The research progress of posterior atlantoaxial internal fixation techniques / 医学研究生学报

Atlantoaxial instability or dislocation is a common upper cervical disease which can lead to serious outcomes including sensory and motor deficit or even sudden death. Therefore, active surgical intervention is often recommended. The most popular surgical procedure for atlantoaxial instability is posterior bone graft and internal fixation. Posterior stabilization techniques mainly include wiring techniques, interlaminar clamp fixation, C1-C2 transarticular screw fixation (Magerl technique), screw-plate systems, and screw-rod systems. Each technique has its advantage and shortcoming. The screw-rod systems, along with various modifications, has become the most popular internal fixation technique for posterior atlantoaxial stabilization in clinic. This article reviews the evolution, characteristics and new advancement of some prevail posterior atlantoaxial fixation techniques in purpose of giving a reference for surgeons to have a better understanding of posterior fixation techniques and make a reasonable choice in clinical practice.

Advances in prostate-specific membrane antigen-mediated antitumor drugs / 药学学报

Prostate cancer is the most prevalent male malignancy in the United States, and remains the second leading cause of cancer-related death in the male population. Prostate specific membrane antigen (PSMA) is a type of Ⅱ transmembrane glycoproteins that is over-expressed in prostate cancer cell. More importantly, its expression is increased with cancer progression. PSMA has been a major target for imaging and therapeutic applications in prostate cancer. PSMA, also known as N-acetylated α-linked acidic dipeptidase Ⅰ and folate hydrolase, can catalyze the hydrolysis of α-or γ-linked glutamates from peptides or small molecules. This article provides a review of the recent applications of ligand-drug conjugates targeting PSMA and prodrugs activated by PSMA.

Glycemic Variation in Tumor Patients with Total Parenteral Nutrition / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hyperglycemia is associated with poor clinical outcomes and mortality in several patients. However, studies evaluating hyperglycemia variation in tumor patients receiving total parenteral nutrition (TPN) are scarce. The aim of this study was to assess the relationship between glycemia and tumor kinds with TPN by monitoring glycemic variation in tumor patients.</p><p><b>METHODS</b>This retrospective clinical trial selected 312 patients with various cancer types, whose unique nutrition treatment was TPN during the monitoring period. All patients had blood glucose (BG) values assessed at least six times daily during the TPN infusion. The glycemic variation before and after TPN was set as the indicator to evaluate the factors influencing BG.</p><p><b>RESULTS</b>The clinical trial lasted 7.5 ± 3.0 days adjusted for age, gender, family cancer history and blood types. There were six cancer types: Hepatic carcinoma (HC, 21.8%), rectal carcinoma (17.3%), colon carcinoma (CC, 14.7%), gastric carcinoma (29.8%), pancreatic carcinoma (11.5%), and duodenal carcinoma (DC, 4.8%). The patients were divided into diabetes and nondiabetes groups. No statistical differences in TPN glucose content between diabetes and nondiabetes groups were found; however, the tumor types affected by BG values were obvious. With increasing BG values, DC, HC and CC were more represented than other tumor types in this sequence in diabetic individuals, as well as in the nondiabetic group. BG was inclined to be more easily influenced in the nondiabetes group. Other factors did not impact BG values, including gender, body mass index, and TPN infusion duration time.</p><p><b>CONCLUSIONS</b>When tumor patients are treated with TPN, BG levels should be monitored according to different types of tumors, besides differentiating diabetes or nondiabetes patients. Special BG control is needed for DC, HC and CC in both diabetic and nondiabetic patients. If BG overtly increases, positive measurements are needed to control BG values. The ClinicalTrials.gov ID is NCT02024321.</p>

Preparation of cisplatin-impregnated coral hydroxyapatite drug delivery system / 南方医科大学学报

<p><b>OBJECTIVE</b>To prepare a cisplatin-impregnated coral-derived hydroxyapatite (CCHA) drug delivery system (DDS), and evaluate its inhibitory effect on human osteosarcoma cells U-2 OS, human breast cancer and prostatic carcinoma cells PC-3 in vitro.</p><p><b>METHODS</b>The coral-derived hydroxyapatite (CHA) was manufactured by hydrothermal exchange and impregnated with cisplatin by vacuum freeze-drying techniques. The leaching solutions of this DDS was collected at different intervals in a course of 8 weeks and their inhibitory effect on the cells was tested in vitro by MTT assay.</p><p><b>RESULTS</b>Electron microscope showed that cisplatin was distributed homogeneously in the pores of CHA. The inhibition rates of the leaching solution on all the tumor cells exceeded 50% except for PC-3 cells, whose inhibition rate was 29.92% when treated with the solution collected at the eighth week.</p><p><b>CONCLUSION</b>CCHA allows sustained drug release and maintains excellent inhibitory effect on human bone tumor cells within 8 weeks in vitro.</p>

Sensitization of human glioma SWO cell line to tumor necrosis factor-induced apoptosis by blocking phospholipase C-gamma1 signaling pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the role of phospholipase C-gamma1 (PLC-gamma1) in tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis of human glioma SWO cells.</p><p><b>METHODS</b>The PLC-gamma1 pathway was blocked by U73122 in SWO cells, and the inhibitory effect of TNF-alpha on SWO glioma cell proliferation with or without U73122 treatment was investigated by MTT assay. The cell apoptosis induced by TNF-alpha along or in combination with U73122 was detected by flow cytometry with PI staining. The expression of caspase-3 and Bcl-2 was detected by Western blotting.</p><p><b>RESULTS AND CONCLUSION</b>U73122 can sensitize SWO glioma cells to TNF-alpha-induced apoptosis. Blocking the PLC-gamma1 pathway may not induce apoptosis of SWO glioma cells, but can sensitize SWO glioma cells to small-dose TNF-alpha-induced apoptosis, the mechanism of which may involve down-regulation of bcl-2.</p>