The process of embryo implantation is a multifaceted and intricate dynamic event that includes the development of endometrial receptivity, embryo localization, adhesion, and invasion. Adhesion molecules, acting as crucial mediators of communication between cells or between cells and the extracellular matrix, are essential for the maintenance of endometrial receptivity and the regulation of embryo localization, adhesion, and invasion. However, the mechanisms by which adhesion molecules of maternal and embryo are organized to regulate key events in the peri-implantation period have yet to be fully explored. Based on recent research findings, this review provides a summary of the functions of different adhesion molecules at the maternal-fetal interface and their potential regulatory mechanisms according to the key progress of embryo implantation. In particular, we discussed the interactions between decidual immune cells and other cells mediated by adhesion molecules during the invasion process, which will provide novel perspectives into the role of adhesion molecule dysfunction in contributing to implantation failure.

The process of embryo implantation is a multifaceted and intricate dynamic event that includes the development of endometrial receptivity, embryo localization, adhesion, and invasion. Adhesion molecules, acting as crucial mediators of communication between cells or between cells and the extracellular matrix, are essential for the maintenance of endometrial receptivity and the regulation of embryo localization, adhesion, and invasion. However, the mechanisms by which adhesion molecules of maternal and embryo are organized to regulate key events in the peri-implantation period have yet to be fully explored. Based on recent research findings, this review provides a summary of the functions of different adhesion molecules at the maternal-fetal interface and their potential regulatory mechanisms according to the key progress of embryo implantation. In particular, we discussed the interactions between decidual immune cells and other cells mediated by adhesion molecules during the invasion process, which will provide novel perspectives into the role of adhesion molecule dysfunction in contributing to implantation failure.

Objective:To analyze the distribution and drug sensitivity of pathogens and cerebrospinal fluid (CSF) related measurements in AIDS patients with central nervous system (CNS) infections in Chongqing, so as to provide guidance for etiological diagnosis and rational use of antibiotics in AIDS patients with CNS infections.Methods:A total of 173 AIDS patients with CNS infections were divided into fungal group, Gram-positive bacilli group, Gram-positive cocci group and Gram-negative bacilli group. During the same period, 198 AIDS patients with non-CNS infection visited this hospital were enrolled into the control group. CSF and blood were collected for bacterial culture. The composition and drug resistance of pathogens were analyzed. The levels of CSF related measurements were determined and compared.Results:A total of 173 strains of pathogens were isolated from the CSF of the AIDS patients with CNS infections. The 173 strains included 101 (58.38%) fungi, 39 (22.54%) Gram-positive bacilli, 24 (13.87%) Gram positive cocci and 9 (5.20%) Gram-negative bacilli; 230 strains of pathogens were isolated from the blood of the AIDS patients with non CNS infections. The 198 strains were composed of 107(54.04%) fungi, 65 (32.83%) Gram positive cocci and 26 (13.13%) Gram-negative bacilli. Antifungal sensitivity testing result of Cryptococcus neoformans showed that MIC of amphotericin B, fluorocytosine, fluconazole, voriconazole and itraconazole were≤4, ≤32, ≤8, ≤1 and ≤1 μg/ml. The resistance rate of Mycobacterium tuberculosis to rifampicin was 7.69%. The result of drug sensitivity of coagulase negative staphylococci isolated from patients with CNS infections and non-CNS infections were consistent. There were significant differences among Staphylococcus aureus, Enterobacteriaceae and Acinetobacter. Compared with the control group, the levels of protein were higher and the levels of chloride and glucose were lower in fungal group, Gram-positive bacteria group, Gram-positive coccus group and Gram-negative bacteria group ( t=3.408-9.249, all P<0.011). The levels of protein, adenosine deaminase (ADA) and lactic dehydrogenase (LDH) in Gram-positive bacilli group were significantly higher than those in fungal group, Gram-positive coccus group, Gram-negative bacteria group and control group ( t=3.836-7.686, all P<0.037). Conclusions:The pathogens causing CNS and blood infections in AIDS patients were widely distributed, mainly dominated by fungus. The CSF related measurements varied with different pathogens, so as to assist in the etiological diagnosis of CNS infections.

[Abstract] Objective: To study the effect and possible mechanism of TGF-β2 on the invasion of glioma stem cells (GSCs). Methods: Tumor tissues of 8 patients with glioblastoma multiforme, who underwent resection at Department of Neurosurgery of the FirstAffiliated Hospital of China Medical University duringApril 2016 toApril 2017, were collected. The primary culture of glioma cells were conducted with trypsin digestion. Partial primary glioma cells were seeded into serum-free DMEM/F12 culture medium containing EGF, bFGF and B27 to obtain suspension of tumor spheres. Immunoflurenscent staining and differentiation assay were used to detect whether the tumor spheres were GSCs. TGF-β2 secretion ability of GSCs was determined by ELISAassay.After transfection of TGF-β2 siRNA, the invasion ability of glioma stem cells was determined by Transwell assay. Western blotting was used to examine the effect of TGF-β2 on expression of matrix metalloproteinases (MMP) in glioma stem cells. Results: The suspended tumor spheres were proved to be GSCs by immunofluorescent staining and differentiation assay; the tumor spheres expressed the marker of GSCs（CD133）and had the ability to multi-differentiate (glia and neuronal cells). Compared with the primary glioma cells, Glioma stem cells exerted significantly improved TGF-β2 secretion ability ([74.13±3.63] vs [46.13±2.61] pg/ml, P<0.05); and TGF-β2 silencing significantly reduced the invasion ability of glioma stem cells ([105.71±8.69] vs [63.67±5.93], P<0.05) and inhibited MMP-2 and MMP-9 expressions. Conclusion: TGF-β2 can promote the invasiveness of glioma stem cells through MMP-2 and MMP-9 pathway.

Ghrelin and motilin (MTL) are mainly secreted by digestive tract,and they both can promote gastrointestinal motility. Disorder of gastrointestinal motility (DGIM)is a gastrointestinal motility or sensory disease mainly caused by neuroregulatory disorder,its main symptoms are nausea,vomiting,abdominal pain and abdominal distension. More and more studies have indicated that ghrelin,MTL and their receptor agonists are closely related to DGIM. This article reviewed the advances in studies on relationship between ghrelin/ GHS-R agonist,MTL/ MTL-R agonist and DGIM.

Objective To investigate the effects of propofol and sevoflurane on adriamycin chemotherapy-induced myocardial damage in rats.Methods Twenty-four healthy male Wistar rats, aged 3 months, weighing 212-270 g, were randomly divided into 4 groups (n =6 each) using a random number table: control group (group C) , adriamycin group (group ADM) , adriamycin-propofol group (group ADM-Pro) , and adriamycin-sevoflurane group (group ADM-Sevo).The equal volume of normal saline was injected intraperitoneally in group C.In group ADM, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times (11 days in total).In group ADM-Pro, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, propofol anesthesia was performed as follows : the total amount of propofol injected intraperitoneally was 200 mg/kg, the initial dose was 100 mg/kg, and 1 h later the remaining amount was added, and the duration of anesthesia was about 2 h.In group ADM-Sevo, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, sevoflurane anesthesia was performed as follows: 1.5％-3.0％ sevoflurane was inhaled for 2 h.After the end of anesthesia, blood samples were collected for determination of serum cardiac troponin (cTnI) concentrations.Myocardial specimens were collected for detection of caspase-3 expression by immuno-histochemistry.Results Compared with group C, the serum cTnI concentration was significantly increased, and the caspase-3 expression was up-regulated in ADM, ADM-Pro and ADM-Sevo groups (P＜ 0.05).Compared with group ADM, the serum cTnI concentration was significantly decreased, and the caspase-3 expression was down-regulated in ADM-Pro and ADM-Sevo groups (P＜0.05).There was no significant difference in the parameters mentioned above between group ADM-Pro and group ADM-Sevo (P＞0.05).Conclusion Propofol and sevoflurane both can mitigate adriamycin chemotherapy-induced myocardial damage in rats, without significant difference in the efficacy.

Aged ; Coronary Artery Disease ; diagnosis ; Coronary Vessel Anomalies ; diagnosis ; Coronary Vessels ; pathology ; Humans ; Male

One hundred and ninety one patients with esophageal carcinoma underwent surgical resection from January 2004 to January 2009. The gastroesophageal anastomosis was performed with auto suture instrument at superior aperture of the thorax in 107 cases (group A) and the instrument anastomosis was performed above or below the aorta arch in 84 cases ( group B ). The electron gastroscopy was performed and biopsy of mucosa at 3cm above the anastomosis was taken during the postoperative follow-up in all patients. Results showed that the incidence rate of reflux esophagitis in group A ( 5% ) was much lower than that in group B (51% ).

ObjectiveTo investigate the role of δ-opioid receptor in remifentanil-induced N-methyl-D-aspartate (NMDA) receptor miniature excitatory postsynaptic currents (mEPSCs) in rat spinal dorsal horn neurons.MethodsMale 14-18 d old Wistar rats weighing 50-60 g were used in this study.The animals were anesthetized with intraperitoneal choral hydrate 400 mg/kg and sacrificed.Their lumbar segments of spinal cord (L1-S1 ) were immediately removed and sliced.Twenty-four slices were randomly divided into 4 groups ( n =6 each): control group (group C) ; glycine group (group G) ; remifentanil group (group R) and remifentanil + naltrindole(a δ receptor antagon) (group RN).Slices were cultured in artificial cerebrospinal fluid (ACSF) (group C) or incubated in ACSF containing glycine 0.24 μmol/L (group G) or remifentanil 4 nmol/L (group R) or remifentanil 4 nmol/L+ naltrindole 1 nmol/L (group RN) for 60 min.Whole cell patch clamp technique was used to measure NMDA receptor mEPSCs.ResultsThe amplitude and frequency of mEPSCs were significantly higher in group R than in groups C and RN ( P ＜ 0.01).There were no significant differences in amplitude and frequency of mEPSCs among gorups C,G and RN ( P ＞ 0.05).ConclusionActivation of δ-receptor can enhance NMDA receptor function in spinal dorsal horn neurons in rats which may be the mechanism of remifentanil-induced hyperalgesia.