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Biomedical subjects

B Hammond

Publications and source records attributed to B Hammond.

At least 19 recordsLinked to original sources
PubMed1992

The use of targeting criteria in hospitalized HMO patients: results from the demonstration phase of the Hospitalized Older Persons Evaluation (HOPE) Study.

OBJECTIVE: To determine the yield of standardized targeting criteria for identifying hospitalized HMO patients who are at high risk for mortality and nursing home placement and, therefore, may be appropriate for comprehensive geriatric assessment. DESIGN: Prospective cohort study. SETTING: Four HMO (Southern California Kaiser-Permanente) hospitals. SUBJECTS: 3,697 patients 65 years of age or older admitted to any inpatient service from July 1 through September 30, 1990. MAIN OUTCOME MEASURES: Screening measures for standardized targeting criteria, administered 24-48 hours after admission. RESULTS: Overall, 35.1% of patients screened met at least one inclusionary criterion, which is considerably higher than other published reports. The most commonly met criteria were incontinence, impairment in performing activities of daily living, malnutrition, and immobility. The percentage of patients meeting at least one criterion and meeting each criterion varied considerably among hospitals. The vast majority of patients (83%) who were judged appropriate for assessment met at least three criteria. CONCLUSIONS: The yield of standardized criteria differs when applied to patients in different health care systems and to patients at different hospitals within a health care system, which may reflect differences in the populations being served and the practice styles of physicians and the delivery system. Because no single criterion identified more than approximately half of patients who were judged appropriate for assessment, it is likely that a battery of criteria will be necessary to identify these patients.

Activities of Daily Living↗
PubMed1991

Urinary excretion of nitrogenous and non-nitrogenous compounds in the chronic ethanol-fed rat.

1. The metabolic consequences of chronic ethanol feeding was investigated by assay of urinary metabolites. Male Wistar rats were fed a liquid diet containing 35% of total energy as ethanol or isovolumetric, isocaloric and isonitrogenous amounts of the same diet in which ethanol was substituted by isocaloric glucose (controls). 2. At 6 weeks the entire skeletal muscle mass was reduced by approximately 20%. The urinary excretion of nitrogen, urea and uric acid increased by between 23 and 128%. Urinary creatinine excretion was not significantly altered. 3. Urinary excretion of magnesium was significantly increased by 43%. Urinary excretion of sodium, potassium, calcium and phosphate was increased slightly (i.e. 5-22%), but this change was not statistically significant. 4. Proton n.m.r. spectroscopic analysis showed that ethanol feeding reduced the urinary excretion of citrate and 2-oxoglutarate (by approximately 50%), suggesting decreased citric acid cycle activity. There was an increased excretion of alanine (44%), but excretion of succinate and acetate was not significantly altered. Ethanol in the urine of ethanol-fed rats comprised approximately 2% of total ethanol intake and less than 1% of total energy intake. 5. Lactose was detectable in urine of ethanol-fed rats, but not in control rats, reflecting the reported decreased intestinal lactase activity and increased gut permeability in alcoholics. Urinary galactose excretion decreased by 41%, but relatively large increases in lactate excretion (50%) did not achieve statistical significance. 6. It was concluded that chronic ethanol feeding causes disturbances in whole-body nitrogen homoeostasis and alterations in intermediary metabolism.

Alanine↗
PubMed1991

An investigation into the effects of aminoguanidine treatment on the plasma and blood of free-fed and dietary-restricted rats.

An investigation has been made into the effect of oral aminoguanidine (50-60 mg kg-1 day-1) on the blood biochemistry of male Wistar rats which either had free access to food or were dietary-restricted (50% of the food consumed by the free access group). In control rats (i.e. without aminoguanidine treatment) three weeks of food restriction caused significant increases in plasma sodium and albumin and the erythrocyte count, haematocrit and haemoglobin. There were reductions in plasma calcium, phosphate, alkaline phosphatase activity, urea, triglycerides, creatinine, glucose and the red cell volume. Similar effects of food restriction were observed in aminoguanidine-treated rats. Aminoguanidine ingestion in free-fed animals caused a reduction in plasma creatinine concentration. In dietary-restricted rats, aminoguanidine ingestion reduced plasma sodium and total plasma proteins (largely as a result of a decline in albumin), and increased plasma urea concentrations. Aminoguanidine was added to plasma of control rats in-vitro to determine whether it interfered with the assay of urea and creatinine. At concentrations of 0.1 to 10 mg mL-1, aminoguanidine had no effect on urea determinations. However, aminoguanidine significantly reduced the apparent concentration of plasma creatinine by between 7 to 81%. The changes in plasma analytes in aminoguanidine-treated rats may be indicative of minor hepatic perturbations or kidney function, but the data also imply that prior nutritional state is a determinant of aminoguanidine effects.

Animals↗
PubMed1990

Activity of cardiac enzymes measured in the coronary sinus in acute myocardial infarction.

Three patients with acute infarction of the anterior wall of the heart underwent catheterisation of the coronary sinus. Samples were taken for estimation of activity of cardiac enzymes. A small gradient was demonstrated between the sinus and the venous blood, suggesting that the coronary sinus is the conduit by which these enzymes are liberated into the systemic circulation.

Aged↗
PubMed1990

Antimicrobial effect of chlorhexidine in a controlled release delivery system.

Chlorhexidine is widely used as a mouth rinse in the prevention and treatment of periodontal diseases and dental caries. The purpose of the present study was to evaluate the in vitro antimicrobial effect of chlorhexidine in a controlled release delivery system. The controlled release dispenser comprised a polymeric inner core matrix containing the medicament with an outer vinyl membrane controlling the drug release. The effect on the following bacteria was studied: Actinobacillus actinomycetemcomitans, Actinomyces viscosus, Streptococcus mutans, Wolinella recta, Bacteroides gingivalis, Bacteroides intermedius, Eikenella corrodens, Pseudomonas aeruginosa, Enterobacter aerogenes, and Enterobacter cloacae. Chlorhexidine-containing vinyl patches with a diameter of 5.5 mm were placed on blood agar plates containing the various bacteria. The plates were incubated aerobically or anaerobically at 37 degrees C for 24 h or longer, when appropriate, and examined for inhibition of bacterial growth. Distinct zones of inhibition were seen surrounding all vinyl patches on all plates with all bacteria. Thus, the vinyl dispenser appeared to be an effective vehicle for releasing chlorhexidine to a localized area such as the surface of a tooth, a periodontal pocket, or a root canal.

Bacteria↗
PubMed1990

Measurement of protein synthesis by the phenylalanine flooding dose technique: effect of phenylalanine and anaesthesia on plasma electrolyte, enzyme and metabolite levels.

Ten minutes after an intravenous flooding dose of phenylalanine to rats, plasma sodium and calcium concentrations were slightly reduced (by 2-7%) but no effects on potassium or phosphate were observed. Creatine kinase activities were significantly increased by phenylalanine injection (by 39%), but alkaline phosphatase, alanine aminotransferase, lactate dehydrogenase and aspartate aminotransferase activities were unaltered. Plasma concentrations of total proteins, albumin, cholesterol, triglycerides, urea, creatinine and glucose were also unaffected. In the presence of anaesthesia, phenylalanine injection had almost identical effects, although the increase in creatine kinase activities did not reach statistical significance. Anaesthesia for 10 min reduced plasma potassium concentrations (by 27%), and calcium (by 5%), though phosphate and sodium were unaltered. The activities of lactate dehydrogenase, creatine kinase and aspartate aminotransferase were reduced by between 36-52%, but alkaline phosphatase and alanine aminotransferase activities were unaltered by anaesthesia. Plasma concentrations of total proteins and albumin were also reduced (both by 9%), but glucose concentrations were increased (by 33%). Anaesthesia had no other significant effects on cholesterol, triglycerides, urea or creatinine concentrations. The qualitative effects of anaesthesia in the presence of raised free phenylalanine concentrations were similar. It was concluded that, except for creatine kinase, determinations of plasma constituents in phenylalanine-injected rats could be made without overt interpretational errors. However, caution is required in interpreting data on plasma constituents from anaesthetized rats.

Alanine Transaminase↗
PubMed1985

The oxygen free radical system: potential mediator of myocardial injury.

The sequential univalent reduction of oxygen gives rise to very reactive intermediate products including superoxide anion radical, hydrogen peroxide and free hydroxyl radicals. Normally, the tissue concentration of these intermediate products of oxygen is severely limited; however, if oxygen free radicals are produced in excess of the capacity of the tissues to eliminate them, they may cause serious damage. The biochemistry and possible sources of free radical generation in animal models of ischemic/reperfusion injury are reviewed. The ability of scavengers of oxygen free radicals to improve mechanical, mitochondrial and sarcoplasmic reticulum function in animal models of ischemic/reperfusion injury suggests that oxygen free radicals are partly responsible for myocardial injury in these models. Future research should be directed at establishing the relevance of oxygen radical-mediated myocardial injury in the experimental setting to analogous clinical situations.

Acute Disease↗
PubMed1985

The pulmonary hypertension of sclerosing agents is prevented by cyclooxygenase inhibitors.

Sodium morrhuate and sodium tetradecylsulfate are injected during endoscopic sclerotherapy to control variceal bleeding. When administered to sheep they cause transient pulmonary hypertension and increase protein poor lung lymph flow. To determine the etiology of these alterations, we studied three groups of sheep after establishing acute lung lymph fistulas. In Group 1, indomethacin or ibuprofen was infused. In Group 2, 2.5 cc of sodium morrhuate was injected alone (2A) or after indomethacin or ibuprofen pretreatment (2B). In Group 3, 2.5 cc of sodium tetradecylsulfate was given intravenously either alone (3A) or after indomethacin or ibuprofen (3B). When sclerosing agents were given alone (Group 2A and 3A) pulmonary artery pressures increased three-fold at 30 seconds postinjection to 37 +/- 4.4 and 39 +/- 5.7 mmHg respectively with a slow return to baseline over two hours. Lymph flow increased significantly from 1.3 +/- 1.5 to 2.7 +/- 1.5 cc/30 minutes after sodium morrhuate and from 1.2 +/- .62 to 2.7 +/- 1.7 cc/30 mins at 30 minutes after sodium tetradecylsulfate and the lymph/plasma albumin ratio fell. Increased lymph flow persisted through 120 minutes. In those animals receiving a sclerosing agent after indomethacin or ibuprofen (2B and 3B) there was no change in pulmonary artery pressure, lymph flow, lymph plasma albumin ratio, or lung wet weight to dry weight ratios. We conclude that the pulmonary hypertension and increased protein poor lymph flow are mediated by prostaglandins.

Animals↗
PubMed1985

Oxygen radicals in the adult respiratory distress syndrome, in myocardial ischemia and reperfusion injury, and in cerebral vascular damage.

Recent work suggests that oxygen radicals may be important mediators of damage in a wide variety of pathologic conditions. In this review we consider the evidence supporting the participation of oxygen radicals in the adult respiratory distress syndrome, in ischemia reperfusion injury in the myocardium, and in cerebral vascular injury in acute hypertension and traumatic brain injury. In the adult respiratory distress syndrome there is active sequestration of polymorphonuclear neutrophils in the pulmonary vascular system. There is evidence that activation of these neutrophils results in the production of oxygen radicals which injure the capillary membrane and increase permeability, leading to progressive hypoxia and decreased lung compliance which are hallmarks of the syndrome. In acute arterial hypertension or experimental brain injury oxygen radicals are important mediators of vascular damage. The metabolism of arachidonic acid is the source of oxygen free radical production in these conditions. In myocardial ischemia and reperfusion injury, the ischemic myocyte is "primed" for free radical production. With reperfusion and reintroduction of molecular oxygen there is a burst of oxygen radical production resulting in extensive tissue destruction. Myocardial ischemia--reperfusion injury shares in common with the other two syndromes activation of the arachidonic acid cascade and acute inflammation. Thus it would appear that the generation of toxic oxygen species may represent a final common pathway of tissue destruction in several pathophysiologic states.

Animals↗
PubMed1982

Release of toxic microvesicles by Actinobacillus actinomycetemcomitans.

Oral isolates of Actinobacillus actinomycetemcomitans (strain Y4) release spherical microvesicles in large numbers during normal growth. The biological activities of these products were studied, and it was estimated that approximately 1/10 of their dry weight was made up of heat- and proteolysis-resistant endotoxin. The chicken embryo lethality and bone-resorbing activity of the microvesicles were heat stable but proteolysis sensitive. Other laboratories have reported the presence of a heat- and proteolysis-sensitive leukotoxin in similar preparations. Accordingly, the microvesicles released by strain Y4 may contain, in addition to endotoxin, several potent substances which are highly toxic and active in bone resorption, and these may be significant factors in the pathogenesis of periodontal diseases.

Actinobacillus↗
PubMed1981

Chemotactic response to some arachidonic acid lipoxygenase products in the rabbit eye.

The effects of arachidonic acid, its cyclo-oxygenase and lipoxygenase products and the synthetic chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (FMLP) on leukocyte accumulation in the aqueous humour and intraocular pressure in the rabbit were studied in vivo. Substances were injected into the anterior chamber of the eyes of anaesthetised rabbits using a closed circuit perfusion system. Injection of arachidonic acid, prostaglandins E1 and E2, and the monohydroperoxy and hydroxy acids of the lipoxygenase pathway did not result in any significant accumulation of leukocytes in the anterior chamber. In contrast, FMLP and 5,12-diHETE (Leukotrine B4) resulted in significant dose dependent accumulation of leukocytes into the aqueous humour. Leukocytes appeared in the aqueous humour between 2 and 3 h after the injection of either FMLP or LTB4 and the response was maximal at 4 h. None of the lipoxygenase products tested had any effect on intraocular pressure in contrast to the profound effects observed with arachidonic acid and the E type prostaglandins. FMLP had a small but significant effect on intraocular pressure at the highest dose tested for leukocyte accumulation. These results indicate that the effects of the cyclo-oxygenase products of arachidonate metabolism are mainly vascular in the rabbit eye in contrast to the predominantly cellular effects of lipoxygenase products. Thus in the eye, the interaction of cyclo-oxygenase and lipoxygenase products of arachidonate metabolism may be important in the development of both acute and chronic ocular inflammation.

Animals↗