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Biomedical subjects

J Ellis

Publications and source records attributed to J Ellis.

At least 37 records · Page 2Linked to original sources
PubMed1991

Muscarinic receptor regulation and protein kinase C: sites for the action of chronic lithium in the hippocampus.

Regulation of muscarinic receptor activity in critical regions of the limbic system may represent a site for the therapeutic action of lithium. Muscarinic receptors in the hippocampus are coupled to phosphoinositide (PI) hydrolysis and the generation of the second messengers inositol (1,4,5) trisphosphate [Ins (1,4,5)P3] as well as diacylglycerol (DAG), which can directly activate protein kinase C (PKC). Since lithium may affect the regeneration of critical receptor-coupled pools of phosphatidylinositol 4,5-bisphosphate, studies in our laboratory have investigated the effects of chronic lithium on the regulation of the muscarinic receptor response. We have recently demonstrated that, following chronic administration of atropine in control and chronic lithium animals, there is an up-regulation of muscarinic receptor binding sites in the hippocampus; however, a concomitant sensitization of the carbachol-stimulated PI response is observed only in control animals. We have so far detected no effects of either in vitro or in vivo lithium on muscarinic receptor interactions with G proteins. However, we have observed a reduction in the in vitro phosphorylation of a major PKC phosphoprotein substrate in the rat hippocampus, following chronic lithium treatment. This effect may be related to long-lasting changes in regulation of receptor activity.

Animals↗
PubMed1979

Activation of macrophages in vivo and in vitro. Correlation between hydrogen peroxide release and killing of Trypanosoma cruzi.

As reported previously, mouse peritoneal macrophages could be activated to kill intracellular trypomastigotes of Trypanosoma cruzi, the agent of Chagas' disease, in either of two ways: by immunizing and boosting the mice (3), or by culturing resident or inflammatory macrophages in spleen cell factor(s) (SCF) in vitro (2). Macrophages activated in vivo became less trypanocidal with time in culture, and cells activated in vitro lost trypanocidal capacity when CSF was removed (2). In the present study, the ability of macrophages to release H2O2 in response to phorbol myristate acetate (PMA) could be induced in vivo and in vitro, and reversed in vitro, in a manner correlating closely with changes in trypanocidal activity. Macrophages could be activated in vitro with SCF in a time-dependent and dose-dependent fashion, so that they released as much H2O2 as macrophages activated in vivo. The sensitivity of epimastigotes and trypomastigotes to enzymatically generated H2O2 suggested that the generation of H2O2 by activated macrophages could be plausible explanation for their trypanocidal activity. Of the biochemical correlates of macrophage activation reported to date, increased ability to release H2O2 seems most closely allied to enhanced capacity to kill an intracellular pathogen.

Animals↗
PubMed1979

Clinical results of a cross-over treatment with pyridoxine and placebo of the carpal tunnel syndrome.

Clinical evaluation was made of cross-over treatments by pyridoxine and a placebo of patient 22 having the carpal tunnel syndrome. Extraordinary monitoring of the specific activities of the erythrocyte glutamic oxaloacetic transaminase proved a severe vitamin B6 deficiency, which was partially corrected by the Recommended Dietary Allowance of 2 mg, and completely corrected by 100 mg. The severity of the syndrome diminished on the Recommended Dietary Allowances and the patient was asymptomatic at the higher dosage. On placebo, both the vitamin B6 deficiency and syndrome reappeared. Retreatment with 100 mg again corrected both the deficiency and syndrome. Measurements (total n = 19) of flexion of proximal interphalangeal joints of the index fingers by a goniometer, and of pinch by the Preston gauge revealed objective normalization. Scores of 17 symptoms revealed reductions at both the 2- (P less than 0.01) and 100-mg (P less than 0.001) dosages. Conduction through the carpal tunnels had improved by electromyography. These and previous data on a total of 22 patients showed the concomitant presence of a deficiency of vitamin B6 and the carpal tunnel syndrome; a causal relationship is apparent.

Adult↗
PubMed1978

Antibody-mediated activation of a defective beta-D-galactosidase: dimeric form of the activatable mutant enzyme.

Sedimentation analyses of AMEF, an activatable mutant beta-D-galactosidase (beta-D-galactoside galactohydrolase, EC 3.2.1.23), and the products of its reaction with Fab fragments of activating antibody show that this enzyme exists mainly as 10S dimers. Activation of AMEF by purified antibody resulted in formation of 16S tetramers. A unifying hypothesis postulating a dimer--tetramer equilibrium accounts for this observation as the counterpart of inactivation, which was shown to involve the breakdown of tetramers into inactive subunits [Roth, R. A. & Rotman, B. (1975) Biochem. Biophys. Res. Commun. 67, 1382--1390]. Conditions are described under which AMEF loses the specific antigenic determinant(s) responsible for binding activating antibody, allowing its subsequent use as an absorption to obtain immunologically purified activating antibody,

Antibodies↗
PubMed1978

Biochemical evidence for a deficiency of vitamin B6 in the carpal tunnel syndrome based on a crossover clinical study.

In a patient with severe carpal tunnel syndrome and a significant deficiency of vitamin B(6), the evidence for the deficiency was an extraordinarily low basal specific activity of the glutamic-oxaloacetic transminase of the erythrocytes (EGOT). This enzyme was also deficient in pyridoxal phosphate. The patient was treated with the recommended dietary allowance of pyridoxine, 2 mg/day, for 11 weeks, then 100 mg/day for 12 weeks, a placebo for 9 weeks, and again pyridoxine at 100 mg/day for 11 weeks. Sixty-one monitorial assays of EGOT over 48 weeks supported the following interpretations. (i) His diet permitted the development of a debilitating carpal tunnel syndrome. (ii) Treatment with pyridoxine at 2 mg/day reduced the deficiency of EGOT activity from about 70% to 50%, maintained a deficiency of pyridoxal phosphate, and relieved but allowed a marginal syndrome. (iii) Treatment at 100 mg/day for 12 weeks nearly achieved a "ceiling" level of EGOT and eliminated the deficiency of pyridoxal phosphate. (iv) After placebo for 7 weeks, the deficiencies of EGOT activity and pyridoxal phosphate reappeared, and clinical symptoms become worse. (v) Retreatment at 100 mg/day reestablished a "ceiling" EGOT, with no deficiency of pyridoxal phosphate, and the patient was asymptomatic. These data also support the concept that a deficiency of vitamin B(6) is significant in the etiology of the carpal tunnel syndrome. Mechanistically, a state of deficiency of the coenzyme seems to lower the level of the apoenzyme; a state of no deficiency of the coenzyme regulates a ceiling level of the transaminase. The latter state is presumably desired for health.

Apoenzymes↗
PubMed1976

A new concept and finding in morbid jealousy.

The authors describe an unexpected coincidental finding in three couples who sought therapy because the husband was pathologically jealous. In the course of treatment they found that during early adolescence each of these men had witnessed his mother engaged in extramarital sexual activity. The authors discuss the implications of this finding for further understanding of the etiology of the syndrome of pathological jealousy, its transactional dimensions, and possible psychotherapeutic approaches. They also present a typology of morbid jealousy that consists of excessive obsessional-delusional, and ego dysfunctional forms.

Adult↗