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Biomedical subjects

A Sumner

Publications and source records attributed to A Sumner.

15 recordsLinked to original sources
PubMed2001

The structure of verbal abilities in young and older adults.

Four language sample measures as well as measures of vocabulary, verbal fluency, and memory span were obtained from a sample of young adults and a sample of older adults. Factor analysis was used to analyze the structure of the vocabulary, fluency, and span measures for each age group. Then an "extension" analysis was performed by using structural modeling techniques to determine how the language sample measures were related to the other measures. The measure of grammatical complexity was associated with measures of working memory including reading span and digit span. Two measures, sentence length in words and a measure of lexical diversity, were associated with the vocabulary measures. The fourth measure, propositional density, was associated with the fluency measures as a measure of processing efficiency. The structure of verbal abilities in young and older adults is somewhat different, suggesting age differences in processing efficiency.

Adult↗
PubMed1999

Hyperinsulinism and sex hormones in young adult African Americans.

Hyperinsulinemia is a risk factor for cardiovascular disease, and is linked with non-insulin-dependent diabetes mellitus (NIDDM), hyperlipidemia, obesity, and hypertension. Sex hormones also play a role in the metabolic alterations associated with the risk for cardiovascular disease. A reduction in sex hormone-binding globulin (SHBG) may be predictive of future NIDDM particularly in women. The postmenopausal decline in estrogen is also associated with an increase in risk factor expression in women. Since African Americans experience a greater prevalence of NIDDM, obesity, and hypertension, conditions associated with hyperinsulinemia, the purpose of this study was to determine if alterations in sex hormone levels are associated with the plasma insulin concentration in young adult African Americans, and to determine if there are sex differences in the effect of insulin on lipids and sex hormones. In a sample of 221 nondiabetic African American men (n = 105) and women (n = 116) with a mean age of 31 years, we examined the relationship of the plasma insulin concentration with the body mass index (BMI), blood pressure, plasma lipids, and sex hormones, including free testosterone, estradiol, and SHBG. Plasma insulin increased with the BMI and other measures of adiposity (P<.001) in men and women. Significant correlations of insulin with plasma lipids were also present in both sexes. There was a significant inverse correlation of insulin with SHBG in both men (r = .28, P = .007) and women (r = .27, P = .02). There was a significant direct correlation of insulin with free testosterone in women (r = .032, P<.001). Stepwise multiple regression analyses with insulin as the dependent variable detected the BMI, triglyceride, and apolipoprotein A1 as significant contributors to the plasma insulin concentration in men. In women, the multiple regression model detected percent body fat, low-density lipoprotein (LDL) cholesterol, and free testosterone as significant contributors to plasma insulin. These data on young African Americans demonstrate a significant relationship between hyperinsulinemia and obesity, atherogenic lipid status, and lower SHBG. In the premenopausal women, the lower SHBG is linked with higher free testosterone, favoring a condition of relative androgen excess.

Adult↗
PubMed1999

Physiological values and procedures in the 24 h before ICU admission from the ward.

Physiological values and interventions in the 24 h before entry to intensive care were collected for admissions from hospital wards. In a 13-month period, there were 79 admissions in 76 patients who had been in hospital for at least 24 h and had not undergone surgery within 24 h of admission to intensive care. Thirty-four per cent of patients underwent cardiopulmonary resuscitation before intensive care admission. Using Acute Physiology and Chronic Health Evaluation II scoring to quantify abnormal physiology in the group as a whole, a significant deterioration in respiratory function before admission was found. During the 6-h period immediately before intensive care admission, 75% of patients received oxygen, 37% underwent arterial blood gas sampling, and oxygen saturation was measured in 61% of patients, 63% of whom had an oxygen saturation of less than 90%. Overall hospital mortality in the study group was 58%. Information collected on the wards identified seriously ill patients who may have benefited from earlier expert treatment.

APACHE↗
PubMed1999

The patient-at-risk team: identifying and managing seriously ill ward patients.

A 'patient-at-risk team', established to allow the early identification of seriously ill patients on hospital wards, made 69 assessments on 63 patients over 6 months. Predefined physiological criteria were not able to reliably predict which patients would be admitted to the intensive care unit. The incidence of cardiopulmonary resuscitation before intensive care admission was 3.6% for patients seen by the team and 30.4% for those not seen (p < 0.005). Of admissions seen by the team, 25% died on the intensive care unit compared with 45% of those not seen (not significant, p = 0.07). Among those not seen by the team, mortality was 40% for those who did not require resuscitation and 57% for those who did (not significant). Many critically ill ward patients had abnormal physiological values before intensive care unit admission. Identification of critically ill patients on the ward and early advice and active management are likely to prevent the need for cardiopulmonary resuscitation and to improve outcome.

APACHE↗
PubMed1998

APACHE II, data accuracy and outcome prediction.

From review of 122 intensive care charts, Acute Physiology and Chronic Health Evaluation (APACHE) II points were determined for eight physiological values. Using a strict interpretation of APACHE II criteria, an average of 20.6% of these points were higher and 6.7% lower than the points entered originally into an intensive care database. The resulting 1.73 points mean increase in APACHE II score increased predicted mortality from 24.8% to 27.8% and decreased the mortality ratio (observed hospital deaths devided by predicted deaths) from 1.52 (95% confidence interval: 1.11-2.03) to 1.35 (95% confidence interval: 0.99-1.81). There were few errors entering the data recorded on the audit form into the intensive care unit database with an optical mark reader and keyboard. Inaccuracy and inconsistency in data collection must be excluded before differences in mortality ratios are ascribed to intensive care unit performance.

APACHE↗
PubMed1998

Outcome of intensive care patients in a group of British intensive care units.

OBJECTIVE: To identify priorities for intensive care unit (ICU) intervention and research. DESIGN: Analysis of a large intensive care database. SETTING: Twenty-four ICUs in the North Thames region of the United Kingdom. PATIENTS: All patients admitted to an ICU between January 1, 1992, and April 31, 1996, on whom data had been entered into the database. Patients who were admitted after cardiac surgery, who had burns, or were <16 yrs of age were excluded from the study, as were data from patients with a previous ICU admission within 6 mos or where ICU or hospital outcome was unknown. Data were excluded from units that had entered <300 patients into the database. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: A total of 23,331 admissions with complete records were available. After exclusions, 12,762 admissions from 15 ICUs were selected for analysis. Hospital mortality was 32.5% with a mortality ratio of 1.14 (95% confidence interval 1.10 to 1.17). Nonsurvivors were older than survivors and had longer ICU stays. Patients admitted from wards had a higher mortality than patients from the operating room/recovery or the emergency department. Observed percentage mortality increased linearly with mortality predicted by Acute Physiology and Chronic Health Evaluation II, although the number of patients who died remained broadly constant across the range of predicted mortality. Twenty-seven percent of all deaths occurred after discharge from the ICU. Patients admitted after cardiopulmonary resuscitation constituted 30% of all deaths. Thirty-four percent of patients were in the ICU for >2 days, and they accounted for nearly 81% of bed days. CONCLUSIONS: Early identification of patients at risk, both before admission and after discharge from the ICU, may allow treatment to decrease mortality. Research and resources may be best directed at patients who die, despite a relatively low predicted mortality. Although these patients are a small percentage of the low-risk admissions, they constitute a large number of ICU deaths. Many patients die after discharge from ICU and this mortality may be decreased by minimizing inappropriate early discharge to the ward, by the provision of high-dependency and step-down units, and by continuing advice and follow-up by the ICU team after the patient has been discharged. Intervention before ICU admission and support of patients after discharge from the ICU should be part of the effort to decrease mortality for ICU patients. Inadequate provision of resources for critically ill patients may result in excess intensive care mortality that is not detected with ICU outcome prediction methods.

APACHE↗
PubMed1990

Electrophysiologic evaluation of peripheral nerve regeneration through allografts immunosuppressed with cyclosporin.

A model was designed to evaluate the long-term in vivo electrophysiology of rat peripheral nerve transplants. The application of this model was demonstrated using cyclosporin (CSA) immunosuppression of recipient animals to facilitate peripheral nerve regeneration through nerve allografts. Isogenic Brown Norway (BN) rats [RT1n] were divided into three groups: two received Lewis (LE) rat [RT1l] allografts and one received BN isografts. One allograft recipient group received CSA immunosuppression for the duration of the investigation (150 days). Successful nerve regeneration in the isograft and the immunosuppressed allograft recipient groups was determined by immunohistochemical methods and serial in vivo electrophysiologic techniques to measure nerve conduction velocity and evoked compound muscle action potential amplitude. Statistical analysis of these results indicate that: (a) CSA immunosuppression of peripheral nerve allograft recipients facilitates peripheral nerve regeneration which is indistinguishable from isograft recipient controls at the functioning axon level; and (b) in vivo electrophysiologic monitoring in this model is particularly useful for long term peripheral nerve transplantation studies permitting serial assessment of regeneration with little morbidity.

Action Potentials↗
PubMed1989

Effect of the venodilated state on sympathetic-induced venoconstriction in normal subjects.

The interaction between venoconstriction induced by application of ice to the forehead and nitroglycerin-induced venodilation was examined in 19 healthy male volunteers, ages 25 +/- 5 years (mean +/- standard deviation). Venous tone was determined by the equilibration technique. Mercury-in-silastic plethysmography was used to measure changes in forearm volume before and after ice application during control conditions, and before and after ice application in the venodilated state (nitroglycerin spray, 0.8 mg). Venous tone and arterial pressure increased significantly after the application of ice to the forehead in both the control and venodilated states, indicating that ice increased sympathetic tone. Nitroglycerin increased venous volume by 0.28 cc/100 cc arm. The venoconstrictive effect of ice after nitroglycerin (a decrease in venous volume of 0.53 cc/100 cc arm) was quantitatively similar to the venoconstrictive effect of ice during control conditions (a decrease in venous volume of 0.54 cc/100 cc arm). These results suggest that sympathetic-induced venoconstriction is not attenuated in the venodilated state.

Adult↗
PubMed1989

Effects of posture on the venodilatory response to nitroglycerin.

To determine the effects of posture on the venodilatory response to nitroglycerin (TNG), the change in forearm venous volume after inflation of an upper arm cuff to 30 mmHg above cuff zero (VV[30]) was measured during control conditions and after TNG (0.8 mg spray) in 18 healthy young volunteers in the supine position and the sitting position. VV[30] was 3.24 +/- 0.98 ml/100 ml arm in the supine position and 2.46 +/- 1.32 ml/100 ml arm in the sitting position. TNG increased VV[30] by 0.56 +/- 0.19 ml/100 ml arm in supine subjects, but by only 0.38 +/- 0.17 ml/100 ml arm in sitting subjects (P = 0.013). When limb volume was measured in the forearm and calf without using a cuff to produce venous congestion, the increase in limb volume with TNG was significantly greater in the sitting than in the supine position. Because the fall in both systolic and diastolic pressure and the rise in heart rate were significantly greater after TNG was administered in the sitting position, it is suggested that a greater reflex venoconstriction occurred in this posture, which antagonized the TNG-induced increase in venous distensibility. In the seated position, the effect of gravity more than compensated for the impaired venodilatory response to TNG. These results suggest that TNG causes a greater reduction in venous return to the heart when administered in the sitting position than in the supine position.

Adult↗
PubMed1985

Relapsing ophthalmoparesis-sensory neuropathy syndrome.

We studied two patients with recurrent sensory neuropathy and weakness of extraocular muscles. There was electrophysiologic evidence of multifocal demyelination of sensory nerves, with relative sparing of somatic motor nerves. Sural nerve biopsy in one patient showed segmental demyelination. We believe that these patients had an unusual form of inflammatory polyneuropathy--possibly a relapsing variant of the Miller-Fisher syndrome of acute idiopathic polyneuritis.

Female↗
PubMed1982

[Electrophysiological and morphological effects of the injection of Guillain-Barré sera in the sciatic nerve of the rat (author's transl)].

Serum from 3 of 4 patients with classical Guillain-Barré syndrome has produced conduction block in a large proportion of motor axons following subperineurial injection into 13 rat sciatic nerves. These effects, although qualitatively similar to those previously described for certain experimental sera (EAN, EAE, and anti-Gal-Cer), are notably slower in evolution. Conduction block does not begin until more than 24 hours after injection and is maximal at about 5 days. Between 6 and 8 days the appearance of long latency responses signals return of conduction in previously blocked axons. Thereafter return to control values is rapid and complete within 10 to 15 days. Six control human sera injected into 13 sciatic nerves have shown no comparable effect. Correlative morphological studies indicate that these Guillain-Barré sera produce focal demyelination which evolves pari passu with conduction block. Demyelination appears to evolve both by vesicular disruption and by macrophage mediated myelin stripping. A factor is present in the serum of some patients with Guillain-Barré syndrome, which given access to the endoneurial environment produces active demyelination with conduction block. We believe that the production of this factor could be responsible for the polyradiculoneuropathy of this disease.

Animals↗
PubMed1979

Skeletal muscle calcium metabolism and contractile force in vitamin D-deficient chicks.

The myopathy associated with vitamin D deficiency has not been well characterized, and it is not known if weakness is a result of a specific effect of vitamin D deficiency on skeletal muscle. Chicks were raised from hatching on a vitamin D-deficient diet, and by 3 wk of age were hypocalcemic and appeared weak. Tension generated by triceps surae during repetitive stimulation of posterior tibial nerve was significantly less than that developed by chicks given vitamin D(3) supplements (309 g tension/g wet weight of triceps surae, SD 60, for vitamin D-deficient chicks; 470, SD 77, for vitamin D(3)-treated chicks, P < 0.01). Histochemical and electron microscopic examination of skeletal muscles of these chicks showed no abnormalities, and there were no electrophysiologic evidences of motor nerve or neuromuscular junction dysfunction. The concentration of ATP in skeletal muscle of the vitamin D-deficient chicks (5.75 mumol/g wet weight, SD 0.17) was not significantly different from that in vitamin D-treated chicks (5.60, SD 0.50). There was no correlation between strength and serum calcium, serum inorganic phosphate, or skeletal muscle inorganic phosphate. Relaxation of tension after tetanic stimulation was slowed in the vitamin D-deficient chicks (20.6 ms, SD 1.7, vs. 15.4, SD 1.3, in vitamin D-treated chicks and 15.3, SD 1.0, in normal control chicks), and in vitro (45)Ca(++) transport by sarcoplasmic reticulum from the vitamin D-deficient chicks was reduced. Calcium content of mitochondria prepared from leg muscles of vitamin D-deficient chicks (24 nmol/mg mitochondrial protein, SD 6) was considerably lower than that of mitochondria from normal control chicks (45, SD 8) or from chicks treated with vitamin D for 2 wk or more (66-100, depending upon level and duration of therapy). Treatment of the vitamin D-deficient chicks from hatching with sufficient dietary calcium to produce hypercalcemia did not significantly raise skeletal muscle mitochondrial calcium content (31 nmol/mg mitochondrial protein, SD 7) and did not prevent weakness. These studies demonstrate objective weakness as a result of myopathy in vitamin D-deficient chicks, and provide evidence that vitamin D deficiency has effects on skeletal muscle calcium metabolism not secondary to altered plasma concentrations of calcium and phosphate.

Animals↗