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Biomedical subjects

C Greiner

Publications and source records attributed to C Greiner.

At least 19 recordsLinked to original sources
PubMed1992

[Acute necrotizing retinitis with amotio retinae. Surgical and medicamentous antiviral therapy].

This report pertains to the case of a 25-year-old patient suffering from acute necrotizing retinitis (ANR syndrome). Initially, one eye revealed clinical signs of diffuse chorioretinitis accompanied by perivasculitis and heavy keratic precipitates, papillitis, and vitreous infiltrates. After initial improvement under antiphlogistic therapy, however, necrotizing retinitis developed, associated with peripapillar hemorrhages, multiple peripheral retinal holes and eventually complete retinal detachment. The subsequently performed retinal detachment surgery, completed with vitrectomy, cerclage and silicone oil tamponade, was successful. At the same time, the patient was put on systemic therapy based on acyclovir. In the literature, similar developments are usually related to HSV and HZV infections. Although in our case a virological diagnostic test did not reveal the presence of any virus, the characteristic symptoms of the ANR syndrome completely disappeared under the above-mentioned therapy. Visual acuity, previously consisting only in light perception, improved to 0.4.

Acyclovir↗
PubMed1991

[Liver abscess caused by Aeromonas hydrophila].

Because of the rare incidence of liver abscess in childhood and of extremely rare observed Aeromonas hydrophila as pathogen of such a disease we report on a 14 7/12 year old girl with a liver abscess. For the last 4 years she had to be enrolled in chronic hemodialysis. The treatment comprised opening of the abscess cavity and drainage, and antibiotic therapy with cefotiam. We were unable to isolate Aeromonas hydrophila in the environment of the hemodialysis center. Some aspects of clinical importance of liver abscess in childhood and of Aeromonas spp. as pathogens in human infections are discussed.

Adolescent↗
PubMed1989

[Treatment of otherwise incurable tumor diseases in childhood using whole-body hyperthermia and chemotherapy].

Conventional methods of treatment having failed in 17 children (aged 9/12 to 16 5/12 years) with incurable solid malignant tumours underwent whole-body hyperthermia (41.8-42.0 degrees C, for 2-3 h), hyperglycaemia (20-25 mmol/l) and polychemotherapy. Five children had neuroblastoma (stage 4), three Wilm's tumour (stage 4 or 5, unfavourable histology), five skeletal sarcoma with metastases, three inoperable malignant liver tumour, and one brainstem tumour of unknown histology. Whole-body hyperthermia was induced by extracorporeal blood warming in an haemodialysis apparatus under neuroleptic analgesia, thermistors measuring the temperature in the oesophagus, rectum, trachea and skin. There were on average four treatment sessions (between one and ten, total 58), a week apart. The result could be assessed in 12 children: one persisting complete remission (19 months-metastasising renal rhabdoid tumour), eight partial or incomplete remissions, and three nonresponders (osteogenic sarcoma; Ewing sarcoma; brainstem tumour). If the risk can be satisfactorily judged the method is useful and of bearable toxicity. The results point to a high antitumour effectiveness of combined hyperthermia and chemotherapy.

Adolescent↗
PubMed1989

Summary of complementation groups of UV-sensitive CHO cell mutants isolated by large-scale screening.

A summary is given for the lineage and complementation group assignments of 153 UV-sensitive mutants of the CHO AA8 cell line. The distribution of mutants among six complementation groups was highly non-random, with the great majority of the isolates belonging to groups 1 and 2. This asymmetry is consistent with the known hemizygosity of these two linked loci in CHO cells. The relative numbers of mutants induced in group 2 was found to depend greatly on the type of mutagen used. Mutagenesis with UV radiation, ethyl methanesulfonate (EMS), N-methyl-N'-nitro-N-nitrosoguanidine and 7-bromomethylbenz[a]anthracene produced high frequencies of group 2 mutants. In contrast, ICR170 and ICR191, which are thought to produce mostly frameshift mutations, yielded very few mutants in group 2. These results are of particular importance in light of the recent finding that the human ERCC2 gene, which corrects group 2 mutants, has very strong homology with the yeast gene RAD3. RAD3 is an essential gene for viability in yeast, and the low recovery of group 2 mutants using the frameshift agents strongly suggests that frameshift mutations tend to be lethal in the hamster ERCC2 locus. Several mutagen-sensitive double mutants were isolated in two-step selections from EMS-, mitomycin C- or UV-sensitive parental cells, including the line UVU1, the first mammalian line with two mutations that affect UV sensitivity. The first mutation inactivated excision repair, and the second mutation appears to have affected some other recovery process. UVU1 should be useful for studying recovery processes that are separate from nucleotide excision repair.

Animals↗
PubMed1988

Guanine nucleotide-independent inhibition of adenylate cyclase by a stimulatory hormone.

Stimulation of basal adenylate cyclase activity in membranes of neuroblastoma x glioma hybrid cells by prostaglandin E1 (PGE1) is half-maximal and maximal (about 8-fold) at 0.1 and 10 microM respectively. This hormonal effect requires GTP, being maximally effective at 10 microM. However, at the same concentrations that stimulate adenylate cyclase in the presence of GTP, PGE1 inhibited basal adenylate cyclase activity when studied in the absence of GTP, by maximally 60%. A similar dual action of PGE1 was observed with the forskolin-stimulated adenylate cyclase, although the potency of PGE1 in both stimulating and inhibiting adenylate cyclase was increased and the extent of stimulation and inhibition of the enzyme by PGE1 was decreased by the presence of forskolin. The inhibition of forskolin-stimulated adenylate cyclase by PGE1 occurred without apparent lag phase and was reversed by GTP and its analogue guanosine 5'-[gamma-thio]triphosphate at low concentrations. Treatment of neuroblastoma x glioma hybrid cells or membranes with agents known to eliminate the function of the inhibitory GTP-binding protein were without effect on PGE1-induced inhibition of adenylate cyclase. The data suggest that stimulatory hormone agonist, apparently by activating one receptor type, can cause both stimulation and inhibition of adenylate cyclase, and that the final result depends only on the activity state of the stimulatory GTP-binding protein, Gs. Possible mechanisms responsible for the observed adenylate cyclase inhibition by the stimulatory hormone PGE1 are discussed.

Adenylate Cyclase Toxin↗
PubMed1988

Diagnostic significance of flow cytometric DNA analysis applied for the detection of cancer cells in bronchial washing fluid.

Since both DNA aneuploidy and increased proliferative activity are important characteristics of malignant neoplasms, flow cytometric (FCM) analysis was used to examine the cell content in bronchial washing samples obtained via fiberoptic bronchoscopy from 73 patients. The results were compared with the results of histology and conventional cytology. The patients included 30 with bronchial carcinomas, 12 with bronchopneumonia and 31 with no evidence of lung disease. Of the 30 patients with histologically confirmed lung cancers, 25 showed either aneuploid stem lines (19 cases) or high levels of proliferation (6 cases) as determined by analysis of cell-cycle stages. The same rate of cancer cell detection was obtained by cytology. In the 43 cases with neither histologic nor clinical evidence of malignancy, FCM data yielded 5 false-positive results, as compared to 4 erroneous suspicions of cancer by cytology. From these data, it is concluded that FCM measurements of both DNA ploidy and proliferative activity may complement conventional cytology in the recognition of bronchial carcinomas.

Bronchitis↗
PubMed1986

Bradykinin stimulates GTP hydrolysis in NG108-15 membranes by a high-affinity, pertussis toxin-insensitive GTPase.

In membranes of neuroblastoma x glioma hybrid (NG108-15) cells, bradykinin (EC50 approximately equal to 5 nM) stimulates GTP hydrolysis by a high-affinity GTPase (Km approximately equal to 0.2 microM). The octapeptide, des-Arg9-bradykinin, was inactive. Stimulation of GTP hydrolysis by bradykinin and an opioid agonist was partially additive. Treatment of NG108-15 cells with pertussis toxin, which inactivates Ni, eliminated GTPase stimulation by the opioid agonist but not by bradykinin. The data suggest that bradykinin activates in NG108-15 membranes a guanine nucleotide-binding protein which is not sensitive to pertussis toxin and which may be involved in bradykinin-induced stimulation of phosphoinositide metabolism in these cells.

Bradykinin↗