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Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 199 records · Page 11Linked to original sources
PubMed1985

Envelope gene and long terminal repeat determine the different biological properties of Rauscher, Friend, and Moloney mink cell focus-inducing viruses.

The nucleotide sequence of the envelope (env) gene and the long terminal repeat (LTR) of an infectious clone of Rauscher mink cell focus-inducing (R-MCF) virus has been determined and compared with the published env gene and LTR sequences of Friend (F)- and Moloney (M)-MCF viruses. The sequence shows that R-MCF virus, like other MCF viruses, is a recombinant virus. Its env gene contains sequences which were acquired from an env gene in the mouse genome and which confer on the MCF virus its dualtropic host range. Unlike F-MCF and M-MCF viruses, R-MCF virus will not replicate in NIH 3T3 cells. The deduced amino acid sequence for the gp70 of R-MCF differs from that of F- and M-MCF viruses by 15 amino acids between residues 49 and 138 of gp70. These differences in amino acid sequences may be responsible for the inability of R-MCF virus to replicate in NIH 3T3 cells. The host range of two hybrid viruses constructed in vitro is consistent with this hypothesis. R-MCF virus and Friend murine leukemia virus (F-MLV) show 98% identity in their env gene 3' from the acquired env sequences. This contrasts with 82% identity between the env gene of R-MCF virus and M-MLV. The LTR of R-MCF shows 98% identity with the LTR of F-MCF as compared to 88% identity with the LTR of M-MCF. This striking similarity between the sequences of R-MCF, F-MCF, and F-MLV is surprising since the Rauscher virus and the Friend virus are thought to have originated independently. The high degree of similarity suggests that Rauscher and Friend viruses have a common origin. In contrast to M-MLV, which induces predominantly a lymphoid disease, R- and F-MCF viruses induce an erythroproliferative disease in NIH Swiss mice. A hybrid R-MCF virus with a genome derived primarily from R-MCF virus and a 3' end including the U3 region derived from M-MLV induces a lymphoid disease instead of an erythroid disease. This result indicates that it is the U3 region which determines the tissue specificity of the MCF virus-induced disease. It is suggested that the putative viral enhancers in the U3 region play two roles in the process of leukemogenesis: in the Friend and Rauscher disease, the viral enhancers act by increasing the transcription of the MCF env gene; in the thymic lymphoma, the enhancers activate mainly the expression of cellular genes.

Amino Acid Sequence↗
PubMed1985

Acquired immunodeficiency syndrome (AIDS) in pediatric patients. Case report and review.

The first pediatric case of acquired immunodeficiency syndrome (AIDS) observed in Switzerland is described. The 3-year-old African/Swiss patient was most probably vertically infected from her asymptomatic, HTLV-III antibody positive Zairian mother. Clinical symptomatology started at 14 months of age, and diagnosis was made at 22 months when medical care and comprehensive investigation were initiated at this clinic. Review of the literature revealed 125 pediatric patients with AIDS. Based on these data, relevant and practically orientated information is given concerning definition, epidemiology, clinical presentation, laboratory findings, management, and prognosis of this newly recognized entity.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Acquired immunodeficiency syndrome in a child of Swiss origin whose mother died from AIDS].

Report of a now 2 8/12-year-old girl, who presented at the age of 8 months with chronic progressive pneumonia, mucocutaneous candidiasis, diarrhea, failure to thrive and a non-progressive paraplegia. The child's mother presented AIDS with pneumocystis carinii pneumonia and progressive general paralysis one year after the beginning of the child's disease and died within a few months. Additional findings in the child include lymphopenia, hyperimmunoglobulinemia, cutaneous anergy and an abnormal T helper/T suppressor cell ratio. HTLV-III antibodies were positive (ELISA and Western blot virus strip RIA). Prophylactic treatment with Co-trimoxazole relieved pulmonary infections but failure to thrive remained unchanged in spite of a continuous nutritional support. A vertical mode of transmission of AIDS from mother to child seems very probable.

Acquired Immunodeficiency Syndrome↗
PubMed1984

[Acquired immune deficiency syndrome in the region of Zurich. Report on 12 cases].

Observations of 12 patients with AIDS at this institution from March 1981 to April 1984 are reported. Ten patients were homosexuals and two were bisexual. The majority had travelled abroad (USA, Haiti) and reported multiple anonymous sexual contracts. Eleven patients reported symptoms and signs, of 2-12 months' duration, frequently seen in pre-AIDS: fatigue (10), weight loss (10), diarrhea (7), night sweats (5), fever (4), and generalized lymphadenopathy (1). Laboratory studies showed anemia (10), lymphopenia (9), leukopenia (7), decreased T-helper/T-suppressor ratio (10) and cutaneous anergy to multiple skin-test antigens (9). P. carinii pneumonia was diagnosed in three patients, P. carinii pneumonia and Kaposi's sarcoma in one patient and Kaposi's sarcoma in six patients. Another patient had a chronic mucocutaneous infection with herpes simplex and another an intestinal cryptosporidiosis and Kaposi's sarcoma. Alpha-A-interferon was used to treat patients with Kaposi's sarcoma and three patients with limited disease showed a favorable response. Six patients with advanced disease died.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Involvement of 5-hydroxytryptamine-containing neurons in antinociception produced by injection of morphine into nucleus raphe magnus or onto spinal cord.

We studied whether antinociception produced by injection of morphine into the nucleus raphe magnus (NRM) or superfusion onto the spinal cord involved serotonergic neurons that descend from brainstem to spinal cord. Involvement of 5-hydroxytryptamine (5-HT)-containing neurons was determined by correlating morphine-induced analgesia with an increase in turnover of 5-HT and by determining if depletion of cord 5-HT with the neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT) could attenuate the antinociceptive effects of morphine. When injected directly into the NRM, 10 micrograms of morphine produced profound analgesia as measured by the paw-pressure technique, and significantly increased the turnover of 5-HT in both posterior medulla and spinal cord. Depletion of cord 5-HT to less than 10% of control concentrations attenuated the antinociceptive effect of morphine injected into the NRM. When various concentrations of morphine (1, 10 or 50 micrograms) were injected directly into the spinal subarachnoid space, a dose-dependent analgesia was observed. No change in 5-HT turnover in spinal cord was observed with any dose of morphine superfused onto the cord. In addition, depletion of cord 5-HT with 5,7-DHT did not alter the analgesic response to either 1 or 10 micrograms of intrathecal morphine. These results suggest that although 5-HT-containing neurons descending from brainstem into spinal cord are involved with analgesia produced by morphine injection into the NRM, they are not involved in the analgesia induced by applying morphine directly to the cord.

5,7-Dihydroxytryptamine↗
PubMed1984

Factors influencing the cholinesterases of cerebrospinal fluid in the anaesthetized cat.

Both acetylcholinesterase and non-specific cholinesterase are found in cerebrospinal fluid and blood plasma of the cat; the ratio of activities acetylcholinesterase/non-specific cholinesterase is about 1.5 in cerebrospinal fluid and 0.15 in plasma. A search was made for factors capable of influencing the concentration of the two cholinesterases in cerebrospinal fluid. Either the ventricular system was perfused with artificial cerebrospinal fluid from a lateral ventricle to the aqueduct, or the atlanto-occipital membrane was punctured and cerebrospinal fluid was collected continuously from the cisterna magna. Factors studied included: (a) procedures affecting the composition or formation of cerebrospinal fluid, such as changes in the ionic constituents of the perfusate, the inhibition of cerebrospinal fluid formation by acetazolamide or ouabain, or the rapid intra-carotid infusion of hypertonic urea; (b) arousal (noise or stimulation of the central ends of the sciatic nerves), or deepening of anaesthesia; (c) changes in blood pressure; (d) central stimulants and depressants, pyrogens, prostaglandins, antagonists of acetylcholine. Whereas most procedures or drugs tested increased the concentration of acetylcholinesterase, some central depressants (e.g. chlorpromazine) reduced, while another (ether) increased the appearance of acetylcholinesterase in the cerebrospinal fluid. The effect of ether was, in all probability, due to damage to the blood-brain barrier. A rise in acetylcholinesterase concentration was obtained upon stimulation of the central ends of the sciatic nerves; this was inhibited by atropine but not by N-methylatropine, indicating that the rise was due to increased nervous activity and not to the circulatory effects of the stimulation, since the changes in blood pressure caused by the stimulation remained the same after atropine administration. Amphetamine or leptazol raised the levels of acetylcholinesterase but it was not possible to determine whether this was due only to increased central nervous activity, since there was invariably leakage through the blood-brain barrier which by itself would be sufficient to produce the effect. A rise in the level of acetylcholinesterase was seen after administration of pyrogen; this was apparently not a simple effect of warming the body, but due to the action of the pyrogen on centers concerned with temperature control, since warming the animal by external heat failed to produce a similar change.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1983

[Monotherapy of systematic Pseudomonas aeruginosa infections with ceftazidime. The causes of therapeutic failures].

Ceftazidime, a new cephalosporin, is characterized by very good in-vitro action against P. aeruginosa. Nonetheless, clinical and (or) microbiological failure occurred in four patients with severe P. aeruginosa infections being treated with ceftazidime. Main cause infections being treated with ceftazidime. Main cause of the discrepancy between in-vitro and in-vivo results during treatment of three patients was a rapid drop in bacterial sensitivity. Superinfection with resistant microorganisms was excluded by the identity of the isolated bacteria in the different epidemiological markers before and during treatment. This rise in resistance was also demonstrated in-vitro by culturing clinically isolated material in ceftazidime-containing media: a 16-fold decrease in sensitivity was demonstrated within three subcultures. Increased beta-lactamase activity of the resistant strains makes it likely that enzymatic inactivation was part of the resistance mechanism. Good inducibility of beta-lactamases and absent resistance transfer argue for chromosomal localisation of the resistance. Because of the development of resistance, severe infections caused by P. aeruginosa should not be treated by ceftazidime alone. In order early to discover the development of resistance, microbiological samples should be taken periodically and examined for their sensitivity.

Ceftazidime↗
PubMed1983

Ceftazidime in severe infections: a Swiss multicentre study.

A total of 105 patients (mean age 57, range 15 to 90) with serious infections were treated with intravenous ceftazidime, usually 2 g 8-hourly. Most patients had complicating factors such as major surgery, cancer, chronic obstructive lung disease, catheters or anatomical abnormalities. Eighty-seven infectious episodes in 77 patients could be assessed for efficacy. Bacteraemia was diagnosed in 26% of these episodes. Seventy-five per cent of infections were due to Gram-negative bacteria, Pseudomonas aeruginosa being the most frequent. The major sites of infections were the lower respiratory tract (30), the urinary tract (28), the soft tissues (9), the biliary tract (4), bones (4) and the ears (4). Overall, 67% of the patients were cured, 20% improved, 7% relapsed and 6% failed to respond. Among the 27 infections due to Ps aeruginosa, only two failures (in the same patient) and four relapses were recorded. However, in the two failures and in three other cases with persistent Ps. aeruginosa colonisation, the organism had become resistant to ceftazidime. Three failures were recorded in the seven Staphylococcus aureus infections included in this study. Superinfection occurred in four patients. Adverse events included rash (6), Clostridium difficile toxin-induced diarrhoea (3), transaminase elevation (3), weakly positive Coombs test (10). Ceftazidime appears to be safe and effective for the treatment of severe Gram-negative infections, including those caused by Ps. aeruginosa.

Adolescent↗
PubMed1982

[Acquired immunologic deficiency syndrome, opportunistic infections and homosexuality. Presentation of 3 cases studied in Switzerland].

Three cases of multiple opportunistic infections in previously healthy homosexual males were observed in 3 different University Hospitals in Switzerland. Two of the patients died. Infections were multiple, with P. carinii pneumonia (3 cases), chronic mucocutaneous ulcers probably due to Herpes simplex virus (2 cases), mucosal candidiasis (2 cases) and disseminated infections due to cytomegalovirus (1 case) and Mycobacterium avium (1 case). All patients had depressed cellular immunity with marked lymphopenia. These cases are similar to those recently observed in the United States, but two of the patients had never been to the USA although both had vacationed in Haïti where the syndrome has been described. These patients illustrate that this new syndrome should also be suspected outside the USA when a patient (especially a male homosexual) presents with persistent fever of unknown origin and develops opportunistic infections without obvious underlying disease.

Adult↗
PubMed1982

[GRID syndrome].

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Cytomegalovirus↗