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In this study, we investigated sex-specific effects of acute exposure to trimethyltin, a known neurotoxicant on metabolic steroids.

We administered intraperitoneally 2.3 mg/kg trimethyltin to 4-week-old male mice and measured the levels of metabolic steroids 24 h after treatment. We also measured mRNA and protein levels of cytochrome P450 1B1 using real-time polymerase chain reaction and western blotting.

Cortisol levels in the cortex increased in both sexes following acute trimethyltin exposure. The estradiol levels decreased, and the 4-hydroxyestradiol levels increased only in females. We also observed increased cytochrome P450 1B1 mRNA and protein levels only in the female cortex.

Acute trimethyltin exposure induces distinct sex-specific metabolic changes in the brain before significant sexual maturation.

Acute trimethyltin exposure induces distinct sex-specific metabolic changes in the brain before significant sexual maturation.

Combination cancer therapy is currently under investigation. This study examined the effect of cancer combination therapy using the E3 and C1 (E3C1) domains of developmental endothelial locus-1 (Del1) and cisplatin (CDDP) in murine transplanted tumors.

Mice with transplanted tumors (A431, SCCKN or SCC-4 cells) were injected intraperitoneally with CDDP and injected locally with nonviral plasmid vectors encoding E3C1. Histochemical analysis of the transplanted tumors was then performed to assess the effects on prognosis.

The CDDP+E3C1 injected group had reduced tumor growth and longer survival compared to the CDDP injected group. In addition, cell death was observed in the tumor of the CDDP+E3C1 group.. Furthermore, angiogenesis and increased blood vessels were observed together with stromal development.

The CDDP+E3C1 treatment resulted in improved survival and poor tumor stromal development in mice with transplanted tumors.

The CDDP+E3C1 treatment resulted in improved survival and poor tumor stromal development in mice with transplanted tumors.

Estrogen receptor α (ERα) antagonist is the most common treatment for ERα-positive breast cancer. However, compensatory signaling contributes to resistance to ERα antagonists. Thus, to explore the potential agents for targeting compensatory signaling, we screened multiple target inhibitors for breast cancer treatment.

We attempted to build a structure-based virtual screening model that can find potential compounds and assay the anticancer ability of these drugs by overall cell survival assay. The downstream compensatory phosphorylated signaling was measured by immunoblotting.

Hamamelitannin and glucocheirolin were hits for ERα, phosphoinositide 3-kinase (PI3K), and KRAS proto-oncogene, GTPase (KRAS), which were active against estrogen and epidermal growth factor-triggered proliferation. Additionally, we select aminopterin as a hit for ERα, PI3K, KRAS, and SRC proto-oncogene, non-receptor tyrosine kinase (SRC) with inhibitory activities toward AKT serine/threonine kinase 1 (AKT) and mitogen-activated protein kinase kinase (MEK) signaling.

Our structure-based virtual screening model selected hamamelitannin, glucocheirolin, aminopterin, and pemetrexed as compounds that may act as potential inhibitors for improving endocrine therapies for breast cancer.

Our structure-based virtual screening model selected hamamelitannin, glucocheirolin, aminopterin, and pemetrexed as compounds that may act as potential inhibitors for improving endocrine therapies for breast cancer.

The role of glutathione peroxidase 2 (GPX2) expression in urothelial carcinoma (UC) is rarely reported. The aim of this study was to assess the expression status of GPX2 in UC of the bladder.

We collected samples from 112 patients treated with radical cystectomy for immunohistochemical study.

Following immunohistochemical analysis of the specimens, 86 (76.8%) had weak GPX2 expression. In cases with consistent GPX2 expression within the same lesion, the levels of GPX2 showed significant decreases from pTa to pT1 (47.1%) compared to those from pT1 to pT2 (5.9%) (p=0.017). Specimens obtained with transurethral resection before cancer progressed to muscle invasive bladder cancer showed that pT1 had a lower expression for GPX2 than that of pTa (63.3% vs. 93.3%; p=0.009).

The decrease in GPX2 expression among those with UC of the bladder may be involved in the early step of cancer invasion.

The decrease in GPX2 expression among those with UC of the bladder may be involved in the early step of cancer invasion.

Neoadjuvant chemotherapy (NAC) using 5-FU (5-fluorouracil)/CDDP (cisplatin) is a standard therapy for stage II/III thoracic esophageal squamous cell carcinoma (ESCC) in Japan. The aim of this study was to investigate whether 5-FU/CDDP could induce immunogenic cell death in ESCC cell lines.

Tumor samples for immunohistochemistry were obtained from 50 patients (mean age=63.1 years) with pathological stage 0-IVa ESCC who underwent NAC followed by surgery. Cell lines T.T and KYSE30 were used for the in vitro experiments.

The concentrations of HMGB1 were elevated in the cell line supernatants treated with 5-FU/CDDP. Selleck AS101 5-FU/CDDP treated dendritic cells (DCs) showed a mature phenotype, and enhanced T cell proliferation capacity. In addition, mature DCs were observed in surgical specimens with a histological response after treatment with 5-FU/CDDP chemotherapy.

5-FU/CDDP could induce immunogenic cell death in the tumor microenvironment of ESCC.

5-FU/CDDP could induce immunogenic cell death in the tumor microenvironment of ESCC.

Anastomotic leakage is a feared complication in colorectal surgery. Postoperative peritoneal adhesions can also cause life-threatening conditions. Nanofibrous materials showed their pro-healing properties in various studies. The aim of the study was to evaluate the impact of double-layered nanofibrous materials on anastomotic healing and peritoneal adhesions formation.

Two versions of double-layered materials from polycaprolactone and polyvinyl alcohol were applied on defective anastomosis on the small intestine of healthy pigs. The control group remained with uncovered defect. Tissue specimens were subjected to histological analysis and adhesion scoring after 3 weeks of observation.

The wound healing was inferior in the experimental groups, however, no anastomotic leakage was observed and the applied material always kept covering the defect. The extent of adhesions was larger in the experimental groups.

Nanofibrous materials may prevent anastomotic leakage but delay healing.

Nanofibrous materials may prevent anastomotic leakage but delay healing.