Joint hypermobility, obstetrical outcomes, and pelvic floor disorders

Introduction and hypothesis

Benign joint hypermobility syndrome may be a risk factor for pelvic floor disorders. It is unknown whether hypermobility impacts the progress of childbirth, a known risk factor for pelvic floor disorders. Our objective was to investigate the association between joint hypermobility syndrome, obstetrical outcomes, and pelvic floor disorders. Our hypotheses were: (1) women with joint hypermobility are less likely to experience operative delivery and prolonged second-stage labor; and (2) pelvic floor disorders are associated with benign hypermobility syndrome, controlling for obstetrical history.

Methods

Joint hypermobility was measured in 587 parous women (participants in a longitudinal cohort study of pelvic floor disorders after childbirth). Their obstetrical histories were obtained from review of hospital records. Pelvic floor disorders were assessed using validated questionnaires and a structured examination for prolapse. Joint hypermobility and pelvic floor disorders were evaluated at enrollment (5–10 years after first delivery). We compared obstetrical outcomes and pelvic floor disorders between women with and without joint hypermobility, defined as a Beighton score ≥4.

Results

Hypermobility was diagnosed in 46 women (7.8 %) and was associated with decreased odds of cesarean after complete cervical dilation or operative vaginal delivery [odds ratio (OR)?=?0.51; 95 % confidence interval (CI):0.27–0.95]. Anal sphincter laceration was unlikely to occur in women with hypermobility (OR?=?0.19; 95 % CI 0.04–0.80). However, hypermobility was not associated with any pelvic floor disorder considered.

Conclusions

Benign joint hypermobility syndrome may facilitate spontaneous vaginal birth but does not appear to be a risk factor for pelvic floor disorders in the first decade after childbirth.     

Animal model Of cerebral aneurysms: Pathology and pathogenesis of induced cerebral aneurysms in rats

Saccular cerebral aneurysms are induced in rats treated with ligation of one or both of the common carotid arteries, experimental hypertension, and β-aminopropionitrile feeding. Combination of ligation of the carotid artery and experimental hypertension is the minimal requirement for inducing aneurysms within a few months. β-aminopropionitrile makes the arterial wall fragile, increasing the incidence of aneurysmal development. Induced aneurysms are strongly related to haemodynamic stresses. They ere located on the large arteries at the base of the brain. Some of them apparently originate from the apex of bifurcation. The macroscopic and microscopic findings are generally in accordance with those of spontaneous lesions in man. The results of electron microscope and histochemical studies indicate the participation of leukocytes and their lysosomal enzymes in the development and growth of aneurysms. Adventitial cells are also suggested to be responsible for the growth of aneurysms.     

Comparison of magnetoencephalography,functional MRI,and motor evoked potentials in the localization of the sensory-motor cortex

Abstract

To clarify the topographical relationship between peri-Rolandic lesions and the central sulcus, we carried out presurgical functional mapping by using magnetoencephalography (MEG), functional magnetic resonance imaging (f-MRI), and motor evoked potentials (MEPs) on 5 patients. The sensory cortex was identified by somatosensory evoked magnetic fields using MEG (magnetic source imaging (MSI)). The motor area of the hand region was identified using f-MRI, during a hand squeezing task. In addition, transcranial magnetic stimulation localized the hand motor area on the scalp, which was mapped onto the MRI. In all cases, the sensory cortical vein or the lack of any functional activation in the area of peri-lesional edema. MEPs were also unable to localize the entire motor strip. Therefore, at present, MSI is considered to be the most reliable method to localize peri-Rolandic lesions. [Neurol Res 1995; 17: 361-367] cortical vein or the lack of any functional activation in the area of peri-lesional edema. MEPs were also unable to localize the entire motor strip. Therefore, at present, MSI is considered to be the most reliable method to localize peri-Rolandic lesions. [Neurol Res 1995; 17: 361-367]     

Novel nootropic drug sunifiram enhances hippocampal synaptic efficacy via glycine‐binding site of N‐methyl‐D‐aspartate receptor

Sunifiram is a novel pyrrolidone nootropic drug structurally related to piracetam, which was developed for neurodegenerative disorder like Alzheimer's disease. Sunifiram is known to enhance cognitive function in some behavioral experiments such as Morris water maze task. To address question whether sunifiram affects N‐methyl‐D ‐aspartate receptor (NMDAR)‐dependent synaptic function in the hippocampal CA1 region, we assessed the effects of sunifiram on NMDAR‐dependent long‐term potentiation (LTP) by electrophysiology and on phosphorylation of synaptic proteins by immunoblotting analysis. In mouse hippocampal slices, sunifiram at 10–100 nM significantly enhanced LTP in a bell‐shaped dose‐response relationship which peaked at 10 nM. The enhancement of LTP by sunifiram treatment was inhibited by 7‐chloro‐kynurenic acid (7‐ClKN), an antagonist for glycine‐binding site of NMDAR, but not by ifenprodil, an inhibitor for polyamine site of NMDAR. The enhancement of LTP by sunifilam was associated with an increase in phosphorylation of α‐amino‐3‐hydroxy‐5‐methylisozazole‐4‐propionate receptor (AMPAR) through activation of calcium/calmodulin‐dependent protein kinase II (CaMKII) and an increase in phosphorylation of NMDAR through activation of protein kinase Cα (PKCα). Sunifiram treatments at 1–1000 nM increased the slope of field excitatory postsynaptic potentials (fEPSPs) in a dose‐dependent manner. The enhancement was associated with an increase in phosphorylation of AMPAR receptor through activation of CaMKII. Interestingly, under the basal condition, sunifiram treatments increased PKCα (Ser‐657) and Src family (Tyr‐416) activities with the same bell‐shaped dose‐response curve as that of LTP peaking at 10 nM. The increase in phosphorylation of PKCα (Ser‐657) and Src (Tyr‐416) induced by sunifiram was inhibited by 7‐ClKN treatment. The LTP enhancement by sunifiram was significantly inhibited by PP2, a Src family inhibitor. Finally, when pretreated with a high concentration of glycine (300 μM), sunifiram treatments failed to potentiate LTP in the CA1 region. Taken together, sunifiram stimulates the glycine‐binding site of NMDAR with concomitant PKCα activation through Src kinase. Enhancement of PKCα activity triggers to potentiate hippocampal LTP through CaMKII activation. © 2013 Wiley Periodicals, Inc.     

Hemodynamic factor evaluation using computational fluid dynamics analysis for de novo bleb formation in unruptured intracranial aneurysms

Neurological Sciences - Although bleb formation increases the risk of rupture of intracranial aneurysms, previous computational fluid dynamic (CFD) studies have been unable to identify robust...     

Insecticide resistance in potential vector mosquitoes for West Nile virus in Japan

Culex pipiens complex is the significant vector mosquito of West Nile virus. To take stock of the current situation of insecticide susceptibilities and design an ideal mosquito control strategy, we collected Culex pipiens pallens Coquillet, Culex pipiens form molestus Forskal, and Culex quinquefasciatus Say from fields in Japan and conducted bioassays for five larvicides (fenitrothion, temephos, etofenprox, diflubenzuron, and pyriproxyfen) by using a larval dipping method. Among five insecticides tested, obvious reduced susceptibilities were observed for etofenprox, which is the only pyrethroid compound registered as a larvicide in Japan. Twenty-two of 56 colonies exhibited a >10% survival rate at the etofenprox concentration of 5.7 microg/ml, which is a 10 times higher concentration of the working solution. The LC50 of a colony collected from Fukuoka prefecture for etofenprox exceeded 60 microg/ml (resistance ratio >2,307), and this colony also exhibited cross-resistance to other pyrethroids, permethrin (299-fold) and phenothrin (1,200-fold). The insect growth regulators diflubenzuron and pyriproxyfen were found to be sufficiently effective enough to control Culex larvae present, but decreased sensitivities to these insecticides were slightly detected in some colonies of Cx. p. form molestus collected from urban areas. Several etofenprox-resistant colonies of Cx. p. form molestus exhibited simultaneously decreased susceptibilities to other insecticides, including temephos, diflubenzuron, and pyriproxyfen.