Search

Background Wrist motor dysfunction is a common sequela at post-stroke, and the wrist has an important role in improving hand practicality. Therefore, improving the range of motion of the wrist can effectively promote the activities of daily life in post-stroke patients. Although repetitive peripheral magnetic stimulations (rPMS) have been shown to have a significant effect on improving the range of motion of the wrist, the therapeutic effect of different stimulation sites still needs to be further explored. Objective To investigate the effect of rPMS on wrist extensor muscle and radial nerve for the motor function of wrist of subacute stroke patients. Methods A total of 60 subacute stroke patients with wrist motor dysfunction admitted to Rehabilitation Hospital Affiliated to Fujian University of Traditional Chinese Medicine from October 2022 to October 2023 were selected as the study subjects. The included patients were randomly divided into control group (20 cases), muscle stimulation group (20 cases) and nerve stimulation group (20 cases) by simple randomized grouping method using a random number table. Patients in all the three groups received routine rehabilitation training, and those in the muscle stimulation group and nerve stimulation group were additionally managed by rPMS on the wrist extensor muscle and the radial nerve, respectively. Before and after the interventions for 10 times of rPMS, integrated electromyography (iEMG), root mean square (RMS) and median frequency (MF) on the surface of the wrist extensor muscle, the Fugl-Meyer Assessment for upper extremity (FMA-UE), the Action Research Arm Test (ARAT) and the modified Barthel Index (MBI) were measured to assess the upper limb function of the affected side. Results During the intervention period, there were 2 cases of data loss due to voluntary withdrawal or forced termination of the trial, and finally 20 cases were included in the control group, 19 cases in the muscle stimulation group, and 19 cases in the nerve stimulation group. There were no significant differences in iEMG, RMS and MF of wrist extensor muscle among three groups before treatment (P>0.05). After treatment, iEMG, RMS and MF of wrist extensor muscle in muscle stimulation group and nerve stimulation group were significantly higher than those of control group (P0.05). After treatment, FMA-UE, ARAT and MBI scores in muscle stimulation group and nerve stimulation group were significantly higher than those of control group (P

Background: Previous studies have demonstrated that β2-microglobulin (β2M) promotes the growth and survival of a variety of cancer cells and has different regulatory effects on the expression of Bcl-2 and HER2 in HER2- breast cancer cells. However, β2M-mediated signaling in ER+ and ER- breast cancer with HER2- remains unclear.Methods: β2M expression vector and siRNA were transfected into two types of HER2- breast cancer cells, and the possible relevant signaling molecules were subsequently analyzed by real-time PCR and western blotting. These signaling molecules were also analyzed by real-time PCR and immunohistochemistry (IHC) in two types of HER2- breast cancer tissues, and the associations between β2M and these signaling molecules were assessed using Spearman's correlation analysis.Results: β2M silencing downregulated p-SGK1/SGK1 levels and Bcl-2 expression, and β2M overexpression downregulated p-CREB/CREB and significantly upregulated p-SGK1/SGK1 levels and Bcl-2 expression, and both resulting processes did not affect HER2, HIF-1α, VEGF, and ERK signaling in ER+ breast cancer cells with HER2-. β2M silencing upregulated p-CREB/CREB and VEGF protein and significantly downregulated p-ERK/ERK levels, and β2M overexpression downregulated p-CREB/CREB and VEGF, significantly upregulated p-ERK/ERK levels, and both resulting processes did not affect HIF-1α and SGK1 signaling in ER- breast cancer cells with HER2-. β2M expression was positively correlated with p-CREB, p-SGK1, and Bcl-2 expression and had no correlation with HIF-1α, VEGF, and p-ERK1/2, whereas p-SGK1 exhibited a significantly positive correlation with Bcl-2 expression in cancer tissues of patients with luminal A breast cancer, which coincide with the results obtained from the same molecular types of breast cancer cells except CREB signaling. However, β2M expression did not show a significant correlation with HIF-1α, p-CREB, VEGF, p-SGK1, p-ERK1/2, and Bcl-2 expression in cancer tissues of patients with basal-like breast cancer, which was discordant with the results obtained from the same molecular types of breast cancer cells.Conclusions: β2M has a different molecular regulatory mechanism between ER+ and ER- breast cancer with HER2-, and it may promote tumor survival through the SGK1/Bcl-2 signaling pathway in ER+ breast cancer with HER2- and has no regulatory effects on ER- breast cancer with HER2-. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the expression of leucine zipper transcription factor-like1 (LZTFL1) molecule in the gastric cancer tissues, and its relationship to cellular adhesion protein. Methods: Expressions of LZTFLl, E-cadherin, ß-catenin, intercellular cell adhesion molecule-1(ICAM-1) as well as vascular cell adhesion molecule-1 (VCAM-1) in the 133 gastric cancer samples and 40 gastritis samples were evaluated by immunohistochemistry. Levels of mRNA in gastric cancer and latero-cancer tissue were determined by real-time polymerase chain reaction (RT-PCR). Results: Protein levels in gastric tissue decreased. The expression of LZTFL1in gastric cancer tissue correlated with tumor stage (tumor node metastasis staging), degree of tumor differentiation and invasion depth (p < 0.05). Protein expression correlated with E-cadherin positively, and correlated with ß-catenin and ICAM-1 negatively, but had no correlation with VCAM-1. Compared with tissues remote to the cancer, mRNA level of LZTFL1 in gastric cancer decreased significantly. There was no significant difference in LZTFL1 mRNA levels in the various clinical pathological tissues. LZTFL1 mRNA expression did not correlation with various adhesion factors. Conclusion: LZTFL1 is expressed at a low level in gastric cancer tissue. Its protein expression is related to cellular adhesion protein, but not to mRNA level. As a suppressor of invasion of cancer cells, LZTFL1 may be a potential target for targeted therapy of gastric cancer. [ABSTRACT FROM AUTHOR]

Background: A mouse model of metastasis of human gastric cancer is one of the most important tools for studying the biological mechanisms underlying human gastric cancer metastasis. In this paper, we established a mouse model of metastatic human gastric cancer in nude mice that has a higher rate of tumor formation and metastasis than existing models.Methods: To generate the mouse model of metastatic human gastric cancer, fresh tumor tissues from patients that have undergone surgery for gastric cancer were subcutaneously implanted in the right and left groins of nude mice. When the implanted tissue grew to 1 cubic centimeter, the mice were killed, and the tumor tissues were examined and resected. The tumor tissues were implanted into nude mice and subjected to pathological examination, immunohistochemical staining, and real-time PCR for cytokeratin 8/18 (CK8/18), E-cadherin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). The mice were also analyzed for metastasis in their peritoneum, abdominal cavity, and internal organs by histopathological examination. Tissues collected from these organs were examined for pathology.Results: After ten generations of implantation, all mice developed tumor growth at the implanted position, 94% of the mice developed metastasis to the retroperitoneum and viscera. The implanted and metastatic tumor maintained the same histological features across all generations, and metastasis was observed in the esophagus, stomach, spleen, liver, kidney, adrenal, intestine, and pancreas. These metastatic tumors revealed no detectable expression of CK8/18, E-cadherin, VCAM-1, and ICAM-1.Conclusions: This model will serve as valuable tool for understanding the metastatic process of human gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Previous studies have demonstrated that β2-microglobulin (β2M) promotes the growth and survival of a variety of cancer cells and has different regulatory effects on the expression of Bcl-2 and HER2 in HER2- breast cancer cells. However, β2M-mediated signaling in ER+ and ER- breast cancer with HER2- remains unclear.Methods: β2M expression vector and siRNA were transfected into two types of HER2- breast cancer cells, and the possible relevant signaling molecules were subsequently analyzed by real-time PCR and western blotting. These signaling molecules were also analyzed by real-time PCR and immunohistochemistry (IHC) in two types of HER2- breast cancer tissues, and the associations between β2M and these signaling molecules were assessed using Spearman's correlation analysis.Results: β2M silencing downregulated p-SGK1/SGK1 levels and Bcl-2 expression, and β2M overexpression downregulated p-CREB/CREB and significantly upregulated p-SGK1/SGK1 levels and Bcl-2 expression, and both resulting processes did not affect HER2, HIF-1α, VEGF, and ERK signaling in ER+ breast cancer cells with HER2-. β2M silencing upregulated p-CREB/CREB and VEGF protein and significantly downregulated p-ERK/ERK levels, and β2M overexpression downregulated p-CREB/CREB and VEGF, significantly upregulated p-ERK/ERK levels, and both resulting processes did not affect HIF-1α and SGK1 signaling in ER- breast cancer cells with HER2-. β2M expression was positively correlated with p-CREB, p-SGK1, and Bcl-2 expression and had no correlation with HIF-1α, VEGF, and p-ERK1/2, whereas p-SGK1 exhibited a significantly positive correlation with Bcl-2 expression in cancer tissues of patients with luminal A breast cancer, which coincide with the results obtained from the same molecular types of breast cancer cells except CREB signaling. However, β2M expression did not show a significant correlation with HIF-1α, p-CREB, VEGF, p-SGK1, p-ERK1/2, and Bcl-2 expression in cancer tissues of patients with basal-like breast cancer, which was discordant with the results obtained from the same molecular types of breast cancer cells.Conclusions: β2M has a different molecular regulatory mechanism between ER+ and ER- breast cancer with HER2-, and it may promote tumor survival through the SGK1/Bcl-2 signaling pathway in ER+ breast cancer with HER2- and has no regulatory effects on ER- breast cancer with HER2-. [ABSTRACT FROM AUTHOR]