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Biomedical subjects

D Neal

Publications and source records attributed to D Neal.

46 records · Page 3Linked to original sources
PubMed1989

Role of brain in counterregulation of insulin-induced hypoglycemia in dogs.

The role of the brain in directing counterregulation during hypoglycemia induced by insulin infusion was assessed in overnight-fasted conscious dogs. Concomitant brain and peripheral hypoglycemia was induced in one group of dogs (n = 5) by infusing insulin peripherally at a rate of 3.5 mU.kg-1.min-1. In another group (n = 4), insulin was infused as described above to induce peripheral hypoglycemia, and brain hypoglycemia was minimized by infusing glucose bilaterally into the carotid and vertebral arteries to maintain the brain glucose level at a calculated concentration of 85 mg/dl. Glucose was also infused peripherally as needed so that the peripheral glucose levels in both of the protocols were similar (45 +/- 2 mg/dl with and 48 +/- 3 mg/dl without brain glucose infusion, both P less than .05). The responses (in terms of change of area under the curve) of epinephrine, norepinephrine, cortisol, and pancreatic polypeptide when brain glycemia was controlled during insulin infusion were only 14 +/- 6, 39 +/- 12, 17 +/- 8, and 9 +/- 4%, respectively, of those present during insulin infusion without concomitant brain glucose infusion (all P less than .05). Of particular interest was the glucagon response that occurred when head hypoglycemia was minimized; the glucagon level was only 21 +/- 8% of that present when marked brain hypoglycemia accompanied insulin infusion (P less than .05). During hypoglycemia resulting from insulin infusion, endogenous glucose production (EGP), as assessed with [3-3H]glucose, rose from 2.6 +/- 0.1 to 4.4 +/- 0.5 mg.kg-1.min-1 (P less than .05). In contrast, EGP decreased from 2.7 +/- 0.2 to 2.0 +/- 0.3 mg.kg-1.min-1 when brain hypoglycemia was minimized. In an additional set of studies, when insulin was infused at 3.5 mU.kg-1.min-1 and glucose was infused peripherally to maintain both the head and peripheral glucose concentrations at 88 +/- 6 mg/dl, EGP decreased from 2.6 +/- 0.1 to 1.2 +/- 0.2 mg.kg-1.min-1. These results suggest that under marked hyperinsulinemic conditions the brain is the primary director of glucagon release and that it is responsible for approximately 75% of the life-sustaining glucose production.

Animals↗
PubMed1988

Methemoglobinemia due to ingestion of N,N-dimethyl-p-toluidine, a component used in the fabrication of artificial fingernails.

An acute cyanotic episode due to methemoglobinemia occurred in a 16-month old girl following the ingestion of N,N-dimethyl-p-toluidine, a commercially available component used in the production of artificial fingernails. The amount of the parent compound ingested was about 6 mg/kg of body weight. Administration of methylene blue was effective in the reversal of the methemoglobinemia. In vitro studies suggest that the activity of the compound was probably due to its biochemical transformation to the toxic metabolite p-methylphenylhydroxylamine. We expand the list of aromatic amino or nitro compounds and their derivatives capable of producing methemoglobinemia and call attention to the hazard of their ingestion.

Accidents, Home↗
PubMed1988

Immunologically measured serum markers and their role in the management of prostate cancer.

Serum prostatic acid phosphatase and prostate-specific antigen have been measured in a group of 106 cases of newly diagnosed prostate cancer. The serum levels of the tumour markers have been correlated with the clinical and ultrasound staging of the prostate cancer at diagnosis. All patients were managed by a deferred treatment policy. Patients without detectable metastases at presentation have been assessed after a period of 2 years to determine if the level of serum tumour markers at diagnosis could predict subsequent disease progression. The study has demonstrated that a combination of immunologically measured acid phosphatase and prostate-specific antigen is the best method of assessing the prognosis of an individual prostate cancer at the time of presentation.

Acid Phosphatase↗
PubMed1982

Thyroxin-evoked increase of sucrase activity in lower villus in the jejunum of adrenalectomized suckling rats.

Intestinal sucrase activity, absent in the suckling rat, is evoked precociously by thyroid hormones. Since enterocytes migrate from crypt to villus tip, the question arises: at which level of the villus--crypt columns do the enterocytes respond with an increase of sucrase activity to thyroxin (T4)? Suckling rats (11 days old) were injected daily, subcutaneously, with T4 (2 micrograms/g BW/day). They were sacrificed 1, 2, and 3 days later. Sucrase activity was determined in homogenates of the entire jejunal wall and in serial homogenates of the villus-crypt columns using cryostat sectioning. Maximal increase of sucrase activity was seen after 3 days in the lower villus. Experiments were also done using rats adrenalectomized on day 10 to exclude the effect via precocious maturation of adrenal cortex. The same results were obtained. In conclusion, T4-evoked increase of sucrase activity occurs first in enterocytes that are nearest the villus-crypt junction.

Adrenalectomy↗
PubMed1968

Volunteers.

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Education of Persons with Intellectual Disabilitie↗
PubMedDate not supplied

Vancomycin ototoxicity and nephrotoxicity. A review.

Vancomycin has been in clinical use as a potent antistaphylococcal antibiotic for over 30 years. Most reports of ototoxicity and nephrotoxicity have been associated with early, relatively impure, formulations of vancomycin. This paper reviews the literature concerning vancomycin ototoxocity and nephrotoxicity and the evidence for their correlation with the therapeutic serum concentration range. There have been 28 reports of vancomycin-associated ototoxicity published in the medical literature since 1958. It remains unclear whether any diminution in hearing is permanent or reversible. Few patients in the literature had follow-up audiometry and the hearing impairment tends to be at higher frequencies. Several authors reported peak serum vancomycin concentrations, but the exact time these were drawn with respect to the last dose is mostly unclear. In other reports, the 'peak' concentrations noted 3 to 6 hours after the last dose are probably indicative of much higher concentrations because of vancomycin's rapid phase of distribution. More than half the 57 cases of reported nephrotoxicity due to vancomycin occurred within the first 6 years of the drug's use. Many of these patients also had pre-existing renal dysfunction or were concomitantly receiving other nephrotoxic agents. It is unclear whether the coadministration of aminoglycosides produces a synergistic toxicity. The exact incidence of nephrotoxicity is uncertain, but is probably less with the current, relatively pure, product. The correlation of nephrotoxicity with certain serum vancomycin concentrations remains to be clarified. Other aspects also require clarification, such as when to draw samples to determine peak serum concentrations and whether or not routine measurements are necessary at all. In the absence of better guidelines, efforts should be made to tailor individual patient's regimens to produce peak and trough serum vancomycin concentrations to within the widely accepted ranges of 30 to 40 and 5 to 10 mg/L, respectively. In addition, the concomitant use of other potentially nephrotoxic and ototoxic agents should be avoided.

Ear↗
PubMedDate not supplied

The effect of the hepatic nerves on the disposition of a mixed meal by conscious dogs.

We examined the disposition of a mixed meal by nine conscious dogs fasted for 24 hours with surgical hepatic denervation. The results were compared with those from identical studies carried out previously in 13 hepatic-innervated dogs. Net gut release of glucose and gluconeogenic precursors (assessed with the arteriovenous difference technique), the resulting blood glucose and plasma insulin concentrations, and the hepatic glucose load were remarkably similar in the two groups. Net hepatic glucose uptake was 4.8 +/- 3.6 g in hepatic-denervated and 7.7 +/- 3.3 g in hepatic-innervated dogs. Cumulative net hepatic lactate release in hepatic-denervated dogs was 4.3 +/- 1.4 g of glucose equivalents, half the value for hepatic-innervated dogs. Net hepatic carbon intake was similar in the two groups. Hepatic lipogenesis, oxidation, and net glycogen synthesis were qualitatively similar between groups. In conclusion, the disposition of a mixed meal by hepatic-innervated and hepatic-denervated dogs was very similar. Subtle alterations in net hepatic balance of substrates (tendencies toward decreases in net hepatic glucose uptake and lactate release) made net carbon retention in denervated livers virtually identical with that in innervated livers. When other compensatory mechanisms are intact, hepatic denervation does not significantly alter hepatic disposition of a mixed meal.

Amino Acids↗