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Biomedical subjects

M Buck

Publications and source records attributed to M Buck.

At least 145 records · Page 8Linked to original sources
PubMed1987

Atypical responses to morphine in mice: a possible relationship to anorexia nervosa?

According to our previously proposed auto-addiction hypothesis of chronic anorexia nervosa, patients become addicted to an initial period of dieting through endogenous opioid mediated mechanisms. Morphine causes hyperactivity and anorexia in the mouse, symptoms of anorexia nervosa but responses opposite to those of most species including rats and normal human subjects. This suggests that the atypical opioid systems in the mouse may resemble those of the chronic anorexia nervosa patient in contrast to those of most species including the normal human. Characterization of this atypical opioid system may be useful in understanding the pathophysiology of anorexia nervosa.

Animals↗
PubMed1987

Pericardial effusion in women with breast cancer.

Ninety patients with a history of breast cancer and pericardial effusion detected on echocardiography were identified and divided on a clinical basis into three groups. Group 1 consisted of 20 patients who had progressive metastatic breast cancer and echocardiography performed on a routine basis as a part of a clinical trial involving 38 patients. All 20 had small unexpected effusions, and only one patient developed symptomatic malignant pericardial disease late in her clinical course. Group 2 consisted of 32 patients who were without evidence of metastatic disease at the time of positive echocardiography and the etiology was considered benign in all patients. Six patients required pericardiectomy, five for severe radiation induced pericarditis and one for amyloid. No patient developed proven or suspected malignant pericardial disease. Group 3 comprised 38 patients who had known metastatic disease outside the pericardium at the time of positive echocardiography. Nineteen patients in Group 3 had histologically proven malignant involvement during life or at autopsy, and five more had suspected malignant pericardial disease. Ten patients initially were treated with pericardiectomy and 28 patients were managed with systemic therapy alone (24 patients) or with pericardiocentesis (four patients). Among the 12 patients with malignant effusion treated without surgery, proven local progression of pericardial disease occurred in six, with sudden death in two of those patients. No patient treated initially with surgery suffered progression of her pericardial disease. It was concluded that: small, clinically unsuspected pericardial effusions appear to be relatively common in women with metastatic breast cancer; no patient with clinical pericardial disease confirmed on echocardiography and no evidence of metastatic breast cancer developed malignant pericardial involvement; 50% of patients with known metastatic disease and a clinically apparent pericardial effusion had malignant pericardial disease; and nonsurgical therapy in patients with histologically proven or clinically suspected malignant pericardial effusion was associated with a high incidence of progressive pericardial disease.

Adult↗
PubMed1987

Frameshifts close to the Klebsiella pneumoniae nifH promoter prevent multicopy inhibition by hybrid nifH plasmids.

Certain multicopy plasmids bearing promoter sequences of nitrogen fixation (nif) genes inhibit expression of chromosomal genes in Nif+ Klebsiella pneumoniae, hence leading to a Nif- phenotype. This 'multicopy inhibition' has been attributed to the titration of the nif-specific activator protein NifA by the plasmid-borne promoter sequences. We now report that multicopy inhibition by nifH translational fusions is sensitive to frameshifts close to the nifH promoter. Transcriptional nifH fusion plasmids in which translation terminated near the nifH promoter were transcriptionally active and showed multicopy inhibition; introduction of a transcription terminator after the nifH coding sequence in these plasmids prevented their multicopy inhibition. Therefore it seems likely that premature termination of transcription prevents multicopy inhibition by the nifH promoter.

Cloning, Molecular↗
PubMed1987

Positional requirements for the function of nif-specific upstream activator sequences.

The upstream activator sequence (UAS) found in Klebsiella pneumoniae nif promoters and required for the activation of transcription by nifA, is absent from the nifF-nifL intergenic region, but is present downstream from the nifLA transcription start at +59. To determine whether nif upstream activator sequences can function in a 3' position, the nifH UAS was cloned downstream from the NifH transcription start, but no activation of transcription by nifA dependent upon the UAS in its 3' location could be detected. A mild repressive effect was detectable when the nifH UAS was placed downstream of the nifH promoter, but not when the cat promoter was substituted for the nifLA promoter upstream from the motif at +59 described above. However, deletion analysis showed that the UAS motif located downstream of the nifLA promoter has a role in transcription from the nifF promoter, although it is situated at position -263 with respect to the nifF transcription start, about 100 bp further upstream than previously described occurrences of the activator sequence.

Genes, Bacterial↗
PubMed1987

Transcriptional activation of the Klebsiella pneumoniae nitrogenase promoter may involve DNA loop formation.

Transcriptional activation of nitrogen fixation genes by NifA in Klebsiella pneumoniae requires an upstream NifA binding site. We now report that the introduction of half turns of the DNA helix into the DNA separating the upstream NifA binding site from the downstream promoter element of the nifH promoter decreases NifA-mediated activation to a greater extent than does the introduction of full helical turns. Reducing the spacing between the upstream and downstream elements of the nifH promoter also results in a promoter down phenotype. Introduction of a tight protein-binding site, the lac operator, between the upstream and downstream promoter elements did not render activation of the nifH promoter sensitive to occupancy of this site by the lac repressor. These findings indicate that NifA-mediated activation of transcription requires that NifA is bound upstream, and to the correct face of the DNA helix, in order to interact with downstream transcription factors. This implies that the interaction is brought about by the formation of a DNA loop between upstream and downstream promoter elements rather than by NifA sliding downstream.

DNA Restriction Enzymes↗
PubMed1987

Relationship of the ventilatory response to cotton bract extract and the cells and proteins of the lung.

Many healthy subjects who have had no exposure to cotton textile dusts will experience significant reductions in expired flow rate following an inhalational challenge with an aqueous extract of cotton bracts (CBE). Differences noted among individuals in the magnitude of the bronchial response to a standardized preparation of CBE suggest variable airway reactivity. The mechanism of this response and the reasons for its variability among these naive subjects are unknown. We have studied this problem by performing bronchoalveolar lavage on 13 volunteer subjects with no history of textile dust exposure. Two to three months later, a bronchial provocation with aqueous CBE was performed by an investigator blinded to the lavage results. Subjects with greater than 20 percent drop in flow rate at 40 percent of vital capacity during a partial forced expiration (MEF 40 percent [P]) following CBE had a reduction in total recoverable alveolar macrophages, with a resultant increase in the percentage of recoverable lymphocytes. The magnitude of response (MEF 40 percent [P]) correlated directly with the measured lymphocyte percentage (r = 0.69 p less than 0.01) and inversely with the total numbers of recovered cells.

Adult↗
PubMed1987

Treatment of metastatic islet cell carcinoma with a somatostatin analogue (SMS 201-995).

We used an octapeptide analogue of somatostatin, SMS 201-995, in dosages ranging from 150 to 450 micrograms/d administered subcutaneously in three daily doses for 1 to 16 months, to treat 22 patients with advanced malignant islet cell carcinomas. Of the 22 patients, there were 9 with gastrinomas; 3 with glucagonomas; 4 with insulinomas; 1 with ectopic production of parathyroid hormone; and 3 with mixed syndromes. The only biochemical marker in 1 patient was pancreatic polypeptide, and 1 patient had no demonstrable peptide production from the tumor. In 14 patients, dramatic decreases in the levels of circulating peptides (insulin, vasoactive intestinal polypeptide, gastrin, and glucagon) have been accompanied by major alleviations of symptoms. Steatorrhea appears to be the most significant toxicity. This analogue of somatostatin may be appropriate for use as early therapy in patients who have symptoms from syndromes related to islet cell carcinomas but in whom there is no immediate threat from tumor progression.

Adenoma, Islet Cell↗
PubMed1986

Deletion loop mutagenesis of the nifL promoter from Klebsiella pneumoniae: role of the -26 to -12 region in promoter function.

Nine single C-to-T transitions were introduced into the -26 to -12 region of the Klebsiella pneumoniae nifL promoter by bisulphite mutagenesis of M13 heteroduplexes containing a 15 nucleotide single-stranded loop. Mutant promoter fragments were inserted into translational lac fusion vectors to utilise beta-galactosidase activity as a measure of promoter efficiency. Mutations in invariant nucleotides found in the consensus sequence for nif promoters gave a strong 'down' promoter phenotype with respect to transcriptional activation. Mutations in semi-conserved residues had a much weaker down phenotype, whereas a mutation which increased homology to the consensus sequence enhanced promoter strength. One mutant showed increased activation by ntrC and decreased activation by nifA.

Bacterial Proteins↗
PubMed1986

Directed intravascular precipitation of bisantrene for pelvic malignant lesions: preclinical studies.

Bisantrene, a clinically active anticancer drug with limited solubility at physiologic pH, was delivered by selective injection into the internal iliac artery of male calves. The percutaneous transfemoral angiographic techniques used in the calves were identical to those used in adult human patients. Directed intravascular precipitation of bisantrene at the maximal tolerable clinical dose for intravenous administration (260 mg/m2) caused severe tissue damage in 5 of 10 animals that received these intra-arterial injections. (One calf in this study group died of unknown causes 10 days after the drug infusion). A reduced intra-arterial dose (50 mg/m2) was used in seven calves, and no local tissue damage was evident on gross or microscopic examination. Nevertheless, resultant concentrations of bisantrene deposited in the ipsilateral bladder wall were 10- to 100-fold those concentrations found after intravenous administration of a dose 5 times higher. These animal toxicology and pharmacology data support initiation of a phase I clinical trial of directed intravascular precipitation of bisantrene in humans. This clinical trial will be developed for patients with advanced refractory cancers of the anatomic true pelvis, such as those originating in the urinary bladder, prostate, rectum, and uterine cervix.

Angiography↗
PubMed1986

Iron regulated outer membrane proteins of Escherichia coli: variations in expression due to the chelator used to restrict the availability of iron.

Iron restriction was induced in Escherichia coli O 111, E. coli O 164 and E. coli C by growing the organisms in trypticase soy broth containing ovotransferrin, desferal, EDDA (ethylenediamine-dihydroxyphenylacetic acid) or alpha,alpha'-dipyridyl. There were marked qualitative and quantitative differences in the iron regulated outer membrane proteins expressed in the presence of the various iron chelators. Differences in the kinetics of growth were also noted. E. coli C was devoid of a ferric enterobactin iron uptake system.

2,2'-Dipyridyl↗
PubMed1986

Deletion analysis of the Klebsiella pneumoniae nitrogenase promoter: importance of spacing between conserved sequences around positions -12 and -24 for activation by the nifA and ntrC (glnG) products.

The nitrogen fixation promoters of Klebsiella pneumoniae are atypical procaryotic promoters lacking the usual -10 and -35 elements, requiring instead conserved sequences around -12 and -24 for transcriptional activation. By constructing a set of five deletions between the -12 and -24 elements in the nifH promoter, the spacing between the conserved GC and GG motifs at -12 and -24, respectively, has been reduced from the wild-type 10 bases to 9, 8, 6, 5, and 4 bases. The deletion of a single nonconserved nucleotide was sufficient to eliminate transcriptional activation by either nifA or ntrC (glnG). All deletions relieved the multicopy inhibition of chromosomal nif expression normally shown by the nifH promoter. These results demonstrate a stringent requirement for the 10-base spacing found in ntr-activated promoters. In addition, specific sequences around the invariant GG at -24 were shown to be necessary for activation by either nifA or ntrC, with a minimal requirement for nucleotides through to position -27 for this activation.

Bacterial Proteins↗
PubMed1985

Site-directed mutagenesis of the Klebsiella pneumoniae nifL and nifH promoters and in vivo analysis of promoter activity.

The role of conserved nucleotides in nitrogen-fixation promoter function has been examined using both oligonucleotide and chemical mutagenesis to introduce base changes in the Klebsiella pneumoniae nifL and nifH promoters. Among ten mutations analysed, including six spontaneous mutations, base changes at -12, -13, -14, and -26, located in previously identified conserved sequences, perturbed the activity of the promoters, demonstrating that these sequences are required for transcription. Not all base changes produced similar strong promoter down phenotypes when the nifL and nifH promoters were compared: activation of the nifH promoter by the nifA gene product was less sensitive to base changes in conserved nucleotides than was activation of the equivalently altered nifL promoter by the nifA or ntrC products. We have found that the nifH promoter can be weakly activated by the ntrC product; this activation shows the same down response to base changes seen with ntrC activation of the nifL promoter. We present evidence that the efficient activation of the nifH promoter by nifA (but not ntrC) can be attributed to specific upstream sequences present in the nifH promoter.

Anti-Bacterial Agents↗