nitrophenols and Hypertrophy

Indications for tonsillectomy in recurrent tonsillitis are defined according to the number of episodes of acute bacterial infections in a year. However, little is known about the tonsil immune competence status in patients presenting with recurrent tonsillitis with either hypertrophied or atrophied tonsils, or in patients presenting with obstructive sleep apnoea. In this study we examined the tonsil immune status in children with 3-5 acute recurrent infections a year and in children with obstructive sleep apnoea by comparing the activity of tonsil and adenoid tissue nonspecific alkaline and acid phosphatase.. Specific activity of tonsil and adenoid tissue nonspecific alkaline and acid phosphatase was investigated in children who underwent tonsillectomy and adenoidectomy for recurrent infection (72 children) and for obstructive sleep apnoea (10 children). Tissue enzyme activities were measured using p-nitrophenylphosphate as a substrate. Tissue samples were examined by the haematoxylin-eosin histological technique. Statistical analyses were performed using SPSS v. 16 software.. The tissue nonspecific alkaline phosphatase activity was similar in hypertrophied tonsils in the recurrent infection group and in the obstructive sleep apnoea group (3.437+/-1.226 and 3.978+/-0.762 U/mg of protein, respectively). The enzyme activity in both hypertrophied tonsil groups was significantly higher as compared to atrophied tonsils in the recurrent tonsillitis group, p=0.021 and p=0.006, respectively. The enzyme activity was significantly higher in the adenoids compared to the tonsils from all three groups. Contrary to this, no significant differences were noticed for tonsil and adenoid acid phosphatase activities among the groups.. Similar acid phosphatase activity in all three groups implies that all three groups have preserved antigen presenting cell activity. In patients with hypertrophied tonsils similar tissue nonspecific alkaline phosphatase activity suggests preserved B cell tonsil immune activity, regardless of the pathology. Patients with atrophied tonsils had significantly lower alkaline phosphatase activity, indicating relative tonsil B cell immune deficiency. Thus, different immunological status in patients presenting with hypertrophied vs. atrophied tonsils could point to a different underlying pathophysiologic mechanism of the disease.

Topics: Adenoidectomy; Adenoids; Alkaline Phosphatase; Atrophy; B-Lymphocytes; Child; Child, Preschool; Female; Humans; Hydrogen-Ion Concentration; Hypertrophy; Macrophages; Male; Nasal Obstruction; Nitrophenols; Palatine Tonsil; Recurrence; Sleep Apnea, Obstructive; Tonsillectomy; Tonsillitis

T-type Ca2+ channels (TCCs) are involved in cardiac cell growth and proliferation in cultured cardiomyocytes. Underlying molecular mechanisms are not well understood. In this study, we investigated the role of TCCs in signal transduction in cardiac hypertrophy compared with L-type Ca2+ channels (LCCs). Cardiomyocytes dissociated from neonatal mouse ventricles were cultured until stabilization. Cell hypertrophy was induced by reapplication of 1% fatal bovine serum (FBS) following a period (24 h) of FBS depletion. Cell surface area increased from 862+/-73 microm2 to 2153+/-131 microm2 by FBS stimulation in control (250+/-1.8%). T-type Ca2+ current (I(CaT)) was inhibited dose-dependently by kurtoxin (KT) and efonidipine (ED) with IC50 0.07 microM and 3.2 microM, respectively in whole-cell voltage clamp. On the other hand, 1 microM KT which inhibits I(CaT) over 90% did not effect on L-type Ca2+ current (I(CaL)). 10 microM ED had the ability of I(CaL) blockade as well as that of I(CaT) blockade. 3 microM nisoldipine (ND) suppressed I(CaL) by over 80%. The increase in cell surface area following reapplication of FBS as observed in control (250+/-1.8%) was significantly reduced in the presence of 1 microM KT (216+/-1.2%) and virtually abolished in the presence of 10 microM ED (97+/-0.8%) and 3 microM ND (80+/-1.1%). Hypertrophy was associated with an increase in BNP mRNA of 316+/-3.6% in control and this increase was reduced as well in the presence of 1 microM KT (254+/-1.8%) and almost abolished in the presence of 10 microM ED (116+/-1.1%) and 3 muM ND (93+/-0.8%). Immunolabeling showed that translocation of nuclear factor of activated T cells (NFAT3) into the nucleus in response to FBS stimulation was markedly inhibited by either KT or ED as well as ND. Calcineurin phosphatase activity was upregulated 2.2-fold by FBS, but KT, ED and ND decreased this upregulation (1.7-fold, 0.8-fold, and 0.7-fold with KT, ED and ND respectively). These results suggest that blockade of Ca2+ entry into cardiomyocytes via TCCs may block pathophysiological signaling pathways leading to hypertrophy as well as via LCCs. The mechanism may be the inhibition of calcineurin-mediated NFAT3 activation resulting in prevention of its translocation into the nucleus.

Topics: Active Transport, Cell Nucleus; Animals; Calcineurin; Calcium Channel Blockers; Calcium Channels, L-Type; Calcium Channels, T-Type; Cattle; Cells, Cultured; Dihydropyridines; Hypertrophy; Mice; Myocardium; Myocytes, Cardiac; Natriuretic Peptide, Brain; Neurotoxins; NFATC Transcription Factors; Nisoldipine; Nitrophenols; Organophosphorus Compounds; Patch-Clamp Techniques; Scorpion Venoms

Esterolytic activity of blood serum was determined in infants with hypertrophic pyloric stenosis and in healthy control children. The substrates hydrolyzed mainly by arylesterase (EC. 3.1.1.2), i.e. p-nitrophenyl esters of acetic, propionic and butyric acid were used. It was found that in infants with hypertrophic pyloric stenosis the rate of p-nitrophenyl propionate hydrolysis was significantly higher than that of the acetate or butyrate. In control group children all three substrates were hydrolysed at similar rates, and these were significantly lower than in infants with hypertrophic pyloric stenosis.

Topics: Carboxylic Ester Hydrolases; Female; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Nitrophenols; Pyloric Stenosis; Substrate Specificity

Topics: Carboxylic Ester Hydrolases; Female; Humans; Hydrolysis; Hypertrophy; Infant; Male; Nitrophenols; Pyloric Stenosis