Biomedical subjects
M Kemp
Publications and source records attributed to M Kemp.
[Penicillin resistant pneumococci--not a threat in Denmark yet?].
The occurrence of penicillin resistance in clinical isolates of pneumococci was investigated in two clinical microbiological laboratories in Copenhagen, Denmark. One of the laboratories predominantly received samples from patients with frequent use of antibiotics mainly because of chronic lung diseases. In this laboratory, 6.3% of 245 isolates of pneumococci had intermediate resistance to penicillin. In the other laboratory, which received samples from a number of hospitals and general practice, only 1.3% of isolates of pneumococci had reduced sensitivity to penicillin. Penicillin-resistant pneumococci are rare in Denmark, but are more prevalent in patients who frequently use antibiotics.
Socio-economic and dietary influences on leg length and trunk length in childhood: a reanalysis of the Carnegie (Boyd Orr) survey of diet and health in prewar Britain (1937-39).
Social class differences in height have been recognised for many centuries. However, few studies have examined the extent to which these differences are made up of differences in leg length or trunk length. This paper reanalyses cross-sectional information on children examined in Britain in the 1930s. We assess associations between socio-economic status and diet and the components of childhood stature. The analyses were based on the records of 2990 children aged 2 years to 14 years 9 months who were examined in the Carnegie (Boyd Orr) survey of diet and health (1937-39). z-Scores for the measures of childhood stature were calculated using polynomial regression techniques with the study population as the standard. Univariable and multivariable statistical techniques were used to assess the relationships between childhood height, leg length and trunk length, and dietary and socio-economic factors measured at the level of the household. Leg length was the component of stature most strongly associated with measures of childhood diet and socio-economic status. A greater part of the difference in stature between socio-economic groups was caused by differences in leg length rather than trunk length. In multiple regression analyses, district of residence and family food expenditure were generally the two factors most strongly related to stature. In a subsample of the surveyed children, for whom birthweight information was available, trunk length and leg length were equally strongly related to birthweight. Leg length appears to be a particularly sensitive indicator of childhood socio-economic circumstances. Although contemporary studies highlight the importance of biological factors in determining childhood height, the data analysed in this study suggest that socio-economic circumstances were also important in explaining height differentials in prewar Britain.
Humoral and cellular immune responses to synthetic peptides of the Leishmania donovani kinetoplastid membrane protein-11.
Native kinetoplastid membrane protein-11 (KMP-11), purified from crude extracts of Leishmania donovani parasites, activates T cells from individuals who have recovered from visceral leishmaniasis. In this work we used three 38-mer peptides spanning the amino acid sequence of the L. donovani KMP-11 as solid-phase ligands in enzyme-linked immunosorbent assays (ELISAs) and as stimulating antigens in lymphoproliferative assays in order to evaluate humoral and cellular immune responses to well-defined sequences of the protein. Antibody reactivity against the three peptides was measured in plasma from 63 Sudanese visceral leishmaniasis patients (VL) and the percentage of patients with anti-KMP-11 antibodies in ELISA were 37% (KMP-11-1), 30% (KMP-11-2) and 58% (KMP-11-3). The fraction of VL patients with measurable antibody reactivity in one or more of the three ELISAs was 79%. Cross-reactivity to the KMP-11 peptides was detected in plasma from Sudanese patients suffering from Leishmania major infections and in plasma from Sudanese and Danish patients infected with Plasmodium falciparum. In lymphoproliferative assays, 10 of 17 PBMC isolates from donors previously infected with L. donovani showed a response to one or more of the three KMP-11 peptides.
Gastro-intestinal protein loss in late survivors of Fontan surgery and other congenital heart disease.
AIMS: Protein losing enteropathy is a serious complication of Fontan surgery. The aim of this study was to investigate gastro-intestinal protein loss in adults with congenital heart disease, both with and without Fontan surgery, and to correlate findings with systemic venous pressure. METHODS AND RESULTS: Forty eight patients were studied. The first group included adult survivors of Fontan surgery. The second and third groups were control patients with congenital heart disease who had not had Fontan surgery and had either normal or chronically elevated systemic venous pressure. Gastro-intestinal protein loss was assessed by measurement of faecal alpha-1-antitrypsin. Faecal alpha-1-antitrypsin levels were significantly higher in the Fontan group (0.55 +/- 0.15 mg. g-1 faeces, P = 0.002) and the control group with chronically elevated venous pressure (0.60 +/- 0.30 mg. g-1 faeces, P < 0.001) compared to the controls with normal venous pressure (0.29 = 0.12 mg. g-1 faeces). Of the 15 subjects who were found to have increased gastro-intestinal protein loss, only four had clinical protein-losing enteropathy. The degree of gastro-intestinal protein loss correlated significantly with venous pressure (P = 0.01) and with serum aspartate transaminase (P = 0.04). CONCLUSION: Increased gastro-intestinal protein loss is common in this select group of late survivors of Fontan surgery and in other subjects with congenital heart disease and chronic elevation of systemic venous pressure, and was present in patients who did not have protein-losing enteropathy. Increased faecal alpha-1-antitrypsin is an important finding in these patients as intervention at this stage, before the onset of florid protein-losing enteropathy, might prevent the development of further complications.
The Leishmania promastigote surface antigen-2 (PSA-2) is specifically recognised by Th1 cells in humans with naturally acquired immunity to L. major.
The promastigote surface antigen-2 (PSA-2) is a Leishmania parasite antigen, which can induce Th1-mediated protection against murine leishmaniasis when used as a vaccine. To evaluate PSA-2 as a human vaccine candidate the specific T-cell response to PSA-2 was characterised in individuals immune to cutaneous leishmaniasis. Peripheral blood mononuclear cells from Sudanese individuals with a past history of self-healing cutaneous leishmaniasis proliferated vigorously in response to PSA-2 isolated from Leishmania major, whereas the antigen did not activate cells from presumably unexposed Danes. Peripheral blood mononuclear cells from individuals with previous L. major infection had varying proliferative responses to PSA-2 derived from L. donovani promastigotes. Peripheral blood mononuclear cells activated by PSA-2 from L. major produced high amounts of interferon-gamma and tumour necrosis factor-beta, and little interleukin-4, thereby showing a Th1 cytokine pattern. Parallel cultures showed clear Th1 and Th2 response patterns to purified protein derivative of tuberculin or tetanus toxoid, respectively. Flow cytometric analysis revealed that PSA-2 induced blastogenesis in the CD3 positive population and that these cells were the major source of interferon-gamma. The results show that Th1-like cells recognising PSA-2 are expanded during infection by L. major and that they maintain their Th1-like cytokine profile upon reactivation in vitro. Since immunity to cutaneous leishmaniasis is mediated by antigen-specific Th1-like cells, PSA-2 might be considered a vaccine candidate for human leishmaniasis.
Intraoperative release of troponin T in coronary venous and arterial blood and its relation to recovery of left ventricular function and oxidative metabolism following coronary artery surgery.
OBJECTIVE: To investigate the intraoperative release of troponin T during uncomplicated coronary artery surgery and to determine its relation to ischaemic time and to recovery of left ventricular function and oxidative metabolism. DESIGN: A prospective observational study. SETTING: Cardiac surgical unit in a tertiary referral centre. METHODS: Troponin T, creatine kinase, and lactate were analysed from arterial and coronary sinus samples taken before operation, and 1, 4, 6, 10, 20, 35, and 45 minutes after cross clamp release. Net myocardial troponin T release and lactate extraction were derived from their respective arteriovenous differences. Haemodynamic measurements were made using a thermodilution pulmonary artery catheter. PATIENTS: 45 patients, mean (SD) age 62 (9) years, with two or three vessel coronary artery disease and chronic stable angina undergoing routine coronary artery surgery. RESULTS: Before operation, troponin T concentrations were not raised, but within one minute of cross clamp release they increased progressively in both coronary sinus and arterial blood for the entire 45 minutes of reperfusion studied. Coronary sinus troponin T concentrations were consistently higher than arterial concentrations at all time points (p < 0.001), indicating net troponin T release by the myocardium. Peak net troponin T release and area under the curve of net troponin T release correlated closely with ischaemic time (r = 0.58 and r = 0.61, p < 0.0001 for both). Area under the curve of arterial troponin T concentration was also significantly correlated with ischaemic time (r = 0.44, p < 0.01). Patients with cross clamp times longer than 72 minutes (upper quartile for ischaemic time) had greater troponin T release, delayed reversion to lactate extraction, and lower left ventricular stroke work index three hours after surgery, compared with patients who had short (< 50 minutes, lower quartile) and intermediate (51-71 minutes, interquartile) cross clamp times. Peak net troponin T release and area under the curve of arterial troponin T concentration were inversely correlated with left ventricular stroke work index three hours after surgery (r = -0.57, r = -0.38, p < 0.01). CONCLUSIONS: Troponin T concentrations increased in every patient after cross clamp release, and were consistently higher in coronary sinus blood than in arterial blood, indicating net myocardial release of troponin T during the period of reperfusion. Intraoperative net troponin T release has functional significance, as it is closely related to ischaemic time and reflects delayed recovery of left ventricular function and oxidative metabolism; therefore, its measurement may contribute to the perioperative assessment of myocardial injury sustained during coronary artery surgery.
Why is learning American Sign Language a challenge?
In recent years there has been an explosion of interest in American Sign Language (ASL), the language used by Deaf Americans. As a result, an unprecedented number of schools and agencies now offer ASL classes. This welcome development signals growing awareness of and respect for the American Deaf community and ASL. Unfortunately, misconceptions persist about ASL. One major misconception is that it is an easily learned, picture-like language. This understanding is due partly to the fact that some of the first basic signs learned may be thought of as iconic (e.g., signs for eat, sleep, and drink). This even leads some new ASL learners to believe they can become instructors after one or two classes. This mistake is not made among people learning a spoken language. ASL is a complete and complex language, with all the nuances and subtleties of a spoken language. Like all languages, it is not mastered easily beyond a basic level. Mastery requires extensive exposure and practice. Presently, there is no consensus on where ASL might fall on a learnability continuum for native English speakers. Nonetheless, this article posits that learning ASL should be approached with respect and with the knowledge that mastery only occurs over a substantial period of time.
Can C reactive protein or troponins T and I predict outcome in patients with intractable unstable angina?
OBJECTIVE: To determine whether a single blood test for the measurement of C reactive protein, or troponin I or T concentrations could be used to stratify patients with intractable unstable angina awaiting transfer for coronary angiography by correlating these values with coronary anatomy and transient myocardial ischaemia. DESIGN: Prospective study. SETTING: Tertiary cardiac unit. PATIENTS: All patients admitted to their local hospital with ischaemic chest pain, uncontrolled by medical treatment, in whom acute myocardial infarction had been excluded by serial measurement of creatine kinase and lack of Q waves on ECG. INTERVENTION: Coronary angiography and ST segment monitoring for 24 hours. MAIN OUTCOME MEASURES: Concentrations of C reactive protein, troponins T and I, coronary anatomy, presence of transient myocardial ischaemia. RESULTS: Median C reactive protein, troponin I, and troponin T concentrations were 17.1 mg/dl (4.8 to 203.9), 0.05 microgram/l (0 to 7.8), and 0.0 microgram/l (0 to 2.51), respectively. Seven patients (10%) had normal coronaries and 14, 20, and 31 had one, two, or three vessel coronary disease, respectively. Nineteen (26%) had transient myocardial ischaemia, 33 (46%) had complex lesion morphology, and six (8%) had intracoronary thrombus. Of the three markers, troponin T alone was higher in patients with multivessel disease (p < 0.05) and in those with transient myocardial ischaemia (p < 0.05), but there was no significant relation between C reactive protein, troponin T or I and lesion morphology or thrombus. CONCLUSIONS: In patients transferred to a tertiary centre with intractable chest pain, C reactive protein and troponin I are not predictive of transient myocardial ischaemia or lesion morphology, both of which are surrogate markers of outcome. Troponin T is, however, raised in patients with multivessel disease or transient myocardial ischaemia. These serum protein assays cannot be used to stratify the risk of patients with unstable angina who are awaiting transfer to the tertiary centre.
Random blood glucose alone in the diagnosis of cystic fibrosis related diabetes.
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Excretion of ciprofloxacin in sweat and multiresistant Staphylococcus epidermidis.
BACKGROUND: Staphylococcus epidermidis develops resistance to ciprofloxacin rapidly. That this antibiotic is excreted in apocrine and eccrine sweat of healthy individuals might be the reason for the development of such resistance. We assessed whether S epidermidis isolated from the axilla and nasal flora of healthy people could develop resistance to ciprofloxacin after a 1-week course of this antibiotic. METHODS: The concentration of ciprofloxacin in sweat was measured in seven volunteers after oral administration of 750 mg ciprofloxacin twice daily for 7 days, and the development of resistance in S epidermidis from axilla and nostrils was monitored during and 2 months after the treatment. Genotyping of S epidermidis was done by restriction fragment length polymorphism. FINDINGS: The mean concentration of ciprofloxacin in sweat increased during the 7 days of treatment-from 2.2 micrograms/mL 2.5 h after the first tablet to 2.5 micrograms/mL after the fifth tablet, and 5.5 micrograms/mL after the 13th tablet. All persons harboured susceptible S epidermidis (minimal inhibitory concentration [MIC] 0.25 microgram/mL) in axilla and nostrils before treatment. Four resistant strains were detected, two intermediate-level (MIC 4-12 micrograms/mL) and two high-level (MIC > 32 micrograms/mL). Three of these strains were found in all the participants, and a ciprofloxacin-sensitive variant of one of the high-level resistant strains was also found before the start of the treatment. The high-level resistant strains were also resistant to methicillin, erythromycin, gentamicin, sulphonamide, and trimethoprim. A mean of 2.7 days after the start of the treatment, development of ciprofloxacin resistance was detected in S epidermidis from the axilla of all persons, compared with 11 days for the appearance of resistant S epidermidis in nostrils. The resistant strains persisted for an average of 37 and 39 days in axilla and nostrils, respectively, after the end of the treatment. INTERPRETATION: The rapid development of resistance to ciprofloxacin due to excretion of this drug into the sweat might be involved in the development of multiresistant S epidermidis and possibly other skin bacteria in hospitals and in communities with high use of ciprofloxacin or related drugs.
Effects of age and ischemic times on biochemical evidence of myocardial injury after pediatric cardiac operations.
INTRODUCTION: The vulnerability of pediatric myocardium to ischemia is poorly documented in the clinical setting. METHODS: Serial measurements of serum concentrations of myoglobin, the MB isoenzyme of creatine kinase, and cardiac troponins T and I and their respective areas under the curve were obtained, with particular reference to age and ischemic time, in 80 children undergoing cardiac operations. Sixteen (the control group) did not require cardiopulmonary bypass and 64 did. RESULTS: In the control group there were increases (p < 0.01) in myoglobin and creatine kinase MB isoenzyme but no increase in cardiac troponin T or I; by contrast, the group treated with cardiopulmonary bypass had significant increases in all four markers but with differing temporal patterns. Younger age (especially < 12 months) was a highly significant explanatory variable only for the release of cardiac troponins T and I, and ischemic time was a significant explanatory variable for the release of creatine kinase MB isoenzyme, cardiac troponins T and I, but not myoglobin. In comparison with previous studies in adults, creatine kinase MB and cardiac troponin T concentrations were three times greater in children than in adults. CONCLUSIONS: This study supports the specificity of cardiac troponins T and I as markers of myocardial injury after pediatric cardiac operations and defines the importance of age and ischemic time in determining their release. In comparison with previous data in adults, our results raise the possibility that the pediatric heart may be more vulnerable to the effects of ischemia and reperfusion. Cardiac troponins will permit comparison of new myocardial protective strategies or other potentially therapeutic myocardial interventions.
Tumor necrosis factor and steroid metabolism in chronic heart failure: possible relation to muscle wasting.
OBJECTIVES: We sought to assess the possible relations between clinical severity of chronic heart failure and catabolic factors, specifically tumor necrosis factor (TNF), soluble TNF receptors 1 and 2 (sTNFR-1 and sTNFR-2), cortisol, testosterone and dehydroepiandrosterone (DHEA). BACKGROUND: Chronic heart failure is associated with loss of muscle bulk that may be related to alteration of the balance between catabolism and anabolism. METHODS: Sixty-three patients (average age +/- SD 60.4 +/- 11.3 years) with stable chronic heart failure and 20 control subjects aged 52.8 +/- 11.4 years were studied. We measured body mass index (BMI) and obtained maximal incremental exercise testing with metabolic gas exchange measurements and measurements of venous levels of TNF, sTNFR-1 and sTNFR-2, cortisol and DHEA. RESULTS: There was no difference in total TNF-alpha levels between patients and control subjects (9.76 +/- 8.59 vs. 6.84 +/- 2.7 pg/ml). sTNFR-1 (128.9 +/- 84.5 vs. 63.6 +/- 23.3 pg/ml, p < 0.003) and sTNFR-2 (250.1 +/- 109.5 vs. 187.9 +/- 92.2 pg/ml, p = 0.03) were higher in patients. DHEA was lower in patients (9.88 +/- 6.94 vs. 15.64 +/- 8.33 nmol/liter, p = 0.004). The ratio of log cortisol to log DHEA correlated with log TNF level (r = 0.50, p < 0.001 for the patients alone; r = 0.48, p < 0.001 for the group as a whole). Peak oxygen consumption correlated with both sTNFR-1 and sTNFR-2 (r = -0.51, p < 0.001 and r = -0.39, p < 0.001, respectively). There was a negative correlation between BMI and TNF levels (r = -0.43, p < 0.001 for the patients) and the cortisol/DHEA ratio (r = -0.32, p = 0.01 for the patients). CONCLUSIONS: There is an increase in TNF and its soluble receptors in chronic heart failure. This increase is associated with a rise in the cortisol/DHEA (catabolic/anabolic) ratio. These changes correlate with BMI and clinical severity of heart failure, suggesting a possible etiologic link.