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Biomedical subjects

J Ellis

Publications and source records attributed to J Ellis.

At least 325 records · Page 18Linked to original sources
PubMed1981

Bioenergetics in clinical medicine. XVI. Reduction of hypertension in patients by therapy with coenzyme Q10.

Six untreated hypertensive patients and ten on therapy, but having elevated blood pressures, were treated with coenzyme Q10(CoQ10); 14/16 patients showed reductions (p less than 0.05-less than 0.001) in systolic pressures; 11/16 showed reductions (p less than 0.05-less than 0.001) in diastolic pressure; 9/10 showed reductions of elevated pressures to a normal range. By impedance cardiography and electrocardiography, there were no changes in cardiac outputs, stroke volumes and Heather Indices except for a few patients with changes of doubtful biological significance. 3/16 patients had exceptionally low basal specific activities of the succinate dehydrogenase-coenzyme Q10 reductase in blood which increased to a normal range on treatment. A greater deficiency of CoQ10 in the vascular system than in blood is likely. We consider that (1) the mechanism of reduction of elevated blood pressures by CoQ10 is based upon normalization or autoregulation of peripheral resistance rather than cardiac regulation, and (2) that the therapeutic activity of CoQ10 is not pharmacodynamic, but results from a translational increase in levels of CoQ10-enzymes in vascular tissue during ca. 4-12 weeks.

Blood Pressure↗
PubMed1981

Therapy with vitamin B6 with and without surgery for treatment of patients having the idiopathic carpal tunnel syndrome.

Blood samples from four patients at the time of surgery to relieve the compression of the carpal tunnel syndrome, which was diagnosed by clinical and electromyographic evaluation, were differentially assayed to determine the specific activities and the % deficiencies of the erythrocyte glutamic oxaloacetic transaminase (EGOT). The data from these assays revealed that these four patients had a severe deficiency of vitamin B6. These data, in conjunction with previous biochemical and clinical results over five years, underscore the desirability, and even necessity, of testing by the EGOT analysis for the presence of a severe deficiency of vitamin B6 in all such patients before surgery. Treatment with vitamin B6 (pyridoxine) for a minimum period of 12 weeks, depending upon the duration and severity of the symptoms, has been effective without exception. Surgery may relieve compression, but does not correct a deficiency of vitamin B6. Surgery in addition to therapy with vitamin B6 should be reserved for those patients who have had the deficiency for so many years that much tissue damage is irreversible by pyridoxine, and additional relief from pain can be achieved through the surgery.

Adult↗
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↗