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Biomedical subjects

J Peters

Publications and source records attributed to J Peters.

At least 415 records · Page 23Linked to original sources
PubMed1992

Sympathetic blockade by thoracic epidural anaesthesia suppresses renin release in response to hypotension, but activates the vasopressin system.

To determine whether or not the blockade of sympathetic efferents by epidural anaesthesia blunts the normal increase in plasma renin activity in response to hypotension, we assessed the effect of hypotensive thoracic epidural anaesthesia with widespread sympathetic blockade on plasma renin activity. Plasma renin activity and vasopressin concentration, arterial pressure, and serum osmolality were measured in 17 patients before and after random epidural injection of either 6.7 ml of 0.75% bupivacaine (n = 7) or the same volume of saline (n = 10). As an indicator for efferent sympathetic drive, skin temperatures were measured on the hand and foot. A decrease in mean arterial pressure by more than 25% of baseline values was prospectively defined as hypotension requiring intervention. Thoracic epidural anaesthesia induced a decrease in mean arterial pressure of 24 mmHg (range 16-47) from 101 mmHg to 77 mmHg (P less than 0.001 vs. saline). Despite hypotension, plasma renin activity remained unchanged [medians 2.9 ng ml-1 h-1 (0-9.1) vs. 3.4 ng ml-1 h-1 (0-13.8)]. In contrast, vasopressin concentrations increased from a median of 3.8 pg ml-1 (0.5-8.2) to 6.0 pg ml-1 (4.2-33.6; P = 0.025). Both hand and foot skin temperatures increased significantly indicating widespread extent of sympathetic blockade. Serum osmolality did not change. With epidural saline, variables remained unchanged. Thus, during hypotension induced by widespread attenuation of efferent sympathetic drive through thoracic epidural anaesthesia, renin activity did not change, whilst vasopressin concentrations increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Epidural↗
PubMed1991

Adenosine deaminase, Ada, is in mouse chromosome 2H3, and is not allelic with wasted, wst.

The adenosine deaminase locus (Ada) in the mouse has been localized by in situ hybridization to band 2H3. Linkage analysis of backcross data has shown that Ada is 13.8 +/- 2.7 cM from the coat texture mutant, ragged, Ra. From the results of earlier work (Abbott, C. M., et al., Proc. Natl. Acad. Sci. USA 83:693, 1986), it had been suggested that wst was a low-activity allele of Ada, but this cannot be so because Ada and wst have been found to be nonallelic.

Adenosine Deaminase↗
PubMed1991

The molecular characterization of an A:T to G:C transition in the Hbb-b1 gene of the murine homologue of hemoglobin Rainier.

An N-ethyl-N-nitrosourea (ENU)-induced mutation in the Hbb-b1 gene of the mouse hemoglobin-beta complex (Hbb) has been shown to result in a high-oxygen affinity hemoglobin, homologous with hemoglobin Rainier in man (Peters, J., et al., Genetics 110:709, 1985). Substitution of beta 145 tyrosine by cysteine had occurred in both human and mouse forms, probably as the result of a point mutation. Provided that sufficient sequence information is available, point mutations can be directly and rapidly analyzed by allele-specific amplification (ASA), as this technique is sensitive enough to detect single nucleotide differences. We report the use of ASA to detect and characterize the mutation in the murine beta-globin gene, Hbb-b1d-m1, and find that the codon for beta 145 tyrosine (TAC) has been replaced by the codon for cysteine (TGC). Therefore, ENU induced an A:T----G:C transition.

Alleles↗
PubMed1991

Electrophoretic variation in multiple recessive tester, T, stock mice.

The multiple recessive tester stock, homozygous for seven recessive visible markers, has been used since the 1950s in the specific locus test of mutagenicity in the mouse. The stock was developed by W.L. Russell in Oak Ridge, sent to the MRC Radiobiology Unit (Harwell) in 1953 and then passed to Research Triangle Institute (RTI) in 1988. Stocks are maintained by random mating in all three centres. and in addition stocks that have been selected for homozygosity at certain enzyme and protein markers are kept at both Harwell and RTI. The extent of electrophoretic variation was investigated in the random bred tester stocks at Harwell in 1981 and 1990, and in both random bred and fixed tester stocks at RTI in 1990. Altogether 44 loci were scored and eight of these (Acy-1, Es-3, Gpi-1, Hba, Hbb, Idh-1, Mod-1 and Pgd) have been polymorphic in one or more colonies at various times. Three loci (Es-3, Hbb and Mod-1) had low levels of polymorphism in 1981 and had become monomorphic by 1990. Despite this slight loss of variation, overall the tester stocks show considerable variability. The proportion of polymorphic loci and mean heterozygosity is of the same order of magnitude as island populations of wild mice or other isolated random bred laboratory populations. Contamination of tester stocks with other stocks can be ruled out, and thus tester stocks can be considered to be characteristic island populations. The retention of an appreciable amount of genetic variability in tester stocks is of practical importance in designing new mutation tests involving these mice. When using these stocks, care must be taken to ensure that they are homozygous for the loci under test.

Alleles↗
PubMed1991

CSF chromogranin A-like immunoreactivity in schizophrenia. Assessment of clinical and biochemical relationships.

Chromogranin A (CgA) is co-released with catecholamines and peptides and has a wide distribution in the brain. Chromogranin A provides a measure of tonic arousal. CSF CgA-like immunoreactivity (CgA-LI) was studied in 42 drug-free male schizophrenic patients. 33 of these patients were first studied during chronic haloperidol maintenance treatment. Withdrawal from haloperidol maintenance treatment was associated with a significant increase in CSF CgA-LI, particularly in the patients who did not relapse. Contrary to expectation CSF CgA-LI was higher in drug-free patients who slept longer the night before the lumbar puncture. Significant relationships were observed between CSF CgA-LI and CSF homovanillic acid, acetylcholinesterase, neuropeptide Y-LI and 5-hydroxy-indole acetic acid, but not with CSF norepinephrine or 3-methoxy-4-hydroxyphenylglycol. Ventricular brain ratios correlated negatively with CSF CgA-LI levels.

Adult↗
PubMed1991

Successful prophylaxis for fungal peritonitis in patients on continuous ambulatory peritoneal dialysis: six years' experience.

Fungal peritonitis as a serious complication of continuous ambulatory peritoneal dialysis (CAPD) is often associated with severe morbidity, CAPD "drop-out" and, occasionally, death. Most episodes of fungal peritonitis occur during or after a period of antibiotic treatment of various bacterial infections, usually bacterial peritonitis. From April 1979 to December 1982 (period I), 10 episodes of fungal peritonitis occurred during 415 patient-months, ie, 10.5% of all peritonitis episodes recorded in our CAPD program. After the introduction of oral prophylaxis with 3 x 500,000 IU [corrected] nystatin during every course of antibiotic treatment, only four episodes of fungal peritonitis occurred during 2,102 patient-months, ie, 3.1% of all peritonitis episodes from January 1983 to March 1989 (period II). This difference between the first and second periods is significant (P less than 0.05). Moreover, none of the four patients who contracted fungal peritonitis in the second period received nystatin prophylaxis. Thus, the simple measure of oral prophylaxis using this nonabsorbable antifungal agent in every case of an antibiotic treatment largely eliminates the risk of fungal peritonitis in patients on CAPD.

Administration, Oral↗
PubMed1991

Surface Charge-Mediated Effects of Mg on K Flux across the Chloroplast Envelope Are Associated with Regulation of Stromal pH and Photosynthesis.

Studies of Spinacia oleracea L. were undertaken to characterize further how Mg(2+) external to the isolated intact chloroplast interacts with stromal K(+), pH, and photosynthetic capacity. Data presented in this report were consistent with the previously developed hypothesis that millimolar levels of external, unchelated Mg(2+) result in lower stromal K(+), which somehow is linked to stromal acidification. Stromal acidification directly results in photosynthetic inhibition. These effects were attributed to Mg(2+) interaction (binding) to negative surface charges on the chloroplast envelope. Chloroplast envelope-bound Mg(2+) was found to decrease the envelope membrane potential (inside negative) of the illuminated chloroplast by 10 millivolts. It was concluded that Mg(2+) effects on photosynthesis were likely not mediated by this effect on membrane potential. Further experiments indicated that envelope-bound Mg(2+) caused lower stromal K(+) by restricting the rate of K(+) influx; Mg(2+) did not affect K(+) efflux from the stroma. Mg(2+) restriction of K(+) influx appeared consistent with the typical effects imposed on monovalent cation channels by polyvalent cations that bind to negatively charged sites on a membrane surface near the outer pore of the channel. It was hypothesized that this interaction of Mg(2+) with the chloroplast envelope likely mediated external Mg(2+) effects on chloroplast metabolism.

Journal Article↗
PubMed1991

Glial ion transport and volume control.

K(+)-induced glial swelling results from an intricate interaction of transport and diffusion processes and metabolic stimulation, with many open questions remaining. Our concept of the major mechanisms involved can be summarized as follows: high extracellular K+ causes a burst-like stimulation of Na+/K+ ATPase and, hence, increases the metabolic demands. Lactate is produced; the cell is slightly acidified. To maintain a normal intracellular pH, the Na+/K+ antiporter extrudes protons and supplies Na+ for further Na+/K+ exchange. In addition, K+ ions enter the cell via membrane channels or furosemide-inhibitable transport. K+, Cl-, and lactate- ions accumulate as the osmotic basis for cell swelling. Later, cell volume normalizes slowly, a process involving lactate export and other, so far unidentified mechanisms. Taken together, the temporary swelling of glia at high K+ concentrations is the result of a homeostatic function, for the maintenance of a constant extracellular potassium concentration. Ion control ranges over volume control. In pathophysiologic states the loss of cell volume regulation may become a clinical problem, if cerebral swelling leads to an increase in intracranial pressure. It should be kept in mind, however, that elevation of the extracellular K+ concentration is not the only cause of glial swelling. Tissue acidosis, the release of neurotransmitters, especially glutamate, or free fatty acids are other mediator mechanisms initiating the swelling of glial elements. Only under controlled in vitro conditions can the individual significance of these factors be evaluated on a quantitative basis. Therapeutic approaches should be selected very carefully in order to maintain homeostatic mechanisms that are of utmost importance, especially after an insult to the brain.

Biological Transport↗
PubMed1991

Nucleotide and derived amino acid sequences of the major porin of Comamonas acidovorans and comparison of porin primary structures.

The DNA sequence of the gene which codes for the major outer membrane porin (Omp32) of Comamonas acidovorans has been determined. The structural gene encodes a precursor consisting of 351 amino acid residues with a signal peptide of 19 amino acid residues. Comparisons with amino acid sequences of outer membrane proteins and porins from several other members of the class Proteobacteria and of the Chlamydia trachomatis porin and the Neurospora crassa mitochondrial porin revealed a motif of eight regions of local homology. The results of this analysis are discussed with regard to common structural features of porins.

Amino Acid Sequence↗
PubMed1991

Detection of rubella virus gene sequences by enzymatic amplification and direct sequencing of amplified DNA.

We developed a rapid and sensitive polymerase chain reaction (PCR) assay for detecting and identifying rubella virus (RV). A segment of the RV gene which encodes the E1 membrane glycoprotein of RV was selected as a target for PCR amplification. Single-stranded viral RNA, extracted from infected cells or released from virions, was used as a template for reverse transcription followed by PCR amplification with two different sets of primer pairs, one nested within the other. The amplified E1 gene sequences were detected in ethidium bromide-stained agarose minigels, and their identities were verified by restriction enzyme digestion and hybridization to a probe directed at a site within the PCR target. Single-stranded DNA generated by asymmetric amplification of the target was directly sequenced by using fluorescent dideoxy-terminators and an automated procedure in order to confirm the target sequence. This PCR assay provides a rapid confirmatory test for the detection of RV by cell culture and appears to have considerable potential for the direct detection of RV in clinical specimens. The strategy used in the development of this PCR assay should be useful for developing other diagnostic PCR assays for viruses.

Animals↗
PubMed1991

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation.

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

Animals↗
PubMed1991

Isochronic mapping: a preliminary report of a new technique.

A new technique which we have named 'isochronic mapping' is described. The conventional technique of plotting isopotential maps shows little or no contrast for far-field potentials such as the auditory brainstem response (ABR). However, by modifications to the mapping software, the latency values of a peak can be plotted and lines of equal time or isochronic maps can be produced. Data from a normal subject has been obtained for both the compound and derived ABRs and are described in detail. The data are clear but the time delays between earliest and latest projections of a peak are hard to interpret. For monaural click stimulation, wave JV of the ABR projects first to the contralateral side of the head then moves towards the stimulated ear arriving some 0.3 ms later. Possible interpretations of this finding are discussed but further experimentation is needed to develop our understanding of these data.

Acoustic Stimulation↗
PubMed1991

[Paraplegia following removal of an epidural catheter].

Acute paraplegia caused by an epidural hematoma developed in a patient following the removal of an epidural catheter. This catheter had been used for 3 days for postoperative pain relief with no apparent complications. Heparin (10,000 units/day) had been infused for thrombosis prophylaxis and was associated with a normal activated partial thromboplastin time (aPTT) for the first two postoperative days. However, test results from blood drawn prior to catheter removal revealed, in retrospect, an unexpected prolongation of the aPTT (75 s) and PT (56%, Quick's method). An epidural hematoma extending from T12 to L4 was evacuated during emergency laminectomy and neurologic deficits resolved completely over the next days. Thus, the removal of an epidural catheter has the potential for inducing formation of an epidural hematoma. Accordingly, it may be safest to leave epidural catheters in place if test results demonstrate a bleeding diathesis or if a potential for bleeding is suspected on clinical grounds.

Analgesia, Epidural↗