L and ALT/AST ratios. In the training cohort, 66 patients with high APRI had poorer survival (p<0.001) than did 92 patients with low APRI. Using the same cut-off value of APRI, 61 patients with high APRI had poorer survival (p<0.001) than did 96 patients with low APRI in the validation cohort. Furthermore, a nomogram, including the APRI, TACE cycles, tumour size, and tumour number, was built based on the training cohort, and validated well in the validation cohort (concordance index [C-index] 0.713). CONCLUSION: The APRI is a promising marker to predict treatment response and outcome for HCC patients after TACE treatment.

Hepatic resection for synchronous hepatic metastasis from gastric cancer.

BACKGROUND: The role of surgical resection for synchronous hepatic metastases arising from gastric adenocarcinoma has not been established. This study was designed to explore the clinicopathologic features and surgical results of these patients. METHODS: Twenty-five (4.8%) of 526 patients diagnosed with synchronous hepatic metastatic gastric cancer received hepatectomy and gastrectomy at the same time; 2 cases underwent repeat hepatectomy after intrahepatic recurrence. Clinicopathologic parameters of the hepatic metastases and the surgical results for all 25 patients were analysed. RESULTS: The 1-, 3-, and 5-year overall survival (OS) and recurrence-free survival (RFS) rates after resection were 96.0%, 70.4%, and 29.4%, respectively, and 56.0%, 22.3%, and 11.1%, respectively. Five patients survived for more than 5 years after surgery, and no mortality has occurred within 30 days after resection. Univariate analysis revealed that patients with multiple hepatic metastases suffered poorer OS (P = 0.026) and RFS (P = 0.035) than those with solitary hepatic metastasis. Postoperative adjuvant chemotherapy was a significant indicator of a favourable OS (P = 0.022). Number of metastatic lesions remained significant in the multivariate analysis of OS and RFS (P = 0.039, P = 0.049, respectively). None of variables of the primary lesion was a significant prognostic factor for those patients. CONCLUSIONS: Gastric cancer patients with a solitary synchronous liver metastasis may be good candidates for hepatic resection. Postoperative adjuvant chemotherapy may provide a benefit by aiding in OS.

Serum resistin level in essential hypertension patients with different glucose tolerance.

AIMS: To investigate resistin concentrations in patients with essential hypertension and different glucose tolerance and the relationship between serum resistin level and blood glucose. METHODS: Sixty-five patients with essential hypertension [13 with Type 2 diabetes mellitus (DM), 26 with impaired glucose tolerance (IGT), and 26 with normal glucose tolerance (NGT); 30 males, 35 females] were studied. Fasting serum resistin concentrations were measured by enzyme immunoassay (EIA). Oral glucose tolerance tests and insulin release tests were used to calculate glucose area under the curve (AUCG), the ratio of insulin to glucose (DeltaI30/DeltaG30), and insulin sensitivity index (ISI) according to Cederholm's formula. RESULTS: Fasting serum resistin concentrations (microg/l) in DM (34.9 +/- 10.2) patients were significantly higher than those in IGT (25.1 +/- 10.4) (P < 0.05) and in NGT (21.5 +/- 7.9) (P < 0.05) patients. Pearson correlation showed that fasting serum resistin concentration was correlated with AUCG (r = 0.445, P < 0.001), ISI (r = -0.322, P < 0.01) and DeltaI30/DeltaG30 (r = -0.366, P < 0.01), but not body mass index and waist-hip ratio. After adjustment for gender, age and body mass index (BMI), partial correlation analysis showed that the fasting serum resistin concentrations were still correlated with AUCG (r = 0.327, P < 0.01) and DeltaI30/DeltaG30 (r = -0.348, P < 0.01), but ISI. CONCLUSION: Resistin may be involved in the development of diabetes in humans.

[HarpinPss elicited early defense responses of tobacco cells and involvement of calcium].

HarpinPss can induce hypersensitive reaction (HR) in tobacco leaves. As superoxide dismutase can inhibit but catalase can not inhibit the development of HR induced by harpinPss, superoxide anion is required for this response. HarpinPss can also induce the release of active oxygen and extracellular alkalinization, two early defence responses in tobacco suspension culture. Diphenylene iodoium, can completely inhibit the induction of HR in tobacco leaves, and the release of active oxygen in the suspension culture system, superoxide anion in these system may be produced by the activation of NADPH oxidase. Ethyleneglycol-bis (beta-aminoethyl) N, N, N'N'-tetraacetic acid (EGTA) can inhibit the development of harpinPss-induced HR and these two early defence responses in suspension culture system. Adding Ca2+ into the medium again, these responses can return to normal level in a short time. Lanthanum chloride, verapamil, neomycin, U-73122, and LiCl can also inhibit these harpinPss-induced responses. Therefore, the influx of Ca2+ mediated by calcium channel and the release of Ca2+ from internal Ca2+ pool may be involved in the two early defense responses induced by harpinPss. Cycloheximide and actinomycin D have no effect on the release of active oxygen but can inhibit harpinPss-induced HR even added them in the intermediate process for inducing HR. It indicates superoxide is just a trigger for HR, and HR is a more complex process that needs the sustained expression of some genes.

[Involvement of anion channel in signal transduction of early defense responses elicited by harpinPss in tobacco].

No matter when anion channel inhibitors, DIDS (4, 4'-diisothiocyanatostilbene-2, 2'-disulfonic acid) and A9C (anthracene-9-carboxylic acid) added (before, at the same time of or after harpinPss treatment), they can inhibit harpinPss-induced hypersensitive response in tobacco seedlings and release of active oxygen and extracellular alkalinization in tobacco suspension cells. DIDS and A9C also inhibit harpinPss-induced Ca2+ influx. In all these cases, DIDS is more efficient than A9C. It is postulated that anion channel positively regulates calcium channel in plasma membrane, and harpinPss may function through signal transduction mediated by anion channel and calcium channel to regulate cellular Ca2+ concentration and defense responses.