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Biomedical subjects

J Goodson

Publications and source records attributed to J Goodson.

At least 19 recordsLinked to original sources
PubMed1998

Long-term changes in compliance with clinical guidelines through computer-based reminders.

We evaluate the effectiveness of computer-based reminders in improving compliance with preventive medicine screening guidelines and examine the long-term impact of these reminders. Physicians in an ambulatory care practice were given a summary health maintenance report of preventive screening items at each scheduled patient visit. The electronic medical record (COSTAR) in use in this practice was programmed to integrate 13 clinical guidelines into the routine flow of care. Mean performance of 10 out of 13 health maintenance measures improved in the year following introduction of the integrated guideline report (p less than .001 by chi-square test for 8 items, p less than .01 for 2 items). Five years after the report was introduced, improvement in mean performance persisted for 7 measures (p less than .001 by chi-square test), compliance improved for one additional measure (p less than .001), and improvement disappeared for three measures that had shown improvement in the first year of the intervention.

Evaluation Studies as Topic↗
PubMed1996

Biological predictors of 1-year outcome in schizophrenia in males and females.

This paper describes a prospective study designed to ascertain the predictive value of biological factors associated with schizophrenia in males and females. In a sample of 59 medication-free schizophrenic inpatients (41 males; 18 females), we assessed the correlation of four factors--rapid eye movement (REM) sleep latency, delta (slow-wave) sleep, dexamethasone suppression test (DST) cortisol levels, and ventricle-brain ratio (VBR)--with several dimensions of outcome at 1-year post-discharge. In the total sample, shorter REM latency was associated with poor outcome on all dimensions measured: rehospitalization, employment, social activity, symptomatology, and global functioning. However, none of the other biological factors were associated with any measure of outcome. The predictive value of REM latency appeared to be gender-specific; in general, the relationships between reduced REM latency and poor outcome were consistently noted in females, but were not significant in males. These results suggest that a common, possibly gender-related, pathophysiological mechanism might underlie both abnormal REM latency and poor outcome. The findings underscore the importance of considering gender differences in studies of schizophrenia.

Electroencephalography↗
PubMed1992

Electroencephalographic sleep abnormalities in schizophrenia. Relationship to positive/negative symptoms and prior neuroleptic treatment.

Polysomnographic abnormalities in schizophrenia are not well characterized and their associations with schizophrenic symptomatology have not been adequately assessed. To address these issues, we recorded electroencephalographic sleep in 20 drug-naive schizophrenics, 20 drug-free but previously medicated schizophrenics, and 15 normal controls. Drug-naive and previously medicated patients had significantly greater impairment of sleep continuity and shorter rapid eye movement latency when compared with controls. In the previously medicated group, findings were significantly influenced by duration of drug-free status. Rapid eye movement latency was inversely correlated with the severity of negative symptoms (r = -.52) but was unrelated to depressive symptoms. Slow-wave sleep did not differ between schizophrenic patients and normal controls and was unrelated to any clinical parameter. Mechanisms underlying the observed associations between rapid eye movement sleep abnormalities and negative symptoms in the acute phase of schizophrenic illness need to be explored.

Adult↗
PubMed1992

Effect of anticholinergics on positive and negative symptoms in schizophrenia.

Anticholinergic drugs have been assumed to have no effects on schizophrenic symptomatology. Some studies suggest, however, that anticholinergic agents may antagonize the beneficial effect of neuroleptics on positive symptoms and partially ameliorate negative symptoms. Virtually all studies have been conducted in patients receiving concomitant neuroleptic treatment, raising the possibility that neuroleptics may obscure or modify any "true" anticholinergic effect on schizophrenic symptoms. To evaluate the hypothesis that anticholinergics may increase positive and decrease negative schizophrenic symptoms, we assessed the effect of biperiden on symptoms in the medication-free state. We studied the effect of biperiden 8 mg/day for 2 days on positive and negative symptoms in 40 otherwise drug-free schizophrenic inpatients. Biperiden produced a significant increase in positive symptoms (t = 6.7, p < .001) and reduction in negative symptoms (t = -3.4, p < .01). These data indicate that cholinergic modulation significantly affects positive and negative schizophrenic symptoms and suggest the need for systematic trials of cholinergic and anticholinergic agents in the treatment of positive and negative symptoms of schizophrenia, respectively.

Adult↗
PubMed1991

Stability of positive and negative symptom constructs during neuroleptic treatment in schizophrenia.

To assess the structural stability of positive and negative symptom ratings, we rated 40 schizophrenic inpatients on the Brief Psychiatric Rating Scale (BPRS) and the Scale for the Assessment of Negative Symptoms (SANS) at medication-free baseline and after 4 weeks of neuroleptic treatment. Positive symptom variables consisted of six BPRS items, and the negative symptom variables consisted of the five SANS subscale global scores. On principal components analysis, a three-factor, oblique-rotated solution resulted, with a negative symptom factor, a positive symptom factor, and an unstable behavioral agitation factor. The pre- and posttreatment factor loading patterns were similar. The findings suggest that BPRS-positive symptom items and the SANS measure distinct clinical dimensions and that the construct is stable, as demonstrated by minimal structural change with time.

Adult↗
PubMed1988

Effects of an abrupt diet change from hay to concentrate on microbial numbers and physical environment in the cecum of the pony.

Microbial numbers, pH, fluid volume, and turnover rate in the pony cecum were measured during an abrupt change from an all-forage to an all-concentrate diet, both fed at maintenance energy levels. Concentrate feeding resulted in increased (P less than 0.01) numbers of total viable anaerobic bacteria. The numbers of organisms growing on selective starch medium increased (P less than 0.01) when concentrate was fed, while numbers on xylan and pectin media decreased (P less than 0.025). Seven days after the diet change to concentrate, the number of bacteria growing on lactate medium increased (P less than 0.01), followed by a gradual decline. Cellulolytic bacteria occurred in low numbers, ranging from 1.1 x 10(4) to 4.4 x 10(4) per g of cecal contents. Feeding all concentrate decreased both the number of genera (P less than 0.01) and total protozoan numbers (P less than 0.01) in the cecum. Minimum cecal pH values of 6.4 and 5.8 were obtained when forage and concentrate, respectively, were fed, with the minimum pH occurring 6 h postfeeding. Dry-matter percentage of cecal contents followed a diurnal pattern which was the inverse of the pH curve. During forage feeding, the cecum contained an average of 2.2 liters (1.6 to 3.4 liters), which turned over 3.9 times per day. When concentrate was fed, cecal volume averaged 3.9 liters (0.6 to 8.6 liters), with a mean liquid turnover of 4.2 times per day. Microbial numbers and pH changes in the pony cecum associated with an abrupt change in diet from hay to concentrate resembled those which occur in the rumen under similar feeding conditions.

Animal Feed↗
PubMed1987

Determination of the quantity of acetyl CoA carboxylase by [14C]methyl avidin binding.

Conditions are described under which monomeric [14C]methyl avidin binds to SDS-denatured biotin enzymes and remains bound through polyacrylamide gel electrophoresis. The location of radioactive proteins on the dried gel was determined by fluorography and their identity was established by subunit molecular weight. The relative quantity of bound radioactive avidin, stoichiometrically equivalent to the molar quantity of biotin protein, can be determined by scanning the fluorograph with a soft laser densitometer. To determine the absolute quantity of biotin protein, the radioactive areas of the dried gel were cut out, resolubilized, and assayed for radioactivity. Since the specific radioactivity of the [14C]methyl avidin was known, the quantity of avidin bound and therefore the quantity of biotin enzyme could be calculated. The method is illustrated by the analysis of purified acetyl CoA carboxylase and is applied to the analysis of biotin enzymes in isolated rat liver mitochondria.

Acetyl-CoA Carboxylase↗
PubMed1985

Dietary dependent distribution of acetyl CoA carboxylase between cytoplasm and mitochondria of rat liver.

Biotinyl proteins in cytoplasm and mitochondria of rat liver were examined by fluorography and the quantity of acetyl CoA carboxylase was determined after sodium dodecyl sulfate-denatured proteins were incubated with [14C] methyl avidin and separated by polyacrylamide gel electrophoresis. Results show that one-half of the total acetyl CoA carboxylase in liver of fed rats was associated with mitochondria in a relatively inactive form. Fasting shifted the distribution of the enzyme toward the mitochondrial fraction and refeeding previously fasted rats shifted the distribution towards cytoplasm. Thus, acetyl CoA carboxylase can be added to the list of ambiquitous enzymes whose subcellular distribution varies with physiological conditions.

Acetyl-CoA Carboxylase↗
PubMed1984

Molecular weights of subunits of acetyl CoA carboxylase in rat liver cytoplasm.

Monomeric [14C] methyl avidin was shown to bind to sodium dodecyl sulfate-denatured biotinyl proteins and remain bound through polyacrylamide gel electrophoresis which allowed their detection by fluorography. This method was used to show that purified rat liver acetyl CoA carboxylase contained two high molecular weight forms of the enzyme (MR = 241,000 and 252,000) while rapidly prepared, crude rat liver cytoplasm contained two larger molecular weight (MR = 257,000 and 270,000) forms. Thus, the enzyme had undergone substantial proteolysis during purification. The crude enzyme preparation also contained a smaller biotinyl protein (MR = 141,000) which is likely a proteolytic product of the larger forms of acetyl CoA carboxylase.

Acetyl-CoA Carboxylase↗
PubMed1983

Regulation of purified rat liver acetyl CoA carboxylase by phosphorylation.

Acetyl CoA carboxylase was purified from liver of fasted-refed rats to near homogeneity, based on electrophoretic analysis and biotin content. These preparations contained an endogenous protein kinase that catalyzed the transfer of radioactive phosphate from [gamma-32P]ATP to acetyl CoA carboxylase, accompanied by a decrease in acetyl CoA carboxylase activity. Phosphate incorporated into acetyl CoA carboxylase was removed when the preparation was incubated with partially purified phosphorylase phosphatase catalytic subunit with regain of enzymatic activity. This endogenous protein kinase was shown not to be affected by either cyclic-AMP-dependent protein kinase inhibitor, EGTA, or trifluoperazine. The addition of either cyclic-AMP or purified cyclic-AMP-dependent protein kinase catalytic subunit to the purified acetyl CoA carboxylase preparation increased protein phosphorylation but had no further effect on acetyl CoA carboxylase activity. Purified acetyl CoA carboxylase was shown to act as an ATPase during the phosphorylation reaction.

Acetyl-CoA Carboxylase↗