Outcomes of leadless pacemaker implantation in the United States based on sex.

Background: To determine differences in baseline characteristics and outcomes of leadless pacemaker implantation based on sex.

Methods: For the purpose of this study, data were extracted from the National Inpatient Sample database for years 2016-2020. The study group was then stratified based on sex.

The clustered gamma protocadherin PcdhγC4 isoform regulates cortical interneuron programmed cell death in the mouse cortex.

Cortical inhibitory interneurons (cINs) are born in the ventral forebrain and migrate into the cortex where they make connections with locally produced excitatory glutamatergic neurons. Cortical function critically depends on the number of cINs, which is also key to establishing the appropriate inhibitory/excitatory balance. The final number of cINs is determined during a postnatal period of programmed cell death (PCD) when ~40% of the young cINs are eliminated.

Validation of SNP markers for selection of semi-dwarf and peduncle extrusion in barley.

Unlabelled: This study aimed to validate the use of two SNP markers associated to a allele identified previously in a short barley genotype (ND23049) with an adequate peduncle extrusion which reduces predisposition to fungal disease development. First, the GBS SNP were converted in a KASP marker but only one of them, named TP4712, correctly amplified all allelic variations and had a Mendelian segregation in a F population. To corroborate the association between TP4712 allele with plant height and peduncle extrusion, a total of 1221 genotypes were genotyped and evaluated for both traits.

The Clustered Gamma Protocadherin Pcdhγc4 Isoform Regulates Cortical Interneuron Programmed Cell Death in the Mouse Cortex.

Cortical function critically depends on inhibitory/excitatory balance. Cortical inhibitory interneurons (cINs) are born in the ventral forebrain and migrate into cortex, where their numbers are adjusted by programmed cell death. Previously, we showed that loss of clustered gamma protocadherins (), but not of genes in the alpha or beta clusters, increased dramatically cIN BAX-dependent cell death in mice.