Jarvisklitgaard5629

1 ± 38.6 vs men 39.1 ± 73.5, P= .53), citations (women 14.3 ± 19.1 vs men 17.6 ± 20.8, P= .45), and to be mentioned by news outlets, blogs, patents, Facebook, Wikipedia, Mendeley, Google, LinkedIn, and Reddit. Female first and last authors achieved comparable numbers of publications and H-index scores compared with male authors.

Significant sex-based differences in authorship representation persist, but with favorable improvement in female representation over time. Importantly, citations and high-impact status were independent of author sex. Characterization of the representation of women in academic achievement helps us strive for gender equity in our specialty.

Significant sex-based differences in authorship representation persist, but with favorable improvement in female representation over time. Importantly, citations and high-impact status were independent of author sex. Characterization of the representation of women in academic achievement helps us strive for gender equity in our specialty.

We studied the determinants of hemodynamics and analyzed the incidence, risk factors, and clinical impact of pulmonary homograft dysfunction following Ross surgery, after a 20-year follow-up at our referral center.

From 1997 to 2017, a total of 142 patients underwent surgery using the Ross procedure. The development of moderate-severe stenosis (peak transhomograft pressure gradient 36 mm Hg or greater) and surgical or percutaneous Ross homograft reinterventions were evaluated by echocardiography in the immediate postoperative period and at annual intervals.

After 20 years of follow-up, 31% of patients had moderate-severe homograft stenosis, and 9.1% had had to undergo one or two reinterventions, of which, six were valve replacements and seven were percutaneous interventions. At 1, 5, and 20 years, 89.4%, 74.6%, and 69% of these patients, respectively, were free from moderate-severe stenosis; and 99.3%, 95.7%, and 90.9%, respectively, had freedom from homograft reintervention. The pediatric group had a hg the first few years of follow-up, and may have been related to immune responses.GABAA receptors (GABAARs) and glycine receptors (GlyRs) are two principal inhibitory chloride ion channels in the central nervous system. The two receptors do not function independently but cross-talk to each other, i.e., the activation of one receptor would inhibit the other. This cross-talk is present in different patterns across various regions in the central nervous system; however, the factor that determines these patterns is not understood. Here, we show that the pattern of cross-talk between the two receptors is shaped by their relative expression level in a neuron a higher expression level correlates with louder talk. In line with a tendency of decrease in expression level of GlyRs and increase in expression level of GABAARs from the spinal cord, the brainstem to the neocortex, GlyRs talked much louder (i.e. produced greater inhibition) than GABAARs (one-way pattern) in spinal cord neurons, about equally loud as GABAARs (symmetric pattern) in inferior colliculus neurons and less loud (i.e. less inhibition) than GABAARs (asymmetric pattern) in auditory cortex neurons. see more Overexpression of GlyRs in inferior colliculus neurons produced an asymmetric pattern that should otherwise have been observed in spinal cord neurons. These expression level-dependent patterns of cross-talk between the two receptors may suggest how the central nervous system uses an alternative mechanism to maintain a delicate level of inhibition through adjusting the proportion of the two receptors in a neuron along its pathway.Hypoxic-ischemic encephalopathy (HIE) results in high neonatal mortality and severe neurological impairments, and its underlying molecular mechanism underwent extensive investigations. Long non-coding RNA (lncRNA) is considered to be an important regulator on brain development and many neurological diseases. Currently, little is known about the role of Vof-16 (lncRNA) in HIE. We detected the relative expression level of Vof-16 in the cortex and hippocampus of hypoxic-ischemic (HI) models whose successful establishment was verified by TTC staining. Then, Vof-16 knockout rats were generated using the CRISPR/Cas engineering technology to search the specific function of the Vof-16 through a series of behavioral evaluations including Neurological severity scores (NSS), Y-maze test, Morris water maze (MWW) test, open field test, and Rotarod test. The results demonstrated the expression of Vof-16 was substantially up-regulated in the cortex and hippocampus of rats with HI injury. Importantly, Vof-16 knockout facilitated the recovery from long-term HI induced nerve damage and neurobehavioral dysfunctions. In conclusion, this study suggests Vof-16 knockout is a promising treatment target for neonatal HIE.Research focusing on the gut-brain axis is growing, but the interplay of ethanol (alcohol molecule), the gut microbiome, the brain and behavior is poorly understood. In the current study, we remodeled the gut microbiota by providing adult male C57BL/6J mice with a non-absorbable antibiotic cocktail (ABX) in the drinking water and tested ethanol consumption behavior in a binge-like "Drinking in the Dark" model. Notably, 2 weeks of ABX pre-treatment significantly increased ethanol consumption during the 6 weeks of ethanol exposure in the DID paradigm. ABX treatment also appeared to prevent anxiety-like behavior during ethanol withdrawal period. ABX-treated mice expressed reduced bacterial diversity and modified microbiota compositions within cecal samples. There were drastically reduced levels of commensal Firmicutes and increases in the Bacteroidetes and Verrucomicrobia populations. Importantly, the relative abundance of Firmicutes inversely correlated to ethanol intake levels regardless of antibiotic treatment, whereas Bacteroidetes and Verrucomicrobia populations negatively correlated to ethanol intake levels. This is the first report demonstrating that ABX-induced disruption of the gut commensal microbiota leads to increased ethanol consumption in mice. This work reveals an important relationship between the gut microbiota and ethanol consumption behavior and supports the use of microbial-targeted approaches to study gut-brain interactions during alcohol use disorder.