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1.  Feeding requirements of white sharks may be higher than originally thought 
Scientific Reports  2013;3:1471.
Quantifying the energy requirements of animals in nature is critical for understanding physiological, behavioural, and ecosystem ecology; however, for difficult-to-study species such as large sharks, prey intake rates are largely unknown. Here, we use metabolic rates derived from swimming speed estimates to suggest that feeding requirements of the world's largest predatory fish, the white shark (Carcharodon carcharias), are several times higher than previously proposed. Further, our estimates of feeding frequency identify a clear benefit in seasonal selection of pinniped colonies - a white shark foraging strategy seen across much of their range.
doi:10.1038/srep01471
PMCID: PMC3600591  PMID: 23503585
2.  The metabolic activity of gut microbiota in obese children is increased compared with normal-weight children and exhibits more exhaustive substrate utilization 
Nutrition & Diabetes  2011;1(7):e12-.
Objective:
The gut microbiota contribute otherwise impossible metabolic functions to the human host. Shifts in the relative proportions of gut microbial communities in adults have been correlated with intestinal disease and have been associated with obesity. The aim of this study was to elucidate differences in gut microbial compositions and metabolite concentrations of obese versus normal-weight children.
Materials and methods:
Fecal samples were obtained from obese (n=15; mean body mass index (BMI) s.d. score=1.95) and normal-weight (n=15; BMI s.d. score=−0.14) Swiss children aged 8–14 years. Composition and diversity of gut microbiota were analyzed by qPCR and temperature gradient gel electrophoresis (TGGE).
Results:
No significant quantitative differences in gut microbiota communities of obese and normal-weight children were identified. Microbial community profiling by TGGE revealed a high degree of both intra- and intergroup variation. Intergroup comparison of TGGE profiles failed to identify any distinct populations exclusive to either obese or normal-weight children. High-pressure liquid chromatography analysis identified significantly higher (P<0.05) concentrations of short-chain fatty acids (SCFA) butyrate and propionate in obese versus normal-weight children. Significantly lower concentrations of intermediate metabolites were detected in obese children, suggesting exhaustive substrate utilization by obese gut microbiota.
Conclusions:
Our results indicate that a dysbiosis may be involved in the etiology of childhood obesity. In turn, aberrant and overactive metabolic activity within the intestine could dictate survival or loss of individual microbial communities, leading to the altered population ratios previously identified in adult obesity.
doi:10.1038/nutd.2011.8
PMCID: PMC3302137  PMID: 23154580
obesity; pediatric; short-chain fatty acid; gut microbiota; metabolism
3.  Public health training in genitourinary medicine 
Sexually Transmitted Infections  2006;82(3):191-192.
GUM consultants need skills that fall into the broad area of public health
doi:10.1136/sti.2006.021345
PMCID: PMC2564736  PMID: 16731665
public health; genitourinary medicine; sexually transmitted infections; medical careers
4.  Strain rate imaging after dynamic stress provides objective evidence of persistent regional myocardial dysfunction in ischaemic myocardium: regional stunning identified? 
Heart  2005;91(2):152-160.
Objective: To investigate whether persistent ischaemic dysfunction of the myocardium after dynamic stress can be diagnosed from changes in ultrasonic strain rate and strain.
Design: Prospective observational study, with age matched controls.
Setting: University hospital.
Patients and methods: 26 patients (23 men, mean (SD) age 58.9 (8.1) years) with coronary artery disease but no infarction and 12 controls (9 men, aged 56.1 (8.8) years) with normal coronary arteriography and negative exercise test underwent treadmill exercise (Bruce protocol). Tissue Doppler echocardiography was performed at baseline, at peak exercise, and at intervals up to one hour. Systolic and diastolic velocity, strain, and strain rate were recorded in the basal anterior segment of 16 patients with proximal left anterior descending coronary artery disease.
Results: Patients developed ischaemia, since they experienced angina, exercised for less time, and reached a lower workload than the control group, and had ST segment depression (−2.4 mm). Myocardial systolic velocity immediately after exercise increased by 31% and strain rate fell by 25% compared with increases of 92% and 62%, respectively, in the control group (p < 0.05). During recovery, myocardial systolic velocity and strain rate normalised quickly, whereas systolic strain remained depressed at 30 and 60 minutes after exercise, by 21% and 23%, respectively, compared with baseline (p < 0.05 versus controls). Myocardial diastolic velocities and strain rate normalised but early diastolic strain remained depressed by 32% compared with controls for 60 minutes (p < 0.05). Strain during atrial contraction was abnormal for 30 minutes.
Conclusions: Myocardial strain shows regional post-ischaemic dysfunction in systole and diastole and may become a useful diagnostic tool in patients presenting with chest pain with a normal ECG.
doi:10.1136/hrt.2003.027490
PMCID: PMC1768711  PMID: 15657221
stunned myocardium; exercise; tissue Doppler echocardiography; strain rate imaging; Doppler myocardial imaging
5.  Incidence of embolism and paravalvar leak after St Jude Silzone valve implantation: experience from the Cardiff Embolic Risk Factor Study 
Heart  2003;89(9):1055-1061.
Background: Silver coating of the sewing ring (Silzone) was introduced as a modification of the St Jude Medical standard valve to provide antibacterial protection, but the valve has recently been withdrawn.
Objective: To study patients with these prostheses to assess possible adverse effects, and to guide their follow up.
Design: Prospective observational study of risk factors for stroke after valve replacement.
Setting: Cardiology and cardiac surgery departments in a tertiary centre.
Patients: There were 51 patients with Silzone and 116 with St Jude Medical standard valves. Patients undergoing aortic valve replacement were well matched for stroke risk factors. Silzone patients with mitral valve replacement were younger (mean (SD) age 61 (10) v 66 (7) years), more likely to be female (95% v 65%), and had more pulmonary arterial hypertension (100% v 78%), but fewer coronary artery bypass grafts (5% v 33%) than patients with standard mitral valve replacements (all p < 0.05).
Results: Follow up was 100% in the Silzone group (mean duration 3.0 (0.9) years) and 97.4% in the standard group (4.7 (1.4) years). Survival, morbidity, and anticoagulant control were documented over 682 follow up years (153 for Silzone and 529 for standard). There were six embolic strokes and one peripheral embolism in the Silzone group, all within three months after operation, and five embolic strokes and one peripheral embolism in the standard group. Freedom from major thromboembolism at three months was 65% in the Silzone mitral valve replacement group and 100% in the standard mitral valve replacement group (difference 35%, 95% confidence interval 8% to 62%). There was one reoperation for paravalvar leak in the standard group, but none in the Silzone group (NS). Anticoagulant control in the two groups was similar.
Conclusions: Patients with Silzone mitral valves had a high rate of early postoperative embolism but no excess paravalvar leak.
PMCID: PMC1767860  PMID: 12923026
valve prosthesis; Silzone valve; embolism; paravalvar leak
7.  Conduit arterial stiffness is associated with impaired left ventricular subendocardial function 
Heart  2003;89(4):449-450.
PMCID: PMC1769251  PMID: 12639882
conduit arterial stiffness; left ventricular subendocardial function
8.  Cost effectiveness of statins 
Heart  2000;83(6):713.
doi:10.1136/heart.83.6.713a
PMCID: PMC1760882  PMID: 10885942
9.  Cost effectiveness of HMG-CoA reductase inhibitor (statin) treatment related to the risk of coronary heart disease and cost of drug treatment 
Heart  1999;82(3):325-332.
OBJECTIVES—To estimate the cost effectiveness of statin treatment in preventing coronary heart disease (CHD) and to examine the effect of the CHD risk level targeted and the cost of statins on the cost effectiveness of treatment.
DESIGN—Cohort life table method using data from outcome trials.
MAIN OUTCOME MEASURES—The cost per life year gained for lifelong statin treatment at annual CHD event risks of 4.5% (secondary prevention) and 3.0%, 2.0%, and 1.5% (all primary prevention), with the cost of statins varied from £100 to £800 per year.
RESULTS—The costs per life year gained according to annual CHD event risk were: for 4.5%, £5100; 3.0%, £8200; 2.0%, £10 700; and 1.5%, £12 500. Reducing the cost of statins increases cost effectiveness, and narrows the difference in cost effectiveness across the range of CHD event risks.
CONCLUSIONS—At current prices statin treatment for secondary prevention, and for primary prevention at a CHD event risk 3.0% per year, is as cost effective as many treatments in wide use. Primary prevention at lower CHD event risks (< 3.0% per year) is less cost effective and unlikely to be affordable at current prices and levels of health service funding. As the cost of statins falls, primary prevention at lower risk levels becomes more cost effective. However, the large volume of treatment needed will remain a major problem.


Keywords: coronary artery disease; cost effectiveness; statins; primary prevention; secondary prevention
PMCID: PMC1729169  PMID: 10455083
11.  Evidence that an HLA-DQA1-DQB1 haplotype influences susceptibility to childhood common acute lymphoblastic leukaemia in boys provides further support for an infection-related aetiology. 
British Journal of Cancer  1998;78(5):561-565.
Comparison of DQA1 and DQB1 alleles in 60 children with common acute lymphoblastic leukaemia (c-ALL) and 78 newborn infant control subjects revealed that male but not female patients had a higher frequency of DQA1*0101/*0104 and DQB1*0501 than appropriate control subjects. The results suggest a male-associated susceptibility haplotype in c-ALL and supports an infectious aetiology.
PMCID: PMC2063058  PMID: 9744491
12.  Variations in use of cardiology services in a health authority: comparison of coronary artery revascularisation rates with prevalence of angina and coronary mortality. 
BMJ : British Medical Journal  1997;314(7076):257-261.
OBJECTIVE: To explore the relation between rates of coronary artery revascularisation and prevalence of angina to assess whether use of health services reflects need. DESIGN: Prevalence of angina symptoms determined by postal questionnaire on 16750 subjects (18 to 94 years). Comparison of data on use of coronary artery revascularisation with prevalence of symptoms and mortality from coronary heart disease. SETTING: Health authority with population of 530000. SUBJECTS: Patients admitted to hospital for coronary heart disease; patients who died; and patients undergoing angiography, angioplasty, or coronary artery bypass graft. Cohort of 491 people with symptoms from survey. MAIN OUTCOME MEASURES: Pearson's product moment correlation coefficients for relation between variables. RESULTS: Overall, 4.0% (95% confidence interval 3.7% to 4.4%) of subjects had symptoms. Prevalences varied widely between electoral wards and were positively associated with Townsend score (r = 0.79; P < 0.001), as was mortality, but the correlation between admission rates and Townsend score was less clear (r = 0.47; P < 0.01). Revascularisation rate and Townsend score were not associated. The ratio of revascularisation to number experiencing symptoms was inversely related to Townsend score (r = 0.67; P < 0.001). The most deprived wards had only about half the number of revascularisations per head of population with angina than did the more affluent wards. In affluent wards 11% (13/116) of those with symptoms had coronary angiograms compared with only 4% (9/216) in poorer wards (chi 2 = 4.96; P = 0.026). Townsend score also inversely correlated with revascularisations per premature death from coronary heart disease (r = 0.55; P < 0.01) and revascularisations per admission for myocardial infarction (r = 0.47; P < 0.01). CONCLUSION: The use of interventional cardiology services is not commensurate with need, thus exhibiting the inverse care law.
PMCID: PMC2125748  PMID: 9022488
14.  Harm minimisation for drug misusers. 
BMJ : British Medical Journal  1992;304(6839):1441.
PMCID: PMC1882207  PMID: 1628029
15.  Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure. 
Gut  1991;32(1):85-89.
It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.
PMCID: PMC1379220  PMID: 1825077
16.  Opsonic effect of jacalin and human immunoglobulin A on type II group B streptococci. 
Infection and Immunity  1990;58(11):3663-3670.
This study examined the effect of immunoglobulin A (IgA) and the IgA-binding lectin jacalin on the phagocytosis of type II group B streptococci (GBS). Strains possessing the trypsin-sensitive and trypsin-resistant components of the c protein (II/c) and type II GBS lacking the c protein (II) were examined by radiolabeled bacterial uptake, bactericidal assays, and electron microscopy. Type II/c GBS resisted phagocytosis by monocytes (4.9% +/- 0.8% uptake, mean +/- SE, n = 25) compared with type II GBS (8.5% +/- 1.4% uptake, n = 14, P = 0.03). Phagocytic killing by polymorphonuclear leukocytes was also less for the type II/c strain 78-471 than for the type II strain 79-176 (68% +/- 5% versus 86% +/- 4% reduction in CFU at 45 min, P = 0.03). IgA binding did not explain the resistance of type II/c GBS to phagocytosis. The uptake of type II/c GBS was not significantly different after opsonization in cord sera lacking endogenous IgA (5.93% +/- 1.4%) than in the same cord sera after addition of exogenous IgA (5.48% +/- 1.4%, P = 0.69, n = 9). Attempts to remove serum IgA with the IgA-binding lectin jacalin resulted in the binding of IgA-jacalin complexes to II/c GBS. This combination of nonspecific IgA and jacalin increased uptake of II/c GBS from 4.9% +/- 0.8% to 11.8% +/- 1.9% (P = 0.002). Jacalin also combined with specific, immune, monoclonal IgA bound to the surface of Haemophilus influenzae and promoted the uptake of these bacteria. Jacalin and IgA mediated phagocytosis of II/c GBS via receptors that were not dependent on divalent cations and that were not modulated by plating monocytes on antigen-antibody complexes.
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PMCID: PMC313712  PMID: 2228238
17.  Nonimmune binding of human immunoglobulin A to type II group B streptococci. 
Infection and Immunity  1990;58(6):1789-1795.
The binding of 125I-labeled human myeloma immunoglobulin A (IgA) to four type II strains and one nontypable strain of group B streptococci was measured after streptococcal chains were broken by brief sonication. Some IgA binding was observed with all strains, but specific binding (binding that was inhibited by excess unlabeled IgA, was dose dependent, and was saturable) occurred only with those strains possessing the trypsin-sensitive beta component of the c protein. Similar amounts of binding were observed with myeloma IgA and IgA1 purified from normal serum. Specific binding was more rapid at 25 degrees C than at 0 or 37 degrees C and reached a plateau in 6 to 8 h. Binding was drastically reduced (85 to 90%) when streptococci had been heated (90 degrees C for 1 h). Most radioactivity bound to group B streptococci could be displaced (greater than 60% in 3 days) by the addition of excess unlabeled IgA. The binding capacity of one strain (10(8) streptococci in 1 ml of buffer) was saturated by approximately 24 micrograms of IgA. When transformed for Scatchard analysis, these data indicated that there was a specific binding capacity of 16,000 molecules of monomeric serum IgA per single streptococcal cell. The dissociation constant for IgA binding was 19.3 nM. Since enzyme-linked immunosorbent assay studies showed that the myeloma IgA used for the studies described above was IgA1, our quantitative data apply only to the binding of this subclass to group B streptococci. However, an enzyme-linked immunosorbent-filtration assay showed that both IgA1 and IgA2 bound to a type II group B streptococcus bearing the c protein.
PMCID: PMC258724  PMID: 2187808
18.  Effect of differences in antibody and complement requirements on phagocytic uptake and intracellular killing of "c" protein-positive and -negative strains of type II group B streptococci. 
Infection and Immunity  1987;55(5):1243-1251.
The influence of antibody and complement on the polymorphonuclear leukocytic uptake and killing of type II group B streptococci (GBS) was examined with 11 adult sera and three type II strains possessing the trypsin-resistant and trypsin-sensitive components (II/TR+TS) of the "c" (formerly Ibc) protein or two type II strains lacking both components (II/no c) of the c protein. All tested sera mediated a greater than 1 log10 reduction in colony-forming units (CFUR) of a type II/no c strain, even in the absence of measurable type-specific antibody (less than 1.08 micrograms/ml), but only 5 of 11 mediated a greater than 1 log10 CFUR of any type II/TR/TS strain, even in the presence of moderate levels of type-specific antibody. The classical pathway of complement activation appeared to be more important than the alternative pathway, and even absorbed or immunoglobulin G (IgG)-depleted serum (IgG, 10 mg/dl) mediated a greater than 1 log10 CFUR without magnesium ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (magnesium EGTA) chelation. Chelation with magnesium EGTA reduced the CFUR in 4 of 11 test sera and greatly reduced the CFUR in absorbed or IgG-depleted sera for type II/no c strains. Despite variation in the phagocytic killing of two representative strains of type II GBS, both strains were well phagocytized, as measured by radiolabeled bacterial uptake or electron microscopy. This study suggested that poorly killed type II/TR+TS GBS were easily phagocytized but apparently resisted intracellular killing.
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PMCID: PMC260497  PMID: 3552996
19.  Phenolic glycolipid 1 of Mycobacterium leprae causes nonspecific inflammation but has no effect on cell-mediated responses in mice. 
Infection and Immunity  1984;46(3):802-808.
The involvement of the phenolic glycolipid from Mycobacterium leprae in cell-mediated immunity has been investigated in this study. The phenolic glycolipid itself does not appear to stimulate cell-mediated immunity directly, as shown by its failure to elicit a classical delayed-type hypersensitivity response in mice immunized with M. leprae or to stimulate M. leprae-immune lymph node cells in a lymphoproliferative assay. Intradermal vaccination with the phenolic glycolipid failed to influence the growth of M. leprae in mouse footpads. A nonspecific inflammatory response to the sonicated glycolipid was observed in mice vaccinated with whole M. leprae and in control animals. No evidence was obtained for any adjuvant or suppressive effect on cell-mediated immunity by the phenolic glycolipid either to M. leprae or an unrelated antigen (sheep erythrocytes); neither sensitization nor elicitation to either antigen was affected.
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PMCID: PMC261616  PMID: 6389362
20.  Prostacyclin produced by the pregnant uterus in the dog may act as a circulating vasodepressor substance. 
Journal of Clinical Investigation  1981;67(3):632-636.
Uterine production of PGI2 (prostacyclin) was quantitated in late pregnant dogs to evaluate if PGI2 could act as circulating vasodepressor substance in pregnancy. In five anesthetized, laparotomized dogs, the uterine venous plasma concentration of 6-keto PGF1 alpha (the in vitro hydrolysis product of PGI2) was 6.7 +/- 1.9 ng/ml and the arterial plasma concentration was 2.6 +/0 0.8 ng/ml. In four nonpregnant female dogs the arterial plasma concentration of 6-keto PGF1 alpha was consistently below 0.2 ng/ml. In eight pregnant dogs we also evaluated the ability of the pregnant uterus to inactivate PGI2 by comparing the hypotensive response to increasing doses of PGI2 infused into the uterine artery to the hypotensive response to increasing doses of PGI2 infused into the inferior vena cava. In addition, the effect of PGI2 infused into the uterine artery on uterine blood flow and intraamniotic fluid pressure was evaluated. The dose-response curves of intrauterine and intravenous PGI2 in causing systemic hypotension were identical suggesting that the pregnant uterus does not inactivate infused PGI2. Intrauterine PGI2 had no consistent effect on uterine hemodynamics although it did increase intraamniotic fluid pressure significantly. These data demonstrate that the pregnant uterus has the capacity to produce large quantities of PGI2 which is not inactivated in the uterus and therefore can appear in the arterial blood to exert a systemic vasodepressor effect.
PMCID: PMC370611  PMID: 7009646
21.  Effect of the prostaglandin precursor, arachidonic acid, on histamine stimulated gastric secretion in the conscious dog, and observations on the effect of inhibiting endogenous prostaglandin synthesis. 
Gut  1977;18(6):429-437.
The effects of intravenous infusions of prostaglandin E2 (PGE2) and arachidonic acid (AA) on histamine-stimulated gastric secretion have been studied in conscious dogs with either a simple gastric fistula or a denervated Heidenhain pouch. Both compounds produced a dose-related inhibition of acid secretion, though AA was 86-5 to 203-2 times less potent than PGE2. The maximal effect of AA was not achieved until 20 to 40 minutes after the infusion had ceased, suggesting that AA has to undergo some kinetic or metabolic process before it can act. Eicosatetraynoic acid (ETYN) 1-0 microgram.kg-1min-1, an inhibitor of PG biosynthesis, almost totally abolished the anti-secretory effect of AA up to 200 microgram.kg-1min-1. At 400 microgram AA.kg-1min-1, the antisecretory effect was reduced by about one half. The effect of PGE2 was not altered by ETYN. Furthermore, ETYN did not increase the response to histamine stimulation in control studies, which suggests that, in this model at least, prostaglandins are not involved in regulating gastric secretion.
PMCID: PMC1411494  PMID: 873324
23.  Effect of a Protease Inhibitor on the Adhesion of Ehrlich Ascites Cells to Host Cells in vivo 
British Journal of Cancer  1973;28(5):417-428.
Ehrlich ascites tumours (EAT) were grown in mice by injecting 1 × 106 cells intraperitoneally. In mice which received one or more injections of 30 mg soybean trypsin inhibitor (TI) i.p. during tumour growth, the number of recoverable tumour cells was significantly reduced by up to 92%. Also, the mean size of these cells was significantly smaller.
When the rate of labelled thymidine incorporation in vitro was compared in TI-treated and control cells, no significant differences were detected. However, when the population doubling time of EAT cells in vivo was calculated, it was apparent that recoverable TI-treated cells were dividing more rapidly than controls. Consequently, the reduced number of cells recovered from TI-treated mice did not result from a reduced growth rate.
Viability, assessed by trypan blue dye exclusion and rate of labelled chromium release, was the same in TI-treated and control cell populations. Thus TI was nontoxic to EAT cells and the reduced number of cells from treated tumours was not therefore due to cytotoxicity.
Scanning electron microscopy revealed that normal EAT cells did not adhere to internal host surfaces but that after TI treatment they adhered in large numbers to produce an appearance which resembled a confluent monolayer. This binding to host tissue accounted for the reduction in the number of cells recovered from TI-treated animals. We propose that TI acts as a protease inhibitor to prevent intrinsic proteolytic enzyme activity at the tumour cell surface. This activity would normally destroy the binding sites required for adhesion to host tissue.
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PMCID: PMC2008914  PMID: 4271321

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