[Correlation of Rh-positive and Rh-negative factor in maternal and newborn blood].
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The article describes the new two-stage method of determining of Rh-factor belonging. At the first stage tsoliclon "Anti-D-super" (monoclonic anti-D-antibody class IgM) was used. At the second stage Rh-factor belonging is determined in test-tube, using standard universal reagent for definition Rh-factor RhO (D). Combination of negative results at the first stage with positive ones at the second stage is a sign of partial antigen D, most probably category VI. The persons with partial D are qualified as Rh-positive donors and Rh-negative recipients.
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Prior to a clinical trial in humans, we studied the effect and pharmacological distribution of recombinant human basic fibroblast growth-factor (Rh-bFGF) in vivo. Healing experiments on de-epithelialized rabbits corneas (n = 24 animals) compared the efficacy of three bFGF doses to controls and revealed a significantly increased healing rate for both 200 ng and 500 ng per application Rh-bFGF treatment groups compared to the control groups. To assess possible side effects of Rh-bFGF (500 ng topically applied for up to 7 days, twice daily), ten rabbits were involved in a model of an anterior keratectomy wound (performed with Draeger's roto-keratome to a depth of 0.15 mm). Light microscopy of thin sections of treated corneas showed an increased fibrogenesis in the anterior stroma with a more pronounced activation of keratocytes. No evidence for abnormal neovascularization or inflammation was observed when compared to control corneas. Ocular penetration and systemic distribution of topically applied labelled 125I FGF was assessed in three models (iodine vapour epithelial burn, anterior keratectomy and penetrating autokeratoplasty) in 24 rabbits. No intraocular penetration of bFGF occurred as shown by direct gamma counting. Macroautoradiography showed a selective labelling of epithelial basement membrane when denuded and intact, as previously described. Evidence for systemic absorption of breakdown products was confirmed by heparin-sepharose chromatography of blood and urine samples. Under these conditions, we suggest that topical Rh-bFGF promotes corneal wound healing without morphological adverse reaction or intraocular and systemic penetration.
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A statistical research has been carried on 334 pregnant women considering the variation of leucocyte number and leucocyte formula beginning from the 2nd month on. The resulting variations either of the leucocyte number or their formula structure might favour etiological researches for a better understanding of the deep changes caused by pregnancy. These variations refer also to blood group (ABO) and Rh (D) factor.
We investigated the influence of recombinant human tumor necrosis factor alfa (rh-TNF alpha) on the clonal growth of CFU-GM from 14 normal individuals and clonogenic blasts (CFU-L) from 16 patients with acute myeloid leukaemia (AML) in semi-solid cultures in vitro. Recombinant human TNF was produced by the Center of Molecular and Macromolecular Studies of the Polish Academy of Sciences (Lódź, Poland) as a lyophylized powder. This factor was added to the culture medium at the concentrations of 10, 100, 1000 U/ml. A dose-dependent growth inhibition of CFU-GM and AML CFU-L was observed. The inhibitory effect of rh-TNF alpha was significantly greater on CFU-L than CFU-GM.
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The author examined 211 members of 57 families with a genetic (familial) and idiopathic (sporadic) hypophysial nanism of obscure genesis. Rh-negative blood or weakened varieties of the Rh-antigen were revealed in 71 of 211 persons (33.1%), in 44 of 57 families (77.2%). Heterozygotic character of the majority of the positive parents of the sick children, by the Rh-factor, is undoubtful. Analysis of the Rh-factor distribution and of the antigens of the ABO system in the families suffering from hypophysial nanism permitted to exclude the significance of the hematological conflict by these antigens between the mother and the fetus, as a determining factor. It is supposed that there is a possible pathogenetic association between the hypophysial nanism and the absence of the Rh-antigen which is inherited also as an autosomic-recessive sign.
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Stem cell factor (SCF), the ligand of the c-kit receptor, is a potent enhancing cytokine for haematopoietic cells in the presence of IL-3, GM-CSF and erythropoietin (Epo). In the clonogenic assays of 63 MDS patients, the addition of rh-SCF + GM-CSF and/or IL-3 induced a significant increase (p < 0.001) in the number and size of CFU-GM. Never reaching the levels of controls, this increase was seen in all FAB subtypes, but particularly in RA. There was no significant increase in cluster formation, even in RAEB or RAEBt. Rh-SCF (10 ng/ml) led to mean increases of up to 26 times in the number of Epo-dependent BFU-E colonies, particularly in RA (p < 0.001) and RAEB (p < 0.05). Individual responses varied widely (especially in RA) from no response to supranormal levels. Added to the weekly refeed of 37 MDS LTBMC, SCF (10 ng/ml) induced only a 7% mean increase in both cell output and the number of clonogenic cells recovered in the supernatant. Immunohistochemical examination of the supernatant showed significant increases in differentiating myeloid cells in all examined cases, and in erythroid cells in 3 cases; blast cells increased in only 3 cases. These data suggest that rh-SCF is capable of at least partially reversing defective MDS myeloid haematopoiesis, and leads no overt risk of leukaemic transformation. Its potent effect on erythroid cells is encouraging for future clinical applications in patients, particularly if they are selected by means of in vitro tests.
This study was aimed to investigate the molecular genetic basis and serological phenotype of Rh weak D type 15 individuals. Samples were identified by serological tests and genotyped by sequence specific primer-PCR (SSP-PCR), and were sequenced to detect the changes of all ten RHD exons. The number of gene RHD was detected through SSP-PCR. The results showed that in tested individuals of weak D type confirmed by the IAT, 18 cases (56% in weak D) were weak D type 15. Rh factors found in 2 weak D type 15 individuals (11%) were C+c+E+e; Rh factors found in 2 weak D type 15 individuals (11%) were C+c+E-e+; others (78%) were c-c+E+e+. The results by serological tests were consistent with the results genotyped by PCR-SSP method. In all 18 samples, the sequencing result revealed a gene mutation 845G > A at the exon 6 of the RHD and the point mutation changed amino acid G282D of the RhD polypeptide. The zygosity test demonstrated that 2 out of 18 weak D type 15 individuals were RHD(+)/RHD(+) homozygous (two DCe/DcE), 16 cases were RHD(+)/RHD(-) heterozygous (two DCe/dce and fourteen DcE/dce). It is concluded that Weak D type 15 is predominant in weak D individuals of Chinese Han Nationality, and most of them are heterozygous with various RH haplotypes.
The chorionic villi of human placentas, 12 to 40 weeks' gestation, were examined for Rh-D blood group antigens with a direct immunofluorescent (IF) technique. Specific IF-standing was shown on the plasma membrane and cytoplasm of the villous trophoblasts. This staining decreased in intensity as the placenta matured. In addition, the trophoblasts of hydatidiform and destructive moles were also examined. The intensity of the IF-staining in these trophoblastic tumors was about the same as that in the young trophoblasts of the first trimester of pregnancy.
The study presents the frequency of occurrence of newborn haemolitic disease caused by Rh (D) system incompatibility in the years 1980-1999. Serological incompatibility prophylaxis was introduced in 1980. Routine use of anti-D immunoglobulin has led to a significant reduction in the number of newborns with haemalitic disease caused by Rh (D) system incompatibility. In the years 1990-1999 no newborn deaths attributable to this immunization were recorded. Long-term prophylaxis has greatly reduced the occurrence of this pathology in newborns. Nonetheless, in contemporary perinatology we continue to record occasional cases of haemolitic disease in newborns caused by blood group incompatibility between mother and foetus.