Laparoscopic repair with hysteroscopy of cesarean scar diverticulum.

AIM: The aim of this study was to investigate the clinical data of laparoscopic repair with hysteroscopy of cesarean scar diverticulum (CSD). METHODS: We retrospectively evaluated 49 patients with CSD in our hospital who had undergone laparoscopic repair with hysteroscopy from January 2014 to June 2015. All patients had a history of cesarean section deliveries and prolonged postmenstrual spotting (duration 16.1 ± 3.4 days). The diagnosis of CSD was established by using 2-D transvaginal ultrasound. RESULTS: All patients underwent the surgical repair successfully, without evident complications. The mean operation time was 90.4 ± 9.1 min, the mean volume of blood loss was 31.2 ± 14.3 mL, and the mean length of hospital stay was 4.1 ± 0.3 days. All patients were followed for 6 months after the operation; the mean duration of menstruation was 7.5 ± 2.5 days shorter on average than the pre-surgical menstrual days, and the difference was statistically significant (P = 0.001). According to the clinical symptoms assessment, 89.8% (44/49) of the surgeries were effective, while according to the anatomic assessment, 95.9% (47/49) were effective. CONCLUSION: Laparoscopic repair with hysteroscopy of CSD was confirmed to be a safe, effective, and minimally invasive treatment, and should be widely used to treat patients with CSD.

[Protective effects and its mechanism of lipoxins on human umbilical vein endothelial cells under hypoxia].

OBJECTIVE: To investigate protective effects and mechanisms of lipoxinA(4) (LXA(4)) on human umbilical vein endothelial cells (HUVEC) under hypoxia in vitro. METHODS: The HUVEC culture were divided into groups as followed: added M199 culture medium as normal control groups, added CoCl2 to mimic hypoxia in vitro as hypoxia group and added different concentrations of LXA(4) (1, 10, 100 nmol/L) were added to the induced hypoxial HUVEC as agents intervention group. Morphological changes of HUVEC were observed by using inverted phase contrast microscope. The influence of LXA(4) on cell survival was investigated by methyl thiazolyl tetrazolium (MTT) assaying method after the treatment with different concentrations of LXA(4) and 100 nmol/L lipoxinA(4) according to different time (4, 8, 12 and 24 hours). The expression of von-willebrand factor (vWF) was detected by immunocytochemistry method. The changes of cytosolic Ca(2+) were measured by laser scanning confocal microscope. RESULTS: (1) Morphological changes:the cells under hypoxia lost its normal shapes and showed necrosis, while the cells cocultured with 100 nmol/L LXA(4) were normal appropriately. (2) Survival rate: the survival rates of HUVEC under hypoxia was (40.1 +/- 3.9)% and increased to (52.9 +/- 1.4)%, (64.1 +/- 3.3)%, (76.6 +/- 1.6)% respectively when added with LXA(4) with concentration of 1, 10, 100 nmol/L into culture medium. There was significant different survival rate when compared with that of hypoxia group. (3) The level of vWF: The expression of vWF was decreased with the increasing concentrations of LXA(4) added into culture medium, the gray values were 203.9 +/- 0.7 in 1 nmol/L, 204.6 +/- 0.9 in 10 nmol/L, 191.8 +/- 0.5 in 100 nmol/L respectively, which reached statistical difference in comparison with that of hypoxia groups (P < 0.05). (4) Confocal analysis: the intracellular free Ca(2+) concentrations of HUVEC were intensified with LXA(4) treatment. CONCLUSIONS: LXA(4) plays an important role in keeping the normal shape of HUVEC under hypoxia, can enhance survival of hypoxial HUVEC and decrease the level of vWF in cytoplasm. The protective mechanism might be via decreasing mitochondria Ca(2+) overload and increasing cytoplasm Ca(2+) by nucleus Ca(2+) transference.

Formyl-peptide receptor like 1: a potent mediator of the Ca2+ release-activated Ca2+ current ICRAC.

In electrically non-excitable cells, one major source of Ca(2+) influx is through the store-operated (or Ca(2+) release-activated Ca(2+)) channel by which the process of emptying the intracellular Ca(2+) stores results in the activation of Ca(2+) channels in the plasma membrane. Using both whole-cell patch-clamp and Ca(2+) imaging technique, we describe the electrophysiology mechanism underlying formyl-peptide receptor like 1 (FPRL1) linked to intracellular Ca(2+) mobilization. The FPRL1 agonists induced Ca(2+) release from the endoplasmic reticulum and subsequently evoked I(CRAC)-like currents displaying fast inactivation in K562 erythroleukemia cells which expresses FPRL1, but had almost no effect in K562 cells treated with FPRL1 RNA-interference and HEK293 cells which showed no FPRL1 expression. The currents were impaired after either complete store depletion by the sarco/endoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin, or after inhibition of PLC by U73122. Our results present the first evidence that FPRL1 is a potent mediator in the activation of CRAC channels.