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At least 19 recordsLinked to original sources
PubMed2026

Addressing racism as a clinical competence: Robert Wilson, Jr. (1867-1946).

Addressing health inequity is now recognized as a clinical competency in medical education. We examined the career and writings of Robert Wilson Jr. (1867-1946), longtime dean of the Medical College of the State of South Carolina during the Jim Crow Era, using primary and secondary sources within the context of systemic and structural racism, particularly in South Carolina. Wilson used public health data to refute the "Black Extinction Hypothesis" rooted in social Darwinism. He challenged assumptions of inherent Black susceptibility to tuberculosis, linking disease instead to social determinants of health. He also identified disproportionate mortality from kidney and cardiovascular disease among Black populations, anticipating modern health disparities research. Wilson further acknowledged systemic injustice and implicated structural conditions, including housing, in shaping outcomes. In an era of continuing health inequity and racial health disparities, Wilson applied empirical evidence to reject biological determinism, identify outcomes disparities, and advocate for racial justice.

History, 20th Century↗
PubMed1979

Schizophrenia: the nature of the psychological disturbance and its possible neurochemcial basis.

The diagnosis of schizophrenia is established principally by the presence of certain psychological symptoms which although subjective can be reliably assessed by standardized interviewing procedures. The most characteristic symptoms (Schneider's first-rank symptoms) fall into three groups: (a) auditory hallucinations of particular types, (b) 'ego-boundary disturbances', including intrusions into the stream of consciousness attributed to external agencies, and (c) delusional perception. Symptoms closely resembling those seen in schizophrenia can be induced in non-schizophrenic individuals by amphetamine-like drugs, and both these symptoms and those of schizophrenia are ameliorated by neuroleptic drugs (the major tranquillizers). Amphetamines facilitate and neuroleptic drugs diminish neural transmission mediated by the chemical substance dopamine. In recent post-mortem studies on patients who had suffered brom schizophrenia, it was found that dopamine release was not increased. However, in some cases there was evidence of increased sensitivity of the dopamine receptor.

Amphetamine↗
PubMed1978

Neonatal detection and evaluation of infantile polycystic disease by gray scale echography.

Infantile polycystic disease (IPCD) is an uncommon pathologic entity involving the kidneys and liver. Gray scale echography can detect this pathologic process within the kidneys, despite the presence of renal failure. In addition, the sonic study may detect associated hepatic abnormalities even though isotopic liver scan is normal. These capabilities make the ultrasonic examination uniquely suited for evaluating patients with IPCD.

Cysts↗
PubMed1979

Comparative pharmacokinetics of coumarin anticoagulants. XLII: Effect of phenobarbital on systemic availability of orally administered dicumarol in rats with ligated bile ducts.

The purpose of this investigation was to determine if the previously demonstrated inhibitory effect of phenobarbital treatment on the systemic availability of orally administered dicumarol in rats is related to the known effect of phenobarbital on bile output. It was found that phenobarbital had no apparent effect on the systemic availability of an aqueous dicumarol suspension in rats with ligated bile ducts. Compared to results obtained previously on normal rats, bile duct-ligated rats absorbed and eliminated dicumarol much more slowly and absorbed much less of the anticoagulant. On the other hand, the relative inductive effect of phenobarbital treatment on dicumarol elimination was similar in normal and in bile duct-ligated animals. The latter exhibited substantial serum transaminase elevations, indicative of liver damage presumably secondary to cholestasis. These results demonstrate that a drug-drug interaction can depend markedly on the pathophysiological status of the animals.

Animals↗
PubMed1978

Quinacrine fluorescence of Merkel cells in Xenopus laevis.

It has been shown by electron microscopy that, in Xenopus laevis, Merkel cells are usually situated near the ducts of the skin glands. Cells which fluorescence in ultra-violet light after treatment of the skin with quinacrine can be identified with these Merkel cells by their position, shape and size. The method indicates the presence of purine nucleotides, probably ATP. This result is consistent with the view that "large opaque vesicles" are sites of ATP storage.

Animals↗
PubMed1978

Methodological problems in the measurement of drug-induced rotational behaviour: continuous recording reveals time-course differences undetected by previous techniques.

Rats were lesioned unilaterally in the medial forebrain bundle with either the catecholamine neurotoxin 6-hydroxydopamine or the indoleamine neurotoxin 5,6-dihydroxytryptamine. Their rotational responses in automated rotameters to a challenge with the dopamine-receptor agonist apomorphine were compared using four different techniques in current use, and by assessment of complete rotation curves using both conventional statistical procedures and elementary computer-derived elements of curvature. The rotational responses of the two groups, characterized neurochemically by identical depletions of striatal dopamine but with a greater depletion of striatal 5-hydroxytryptamine in 5,6-dihydroxytryptamine-lesioned animals, were indistinguishable using each of the four current techniques. Assessment of rotation curves by both methods revealed significant differences between the two groups, characterised by faster onset and offset of the rotational response in 5,6-dihydroxytryptamine-lesioned animals. Some current techniques may implicitly exclude the detection of such time-course differences in rotational behaviour. Assessment of complete rotation curves may best allow valid comparisons between experimental groups.

5,6-Dihydroxytryptamine↗
PubMed1979

3-Methoxy-4-hydroxyphenylglycol excretion in acutely schizophrenic patients during a controlled clinical trial of the isomers of flupenthixol.

Urinary MHPG excretion in patients with acute schizophrenia was studied before and during a trial of the isomers of flupenthixol and placebo. Pretrial MHPG excretion was not related to severity of illness before the trial or to other pretrial clinical variables. In male subjects higher pretrial MHPG excretion was associated with a better outcome 1 year post-trial. However in females no relationship between MHPG excretion and outcome was established. During the trial there was a reduction in MHPG excretion in patients treated with beta-flupenthixol but no decrease in the group treated with alpha-flupenthixol or chlorpromazine. In patients on placebo there was a reduction in MHPG excretion in those who did well clinically, but not in those who did poorly. Thus low MHPG excretion may be a predictor of poor outcome in schizophrenia, but MHPG excretion also changes both as a function of clinical state and of neuroleptic drug administration.

Adult↗
PubMed1978

The activities of brain dopamine-beta-hydroxylase and catechol-O-methyl transferase in schizophrenics and controls.

It has been suggested that deterioration of central noradrenergic pathways may be responsible for the production of certain schizophrenic symptoms, and that such a degeneration might be reflected in lowered dopamine-beta-hydroxylase (DBH) activity in the brains of schizophrenics. The present study revealed that in rats lowered DBH activity was a sensitive index of noradrenergic degeneration. In the postmortem brains of 12 controls and 12 schizophrenics, however, no significant difference in DBH activity between controls and schizophrenics was found. DBH activity was relatively unstable postmortem and adversely affected by neuroleptic drugs, and these factors may have contributed to the previous finding of lowered DBH activity in the brains of schizophrenics. The activity of catechol-O-methyl transferase, which has also been previously reported as low in the brains of schizophrenics, was found to be no different in the controls of the present study.

Animals↗
PubMed1979

Brain tryptophan metabolism in schizophrenia: a post mortem study of metabolites of the serotonin and kynurenine pathways in schizophrenic and control subjects.

Serotonin (5HT), its chief metabolite 5-hydroxyindoleacetic acid (5 HIAA), its precursor tryptophan, and kynurenine, another metabolite of tryptophan, have been measured in post mortem human brain samples. Concentrations of these metabolites were not found to be significantly different in putamen, hippocampus or temporal cortex from 23 normal subjects compared with 15 subjects in whom a diagnosis of schizophrenia could be restrospectively confirmed. The results have been analysed with respect to cause of death, medication and post mortem changes. Post mortem increases in tryptophan and kynurenine were observed. Some interrelationships between the variables measured within and between the different areas studied are discussed. It is concluded that there is no evidence for a generalised deficit of 5HT in the brain in schizophrenia, nor for gross changes in turnover along the serotonin or kynurenine pathways of tryptophan metabolism in brain.

Aged↗
PubMed1977

The effect of monovalent and divalent cations on the activity of Streptococcus lactis C10 pyruvate kinase.

The pyruvate kinase (ATP: pyruvate 2-O-phosphotransferase, EC 2.7.1.40) from Streptococcus lactis C10 had an obligatory requirement for both a monovalent cation and divalent cation. NH+4 and K+ activated the enzyme in a sigmoidal manner (nH =1.55) at similar concentrations, whereas Na+ and Li+ could only weakly activate the enzyme. Of eight divalent cations studied, only three (Co2+, Mg2+ and Mn2+) activated the enzyme. The remaining five divalent cations (Cu2+, Zn2+, Ca2+, Ni2+ and Ba2+) inhibited the Mg2+ activated enzyme to varying degrees. (Cu2+ completely inhibited activity at 0.1 mM while Ba2+, the least potent inhibitor, caused 50% inhibition at 3.2 mM). In the presence of 1 mM fructose 1,6-diphosphate (Fru-1,6-P2) the enzyme showed a different kinetic response to each of the three activating divalent cations. For Co2+, Mn2+ and Mg2+ the Hill interaction coefficients (nH) were 1.6, 1.7 and 2.3 respectively and the respective divalent cation concentrations required for 50% maximum activity were 0.9, 0.46 and 0.9 mM. Only with Mn2+ as the divalent cation was there significatn activity in the absence of Fru-1,6-P2. When Mn2+ replaced Mg2+, the Fru-1,6-P2 activation changed from sigmoidal (nH = 2.0) to hyperbolic (nH = 1.0) kinetics and the Fru-1,6-P2 concentration required for 50% maximum activity decreased from 0.35 to 0.015 mM. The cooperativity of phosphoenolpyruvate binding increased (nH 1.2 to 1.8) and the value of the phosphoenolpyruvate concentration giving half maximal velocity decreased (0.18 to 0.015 mM phosphoenolyruvate) when Mg2+ was replaced by Mn2+ in the presence of 1 mM Fru-1,6-P2. The kinetic response to ADP was not altered significantly when Mn2+ was substituted for Mg2+. The effects of pH on the binding of phosphoenolpyruvate and Fru-1,6-P2 were different depending on whether Mg2+ or Mn2+ was the divalent cation.

Adenosine Diphosphate↗
PubMed1979

The nephrotoxicity of p-aminophenol. I. The effect on microsomal cytochromes, glutathione and covalent binding in kidney and liver.

p-Aminophenol administration lowered the microsomal cytochrome P-450 and b5 content and decreased the activity of NADPH cytochrome c reductase in kidney, but not in liver. Kidney GSH was depleted to 29% of the control value at 2 h, and only partly restored (50% of control) at 24 h. Liver GSH was transiently decreased, the lowest levels (77% of control) occurring at 30 min. The maximum level of covalently bound radioactivity was at two hours when 16.8% of the total radioactivity in kidney, 1.5% in liver and 3.6% in plasma was protein bound. At this time 81% of the total radioactivity in kidney and 95% of that in the liver was present in the soluble fraction.

Aminophenols↗
PubMed1978

Components of the frequency-following potential in man.

The scalp recorded frequency-following potentials (FFP) are a composite of several FFP's which may be distinguished by comparing simultaneously recorded waveforms from vertical and horizontal derivations in response to tones of very low frequently (below 350 Hz). The two most prominent FFP's were designated FFP1 and FFP2. FFP1 was recorded equally well in vertical and horizontal derivations and at a high stimulus intensities tended to be the predominant FFP. FFP2 followed FFP1 usually by about 1.7 msec and was optimally recorded in the vertical derivation. FFP2 threshold was about 10 dB lower than threshold for FFP1 and in several subjects, FFP2 was observed at 25 dB SL. Two other FFP's, a far-field recorded cochlear microphonic potential and a low-amplitude FFP, the latter presumably of neural origin, were also studied.

Acoustic Stimulation↗
PubMed2026

The Childhood Cancer and Leukemia International Consortium (CLIC): Expanding global collaboration in pediatric cancer etiology research.

Childhood cancers are rare, but incidence has risen modestly in countries with robust registration, partly reflecting improved diagnosis. In high-income countries, cancer is the leading cause of disease-related death in children. Marked inequities in incidence, survival, and research capacity underscore the need for large-scale collaboration to identify environmental, genetic, and contextual determinants of risk. The Childhood Cancer and Leukemia International Consortium (CLIC) was established in 2007 to study the etiology of childhood leukemia and later expanded in 2019 to include other childhood cancers, principally solid tumors. CLIC pools harmonized, individual-level data from case-control and cohort studies, obtained through interviews, record linkage (insurance claims, registries), or geographic information systems, and integrates germline genomic data where available. Membership has grown from 13 studies in 9 countries to 57 studies in 21 countries; recruitment spans the early 1960s to the present and encompasses approximately 150,000 cases across all tumor types and 300,000 controls with clinical, demographic, and exposure data, centralized via harmonized data dictionaries at the Data Coordination Center, established in 2014 at the International Agency for Research on Cancer, and supported by a secure analysis platform. Pooled analyses across diverse populations have implicated parental age, prenatal vitamin or folic acid use, mode of delivery, fetal growth, selected congenital anomalies, occupational or household exposures (e.g., pesticides), paternal smoking, and markers of early-life immune modulation (e.g., breastfeeding, daycare attendance) in leukemia risk, informing carcinogen evaluation and prevention. The integration of genetic ancestry and germline susceptibility data is clarifying ancestry-related differences in leukemia biology and outcomes, while confirming risk loci with population-specific effects. CLIC is now adding polygenic risk scores and exposomic data to refine etiologic subtyping and identify modifiable pathways, while broadening representation from underserved regions through partnership-building and capacity-strengthening.

Humans↗