A meta-analysis of the effects of intramuscular and intravenous injection of oxytocin on the third stage of labor.

BACKGROUND: Clinical studies and trials have shown that oxytocin can effectively reduce postpartum bleeding, whether by intramuscular (IM) injection or intravenous (IV) injection. These two methods are widely used in the prevention and treatment for the third stage of childbirth. However, it is unclear whether the subtle differences between the mode of these routes have any effect on maternal outcomes. OBJECTIVES: To systematically evaluate the efficacy and safety of oxytocin administered intramuscularly or intravenously for prophylactic management of the third stage of labor after vaginal birth. METHODS: Computerized retrieval of PubMed, the Cochrane Library, Web of Science, Embase, and ClinicalTrials.gov was conducted to collect randomized controlled trials (RCT) on the effects of IM and IV oxytocin on the third stage of labor. After independent literature screening, data extraction and evaluation of the bias risk of included studies by two evaluators, RevMan 5.3 software was used for a meta-analysis. RESULTS: Six studies with 7734 women were included in this study. Meta-analysis results showed that: the severe postpartum hemorrhage (PPH) rate [risk ratio (RR) 1.54, 95% confidence interval (95% CI) 1.08-2.20, P = 0.02], PPH rate (RR 1.31, 95% CI 1.11-1.55, P = 0.001), incidence of blood transfusion (RR 2.30, 95% CI 1.35-3.93, P = 0.002) and the need of manual removal of placenta (RR 1.44, 95% CI 1.05-1.96, P = 0.02) for IM group were higher than IV group, but there were no significant differences in the use of additional uterotonics (P = 0.31) and the incidence of serious maternal morbidity and adverse effects between two groups. None of the included studies reported maternal death. CONCLUSION: For clinical practice, intravenous injection oxytocin 10 IU may be a good, safe option in the management of the third stage of labor. Medical conditions, available resources, adverse effects, and women' s preferences should also be considered. If an IV line is already in place at delivery, IV administration may be preferable to IM injection.

[Construction of specific artificial antigen-presenting cells for in vitro activation of CD19 chimeric antigen receptor T cells].

OBJECTIVE: To construct CD19-specific artificial antigen-presenting cells (aAPCs) for in vitro activation and expansion of CD19 chimeric antigen receptor (CAR)-modified T cells (CD19-CAR-T) and investigate their cytotoxic effect. METHODS: CD19-specific aAPCs (NIH3T3-CD19/86, NIH3T3-CD19/86/137L) expressing costimulatory molecules CD86 and/or CD137L were prepared on the basis of NIH3T3 backbone cells by lentivirus-mediated gene transfer. Irradiated CD19-specific aAPCs were co-cultured with CD19-CAR-T cells to activate and amplify CD19-CAR-T cells. The growth curve of CD19-CAR-T cells was determined by trypan blue exclusion assay, and CD19CAR expression and phenotype on CD19-CAR-T cells were detected by flow cytometry. The in vitro cytotoxicity of CD19-CAR-T cells against the target cells was evaluated by bioluminescence-based cytotoxicity assay. RESULTS: Flow cytometry showed that NIH3T3-CD19/86 and NIH3T3-CD19/86/137L expressed high levels of CD19, CD86 and/or CD137L. Both NIH3T3-CD19/86 and NIH3T3-CD19/86/137L cells could amplify CD19-CAR-T cells efficiently, but NIH3T3-CD19/86/137L cells had better amplification effect. After 14 days of co-culture with NIH3T3-CD19/86/137L cells, the number of CD19-CAR-T cells was significantly greater than that of NIH3T3-CD19/86 cells (P<0.05), and the proportion of CD19-CAR-T cells in the total T cells increased significantly (P<0.05). CD19-CAR-T cells amplified by CD19-specific aAPCs produced target-specific cytotoxicity and were able to specifically kill CD19-positive target cells. About 20% central memory T cells were present in the final products expanded by NIH3T3-CD19/86/137L. CONCLUSION: We successfully prepared CD19-specific aAPCs that can specifically amplify functional CD19-CART cells in vitro, which facilitates the acquisition of clinical-scale high-quality CD19-CART cells.

[The effect of leptin on Cx43 expression in protecting mice cerebral ischemia/reperfusion injury].

OBJECTIVE: To explore the effect of leptin on expression of Cx43 after rat cerebral ischemia/ reperfusion injury and its related mechanism. METHODS: Forty-five male kunming mice were randomly divided into 3 groups: sham group, model group and leptin group. Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion in model and leptin group. Mice of leptin group were intraperitoneally injected with 1 mg/kg leptin at 0 minute after ischemia. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury. The histopathological changes in the brain were observed with HE staining. The astrocytes of SD rat cerebral cotex were cultured primaryly and purified, and then divided them into four groups: control, model, leptin 100 microg/L, and leptin 500 microg/L. The cerebral astrocytes with hypoxia/reoxygenation injury were induced. The cellular viability of injury was detected by MTT assay. The effect of leptin on Cx43 expression was detected by Western blot in brain tissues and astrocytes. RESULTS: Compared with the model group, the neurological deficits and cerebral infarct volume of leptin group were reduced (P< 0.05), the histopathological injury in the brain tissues was alleviated and the expression of Cx43 was decreased markedly (P < 0.01). The survival rate of astrocytes was increased significantly in leptin 500 microg/L group (P < 0.01), whereas the Cx43 expression of astrocytes decreased (P < 0.01). But the difference of leptin 100 mcirog/L was not significant (P > 0.05). CONCLUSION: Leptin can ameliorate cerebral pathological changes in the event of IR injury by suppressing the expression of Cx43 both in vivo and vitro experiments.