Kinase regulation of HOX transcription factors

The HOX genes are a group of homeodomain-containing transcription factors that play important regulatory roles in early development, including the establishment of cell and tissue identity. HOX expression is generally reduced in adult cells but is frequently re-established as an early event in tumour formation and supports an oncogenic phenotype. HOX transcription factors are also involved in cell cycle regulation and DNA repair, along with normal adult physiological process including stem cell renewal. There have been extensive studies on the mechanism by which HOX proteins regulate transcription, with particular emphasis on their interaction with cofactors such as Pre-B-cell Leukaemia Homeobox (PBX) and Myeloid Ecotropic Viral Integration Site 1 (MEIS). However, significantly less is known of how the activity of HOX proteins is regulated. There is growing evidence that phosphorylation may play an important role in this context, and in this review, we draw together a number of important studies published over the last 20 years, and discuss the relevance of phosphorylation in the regulation and function of HOX proteins in development, evolution, cell cycle regulation, and cancer

SARS-CoV-2 uses CD4 to infect T helper lymphocytes

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

SARS-CoV-2 uses CD4 to infect T helper lymphocytes

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

La disfagia orofaringea nel soggetto neurochirurgico: uno studio prospettico

Gli scopi del nostro studio sono stati, dunque, quelli di a) analizzare le caratteristiche e l’incidenza delle complicanze della disfagia, b) studiare l’eventuale relazione con il quadro neurologico, c) valutare l’outcome a breve e lungo termine in un gruppo di di soggetti con dsfagia orofaringea, sottoposti ad intervento neurochirurgico per patologie vascolari traumatiche e non traumatiche e lesioni espansive cerebrali

Radiological evidence of subclinical dysphagia in motor neuron disease

I.F. 2.84

Spread of botulinum neurotoxin type a at standard doses is inherent to the successful treatment of spastic equinus foot in cerebral palsy: short-term neurophysiological and clinical study.

To evaluate whether botulinum toxin type A at standard doses spreads to antagonist leg muscles in dynamic equinus foot, we studied 18 ambulatory children with hemiplegic cerebral palsy. The gastrocnemius muscle on the affected side was injected with botulinum toxin type A (Dysport) (mean \ub1 standard deviation, 14.3 \ub1 0.9 U/kg). Compound muscle action potential areas were assessed in the lateral gastrocnemius and tibialis anterior muscles on the treated and untreated sides before botulinum toxin type A injections and on days 10 and 30 after injections. In all patients, compound muscle action potential areas recorded from both the muscles on the treated side decreased from preinjection values at day 10 (P < .05) and 30 (P < .002). After injection, ankle spasticity had diminished (P < .05), equinus foot excursion increased (P < .05), and functional gait improved (P < .05). This study shows that botulinum toxin type A spreads from foot flexors to antagonist extensors and suggests that spread may be partly responsible for improving gait in children with cerebral palsy