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121.
Congenital methemoglobinemia due to NADH-methemoglobin reductase deficiency in three Indian families
Congenital methemoglobinemia is a relatively rare clinical disorder characterized by life-long cyanosis, caused by either an inherited mutant hemoglobin (Hb-M) or deficiency of physiologically active NADH-dependent methemoglobin reductase (NADH-MR). NADH-MR deficiency leads to two different types of recessive congenital methemoglobinemia. In type I, cyanosis is the only major symptom and NADH-MR deficiency is restricted only to the red blood cells. In type II, cyanosis is associated with severe mental retardation and neurological impairment. The objective of this study is to establish the cause of cyanosis in our cases of congenital methaemoglobinemia. Erythrocyte NADH-MR activity was assayed spectrophotometrically. Spectral analysis of the hemolysate treated with potassium ferricyanide was recorded between 400-700 nm and Hb electrophoresis on starch gel at pH 7.0 was done to rule out the presence of Hb-M. NADH-MR deficiency was detected in 3 families. There was a history of consanguinity in one of these cases. The three propositi presented with breathlessness, fever and peripheral cyanosis. There was no history of cardiac illness or exposure to drugs and chemicals. There were no signs and symptoms of mental retardation. The presence of Hb-M was ruled out. Hb-A2, Hb-F, G6PD activity and reduced glutathione levels were normal. NADH-MR activity in all the cases ranged from 4.1 to 9.2 IU/g Hb (normal range 7.0-24.0 IU/g Hb). We describe NADH-MR deficiency in three unrelated cases (age 4 months to 6 years) where the activity of the enzyme was 30-40% of normal. These three cases of congenital methemoglobinemia are due to type-I NADH-MR deficiency without mental retardation. 相似文献
122.
Preimplantation embryo morphology following early luteal phase anti-nidatory treatment with mifepristone (RU486) in the rhesus monkey 总被引:6,自引:0,他引:6
Ghosh D Lalitkumar PG Wong VJ Hendrickx AG Sengupta J 《Human reproduction (Oxford, England)》2000,15(1):180-188
The ultrastructural characteristics of peri-implantation stage embryos recovered on day 6 after ovulation from rhesus monkeys with or without mifepristone (RU486) treatment during the early luteal phase were examined in the present study. Monkeys were randomly allocated to two groups; group 1 animals were injected s.c. with 2 ml vehicle (1:4, benzyl benzoate: olive oil, v/v, n = 21) and group 2 animals received a single dose of mifepristone (2 mg/kg body weight, w/v, n = 30) in the same volume of vehicle on day 2 after ovulation in mated cycles. On day 6 after ovulation, female monkeys of both groups were laparotomized and their reproductive tracts were flushed to retrieve preimplantation stage embryos. Embryos that showed frank degeneration or desynchrony on gross microscopical examination were not included in the present study. Preimplantation embryo growth on day 6 after ovulation was significantly (P < 0.05) affected in the morula-blastocyst transition stage in mifepristone-treated monkeys compared with that in the control group of monkeys. Ultrastructurally, administration of mifepristone on day 2 after ovulation depressed preimplantation stage embryo development, characterized by loss of cell polarity, lack of mitochondrial maturity, and lack of differentiation in trophoblast cells. Furthermore, preimplantation embryos from mifepristone-treated animals displayed a higher occurrence of inter-blastomere space, intra-cytoplasmic vacuoles, myelinoid bodies, accumulation of lipid droplets, lysosomes, lipofuscins, autophagosomes and multivesicular bodies. Collectively, it appears that the developmental potential of preimplantation embryos was significantly compromised in mifepristone-treated cycles. 相似文献
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Two adapter proteins, Grb2 and Shc, have recently been implicated in the transmission of activation signals from the stimulated T cell receptor to Ras. We show here that in vitro stimulation of mouse splenic T cells with crosslinked anti-CD3 antibody leads within 30 s to phosphorylation of both Grb2 and Shc. Treatment with crosslinked anti-CD45 antibody leads to phosphorylation of Grb2 and also to a slight retardation in the mobility of this protein in an SDS polyacrylamide gel; both changes are seen within 30 s of crosslinking. Crosslinked anti-CD4 antibody leads to phosphorylation of Shc and to the phosphorylation of a 30-kDa protein that cross-reacts with anti-Grb2 antibodies. Aging leads to a decline in CD3-stimulated phosphorylation of Shc (but not Grb2), and to an increase in CD4-stimulated phosphorylation of Grb2, Shc, and the 30-kDa Grb2-like protein. Increased tyrosinephosphorylation of Grb2 after exposure to either anti-CD3 or anti-CD45 suggests that Grb2 may be a common substrate for both CD3-linked kinases and the CD45 phosphatase. The differences between T cells from young and old mice suggest that aging may lead to a set of alterations in kinase/substrate coupling that contribute to immune dysfunction in the elderly, and that activation of the Ras pathway might be impaired by aging in T lymphocytes. 相似文献
126.
Algorithms such as convolution superposition, Batho, and equivalent pathlength which were originally developed and validated for conventional treatments under conditions of electronic equilibrium using relatively large fields greater than 5 x 5 cm2 are routinely employed for inhomogeneity corrections. Modern day treatments using intensity modulated radiation therapy employ small beamlets characterized by the resolution of the multileaf collimator. These beamlets, in general, do not provide electronic equilibrium even in a homogeneous medium, and these effects are exaggerated in media with inhomogenieties. Monte Carlo simulations are becoming a tool of choice in understanding the dosimetry of small photon fields as they encounter low density media. In this study, depth dose data from the Monte Carlo simulations are compared to the results of the convolution superposition, Batho, and equivalent pathlength algorithms. The central axis dose within the low-density inhomogeneity as calculated by Monte Carlo simulation and convolution superposition decreases for small field sizes whereas it increases using the Batho and equivalent pathlength algorithms. The dose perturbation factor (DPF) is defined as the ratio of dose to a point within the inhomogeneity to the same point in a homogeneous phantom. The dose correction factor is defined as the ratio of dose calculated by an algorithm at a point to the Monte Carlo derived dose at the same point, respectively. DPF is noted to be significant for small fields and low density for all algorithms. Comparisons of the algorithms with Monte Carlo simulations is reflected in the DCF, which is close to 1.0 for the convolution-superposition algorithm. The Batho and equivalent pathlength algorithms differ significantly from Monte Carlo simulation for most field sizes and densities. Convolution superposition shows better agreement with Monte Carlo data versus the Batho or equivalent pathlength corrections. As the field size increases the DCF's for all algorithms converge toward 1.0. The largest differences in DCF are at the interface where changes in electron transport are greatest. For a 6 MV photon beam, electronic equilibrium is restored at field sizes above 3 cm diameter and all of the algorithms predict dose in and beyond the inhomogeneous region equally well. For accurate dosimetry of small fields within and near inhomogeneities, however, simple algorithms such as Batho and equivalent pathlength should be avoided. 相似文献
127.
We report a rare case of disseminated histoplasmosis in a immunocompetent young adult person involving bone marrow, liver, spleen and oral cavity. He presented with oral ulcers, weight loss and pancytopenia. His bone marrow aspiration examination revealed Histoplasma capsulatum. 相似文献
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