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Biomedical subjects

R Burns

Publications and source records attributed to R Burns.

At least 109 records · Page 6Linked to original sources
PubMed1982

Effects of reductive methylation on microtubule assembly. Evidence for an essential amino group in the alpha-chain.

Microtubule protein from bovine brain was reacted at pH 6.7 with formaldehyde and NaCNBH3. These reagents react specifically with protein amino groups, causing their conversion to mono- and dimethylated forms (Jentoft, N., and Dearborn, D. (1979) J. Biol. Chem. 254, 4359-4365). Reductive methylation both inhibited microtubule assembly and induced extensive depolymerization in assembled microtubules. These effects occurred at low levels of methylation (10%) and appeared to arise from an alteration in tubulin which rendered tubulin assembly incompetent. This alteration had no significant effect on colchicine or GTP binding or on the critical tubulin concentration required for assembly. Comparative methylation studies over a range of formaldehyde concentrations involving microtubule polymer, microtubule protein, and several test proteins suggested that assembly inhibition results from the methylation of one or two highly reactive amino groups in the alpha-chain. The reactivities of these amino group(s) were reduced in the polymerized and denatured states.

Animals↗
PubMed1982

Vasodilator therapy in refractory congestive heart failure: a comparative analysis of hemodynamic and noninvasive studies.

The response to vasodilator therapy was assessed in 12 patients with chronic severe congestive heart failure refractory to conventional treatment. Cardiac output and intraarterial and pulmonary capillary wedge pressures were recorded continuously to assess the hemodynamic response to the vasodilators used. Control and post-treatment M mode echocardiograms and radionuclide angiograms were obtained to assess the change in left ventricular size and ejection fraction concurrent with the hemodynamic improvement. Despite a 33 percent decrease in pulmonary capillary wedge pressure (p less than 0.001) and a 35 percent increase in cardiac index (p less than 0.001), no significant change occurred in left ventricular end-diastolic or end-systolic chamber size on echocardiography or in ejection fraction measured with radionuclide angiography. In this study M mode echocardiography and radionuclide angiography were of no value in monitoring the actual hemodynamic response to vasodilator therapy in this group of patients with a left ventricular ejection fraction of less than 30 percent.

Aged↗
PubMed1982

In vitro cellular effects of hematoporphyrin derivative.

Several in vitro cell systems were exposed to hematoporphyrin derivative (HPD): established lines of rat kangaroo epithelial kidney; normal mouse embryonic fibroblasts; and differentiated neonatal rat myocardial cells. The uptake of HPD (25 to 100 micrograms/ml) by individual cells occurred rapidly over a 2-hr period and leveled off by 24 hr. HPD was excreted from cells by 48 hr after exposure. However, a low level of HPD (above background) was maintained in cells for up to 4 days following cessation of exposure. Intracellular binding of HPD was to mitochondria as demonstrated by fluorescence microscopy. HPD was also shown to have a growth-inhibiting effect on rat kangaroo cells without added light. The growth effects on mouse cells were less marked.

Animals↗
PubMed1981

Genetic aspects of the effects of methylmercury in mice: the incidence of cleft palate and concentrations of adenosine 3':5' cyclic monophosphate in tongue and palatal shelf.

Concentrations of adenosine 3':5' cyclic monophosphate (cAMP) were measured in the tongues and palates of 14.5-day-old fetuses from control and methylmercury-treated mothers of four inbred lines of mice which represent the four possible combinations of two H-2 alleles and two residual genetic backgrounds. The incidence of cleft palate in fetuses from control and methylmercury-treated mothers was also examined. The H-2 alleles significantly affected the degree of reduction of cAMP concentration in palates seen in fetuses from mothers treated with methylmercury. Neither the H-2 allele nor the residual genetic background played a role in the effect of methylmercury on cAMP concentrations in fetal tongues. The magnitude of increase in the incidence of cleft palate with methylmercury treatment was approximately the same for all lines. Thus, methylmercury-induced cleft palate may not be mediated by the reduction of cAMP. Finally, fetuses with cleft lip had increased palatal cAMP levels, whether or not they were from control or methylmercury treated mothers.

Animals↗
PubMed1980

Cortisone-induced cleft palate in the brachymorphic mouse.

Previous studies have shown that the autosomal recessive gene brachymorphic (bm/bm), which is maintained on a C57BL/6J (C57) background, reduces limb growth and sulfation of cartilage proteoglycans. Hydrocortisone administered on gestational days 11-14 resulted in 20% CP in the C57 mouse, but 95% CP in the bm/bm mouse. The bm/bm mouse had a median effective dose for CP of 45 mg/kg, compared to 325 mg/kg for C57 and 40 mg/kg for A/J. Morphometric analysis indicated that the time of palatal elevation was delayed in the bm/bm relative to the C57 mouse both with and without hydrocortisone treatment. The amount of cytoplasmic glucocorticoid receptor protein present in the bm/bm palate on day 14 was the same as the amount found in the C57 palate, and was not elevated as it is in the A/J palate. The levels of cyclic AMP in the bm/bm palate on day 14 were 30-70% higher than that found in the C57 palate with or without hydrocortisone. These results suggest that both bm/bm and A/J exhibit a delay in palatal shelf rotation and elevated levels of cyclic AMP, which appear to be predisposing factors for cortisone-induced cleft palate. These strains differ in that elevated levels of steroid receptors are present in A/J palate, whereas lower levels are found in the C57 and bm/bm mice.

Animals↗
PubMed1979

Cerebrovascular disease.

Cerebrovascular disorders producing transient or permanent symptoms and signs are very common, but they are not the only causes of a sudden neurologic deficit. Careful examination of the cardiovascular system may indicate the likely cause of the lesion, while accurate neurologic localization is also useful in establishing a diagnosis and prognosis. The CT scan is very helpful in distinguishing infarction from haemorrhage. In the management of the acute lesion, treatable disorders such as systemic diseases, potentially fatal rostro-caudal herniation, haematomas and aneurysms always need to be positively exlcuded. Endarterectomy, platelet inhibitors and anticoagulants are advised in certain situations, although their place in the management of cerebrovascular disorders still remains somewhat controversial.

Auscultation↗
PubMed1978

Jaundice associated with polycystic liver disease.

Jaundice is rarely encountered in polycystic disease of the liver. In the present case, pressure from tense cysts at the hilus of the liver caused a marked narrowing of the common hepatic duct and slowing of bile flow with the formation of stasis stones. Decompression of the cysts and removal of debris in the intrahepatic ducts resulted in a rapid decrease of the serum bilirubin level.

Bilirubin↗
PubMed1978

Hypercalciuria related to cadmium exposure.

A work force has been investigated for possible cadmium intoxication. One group who are coppersmiths have an 18.5 per cent prevalence of upper urinary tract stone disease associated with a statistically highly significant hypercalciuria and reduced serum inorganic phosphate. Proof of exposure to cadmium has been confirmed in all workers. The trace element cadmium should be kept in mind when investigating stone formers who exhibit an unexplained hypercalciuria.

Cadmium↗
PubMed1975

Systemic heparinization during percutaneous coronary angiography: evaluation of effectiveness in decreasing thrombotic and embolic catheter complications.

Systemic heparinization has been advocated as preventive for thrombotic and embolic complications of arterial catheterization. To test this hypothesis, 95 patients undergoing coronary angiography via the percutaneous femoral arterial approach were randomized into heparinized and nonheparinized groups. Evaluation for thrombotic and embolic complications by clinical means and non-invasive electrical impedance flow measurements in the lower limbs was performed precatheterization, postcatherization, and at 4 and 24 hr. Clinical data reveal loss of distal leg pulses in 11% (5/74) of the nonheparinized group, with two of these individuals developing signs of claudication and requiring embolectomy. No individuals (0/48) in the heparinized group lost distal leg pulses. Immediate, 4-hr, and 24-hr post-catheterization bloodflow was 12%, 10%, and 12% lower, respectively, in the catheterized limb of those in the nonheparinized group. At 24 hr 52% of the nonheparinized group had bloodflow levels lower than the precatheterization levels in the right (catheterized) extremity, while 2% (2/48) of the heparinized group had a similar reduction. One possible complication of excess bleeding was noted with heparin. It is concluded that systemic heparinization is safe and can be an important adjunct in the reduction of thromboembolic complications of percutaneous coronary angiography.

Angiocardiography↗
PubMed1974

Reversible encephalopathy possibly associated with bismuth subgallate ingestion.

Four patients who had undergone abdominoperineal resection for carcinoma of the colon and who had been taking oral bismuth subgallate developed a stereotyped recurrent and reversible neurological syndrome. This was characterized by confusion, tremulousness, clumsiness, myoclonic jerks, and an inability to walk. All patients were extensively investigated and no cause could be found, but symptoms regressed when the intake of bismuth was stopped. Postmortem examination in one patient failed to show any appreciable abnormality apart from a loss of Purkinje cells in the cerebellum. In the other three patients amino-acid chromatography performed on urine showed the presence of an abnormal unidentified constituent. It is thought that these four patients developed an encephalopathy associated with their bismuth subgallate ingestion.

Adult↗