a, and identify a novel biomarker of preictal state an upward trend in HFO rate leading into seizures in some patients. Overall, our findings provide preliminary evidence that HFOs can function as a temporal biomarker of seizure onset.

Engorgement is the overfilling of breasts with milk, often occurring in the early days postpartum. It results in swollen, hard, painful breasts and may lead to premature cessation of breastfeeding, decreased milk production, cracked nipples and mastitis. Various treatments have been studied but little consistent evidence has been found on effective interventions.

To determine the effectiveness and safety of different treatments for engorgement in breastfeeding women.

On 2 October 2019, we searched Cochrane Pregnancy and Childbirth’s Trials Register, ClinicalTrials.gov, the WHO International Clinical Trials Registry Platform (ICTRP), and reference lists of retrieved studies.

All types of randomised controlled trials and all forms of treatment for breast engorgement were eligible.

Two review authors independently assessed trials for eligibility, extracted data, conducted ‘Risk of bias’ assessment and assessed the certainty of evidence using GRADE.

For this udpate, we included 21 studies (2170 women romising for the treatment of breast engorgement, such as cabbage leaves, cold gel packs, herbal compresses, and massage, the certainty of evidence is low and we cannot draw robust conclusions about their true effects. selleck products Future trials should aim to include larger sample sizes, using women – not individual breasts – as units of analysis.

Although some interventions may be promising for the treatment of breast engorgement, such as cabbage leaves, cold gel packs, herbal compresses, and massage, the certainty of evidence is low and we cannot draw robust conclusions about their true effects. Future trials should aim to include larger sample sizes, using women – not individual breasts – as units of analysis.

The efficacy of conventional systemic antibiotic therapy for eradication of Helicobacter pylori has been seriously challenged by antibiotic resistance. Identification of alternative therapeutic strategies might help to overcome this limitation. The aim of this study was to update previous meta-analyses that investigated the effect of periodontal treatment on gastric H.pylori eradication.

A systematic electronic search of the literature was conducted to identify all published clinical trials that compared the effect of adjunct periodontal treatment on conventional systemic H. pylori eradication therapy.

The updated analysis (consisting of 541 participants representing six studies) demonstrated that, compared with conventional systemic eradication therapy alone, the addition of periodontal treatment resulted in improvements in gastric H.pylori eradication rates with OR 4.11 (P=0.01). Moreover, not to lose any data, the previously presented Chinese results that could not be assessed by any available mechaniodontal treatment with systemic eradication therapy may be a wise strategy, enhancing the efficacy of H.pylori eradication therapy. Systematic review registration in PROSPERO ID number CRD42019119347.

Although the inclusion of five additional clinical trials in this updated meta-analysis has not changed the result of the previous review, the current meta-analysis is superior for having removed one study involving the use of chlorhexidine, which did not meet appropriate criteria for inclusion. Our results strengthen the value of periodontal treatment as an adjunctive remedy. Consistency of these results suggests that the incorporation of professional periodontal treatment with systemic eradication therapy may be a wise strategy, enhancing the efficacy of H. pylori eradication therapy. Systematic review registration in PROSPERO ID number CRD42019119347.

Childhood epilepsy with centrotemporal spikes (CECTS) is a common, focal, transient, developmental epilepsy syndrome characterized by unilateral or bilateral, independent epileptiform spikes in the Rolandic regions of unknown etiology. Given that CECTS presents during a period of dramatic white matter maturation and thatspikes in CECTS are activated during non-rapid eye movement (REM) sleep, we hypothesized that children with CECTS would have aberrant development of white matter connectivity between the thalamus and the Rolandic cortex. We further tested whether Rolandic thalamocortical structural connectivity correlates with spike rate during non-REM sleep.

Twenty-three children with CECTS (age = 8-15years) and 19 controls (age = 7-15years) underwent 3-T structural and diffusion-weighted magnetic resonance imaging and 72-electrode electroencephalographic recordings. Thalamocortical structural connectivity to Rolandic and non-Rolandic cortices was quantified using probabilistic tractography. Developmentalof CECTS. Our data further suggest that the abnormalities in these tracts do not recover, but are increasingly dysmature over time, implicating a permanent but potentially compensatory process contributing to disease resolution.

These data provide evidence that abnormal maturation of thalamocortical white matter circuits to the Rolandic cortex is a feature of CECTS. Our data further suggest that the abnormalities in these tracts do not recover, but are increasingly dysmature over time, implicating a permanent but potentially compensatory process contributing to disease resolution.

Neuroinflammation is a major theme in epilepsy, which has been characterized in acquired epilepsy but is poorly understood in genetic epilepsy. γ-Aminobutyric acid type A receptor subunit gene mutations are significant causes of epilepsy, and we have studied the pathophysiology directly resulting from defective receptor channels. Here, we determined the proinflammatory factors in a genetic mouse model, the Gabrg2

knockin (KI). We have identified increased cytokines in multiple brain regions of the KI mouse throughout different developmental stages and propose that accumulation of the trafficking-deficient mutant protein may increase neuroinflammation, which would be a novel mechanism for genetic epilepsy.

We used enzyme-linked immunosorbent assay, immunoprecipitation, nuclei purification, immunoblot, immunohistochemistry, and confocal microscopy to characterize increased neuroinflammation and its potential causes in a Gabrg2

KI mouse and a Gabrg2

knockout (KO) mouse, each associated with a different epilepsy syndrome with different severities.