Talwar, Panda, Sarin & Tolani (1962) reported that growth hormone causes a significant increase in the incorporation in vivo of [32P]orthophosphate into the nuclear and microsomal fractions of ratliver RNA.
Growth hormone stimulates the synthesis of RNA in hypophysectomized rat liver. The question whether the hormonal stimulation of RNA synthesis is due to the activation of repressed cistrons or to other factors was studied. Nuclear RNA from the livers of adult female hypophysectomized and growth-hormone-treated rats was examined for molecular homology by hybridization techniques: no new species of RNA were detected after hormone treatment. The template activity of the chromatin for RNA synthesis is also not increased by the action of growth hormone. Short- and long-pulse-labelling experiments demonstrate that the hormonal stimulation of RNA synthesis is most marked in experiments where the period of incorporation of radioactive precursors is limited to 1-2hr. It is concluded that the hormone influences essentially the rate of RNA synthesis in these tissues.
Introduction:
Inflammation may mediate the association of mitral valve prolapse (MVP) with ventricular scarring and arrhythmia. The purpose of this study is to investigate the association of neutrophil- and platelet-to-lymphocyte ratios (NLR, PLR) with ventricular arrhythmia in MVP.
Hypothesis:
We hypothesized that hematological markers of inflammation predict ventricular arrhythmia in MVP.
Methods:
Clinical and demographic data were extracted from electronic medical records for all patients aged 18-90 years with MVP on echocardiography between 2016-19 at our institution. We studied 65 patients who had a differential blood count within six months prior to an ambulatory ECG (A- ECG) monitor (median age [IQR] 69.6 [60.5-77.1] years; 61.5% female; 12.3% African American). Patients with surgery or infection within six months prior to CBC were excluded. PVC burden and complex ventricular ectopy (cVE) on A-ECG were compared with NLR and PLR. Logistic and bivariate regression was used to analyze clinical, ECG, and echocardiographic factors associated with NLR and PLR.
Results:
Factors associated with NLR were congestive heart failure (p=0.005), male sex (p=0.015), age (p=0.033), and bileaflet MVP (p=0.036). NLR was associated with absolute PVC burden (R2 0.08, p=0.023) and cVE (median [IQR] 3.1 [1.6 - 5.8]), versus without cVE (1.7 [1.6-3.1], p=0.044). An NLR of 5.6 yielded 50% sensitivity and 90% specificity for PVC burden >1% (AUC 0.69). No significant association was found between PLR and PVC burden or cVE.
Conclusions:
NLR is associated with PVC burden and complex ventricular ectopy in MVP, suggesting that inflammation is a significant factor in the pathogenesis of ventricular arrhythmia in this condition.
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