[Chronic hepatitis C--clinical course and genotypical pattern of distribution in patients of a Berlin infection clinic].
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Biomedical subjects
Publications and source records attributed to R Baumgarten.
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We generated a new lymphoma cell line carrying the translocations (8;14) and (14;18) and studied the genomic organization and expression of the BCL-2 and MYC genes. Polymerase chain reaction (PCR) and Southern analysis showed that the breakpoints of t(14;18) were located in the major breakpoint region (mbr) of the BCL-2 gene and just 5' of JH6 in the IgH locus. The breakpoints of the t(8;14) were located upstream of exon 2 in the non-coding region of the MYC gene and near the switch region of the IgH locus. Both IgH loci were involved in chromosomal translocations resulting in the absence of a functional B-cell receptor. Normal BCL-2 and truncated MYC transcripts were detected in these cells. The BCL-2 protein was expressed.
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Addiction, because of its associated psychological and physical diseases, is producing increasing expenses through social burden and influencing the epidemiological situation of the whole population via sexual or simple intimate social contacts. Outstanding infectious diseases with a high incidence in drug addicts are tuberculosis, hepatitis A, hepatitis B and the classical notifiable venereal diseases. Preventive measures are required, involving immunization and isolation. HIV infection is another increasing problem in drug addicts. The relatively long asymptomatic course in this population also raises the potential for the spread of AIDS to the general population. There is no ideal method for preventing this danger, but because the traditional abstinence paradigm has not been successful, methadone substitution is improving the medical compliance of this difficult clientele, reducing crime and prostitution and, at the same time, drug-associated risks for the general population.
A total of 37 patients with histologically confirmed chronic viral hepatitis B and presence of HBV-DNA and HBsAg in the serum were treated in a randomized, prospectively controlled multicenter trial either with recombinant IFN alpha-2b alone or a combination of IFN alpha-2b and recombinant IL-2. Twenty-two patients from group A were treated with 3 MU of IFN alpha-2b s.c. thrice weekly for 5 months. Starting at month 2 IL-2 was added: priming doses of 1.5 million CU were given s.c. on the first 2 days of each of the remaining 3 months, followed by maintenance doses of 0.3 million CU daily for 5 days per week. Fifteen patients from group B received 5 MU of IFN alpha-2b s.c. thrice weekly for 5 months. Five patients from group A (24%) and 4 patients from group B (28%) cleared HBV-DNA and HBeAg from the serum, and normalized elevated serum aminotransferase activities. The response rate in both groups did not differ significantly. Since side effects were more pronounced during combination therapy than in IFN alpha-2b monotherapy, it is suggested that treatment with IFN alpha-2b alone is preferable to a regimen of IFN alpha-2b/IL-2 applied according to the above schedule.
Fifty eight patients with chronic viral hepatitis B (HBV) were randomised in a prospectively controlled trial. Thirty patients were treated with 3 million units (MU) of interferon alfa-2b subcutaneously thrice weekly for four months. Twenty eight controls received no treatment. The follow up period after treatment was six months. Twenty eight treated patients and 27 controls completed the protocol. One woman in the treatment group showed a complete response, and eight other treated patients (32%) showed a partial response. Three patients in the control group (11%) lost hepatitis B e antigen and HBV-DNA spontaneously. This finding is statistically significant (p < 0.05). The elimination of HBV markers from the serum was associated with a return to normal of serum aminotransferase activities. Reactivation of hepatitis was not observed after seroconversion.
Major phenotypic changes occur in red cell membranes during the perinatal period, but the underlying molecular explanations remain poorly defined. Aquaporin CHIP, the major erythroid and renal water channel, was studied in perinatal rats using affinity-purified anti-CHIP IgG for immunoblotting, flow cytometry, and immunofluorescence microscopy. CHIP was not detected in prenatal red cells but was first identified in circulating red cells on the third postnatal day. Most circulating red cells were positive for CHIP by the seventh postnatal day, and this proportion rose to nearly 100% by the 14th day. The ontogeny of red cell CHIP correlated directly with acquisition of osmotic water permeability and inversely with Arrhenius activation energy. Only minor alterations in the composition of red cell membrane lipids occurred at this time. Immunohistochemical analysis of perinatal kidneys demonstrated a major induction of CHIP in renal proximal tubules and descending thin limbs at birth, coincident with the development of renal concentration mechanisms. Therefore, water channels are unnecessary for oxygen delivery or survival in the prenatal circulation, however CHIP may confer red cells with the ability to rehydrate rapidly after traversing the renal medulla, which becomes hypertonic after birth.
N-Acetylation and debrisoquine hydroxylation phenotypes were determined in 54 patients with Gilbert's syndrome and in 247 (sulfamethazine) and 76 (debrisoquine) non-related healthy volunteers, respectively. 40 (74.1%) of the patients and 135 (54.7%) of healthy volunteers were slow acetylators (chi 2 = 6.87). In patients, the cumulative urinary excretion (CUE) of sulfamethazine (0-6 hours) was significantly reduced. No differences between the debrisoquine poor metabolizers were observed: Gilbert's syndrome 5/54 (9.3%), healthy volunteers 5/76 (6.6%). The metabolic ratios were similar in both groups as well as the CUE of debrisoquine and its metabolite. Gilbert's syndrome seems to be related in some way to N-acetylation but not to debrisoquine hydroxylation polymorphism.
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Male copulatory stimuli in various animal species abbreviate the length of the period of their female conspecifics' heat. Such effect can be explained in some species as the result of copulation-induced alterations in ovarian hormone secretion (e.g. reflex ovulators). Other species require a different explanation: specifically, interactions in the hypothalamus between effects of steroid hormones and inhibitory neural afferents from the genital area have been hypothesized to play a role in some laboratory animals such as guinea pigs, hamsters and rats. However, the evidence in support of heat abbreviation through copulatory stimuli in rats is at best equivocal. There is obvious need for its unequivocal demonstration prior to any further analysis of the potential mechanism of action. The present study intended to find a model in support of the concept of 'centrally induced' heat abbreviation in rats. Virgin rats during 'natural heat' were examined with or without allowing them the opportunity to pace male copulatory activities. Ovariectomized, steroid hormone-treated rats were studied with minor or ample experience with sexual activities in prior tests and, also, with or without the opportunity to 'pace' male sexual acts. None of the experimental models revealed unequivocal support for detrimental effect of large numbers of intromittive copulations on 'central mechanisms' regulating heat duration. It rather seemed that frequent intromittive copulations and ejaculates affected the 'peripheral' genital tract (vulva, vagina, cervix) making further copulation of a highly aversive quality so that sexual encounters were avoided or prevented. This effect was noticed with great inter-individual variability. The conclusion is drawn that rats do not show the counterpart of heat abbreviation reportedly occurring rapidly and reliably in guinea pigs after a limited amount of vaginal/cervical stimulation through copulation or insertions of a glass-rod.
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