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At least 739 records · Page 41Linked to original sources
PubMed1996

[A new strategy for treating small cell lung cancer].

Recent results from molecular biology have shown that lung cancer is characterized by multiple, sequentially appearing molecular changes that include genetic and epigenetic alterations. Among all types of lung cancer, small cell lung cancer (SCLC) is associated with the lowest rate of 5-year survival. In this symposium, we introduce our findings regarding the c-kit oncogenes in SCLC. We found that the c-kit gene is strongly expressed in SCLC. The c-kit gene was not expressed in normal bronchial epithelial cells, which indicates that this gene is abberantly transcribed in SCLC. In addition, c-kit-positive cases of SCLC showed autophosphorylation in response to recombinant human stem cell factor. Furthermore, adding rh stem cell factor of SCLC cell lines induced a significant chemotactic response and moderate in vitro cell growth. These results strongly suggest that abnormal expression of the c-kit gene may be involved in the pathogenesis of SCLC by autocrine/paracrine stimulation via the c-kit/SCF signal pathway. To overcome drug resistance, we assessed the efficacy of a chimeric toxin targeted to c-kit receptors.

Carcinoma, Small Cell↗
PubMed1991

Genetic markers in the blood of multiple sclerosis patients.

Poligenetically determined predisposition to multiple sclerosis (MS) defines the way of immunological reaction to environmental factors and leads to clinically manifest disease. Although the connection between MS and some loci of the HLA system has been established, the hereditary predisposition to MS remains to be elucidated. We determined the phenotypes of monogenic hereditary characteristics linked to the surface of red blood cells that were obtained from 45 MS patients and 458 healthy subjects. The antigens on the erythrocytic surface of the ABO, Rh, MN, Ss, Kell, Kidd, Duffy, P and Lewis system were analyzed. Our results demonstrate that the MS patients differ from the normal subjects with regard to the Rh, ABO and Lewis erythrocytic antigens. The Rh positive factor was present in 95.55% of the MS patients compared to 84.29% of the controls, whereas the Rh negative factor was found in only 4.45% of the MS patients and 15.71% of the healthy subjects. The blood group O was demonstrated in 22.22% of the MS patients compared to 40.42% of the healthy persons. The MS patients had the blood group A in 15.11% of the cases as opposed to 43.99% of the subjects in the control groups. The blood group B was found in 22.22% of the MS patients compared to 11.10% of the controls. The distribution of the Lewis system in the MS patients was also demonstrated to be different from that in the general population. The MS patients were found to have less frequently the Le a+b- phenotype (11.12%) and more frequently Le a- b- (13.33%) compared to the healthy subjects who had the Le a+b- phenotype in 12.00% of the cases and Le a- b- in 5.00%.

Blood Group Antigens↗
PubMed1990

Atrial natriuretic factor in hydrops fetalis caused by Rh isoimmunisation.

Plasma concentrations of atrial natriuretic factor were determined by radioimmunoassay in 16 human fetuses of between 19 and 38 weeks' gestation. Fifteen fetuses had varying degrees of anaemia as a result of Rh isoimmunisation, and one fetus was normal. Eight fetuses had ultrasonographic evidence of severe hydrops fetalis and an additional three fetuses had mild hydrops. Severely hydropic fetuses were more anaemic and immature than those with mild or no hydrops. Among fetuses from which samples were taken before in utero transfusion, concentrations of atrial natriuretic factor were higher in those with severe hydrops than in the other groups. An inverse relationship between the haemoglobin concentration and that of atrial natriuretic factor was found. In four fetuses in which severe hydrops resolved after intravascular transfusions in utero, there were significant decreases in plasma atrial natriuretic factor concentrations; in the fifth fetus the decrease was less pronounced. Raised concentrations of atrial natriuretic factor in fetuses with severe anaemia and hydrops may be the result of atrial natriuretic factor release induced by hypoxia.

Atrial Natriuretic Factor↗
PubMed1976

[Haemolytic disease of the new-born by blood-factor incompatibility other than Rh(d) and ABO (author's transl)].

Rare forms of incompatibility were observed over a period of 20 years in 41 (2%) of 2088 new-borns with haemolytic disease. Antibodies involved were anti-c (n = 27), anti-E (n = 6) and anti-K (n = 4), as well as one case each of anti-E + Fya, -C, -Fya and -Jka. Amniotic fluid was examined during pregnancy in nine cases, three children were given intra-uterine infusions, while in the remainder the haemolytic process was mild or only moderately severe. One infant died of toxoplasmosis, another one of immaturity and respiratory distress syndrome. Kernicterus was always prevented. In haemolytic disease of the newborn caused by anti-c and anti-E, prenatal damage is markedly rarer than with D erythroblastosis, but must be considered during the pregnancy. In anti-K haemolytic disease the severity of the disease is similar to that of D erythroblastosis. All three incompatibilities may lead to kernicterus in the first few days after birth so that exchange transfusions are often necessary. In most of the other incompatibilities the course is similar to that seen with ABO erythroblastosis.

Adult↗
PubMed1998

Contribution of nitric oxide to reactive hyperemia: impact of endothelial dysfunction.

Our objectives were to (1) test the hypothesis that nitric oxide (NO) contributes to peak reactive hyperemia (RH) in the human peripheral vasculature, (2) examine the impact of atherosclerosis and its risk factors on RH, and (3) investigate whether L-arginine will improve RH in patients with endothelial dysfunction. The endothelium contributes to shear stress-mediated vasomotion by releasing a variety of dilating factors, including NO, but the contribution of NO to peak RH in patients with and without endothelial dysfunction is unknown. Endothelium-dependent and endothelium-independent function was assessed with intrafemoral arterial acetylcholine (ACh) and sodium nitroprusside. RH was produced by occlusion of blood flow to the leg for 3 minutes. The study was repeated after NG-monomethyl-L-arginine (L-NMMA) in 44 subjects and L-arginine in 9 patients with atherosclerosis. There were 15 normal control subjects without risk factors for atherosclerosis and 29 patients with risk factors or angiographic atherosclerosis. Microvascular vasodilation in response to ACh, but not to sodium nitroprusside, was lower in the patients with risk factors or atherosclerosis compared with normal control subjects, P=0.048, and the inhibition of ACh-induced microvascular dilation by L-NMMA was also greater in normal control subjects (P=0.045). Similarly, RH, including the peak response, was inhibited by L-NMMA in normal control subjects (P=0.0011) but not in patients with risk factors or atherosclerosis, suggesting that the contribution of NO to both ACh-induced dilation and RH was diminished in patients with risk factors or atherosclerosis. L-Arginine did not affect vasodilation in response to ACh, sodium nitroprusside, or RH. We concluded that (1) NO contributes to all phases of RH in the normal human peripheral vasculature, (2) patients with atherosclerosis or its risks have abnormal NO bioactivity in response to pharmacological and physiological stimulation, and (3) L-arginine does not improve RH in atherosclerosis. Reduced physiological vasodilation in atherosclerosis may contribute to or exacerbate hypertension and ischemia.

Acetylcholine↗