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Biomedical subjects

D Kaye

Publications and source records attributed to D Kaye.

At least 37 records · Page 2Linked to original sources
PubMed2001

Sympathetic nerve biology in essential hypertension.

1. Although the importance of sympathetic nervous activation in the pathogenesis of essential hypertension is well documented, the exact pathophysiology of the sympathetic nervous dysfunction present remains to be delineated. There are several possible explanations for the increased spillover of noradrenaline from the kidneys and heart to plasma, a key piece of evidence supporting the neurogenic basis of essential hypertension, in addition to the obvious one of an increased rate of sympathetic nerve firing. 2. The possibility that there may be an increase in the density of sympathetic innervation in human hypertension, well documented in the spontaneously hypertensive rat, is currently under investigation by us. 3. Adrenaline cotransmission is present in the cardiac sympathetic nerves of patients with essential hypertension, presumptive evidence of their exposure to high levels of stress and a possible basis for the observed increase in cardiac noradrenaline spillover, through presynaptic augmentation of noradrenaline release. 4. Phenotypic evidence exists also of faulty noradrenaline reuptake into the sympathetic nerves of the heart in essential hypertension, an abnormality that would amplify the sympathetic neural signal by impairing removal of noradrenaline from the synaptic cleft.

Aging↗
PubMed2001

Domestic violence and induced-abortion: report of three cases.

Domestic violence not only violates women's rights, but is also associated with adverse consequences ranging from physical injury to psychological morbidity. Several studies have associated domestic violence with risk of having an induced-abortion. The following three cases indicate that domestic violence may not cause unwanted pregnancy, but may be the reason that leads victims to resort to abortion.

Abortion, Induced↗
PubMed2001

Risk factors for preterm premature rupture of membranes at Mulago Hospital, Kampala.

OBJECTIVE: To evaluate the epidemiological risk factors in patients admitted at Mulago Hospital with preterm premature rupture of the membranes from their socio-demographic characteristics and reproductive history. DESIGN: Cross-sectional case control study. SETTING: Labour ward, Mulago Hospital, Kampala, Uganda. METHODS: Cases were enrolled at admission while controls were enrolled after a term delivery not preceded by pre-mature rupture of the membrane (PROM). Controls were matched for age range (age +/- 2 years) and parity with the cases. A detailed history of socio-demographic characteristics, past medical and surgical illness and past reproductive history were obtained and data entered into a coded questionnaire. Endocervical swabs and amniotic fluid samples were taken from the cases during labour. Validity was assessed using Chi-square with a p-value of less than 0.05 considered significant. RESULTS: Maternal socio-demographic characteristics were similar for cases and controls. A history of hypertension, abortion, prior PROM, Caesarean section, cervical cerclage, cervical incompetence or abnormal vaginal discharge were significant risk factors for preterm PROM (p < 0.05). CONCLUSION: There are factors by which mothers at risk of preterm PROM can be identified before onset of rupture.

Abortion, Spontaneous↗
PubMed2000

Risk factors for infective endocarditis: oral hygiene and nondental exposures.

BACKGROUND: The risks of infective endocarditis (IE) associated with various conditions and procedures are poorly defined. METHODS AND RESULTS: This was a population-based case-control study conducted in 54 Philadelphia, Pa-area hospitals from 1988 to 1990. Community-acquired IE cases unassociated with intravenous drug use were compared with matched community residents. Subjects were interviewed for risk factors. Diagnoses were confirmed by expert review of medical record abstracts with risk factor data removed. Cases were more likely than controls to suffer from prior severe kidney disease (adjusted OR [95% CI]=16.9 [1.5 to 193], P:=0.02) and diabetes mellitus (adjusted OR [95% CI]=2.7 [1.4 to 5.2], P:=0.004). Cases infected with skin flora had received intravenous fluids more often (adjusted OR [95% CI]=6.7 [1.1 to 41], P:=0.04) and had more often had a previous skin infection (adjusted OR [95% CI]=3.5 [0.7 to 17], P:=0.11). No association was seen with pulmonary, gastrointestinal, cardiac, or genitourinary procedures or with surgery. Edentulous patients had a lower risk of IE from dental flora than patients who had teeth but did not floss. Daily flossing was associated with a borderline decreased IE risk. CONCLUSIONS: Within the limits of the available sample size, the data showed that IE patients differ from people without IE with regard to certain important risk factors but not regarding recent procedures.

Adolescent↗
PubMed2000

Multidrug-resistant Pathogens: Mechanisms of Resistance and Epidemiology.

Resistance to antimicrobial agents among bacteria and fungi is a persistent problem complicating the management of critically ill patients. To understand the issues involved in resistance in critical care, it is essential to understand the epidemiology and mechanisms of resistance. beta-lactam resistance in pneumococci, and penicillin and chloramphenicol resistance in Neisseria meningitidis, have complicated the management of meningitis. Vancomycin resistance in enterococci and methicillin resistance in Staphylococcus aureus have disseminated among hospitals, nursing homes and, in some cases, community patients. Glycopeptide resistance in S. aureus has recently been described in clinical isolates; the potential for spread of this resistance trait is concerning. Resistance to broad-spectrum cephalosporins is a persistent challenge in the management of infections caused by Pseudomonas areuginosa, and Enterobacter species, as well as other Enterobacteriaceae. Azole resistance in Candida species. has also complicated the treatment of nosocomial infections. Resistance to antimicrobial drugs is a persistent and emerging problem and presents major therapeutic challenges.

Journal Article↗
PubMed2000

Principles of selection and use of antibacterial agents. In vitro activity and pharmacology.

The selection of an antimicrobial treatment regimen is based on many factors, including the nature of the infection, the identity and susceptibility pattern of the infecting organisms, and the pharmacokinetics and pharmacodynamics of the antibacterial drugs. This article discusses principles of susceptibility testing, pharmacology, and monitoring of therapy.

Anti-Bacterial Agents↗
PubMed2000

Antibiotic agents in the elderly.

Changes that occur in the pharmacology of drugs in the elderly must be considered in the use of antimicrobial agents. Although absorption of orally administered drugs is not affected in a significant way, renal function decreases, drug-drug interactions increase, compliance with regimens may be decreased, and drug toxicity is increased. The most frequent infections occurring in the elderly are pneumonia, urinary tract infection, and soft-tissue infection. CDAD is usually a complication of antibiotic therapy. Pneumonia can be categorized as community-acquired, LTCF, and hospital-acquired. Therapeutic approaches vary according to which of these sites is involved. Urinary tract infection is divided into upper tract infection, lower tract infection, and asymptomatic bacteriuria. Upper tract infection is treated for a longer period than lower tract infection; with few exceptions, asymptomatic bacteriuria is usually not treated. Soft-tissue infection is usually caused by an infected pressure ulcer or cellulitis (which may be a complication of a diabetic foot ulcer or an ulcer due to peripheral vascular disease). These infections have different microbial causes and require different therapeutic approaches.

Aged↗
PubMed2000

Measurement of sympathetic nervous system activity in heart failure: the role of norepinephrine kinetics.

Recent demonstration that the level of sympathetic nervous drive to the failing heart in patients with severe heart failure is a major determinant of prognosis, and that mortality in heart failure is reduced by beta-adrenergic blockade, indicate the clinical relevance of heart failure neuroscience research. The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with the application of isotope dilution methods for measuring cardiac norepinephrine release to plasma indicating that in untreated patients cardiac norepinephrine spillover is increased as much as 50-fold, similar to levels of release seen in the healthy heart during near maximal exercise. This preferential activation of the cardiac sympathetic outflow contributes to arrhythmia development and to progressive deterioration of the myocardium, and has been linked to mortality in both mild and severe cardiac failure. Although the central nervous system mechanisms involved in the sympathetic nervous activation at present remain uncertain, increased intracardiac diastolic pressure seems to be one peripheral reflex stimulus, and increased forebrain norepinephrine turnover an important central mechanism.Additional neurophysiological abnormalities present in the failing human heart include release of the sympathetic cotransmitters, epinephrine and neuropeptide Y, at high levels more typical of their release during exercise in healthy subjects, and the possible presynaptic augmentation of norepinephrine release from the cardiac sympathetic nerves by the regionally released epinephrine. Following on the demonstrable benefit of beta-adrenergic blockade in heart failure, additional antiadrenergic measures (central suppression of sympathetic outflow with imidazoline binding agents such as clonidine, blocking of norepinephrine synthesis by dopamine-beta-hydroxylase inhibition, antagonism of neuropeptide Y) are now under active investigation.

Adrenergic beta-Antagonists↗
PubMed2000

Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease.

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.

Heart Diseases↗
PubMed2000

Quality of midwifery care in Soroti district, Uganda.

OBJECTIVES: To determine the quality of care provided by midwives in Soroti district; and specifically, to identify training needs, gaps in knowledge and other barriers to accessibility of emergency obstetric care (EmOC) services in Soroti district. DESIGN: Cross-sectional descriptive study. SETTING: One regional hospital, one district hospital, two health centres and four dispensaries, all health units in the district. SUBJECTS: Patients admitted in the health units with pregnancy complications; attendants of patients (above); midwives delivering health care at the health units; pregnant women exiting from (after attending) antenatal clinics; and health unit records. INTERVENTIONS: Participatory observation, midwife and client interviews, records review, facility assessment and focus group discussions with clients and patients. MAIN OUTCOME MEASURES: Ability of midwives to provide antenatal care of a minimum standard, or recall causes, signs, symptoms or the management of common obstetric complications; and patients and patient attendants' perception of care received. RESULTS: Many midwives were providing care of poor quality for both antenatal and delivery care due to their inability to identify and manage women with or at risk of pregnancy complications. CONCLUSION: The main factors identified as responsible for the poor quality of care were inadequate pre-service and in-service training, lack of technical support supervision and absence of standard treatment guidelines.

Clinical Competence↗
PubMed1999

Immune response to influenza vaccination in a large healthy elderly population.

Elderly individuals not only demonstrate a greater risk of morbidity and mortality from influenza than the young, but also have greater difficulty mounting a protective response to influenza vaccine. The mechanism of the decreased efficacy of influenza vaccination in the elderly is not well understood. The present study was designed to assess the interaction between cell-mediated and humoral immune responses to influenza vaccine in a large population (n = 233) of healthy elderly individuals (mean age = 80.7) living in six continuing care retirement communities (CCRCs). While influenza vaccination resulted in significant increases in the mean anti-influenza antibody titres and mean proliferative responses of peripheral blood mononuclear cells to purified subvirion trivalent influenza vaccine one month after vaccination, only 48.9% and 30.0% of subjects had intact humoral and cell-mediated immune responses, respectively. No association was observed between intact cell-mediated and humoral responses: 14.7% of subjects had an intact cell-mediated, but not humoral response, and 32.6% of subjects had an intact humoral, but not cell-mediated response. However, IFNgamma production was significantly correlated with both antibody and cell-mediated responses to influenza vaccination, a finding not previously reported in the elderly. These results indicate that there is considerable heterogeneity among immune responses of the elderly to influenza vaccination. This heterogeneity needs to be a major consideration in evaluation of new vaccine preparations.

Aged↗
PubMed1999

Leptin is released from the human brain: influence of adiposity and gender.

Leptin, a 16-kDa circulating protein primarily derived from adipocytes, is an important factor in the regulation of appetite and energy expenditure. Using simultaneous arterio-venous blood sampling, several organs were assessed with regard to their individual roles in leptin metabolism in healthy male and female subjects constituting a range of body mass indices. Plasma leptin levels were unchanged after passage through the hepatosplanchnic and forearm circulations. In contrast, concentrations in the renal vein were consistently lower than those in the renal artery (-15%; P<0.005), indicating net extraction, whereas the brain was observed to be a net leptin releaser. Concentrations in the internal jugular vein were significantly higher than arterial levels in lean females (change, 3.0+/-1.2 ng/mL; P<0.02) and in obese males (body mass index, >28 kg/m2), but not lean (change, 2.3+/-2.3 vs. 0.1+/-0.1 ng/mL, respectively; P<0.05), indicating a probable influence of both gender and adiposity on brain leptin release. An attempt to grossly localize the site of brain release by using cerebral venous scans to distinguish between jugular venous drainage from cortical and subcortical brain areas revealed no region-specific secretion. These data raise the possibility that the brain is a nonadipose source of leptin. In addition, the higher level of brain release observed in females may contribute to the well documented gender differences in overall plasma leptin levels.

Adipose Tissue↗
PubMed1998

Dental and cardiac risk factors for infective endocarditis. A population-based, case-control study.

BACKGROUND: Although antibiotic prophylaxis against infective endocarditis is recommended, the true risk factors for infective endocarditis are unclear. OBJECTIVE: To quantitate the risk for endocarditis from dental treatment and cardiac abnormalities. DESIGN: Population-based, case-control study. SETTING: 54 hospitals in the Philadelphia area. PATIENTS: Persons with community-acquired infective endocarditis not associated with intravenous drug use were compared with community residents, matched by age, sex, and neighborhood of residence. MEASUREMENTS: Information on demographic characteristics, host risk factors, and dental treatment was obtained from structured telephone interviews, dental records, and medical records. RESULTS: During the preceding 3 months, dental treatment was no more frequent among case-patients than controls (adjusted odds ratio, 0.8 [95% CI, 0.4 to 1.5]). Of 273 case-patients, 104 (38%) knew of previous cardiac lesions compared with 17 controls (6%) (adjusted odds ratio, 16.7 [CI, 7.4 to 37.4]). Case-patients more often had a history of mitral valve prolapse (adjusted odds ratio, 19.4 [CI, 6.4 to 58.4]), congenital heart disease (adjusted odds ratio, 6.7 [CI, 2.3 to 19.4]), cardiac valvular surgery (adjusted odds ratio, 74.6 [CI, 12.5 to 447]), rheumatic fever (adjusted odds ratio, 13.4 [CI, 4.5 to 39.5]), and heart murmur without other known cardiac abnormalities (adjusted odds ratio, 4.2 [CI, 2.0 to 8.9]). Among case-patients with known cardiac lesions--the target of prophylaxis--dental therapy was significantly (P = 0.03) less common than among controls (adjusted odds ratio, 0.2 [CI, 0.04 to 0.7] over 3 months). Few participants received prophylactic antibiotics. CONCLUSIONS: Dental treatment does not seem to be a risk factor for infective endocarditis, even in patients with valvular abnormalities, but cardiac valvular abnormalities are strong risk factors. Few cases of infective endocarditis would be preventable with antibiotic prophylaxis, even with 100% effectiveness assumed. Current policies for prophylaxis should be reconsidered.

Adolescent↗
PubMed1998

Increased sympathetic nervous system activity and its therapeutic reduction in arterial hypertension, portal hypertension and heart failure.

Although the underlying mechanisms no doubt differ, activation of the sympathetic nervous system is an important pathophysiological feature in primary arterial hypertension, in portal hypertension accompanying hepatic cirrhosis, and in heart failure, and is a logical therapeutic target for centrally acting sympathetic nervous system suppressant drugs. Portal hypertension: The sympathetic outflows to skeletal muscle vasculature, the heart, the kidneys and to the hepatomesenteric circulation are stimulated in patients with alcoholic cirrhosis of the liver, perhaps as a reflex response to the vasodilatation and vascular shunting present. Acute dosing with clonidine produces dose dependent reduction in noradrenaline spillover from visceral organs and reduction in hepatic vein wedge pressure, with preservation of hepatic blood flow and negligible fall in arterial pressure. These findings indicate the clinical potential of drugs such as clonidine, moxonidine and rilmenidine for chronically lowering portal venous pressure in cirrhosis. Arterial hypertension: Activation of the sympathetic outflow to the heart, kidneys and skeletal muscle vasculature is commonly present in younger (< 45 years) patients with essential hypertension. The sympathetic stimulation appears to have adverse consequences in hypertensive patients beyond blood pressure elevation. Neural vasoconstriction in skeletal muscle has metabolic effects by impairing glucose delivery, which is a basis for insulin resistance and hyperinsulinemia. Within the heart a trophic effect of sympathetic activation on cardiac growth, contributing to the development of left ventricular hypertrophy, and an arrhythmogenic effect are also likely. Cardiac failure: The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with norepinephrine release from the failing heart at rest being increased as much as 50-fold, similar to the level seen in healthy people during near maximum exercise. This preferential activation of the cardiac sympathetic outflow contributes to arrhythmogenesis and possibly to progression of the heart failure, and has been directly linked to mortality; a high rate of spillover of noradrenaline from the heart is a strong, independent predictor of poor prognosis in severe cardiac failure. The mechanisms underlying sympathetic nervous stimulation are not entirely clear. Increased intracardiac diastolic pressure seems to be one peripheral signal, and increased forebrain norepinephrine turnover an important central mechanism. Following the demonstration of the beneficial effect of the beta-adrenergic blocker, carvedilol, and with second generation centrally acting sympathetic suppressants now under clinical investigation, elucidation of the abnormalities in central nervous control of sympathetic outflow in heart failure has become clinically relevant.

Animals↗
PubMed1998

Fatal Legionella longbeachae infection following heart transplantation.

A case of fatal Legionella longbeachae infection following heart transplantation is described. Gram stains of respiratory secretions on day 17 posttransplant revealed leucocytes and gram-negative bacilli, but there was no growth on routine bacterial culture. Legionella longbeachae serogroup 1 was isolated from respiratory specimens, blood, and postmortem lung tissue. Legionella longbeachae is a common cause of legionellosis in Australia, and infection has been associated with exposure to potting mixes. Specific culture for Legionella spp. should be performed for any patient who develops pneumonia following organ transplantation.

Cross Infection↗
PubMed1997

Adrenergic nervous system in heart failure.

Recent demonstration that the level of sympathetic nervous drive to the failing heart in patients with severe heart failure is a major determinant of prognosis, and that mortality in heart failure is decreased by beta-adrenergic blockade with carvedilol, indicates the clinical relevance of cardiac neuroscience research. Important initial findings were observations that the plasma concentration of the sympathetic neurotransmitter, norepinephrine, is elevated in heart failure, and that overall clinical outcome is related to plasma norepinephrine concentration (although heart failure severity may be a confounder). Sympathetic nerve recording (clinical microneurography) and radiotracer methods measuring regional sympathetic activity in the heart (cardiac norepinephrine "spillover") have now largely supplanted antecubital venous norepinephrine measurements as research tools, with newer methods providing information on regional sympathetic function that was previously lacking. The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with norepinephrine release from the failing heart at rest in untreated patients increased up to 50-fold, which is similar to the level of release in healthy hearts during near maximal exercise. There is lesser stimulation of the sympathetic outflows to the kidneys and skeletal muscle. In early mild heart failure, it is only the cardiac sympathetic nerves that are activated. This preferential activation of cardiac sympathetic outflow contributes to arrhythmia development and probably to progression of heart failure and has been linked to mortality in mild and severe heart failure. The central nervous system mechanisms involved in the sympathetic nervous activation present in patients with heart failure remain uncertain. Increased intracardiac diastolic pressure seems to be one peripheral reflex stimulus with increased forebrain norepinephrine turnover being an important central mechanism.

Disease Progression↗