Propranolol inhibits the proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms

The aim of this study was to investigate the mechanism of propranolol on the regression of hemangiomas. Propranolol-treated hemangioma tissues were collected and the expression of hypoxia inducible factor-1α (HIF-1α) was examined. We also established HIF-1α overexpression and knockdown hemangioma cells, and determined the effects of HIF-1α on the hemangioma cells proliferation, apoptosis, migration and tube formation. Significantly increased HIF-1α level was found in the hemangioma tissues compared to that in normal vascular tissues, whereas propranolol treatment decreased the HIF-1α level in hemangioma tissues in a time- and dose-dependent manner. Moreover, propranolol treatment significantly decreased cell proliferation, migration and tube formation as well as promoted cell apoptosis in HIF-1α overexpression and knockdown hemangioma cells. Propranolol suppressed the cells proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms. HIF-1α could serve as a novel target in the treatment of hemangiomas.

Perinatal mortality rate in a south Indian population.

Perinatal mortality rate was assessed for 13964 consecutive births in SAT Hospital, Trivandrum, South India, during a period of one year. The overall perinatal mortality rate was 42.75, stillbirth rate 24.41 and early neonatal mortality rate 18.79. The perinatal mortality rate in multiple pregnancy was 156.65. Preventable causes of perinatal mortality still make a major contribution to perinatal deaths in developing countries.

Growth faltering and developmental delay in children with PEM.

Anthropometric measurements, Somatic Quotient (SQ), Development Quotient (DQ), Motor Quotient (MoQ) and Mental Quotient (MeQ) in 136 children in the age group 1-24 months with varying degrees of protein energy malnutrition (PEM) were compared with an equal number of comparable well nourished children. There was a progressive reduction in SQ, DQ, MoQ and MeQ as the degree of PEM advanced. There was a direct linear correlation between SQ and DQ and between height and DQ in 4 degrees PEM. However, there was no direct correlation between head circumference and either DQ or MeQ.

The first attack of acute rheumatic fever in childhood--clinical and laboratory profile.

One hundred consecutive cases of 'first attack' of acute rheumatic fever were studied. There were 52 males and 48 females, constituting 1.12% of total hospital admissions. Nearly 10% of children were below the age of 5 years, stressing the early onset of rheumatic fever in tropics. Only 47% gave a definite history of overcrowding at home. Sore throat was present in 67%, overt arthritis in 66%, carditis in 57%, arthralgia alone in 22% of which 45.45% had carditis. Small joint involvement was noticed in 23% of cases of which 73.91% had carditis. Only 33.33% had congestive cardiac failure. Ten per cent of children had chorea, while subcutaneous nodules were seen in 4% of cases, all of whom had associated carditis. Erythrocyte sedimentation rate (ESR) showed good correlation with clinical profile. Throat cultures were positive for beta hemolytic streptococci only in 12% of cases. Anti-streptolysin 'O' (ASO) titre showed significant titres on 68% of cases, anti-deoxyribonuclease "B" (ADN-B) in 69.32%, antibody to group A carbohydrate (ACHO) in 70.65%. ASO, ADN-B, and ACHO titres together gave 87.5% positivity while estimations in paired sera showed ASO 79.54%, ADN-B 82.27% and ASO, ADN-B together 99.92% significant titres. Study of blood groups showed A group children to be more vulnerable to rheumatic fever (37.5%) and rheumatic carditis (47.37%). Mortality in the present study was nil.

Effect of retinol on the hemolysis and lipid peroxidation in vitamin Ε deficiency.

A study on the effect of retinol in vitro on the hemolysis of vitamin Ε deficient rat red blood cells showed that retinol enhanced the lysis of the Ε deficient cells as compared to the lysis of normal cells. The lipid peroxidation present during hydrogen peroxide induced lysis of Ε deficient cells was however markedly inhibited in the presence of retinol without affecting the rate of lysis. In an actively peroxidising system of non-enzymatic lipid peroxidation of rat liver or brain homogenates and of brain lysosomes incubated with human erythrocytes, no lysis was obtained; incorporation of retinol in such systems resulted in lysis but no peroxidation. Hydrogen peroxide generating substances almost completely inhibited the lysis of normal human erythrocytes by retinol, but linoleic acid hydroperoxide and auto-oxidised liver or brain homogenates and ox-brain liposomes increased the lysis. It is concluded that vitamin Ε deficient erythrocyte hemolysis may be augmented by retinol, an anti-oxidant, having a lytic function without the peroxidation of stromal lipids.

Fructose diphosphate aldolase-Class I (Schiff base) from Mycobacterium tuberculosis H37Rv.

An aldolase was partially purified from fermenter grown Mycobacterium tuberculosis H37Rv cells. The aldolase has a molecular weight of 150,000, possesses a tetrameric structure and cleaves both fructose diphosphate and fructose- 1-phosphate, the former being cleaved 17 times faster. The enzyme was inactivated by treatment with NaBH4 in the presence of fructose diphosphate or dihydroxyacetone, phosphate suggesting Schiff base formation during its catalytic function. Thiol reagents, EDTA and metal ions had no apparent effect on the aldolase activity. These results show that aldolase is of Class I type. However, this enzyme, unlike the mammalian Class I aldolase, was unaffected by carboxypeptidase A. Nethylmaleiniide and dithionitrobenzoic acid.

Studies on hemolysis of human erythrocytes by linoleic acid.

The results presented in this paper show that lysis of human erythrocytes by linoleic acid is not caused by peroxidation of the fatty acid. Peroxidase, superoxide dismutase and scavengers of Ο · and OH had no effect on the lysis while catalase showed only marginal inhibition suggesting that Ο , OH , O and H2O2 do not play any direct role in hemolysis by linoleic acid. Generators of H2O2 inhibited the lysis completely and methemoglobin cells were more resistant to hemolysis by linoleic acid. The fatty acid did neither bind to nor fomed complex with red cell ghosts. Membrane oxidation of sulphydryl groups was also not involved in the lysis. β-Carotene, retinol and bile salts enhanced the lysis, while, cholesterol but not cholesterol acetate, inhibited it. Taurocholate-pretreated cells were more susceptible to linoleic acid lysis. These observations suggested-that lysis by linoleic acid may be due to its detergent property.

Alpha-tocopheryl acetate hydrolase in chicken liver. Characterisation and properties.

An enzyme catalysing the hydrolysis of a-tocopheryl acetate was characterised in chicken liver. The enzyme was localised in the microsomes, had an optimum pH 8·6 and a Km value of 0·5 mM. The enzyme did not hydrolyse retinyl acetate, cholesteryl acetate and ethyl acetate, thus indicating a high degree of specificity. a-Tocopheryl acetate hydrolase required bile salts as a specific cofactor. The results suggested a role for this enzyme in the absorption of vitamin E.