Objective To analyze the reasons for in-hospital mortality after a surgical resection for esophageal and cardial cancer and countermeasures.Methods From 1999.1 to 2010.12,7,225 patients with esophageal and cardial cancer were performed surgery in Cancer Institute and Hospital.Retrospectively analyzing the clinical datas of patients in-hospital mortality of these patients.Results 71 cases of 7,225 patients with a surgical resection for esophageal and cardial cancer died in-hospital after surgery.Conclusion Strictly mastering the operative indications,treating the acompaning diseases actively,choose the appropriate surgical approach,careful operation in surgery,reducing surgical time,intensice care after surgery and timely treatment of postoperative complications correctly may play a significant role in the decrease of in-hospital mortality after surgery.

Objective To study preoperatively on TNM staging of esophageal carcinoma by endo-scopes ultrasonography ( EUS). Methods Sixty-one patients with esophageal carcinoma were preoperatively staged by EUS. The results were compared with the postoperative histopathological staging according to the new (1997) TNM classification. Results Clinical staging of T subsets by EUS was reliable with an overall accuracy rate of 86. 9% , while that of N subsets was relatively more difficult with an overall accuracy rate of 52. 5% ; sensitivity and specificity of regional lymph nodal metastases were 88. 9% and 23. 5% respectively. Conclusion EUS is relatively an accurate measure in assessing the depth of tumor infiltration, whereas further efforts are needed to improve the accuracy in N staging. EUS will be helpful in choice of the appropriate therapeutic procedure and predicting the possibility of surgical resection.

Objective To explore the 5-aminolevulinic acid (5-ALA) mediated photodynamic therapy (PDT) for proliferation and apoptosis of gastric cancer cell line MKN-45.Methods The human gastric cancer cell line MKN-45 was cultured in vitro.The MTT method was used to detect fixed lighting processing (laser radiation dose fixed for 25.00 J/cm2,5-ALA photosensitizer concentrations were 0 mmol/L,0.25 mmol/L,0.50 mmol/L,1.00 mmol/L,2.00 mmol/L),fixed photosensitizer concentration treatment (5-ALA photosensitizer concentrations fixed to 1.00 mmol/L,laser radiation dose were 0 J/cm2,6.25 J/cm2,12.50 J/cm2,25.00 J/cm2,50.00 J/cm2,100.00 J/cm2) of the cell apoptosis rate,and then fixed 5-ALA photosensitizer 1 mmol/L and selected the control group,5-ALA group,pure illumination group and PDT group.The promoting effect on cell apoptosis was determined by MTT,electron microscope and flow cytometry.The activity of human gastric cancer cells MKN-45 apoptosis related proteins p65 and the downstream gene regulatory protein bcl-2,bax,caspase-3 and caspase-9 were detected by using Western blot method.Results When laser radiation dose was fixed,5-ALA photosensitizer concentrations in promoting gastric cancer cell apoptosis was positively related to the dominant (P ＜ 0.01).When 5-ALA photosensitizer concentration was fixed,laser radiation dose effect had no longer dominant after 25.00 J/cm2 positive correlation (P =0.613).When 5-ALA photosensitizer concentration was fixed in 1 mmol/L,compared to control group,5-ALA group and pure illumination group,the inhibition of the MKN-45 cell proliferation in PDT group was more apparently,apoptosis rate increased obviously,signal pathways in cell apoptosis protein involved in the NF-kappa B p65 expression was reduced,the downstream gene regulation of target protein bcl-2,caspase-3 and caspase-9 expression were reduced,and bax protein expression was increased.Conclusions 5-ALA mediated photodynamic has a strong inhibitory effect on the growth of gastric cancer cell line MKN-45 in vitro.It can significantly increase the apoptosis rate of gastric cancer cells,and the effect may be carried out by activating the NF-kappa B pathway.

Methicillin-resistant staphylococcus aureus (MRSA) has become the main pathogen for hospital and community acquired infections. Based on the resistance mechanism of MRSA, this article reviews the reducing and eliminating effect of Chinese herb extracts on bacterial drug resistance, by means of PBP2a protein binding, γ-lactamase, plasmid, efflux system, cell structure and biofilmdamage.

Objective To assess the clinical value of endoscopic uhrasonography(EUS)combined with the mini-probe endoscopic uhrasonography(MPUS)in determing tumor invasion depth and lymph node metastases of early superficial esophageal cancer.Methods One hundred and twenty-four superficial esophageal cancer lesions of 121 patients were staged by EUS combined with MPUS,and the results were finally compared with pathological findings of surgical specimens or samples obtained by mucosal resection.Results The diagnostic accuracy of EUS in T staging of superficial esophageal cancer was 82.3%(102/124).The total ratio of lymph node metastases was 5.0%(6/121),with no node metastases in carcinoma in situ,1.3%(1/28)in mucosal carcinoma,11.6%(5/43)in submucosal carcinoma.Conclusion EUS combined with MPUS is accurate in staging of the superficial carcinoma,which can help the choice of therapeutic strategies.

Objective: To study the changes of the sensitivity of the methicillin-resistant Staphylococcus aureus (MRSA) to oxacillin after Chinese herbs. effects, so as to find Chinese medicine that can enhance the sensitivity of MRSA to antibiotics and provide new ideas for the clinical treatment of MRSA infection. Methods: A total of 33 commonly used antibacterial herbs were selected to prepare extracts, which act on clinically isolated MRSA. The broth micro dilution method was used to determine the minimal inhibitory concentration (MIC) of oxacillin on MRSA before and after the action of Chinese medicine. If there is a statistically significant difference (P ＜ 0.05), the medicine is effective. Results:The MIC of oxacillin on MRSA were 128-512 μg·ml-1, after the effect of Bletilla extracts, the change of MIC showed a statistically significant difference (P ＜ 0.05), which could increase the sensitivity of MRSA (271) to oxacillin. Conclusion:Bletilla extracts can enhance the sensitivity of MRSA (271) to oxacillin and the compatibility with antibiotics is expected to restore the efficacy of antibiotic.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.

Background: The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis. Methods: We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved. Results: Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects. Conclusions This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.