Biomedical subjects

J A Pultz

Publications and source records attributed to J A Pultz.

5 recordsLinked to original sources

PubMed2001

Statistical comparison of dissolution curves.

The purpose of this investigation was to develop statistical procedures to determine if two sets of dissolution curves could have come from the same population of curves. The f(2)statistic developed by the Food and Drug Administration, FDA, has been shown to have many limitations and is too liberal in concluding similarity between dissolution profiles. The procedure currently used by the FDA involves computing the mean amount dissolved at each time and then comparing the two mean curves. This approach ignores all of the variability within sets of profiles, which, from a statistical viewpoint, is a serious limitation. This investigation presents three different statistics for comparison of dissolution curves with associated decision rules and power functions. These three statistics are extensions of existing procedures: (1) an extension of the Mann--Whitney test which compares the variability within each set of profiles and between the two sets; (2) an extension of the Kolmogorov--Smirnov D statistic which compares three empirical cumulative distribution functions; and (3) an adaptation of the well known chi-squared test. A computer program, which includes the algorithm for each of the three statistics and varying sample sizes, is also available.

Algorithms↗

PubMed1995

Sigma-1 receptors modulate functional activity of rat splenocytes.

Neuroleptics, opiates, and cocaine are commonly prescribed for or abused by humans. Although primarily used for their actions at other receptors in brain, these compounds also act at sigma receptors. We have previously identified sigma-1 receptors on human peripheral blood leukocytes and rat spleen, and in the present study we demonstrate a correlation between the pharmacology of these receptors and the ability of drugs to suppress concanavalin A-induced splenocyte proliferation. These results support the hypothesis that sigma-1 receptors regulate functional activities of immune cells, and suggest that sigma agonists may cause changes in immune competence in vivo.

Animals↗

PubMed1991

Fluoxetine versus trazodone: efficacy and activating-sedating effects.

BACKGROUND: The efficacy and safety of fluoxetine (N = 65; median sustained dose, 20 mg/day) and of trazodone (N = 61; median sustained dose, 250 mg/day) were compared in a trial in outpatients with major depressive episode. The incidence and temporal patterns of activation and sedation were also assessed. METHOD: Men and women who met DSM-III criteria for nonpsychotic major depressive episode (but with a current episode greater than or equal to 4 weeks) and had a 21-item Hamilton Rating Scale for Depression (HAM-D21) score greater than 20 were selected. After single-blind placebo was administered for 1 week, eligible patients were randomized to double-blind fluoxetine or trazodone treatment for up to 6 weeks. Efficacy (HAM-D21, Clinical Global Impressions Scales for Severity and Improvement, Patient Global Impressions Scale for Improvement, Guild Memory Test) and adverse events were evaluated weekly. RESULTS: The HAM-D21 score improved within both treatment groups (p less than .001). The groups were similar with respect to endpoint mean HAM-D21 improvement. For individual adverse events that developed or worsened during therapy, more fluoxetine-treated patients reported rhinitis and tremor (p less than or equal to .05), while more trazodone-treated patients reported somnolence and dizziness (p less than or equal to .05). More combined events suggesting activation (agitation, anxiety, nervousness, insomnia) were reported with fluoxetine than with trazodone (15.4% vs. 3.3%, p less than or equal to .05), while more combined events suggesting sedation (somnolence, asthenia) were reported with trazodone than with fluoxetine (42.6% vs. 21.5%, p less than or equal to .05). Discontinuation rates for activation and sedation did not differ between treatments. Numerically, more sedation (21.5%) than activation (15.4%) was reported with fluoxetine. CONCLUSIONS: There was little clinical difference between treatments with regard to efficacy and safety. The occurrence and temporal patterns of activation and sedation differed within and between treatments.

Adult↗

PubMed1989

Clinicopathologic findings in dogs with renal amyloidosis: 59 cases (1976-1986).

The medical records of 59 dogs with renal amyloidosis were reviewed. Most dogs with amyloidosis were greater than 6 years old, and females were affected more often than males. Beagles, Collies, and Walker Hounds were at increased risk, whereas German Shepherd Dogs and mixed-breed dogs were at decreased risk. Common historical findings were anorexia, polyuria, polydipsia, lethargy, vomiting, and weight loss. Common laboratory findings were leukocytosis, lymphopenia, nonregenerative anemia, hypercholesterolemia, azotemia, hyperphosphatemia, metabolic acidosis, isosthenuria, cylindruria, and proteinuria. Proteinuria was moderate to severe in most dogs, as assessed by qualitative determination of urine protein concentration, urine protein/urine creatinine ratio, and 24-hour urine protein excretion. Conservative medical management was of little value, and survival ranged from 3 to 20 months in 12 dogs for which this information was available. Moderate to severe diffuse global glomerular amyloidosis was detected in all dogs. Medullary amyloid deposition was multifocal and less severe, but was evident in most dogs. Secondary tubulointerstitial and glomerular lesions were mild or absent in most dogs. Thromboembolism was identified in approximately 14% of affected dogs, underlying inflammatory disease in 37%, and neoplasia in 20%. Laboratory indicators of renal function correlated poorly with histologic lesions, with the exception of glomerular amyloid deposition and "chronic renal disease" index with endogenous creatinine clearance.

Age Factors↗

PubMed1989

Effects on C3H mouse mammary cancer of changing from a high fat to a low fat diet before, at, or after puberty.

A low fat/low calorie (LF/LC) diet is a relative inhibitor of murine mammary cancer. Because the mammary gland may be most sensitive to the action of a carcinogen at or near the age of puberty, we studied whether beginning a LF/LC diet before puberty would decrease C3H/OuJ mouse mammary cancer incidence more than if such a diet was begun at or after puberty. We also studied whether the advancement of the age of puberty by a high fat/high calorie (HF/HC) diet would in itself be a mammary cancer risk factor and whether dietary fat levels would affect mammary cancer metastases. In the first study, mice were changed from a HF/HC diet to a LF/LC diet at 12 days of age, puberty, or 60 days of age. Other groups were always HF/HC or always LF/LC. In a second experiment, mice were fed a high fat diet for the same length of time, i.e., from 21 to 75 days of age (before and through puberty) or 75 to 129 days of age (well after puberty). In one aspect of the first study, puberty was advanced by feeding a HF/HC diet until the first day of puberty. However, tumor latency, incidence, and multiplicity were not statistically different from those of the LF/LC control. Other results of the first study indicated, in general, that mice consuming a LF/LC diet beginning at or before puberty had a longer tumor latency and a lower tumor incidence and multiplicity than mice either beginning a LF/LC diet at 60 days of age or continuously fed a HF/HC diet. Lung metatases were greater in mice fed a HF/HC diet continuously compared to LF/LC continuously. In the second study, beginning the high fat diet before or after puberty did not result in statistically significant differences in tumor latency, incidence, or multiplicity. It was concluded that the longer a LF/LC diet was fed, the lower was the mammary cancer risk. An early puberty in itself was not a mammary cancer risk factor and mouse puberty had no particular significance as an age before which a LF/LC diet should begin.

Animals↗