Cause and effects of renal failure.
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Acute Kidney Injury↗
Biomedical subjects
M Hamilton
Publications and source records attributed to M Hamilton.
Metabolism and disposition of gemcitabine, and oncolytic deoxycytidine analog, in mice, rats, and dogs.
Gemcitabine, 2'-deoxy-2',2'-difluorocytidine, is a broad spectrum oncolytic compound with antitumor activity in solid tumor models. The pharmacokinetics, metabolism, and disposition of gemcitabine was examined in mice, rats, and dogs. All three species metabolize gemcitabine by deamination to the uracil metabolite. However, deamination in the mouse and dog was more extensive than in the rat. The mouse deaminated gemcitabine rapidly with the plasma concentration maximum of the uracil metabolite of gemcitabine being attained at 15 min postdosing compared with approximately 3 and 6 hr in the dog and rat, respectively. The rapid deamination in the mouse was also reflected in the plasma half-life of the parent compound. The mouse exhibited the shortest plasma half-life, approximately 0.28 hr, contrasted with 2.14 and 1.38 hr half-lives in rat and dog, respectively. Plasma AUC for the uracil metabolite of gemcitabine was 73%, 10.5%, and 315% of that for gemcitabine in the mouse, rat, and dog, respectively. Tissue concentrations of gemcitabine-derived radioactivity in the rat and mouse indicated that gemcitabine was rapidly distributed throughout the body. Half-lives of radioactivity in tissues of both the rat and mouse were relatively short, with the longest tissue half-lives of 5.7 and 3.0 hr, respectively. Plasma protein binding is negligible in all three species. The major route of elimination is via the urine in all three species with 76-86% of the dose excreted in the first 24 hr. The predominant radiolabeled component isolated from urine was gemcitabine in the rat and its uracil metabolite in the mouse and dog.
Animals↗
Nonoperative management of acute epidural hematoma diagnosed by CT: the neuroradiologist's role.
PURPOSE: To determine whether certain patients with epidural hematomas would benefit from conservative treatment and to assess the neuroradiologist's role in decision-making. METHODS: We reviewed the CT scan findings, clinical presentation and outcome of 48 consecutive patients with epidural hematoma managed at our institution within the past 5 years. In 18 patients, initial management was nonsurgical, and only one of these went on to require surgery due to clinical deterioration and evidence of enlargement of hematoma on CT. The remainder of these 18 did well without surgery. OBSERVATIONS AND CONCLUSIONS: Clinical indicators of neurologic dysfunction (decrease in Glasgow coma scale score, pupillary dilatation, and hemiparesis) in the presence of even small epidural hematomas usually dictates the need for surgical management. The role of the neuroradiologist is most important when the patient presents in a good clinical state, when identification of both favorable and unfavorable prognostic factors on Ct is essential. The initial diameter of nonsurgically managed epidural hematomas generally must be small (mean, 1.26 cm in our series, all under 1.5 cm), and midline shift should be minimal (mean, 1.8 mm in our series). The identification of lucent areas within the epidural hematoma (suggesting active bleeding), or CT evidence of uncal herniation, can be ominous and the neurosurgeon must be alerted to their presence. Even in the presence of a favorable clinical status, presence of a larger epidural hematoma with significant mass effect or central lucent areas should alert the neuroradiologist and neurosurgeon to the strong possibility of sudden neurologic deterioration, and indicate the probable need for surgical management.
Acute Disease↗
Region X: history of Branch 5, Oregon.
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History, 20th Century↗
The metabolism of 2- and 3-hydroxyacetanilide. Determination of metabolic products by liquid chromatography/electrochemistry.
The metabolism of 2- and 3-hydroxyacetanilide was examined in incubations with mouse liver microsomes. Metabolic products were determined by a comparison of both chromatographic and electrochemical properties with that of reference materials. Using this technique, 3-hydroxyacetaminophen and 2-acetamidohydroquinone were positively identified as microsomal metabolites of 3-hydroxyacetanilide. Incubation of 2-hydroxyacetanilide with liver microsomes resulted in the formation of 2-acetamidohydroquinone. Deacetylation products, ortho- and meta-aminophenol were observed but were apparently formed through NADPH-independent processes. Tentative identifications were made for the formation of sulfhydryl adducts from 3-hydroxyacetanilide, 2-acetamidohydroquinone, and 2-hydroxyacetanilide but not from 3-hydroxyacetanilide. The microsomal metabolism was compared with in vivo metabolism through the analysis of urine from mice administered 200 mg/kg (ip) dosages of the hydroxyacetanilides. The parent compounds and their dihydroxylated metabolites were excreted primarily as sulfate and glucuronide conjugates. Conjugated o-aminophenol was detected in urine following 2-hydroxyacetanilide administration, but m-aminophenol was not observed in urine from mice receiving the meta isomer. Mercapturates of the above compounds were not detected in any of the urines.
Acetanilides↗
Standardised assessment and recording of depressive symptoms.
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Depression↗
[Use and abuse of rating scales and statistics in psychopharmacology].
Scientific method in clinical work and research is still fully accepted in th world of medicine. There is still much misunderstanding of the principles and errors in its application. Rating scales are particularly useful in the evaluation of treatments, though they have other applications. But they are not absolutely necessary for this purpose and there are simpler methods available, though they are less efficient. Scales provide information in a standard form which permits the making of many different kinds of comparisons. They are not a substitute for sound clinical Judgement applied to properly designed clinical trials. Uncontrolled trials cannot distinguish between good and effective treatments and useless or even harmful ones. Statistical analysis is necessary because all patients are different. Unfortunately, incorrect or inappropriate statistical analysis is still not uncommon. Some examples are given.
Clinical Trials as Topic↗
Depression and endogenicity.
There is evidence from genetic and clinical studies, especially from therapeutic response to biological treatments, that endogenous or constitutional factors are important in some types of depressive illnesses. Unipolar depression is inherited differently from bipolar depression; monozygotic twins have a higher concordance rate than dizygotic twins. Endogenous depressions are cyclic in nature: the length of phases as well as the length of cycles are log-normally distributed. The effectiveness of antidepressants and ECT in endogenous depression points to a biochemical disorder. The author discusses the distinction between endogenous and exogenous depressions or between psychotic and neurotic depressions by reporting the work of Brown and others on "significant vs. stressful" events and on increased vulnerability.
Antidepressive Agents↗
Extended comparison of quality of life between stable heart failure patients and heart transplant recipients.
Heart failure has been associated with poor quality of life, which can improve after heart transplantation. Long-term quality-of-life comparisons between patients with heart failure stabilized with medical therapy and heart transplant recipients have not been performed. We assessed quality of life at the time of heart transplantation evaluation and again after 41 months in 12 patients with advanced heart failure stabilized with medical therapy and in 19 patients who had gone on to undergo heart transplantation. Quality of life was measured by three questionnaires. Both groups had similar quality-of-life and clinical features during the transplantation evaluation. Over time, feelings of anxiety and depression, psychologic adaptation, and perceived functional capability improved in the transplant recipients. However, transplant recipients reported more weakness after surgery; this was the major symptom that limited activities. At follow-up 41 months later, we found no significant differences in quality-of-life changes over time between patients stabilized with medical therapy and heart transplant recipients. Overall quality of life for patients who remain stable while receiving medical therapy may not be significantly different from patients who have undergone transplantation.
Aged↗
Does short-course induction with OKT3 improve outcome after heart transplantation? A randomized trial.
OKT3 is often used routinely for induction immunotherapy or selectively to avoid acute cyclosporine nephrotoxicity in heart transplant recipients at high risk for immediate postoperative kidney failure. It has not been shown in a randomized trial to be useful in patients at low risk for early kidney failure. We randomized 30 patients with a serum creatinine level of less than 1.4 mg/dl before heart transplantation to be treated with triple-drug immunotherapy with cyclosporine, which was started before surgery, (group 1) or to be treated with OKT3 for 4 to 6 days after surgery with oral cyclosporine, which was started between days 2 and 4, after renal function had stabilized (group 2). Follow-up for 6 months revealed no significant differences in the total number of rejection episodes, total number of infections, or in the serum creatinine level. Four patients in group 1 and five patients in group 2 have had no rejection. OKT3 showed a trend to delay time to first rejection (p = 0.10), as has been reported for the 14-day induction course of OKT3. A short course of OKT3 induction in heart transplant recipients at low risk for immediate postoperative kidney failure prolongs the time to first rejection for most patients but does not appear to reduce the total incidence of rejection in the first 6 months after heart transplantation.
Creatinine↗