bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is cocaine use recognised as a risk factor for acute coronary syndrome by doctors in the UK?
Authors: Wood David M , Hill Duncan , Gunasekera Awini , Greene Shaun L , Jones Alison L , Dargan Paul I 
Published: May 2007

Abstract

Background
Cocaine is a sympathomimetic agent that can cause coronary artery vasospasm leading to myocardial ischaemia, acute coronary syndrome and acute myocardial infarction (ACS/AMI). The management of cocaine-induced ACS/AMI is different to classical atheromatous ACS/MI, because the mechanisms are different.

Methods
Knowledge study—Junior medical staff were given a scenario of a patient with ACS and asked to identify potential risk factors for ACS and which ones they routinely asked about in clinical practice. Retrospective study—Retrospective notes reviews of patients with suspected and proven (elevated troponin T concentration) ACS were undertaken to determine the recording of cocaine use/non-use in clinical notes.

Results
Knowledge study—There was no significant difference in the knowledge that cocaine was a risk factor compared to other “classical” cardiovascular risk factors, but juniors doctors were less likely to ask routinely about cocaine use compared to other “classical” risk factors (52.9% vs &gt;90%, respectively). Retrospective study—Cocaine use or non-use was documented in 3.7% (4/109) and 4% (2/50) of clinical notes of patients with suspected and proven ACS, respectively.

Discussion
Although junior medical staff are aware that cocaine is a risk factor for ACS/AMI, they are less likely to ask about it in routine clinical practice or record its use/non-use in clinical notes. It is essential that patients presenting with suspected ACS are asked about cocaine use, since the management of these patients is different to those with ACS secondary to “classical” cardiovascular risk factors.
The challenge of providing mentorship in primary care
Authors: MacLeod Sheona 
Published: May 2007

Abstract
In the changing National Health Service, there is an increasing awareness of stress related problems in the medical workforce. Mentorship has been shown to help with both stress reduction and adaptation to change. There are recognised difficulties with providing mentorship for doctors but there are ways in which these can be overcome. The medical profession is now considering revalidation, re-certification, and the standards required for these. Perhaps it is also time to consider ways in which mentorship can be provided to support the medical workforce, promote ongoing development and thus improve our ability to care for patients.
False cardiac arrests: the right time to turn away?
Authors: Kenward Gary , Robinson Alan , Bradburn Sandra , Steeds Richard 
Published: May 2007

Abstract

Aim
Cardiac arrest teams may be activated only to find that the patient does not require cardiac or respiratory resuscitation. Members of the cardiac arrest team are drawn from medical personnel with other responsibilities who may disperse quickly, leaving ongoing care of the patient to existing ward staff. The outcome for such false cardiac arrests, however, is rarely reported. The objective of this study was to determine the causes of false cardiac arrest team alerts (FCAs) and to assess the outcome of these patients relative to the general hospital population.

Setting
Tertiary care hospital.

Participants
Patients subject to a cardiac arrest call who were found not to require basic or advanced cardiac life support on arrival.

Results
In 512 events over a 1-year period, patients suffering FCAs were more likely to survive compared to patients suffering cardiac arrest (15% vs 73%, odds ratio (OR) 14.95; χ2 p⩽0.0001), but significantly less likely to survive than the general hospitalised population (73% vs 97%, OR 14.15; χ2 p⩽0.0001). The cause of the FCA was often minimised as collapse or vasovagal syncope; in 58% (87/150) of cases no further action was taken by the attending medical team. Patients suffering FCAs tended to be long-stay patients with a worse outcome at weekends.

Conclusion
In areas lacking a medical alert, outreach or patient at risk system, particular attention should be paid to optimising care of those suffering FCAs.
Hypervirulent strains of Clostridium difficile
Authors: Cookson Barry 
Published: May 2007

Abstract
North America has seen increasing numbers of hospitalised patients and others in nursing homes and the community, with more severe Clostridium difficile associated diarrhoea. This is also described in Northern Europe and surveillance systems are being developed or improved to monitor the situation. One strain (ribotype O27) is described in detail and, like other emerging strains, is demonstrating increasing antimicrobial resistance, notably to quinolone antibiotics. However, its association with increased virulence is not straightforward, probably reflecting the interactions with differing patient case mix. There are many subtypes of the strain and more sophisticated typing and virulence assessment systems need to be developed using isolates carefully collected to test different epidemiological hypotheses. There are also environmental factors relating to treatment such as antimicrobials, cytotoxics and proton pump inhibitors. An emerging theme is the importance of aspects of healthcare delivery in contributing to the problem; this includes poorly maintained and cleaned healthcare premises, overcrowded hospitals and increased staffing workloads leading to poor compliance with infection control.
Can we detect the development of baroreflex sensitivity in humans between 11 and 20 years of age?
Authors: Zavodna Eva , Honzikova Natasa , Hrstkova Hana , Novakova Zuzana , Moudr Jiri , Jira Miroslav , Fiser Bohumil 
Published: May 2007

The aim of the study was to determine changes of baroreflex sensitivity in humans between 11 and 20 years of age. Continuous 5 min blood pressure recordings using a Finapres were taken in 415 healthy subjects while in a sitting, resting position (breathing at a frequency of 0.33 Hz). Beat-by-beat values of interbeat intervals (IBI) or heart rate, and systolic and diastolic blood pressures were measured. Baroreflex sensitivity in ms/mmHg (BRS) and in mHz/mmHg (BRSf) was determined at an average frequency of 0.1 Hz by spectral analysis. BRS did not correlate with age, but BRSf significantly decreased with age (p < 0.001). BRS correlated with mean IBI (p < 0.001) in all subjects and also in the particular subgroups, but BRSf was IBI-independent. Results of multiregression equations were BRS = 1.37 – 0.56 × age (years) + 0.02 × IBI (ms) (p < 0.001 for BRS vs. age and for BRS vs. IBI); BRSf = 34.74 – 0.97 × age (years) – 0.001 × IBI (ms) (p < 0.001 only for BRS vs. age), where age was measured in years and IBI was measured in ms. The limits of BRS were estimated for the total group: 5th percentile, 3.9; 50th percentile, 9.1; and 95th percentile, 18.7 ms/mmHg; and limits for BRSf were 5th percentile, 8.5; 50th percentile, 16.4; and 95th percentile, 33.6 mHz/mmHg. We conclude that IBI-dependent BRS was unchanged in the particular age groups, but the standardization of BRS on IBI decreased with age. BRSf was IBI-independent and better reflected the development of the BRS.
Increased expression of endothelial nitric oxide synthase and caveolin-1 in the aorta of rats with isoproterenol-induced cardiac hypertrophy
Authors: Krenek P. , Klimas J. , Kroslakova M. , Gazova A. , Plandorova J. , Kucerova D. , Fecenkova A. , Svec P. , Kyselovic J. 
Published: May 2007

Isoproterenol-induced cardiac hypertrophy is associated with increased expression of endothelial nitric oxide synthase in the aorta but without signs of improved endothelial function. The aim was to examine the hypothesis that increased expression of eNOS allosteric inhibitor caveolin-1 could be associated with unimproved endothelium-dependent relaxations. Rats received isoproterenol (5 mg/kg body mass, i.p., n = 13) or its vehicle (n = 14) during 1 week. Systolic blood pressure (SBP) and heart rate (HR) were measured by the tail-cuff method. Expression of eNOS and caveolin-1 was measured using immunoblotting analysis. Relaxations of isolated aorta to acetylcholine and sodium nitroprusside were evaluated ex vivo. After 1 week of isoproterenol administration, basal SBP and HR were decreased (SBP 110 ± 3 vs. 126 ± 3 mmHg, p < 0.05; HR 342 ± 8 vs. 366 ± 6 beats/min, p < 0.05). Isoproterenol increased the mass of the left ventricle (+33% ± 4% vs. control; p < 0.05) and right ventricle (+40% ± 9%; p < 0.05). Isoproterenol administration increased the expression of eNOS (+53% ± 12%; p < 0.05) and caveolin-1 (+54% ± 20%, p < 0.05) in the aorta. Relaxation of isolated aorta to acetylcholine and sodium nitroprusside showed a trend towards a worsened endothelial function and a lower sensitivity to exogenous NO. Thus, 1 week of isoproterenol administration led to increased eNOS expression in the aorta without amelioration of endothelial vasorelaxation function. Concomitant increase in caveolin-1 expression may be responsible for this paradox.
Expression of breast cancer resistance protein (BCRP/ABCG2) in human placenta throughout gestation and at term before and after labor
Authors: Yeboah D. , Sun M. , Kingdom J. , Baczyk D. , Lye S.J. , Matthews S.G. , Gibb W. 
Published: May 2007

Breast cancer resistance protein, BCRP, is a multidrug resistance protein that is highly expressed in the human placenta. In cancer tissues, this protein actively extrudes a wide variety of chemically and structurally unrelated chemotherapeutic drugs and other compounds. Studies in mice have shown that in the absence of BCRP activity in the placenta, there is a 2-fold increase in the uptake in BCRP substrates into fetus. This suggests that in the placenta, BCRP extrudes compounds that would otherwise cross the syncytiotrophoblast cells into fetal circulation. The purpose of this study was to examine the expression and localization of BCRP in the human placenta throughout gestation. Tissues from 6–13, 16–19, 24–29, 32–35, and 38–41 weeks of gestation were used. Real time RT-PCR analysis demonstrated that the mRNA levels of BCRP in the placenta do not change significantly as gestation progressed. However, Western blot analysis revealed that the protein levels increased towards the end of gestation. We demonstrated that BCRP is localized to the syncytiotrophoblast of the placenta and in some fetal blood vessels within the placenta. Tissues from the early stages of pregnancy (6–13 weeks) showed fewer BCRP positive blood vessels than term tissues (38–41 weeks).
Antinociceptive, anti-inflammatory and antipyretic properties ofMelastoma malabathricumleaves aqueous extract in experimental animals
Authors: Zakaria Z.A. , Raden Mohd. Nor R.N.S. , Hanan Kumar G. , Abdul Ghani Z.D.F. , Sulaiman M.R. , Rathna Devi G. , Mat Jais A.M. , Somchit M.N. , Fatimah C.A. 
Published: May 2007

The present study was carried out to establish the antinociceptive, anti-inflammatory, and antipyretic properties of the aqueous extract of Melastoma malabathricum leaves in experimental animals. The antinociceptive activity was measured using abdominal constriction, hot-plate, and formalin tests, whereas the anti-inflammatory and antipyretic activities were measured using carrageenan-induced paw edema and brewer’s yeast-induced pyrexia tests, respectively. The extract, which was obtained after soaking the air-dried leaves in distilled water for 72 h and then preparing in concentrations of 10%, 50%, and 100% (v/v), was administered subcutaneously 30 min prior to subjection to the above mentioned assays. At all concentrations tested, the extract was found to exhibit significant (P < 0.05) antinociceptive, anti-inflammatory, and antipyretic activities in a concentration-independent manner. Our findings that the aqueous extract of M. malabathricum possesses antinociceptive, anti-inflammatory, and antipyretic activities supports previous claims on its traditional uses to treat various ailments.
Citrobacter rodentiuminfection causes iNOS-independent intestinal epithelial dysfunction in mice
Authors: Skinn Andrew C. , Vergnolle Nathalie , Zamuner Stella R. , Wallace John L. , Cellars Laurie , MacNaughton Wallace K. , Sherman Philip M. 
Published: May 2007

Attaching-effacing bacteria are major causes of infectious diarrhea in humans worldwide. Citrobacter rodentium is an attaching-effacing enteric pathogen that causes transmissible murine colonic mucosal hyperplasia. We characterized colonic inflammation and ion transport at 3, 7, 10, 30, and 60 d after infection of C57Bl/6 mice with C. rodentium. Macroscopic damage score was significantly increased 7 and 10 d after infection. Colonic wall thickness was increased at 7, 10, 30, and 60 d. Myeloperoxidase (MPO) activity was significantly increased at 3, 7, and 10 d and returned to control levels by days 30 and 60. The expressions of inducible nitric oxide synthase and cyclooxygenase-2 were increased by C. rodentium infection. Significant reductions in the epithelial secretory response to carbachol, but not to electrical field stimulation or forskolin, were observed at 3 and 10 d of infection. Translocation of enteric bacteria into the mesenteric lymph nodes was observed 10 d following infection. There was no difference in response to infection between animals deficient in inducible nitric oxide synthase and wild-type controls. The COX-2 inhibitor rofecoxib caused decreased wall thickness and MPO activity at day 10. However, COX-2 inhibition did not alter infection-induced changes in ion transport. Citrobacter rodentium infection causes colonic inflammation, mucosal hyperplasia, and nitric-oxide-independent epithelial dysfunction in association with increased permeability to luminal bacteria.
Insights into the change in brain natriuretic peptide after ST-elevation myocardial infarction (STEMI): why should it be better than baseline?This paper is one of a selection of papers published in this Special Issue, entitled Young Investigators' Forum.
Authors: Ezekowitz Justin A. , Théroux Pierre , Welsh Robert , Bata Iqbal , Webb John , Armstrong Paul W. 
Published: May 2007

While baseline N-terminal brain natriuretic peptide (NT-proBNP) is useful in the prognosis of acute ST-elevation myocardial infarction (STEMI), it is unclear whether a relationship exists between serial NT-proBNP, reperfusion success, and prognosis. We prospectively defined a NT-proBNP analysis in the WEST (Which Early ST-elevation myocardial infarction Therapy) trial that enrolled 304 acute STEMI patients. NT-proBNP (pg/mL) was measured at baseline prior to treatment (n = 258) and 72 to 96 h (n = 247) and 30 days (n = 221) after treatment (ΔNT-proBNP = 72 h value – the baseline NT-proBNP). Reperfusion success was measured by ST-segment resolution at 180 min, infarct size by peak creatine kinase (CK) during the first 24 h, and QRS score at discharge (QRSd). The primary endpoint was a 30 day clinical composite. The ability of either baseline NT-proBNP or ΔNT-proBNP to predict the primary endpoint was compared using single-variable logistic regression and the c-statistic. Median (interquartile range) NT-proBNP in pg/mL was 87 (39–316) at baseline, 864 (338–1857) at 72 h, and 585 (264–1212) at 30 days. ST resolution was inversely correlated with ΔNT-proBNP (r = –0.23, p = 0.002) and 30 day NT-proBNP (30 day NT-proBNP 1016, 828, and 397 for <30%, 30%–70%, ≥70% STR, respectively, p < 0.001). Infarct size was correlated with ΔNT-proBNP by CK (r = 0.41, p < 0.001) and QRSd (r = 0.31, p < 0.001); the 30 day NT-proBNP relationship was similar for CK (r = 0.48, p < 0.001) and QRSd (p = 0.003). The baseline NT-proBNP was associated with an increased 30-day composite endpoint (Q1, 19%; Q2, 20%; Q3, 15%; Q4, 38%; p = 0.03 for trend) as was ΔNT-proBNP (Q1, 16%; Q2, 18%; Q3, 19%; Q4, 37%; p = 0.009 for trend). The c-statistic for baseline, 72 to 96 h, and ΔNT-proBNP was 0.59, 0.61, and 0.62 for the 30-day composite and 0.64, 0.62, and 0.62 for the 90-day composite, respectively. ΔNT-proBNP clearly predicts short-term adverse cardiac events and is superior to baseline NT-proBNP, but similar to the 72 to 96 h NT-proBNP in predicting clinical events after STEMI. This likely reflects the variability in NT-proBNP at presentation and the ability to integrate subsequent important physiologic sequelae of STEMI such as reperfusion and infarct size.
Beneficial effects of carvedilol as a concomitant therapy to angiotensin-converting enzyme inhibitor in patients with ischemic left ventricular systolic dysfunction
Authors: Gandhi Purvi S. , Goyal Ramesh K. , Jain Anil R. , Mallya B. Srinivas , Gupta Vishal M. , Shah Dhiren S. , Trivedi Bharat R. , Shastri Naman A. , Mehta Chirag B. , Jain Kalpana A. , Bhavasar Niren S. , Shah Urmi J. 
Published: May 2007

Studies are scant on the effects of short-term carvedilol treatment as an adjuvant to angiotensin-converting enzyme (ACE) inhibitor in patients with left ventricular (LV) systolic dysfunction. The objective of this study was to find the effects of short-term treatment of carvedilol on patients with ischemic LV systolic dysfunction (defined as LV ejection fraction (LVEF) ≤30% on 2D echocardiography) undergoing coronary artery bypass surgery (CABG). There were 74 patients that received ACE inhibitor without any β-blocker (control) and 67 patients that received carvedilol in addition to ACE inhibitor following CABG (carvedilol group). After 1 month of drug administration following CABG, the control group was found to have significantly greater percent improvement in LVEF (29.1% ± 5.39%) as compared with the carvedilol group (15.3% ± 4.89%). However, after 3 and 6 months, LVEF levels were found to be significantly greater in the carvedilol group as compared with the control group. Further, at 6 months of drug administration, LV end systolic diameter was significantly less in the carvedilol group (39.11 ± 1.10 mm) as compared with the control group (43.49 ± 1.39 mm). Thus, carvedilol produces beneficial effect on short-term administration in terms of LV contractility when given along with ACE inhibtior as compared with ACE inhibitor therapy alone.
Combining ursodeoxycholic acid or its NO-releasing derivative NCX-1000 with lipophilic antioxidants better protects mouse hepatocytes against amiodarone toxicity
Authors: Ouazzani-Chahdi Amine , Elimadi Aziz , Chabli Allal , Spénard Jean , Colin Patrick , Haddad Pierre S. 
Published: May 2007

Nonalcoholic steatohepatitis (NASH) is a common and potentially severe form of liver disease. This study aimed to determine the effect of ursodeoxycholic acid and its NO-releasing derivative NCX-1000 alone or in combination with antioxidants on cultured mouse hepatocytes treated with amiodarone to mimic certain aspects of hepatocyte injury found in NASH. Isolated mouse hepatocytes were incubated with ursodeoxycholic acid or NCX-1000 (0–100 μmol/L) combined or not combined with the hydrophilic antioxidants butylated hydroxytoluene and ascorbic acid (0–100 μmol/L) or with the lipophilic antioxidant α-tocopherol (0–100 μmol/L) 15 min before adding amiodarone (50 μmol/L) to the culture medium. Twenty hours later, necrosis, apoptosis, superoxide anion production, and malondialdehyde levels were assessed in cultured cells. Amiodarone led to a dose-dependent decrease in cell viability with an LD50of 50 μmol/L and increased production of superoxide anion and lipid peroxidation. NCX-1000 showed a better protective potential than ursodeoxycholic acid against the toxic effects of amiodarone. The hydrophilic antioxidants had no effect on the toxicity of amiodarone, whereas α-tocopherol at a concentration >100 μmol/L almost completely suppressed it. Ursodeoxycholic acid and NCX-1000 protection was additive only when they were combined with α-tocopherol, not with butylated hydroxytoluene or ascorbic acid. In addition, all the antioxidants tested reduced the superoxide anion detected, but only α-tocopherol prevented lipid peroxidation induced by amiodarone. The combination of lipophilic antioxidants with ursodeoxycholic acid or NCX-1000 enhances their protective potential and could represent an interesting therapeutic approach to explore for the treatment of NASH.
Altered PKC expression and phosphorylation in response to the nature, direction, and magnitude of mechanical stretch
Authors: Bullard Tara A. , Hastings Joshua L. , Davis Jeffrey M. , Borg Thomas K. , Price Robert L. 
Published: May 2007

Protein kinase C (PKC) isozymes have been shown to play a role in mechanotransduction in a variety of cell types. We sought to identify the PKC isozymes involved in transducing mechanical (cyclic vs. static), direction and intensity of stretch by examining changes in protein expression and phosphorylation. We used a 3-dimensional culture system with aligned neonatal rat cardiac myocytes on silastic membranes. Myocytes were subjected to either cyclic stretch at 5 cycles/min or static stretch for a period of 24 h at intensities of 0%, 2.5%, 5%, or 10% of full membrane length. Stretch was applied in perpendicular or parallel directions to myocyte alignment. PKC δ was most sensitive to stretch applied perpendicular to myocyte alignment regardless of the nature of stretch, while phospho PKC δ T505 increased in response to static-perpendicular stretch. PKC ε expression was altered by cyclic stretch but not static stretch, while phospho PKC ε S719 remained unchanged. PKC α expression was not altered by stretch; however, phospho PKC α S657 increased in a dose-dependent manner following cyclic-perpendicular stretch. Our results indicate that changes in PKC expression and phosphorylation state may be a mechanism for cardiac myocytes to discriminate between the nature, direction, and intensity of mechanical stretch.
Impact of puma predation on the decline and recovery of a mule deer population in southeastern Idaho
Authors: Laundré J.W. , Hernández L. , Clark S.G. 
Published: May 2007

We modeled the impact of puma ( Puma concolor (L., 1771)) predation on the decline and recovery of mule deer ( Odocoileus hemionus (Rafinesque, 1817)) in southern Idaho based on estimates of puma numbers, predation rates of pumas, and reproductive variables of deer. Deer populations peaked in 1992–1993, then declined more than 55% and remained low for the next 11 years. Puma numbers peaked 4–6 years after deer populations peaked but then declined to original levels. Estimated puma predation on the deer population before and after the decline was 2.2%–3.3% and 3.1%–5.8%, respectively. At high puma densities (>3 pumas/100 km2), predation by pumas delayed deer recovery by 2–3 years. Percent winter mortality of fawns (r2 = 0.62, P < 0.001) and adult female deer (r2 = 0.68, P < 0.001) correlated positively with December–January snowfall. Incorporation of winter snowfall amounts in the model produced a pattern of deer population change matching estimated changes based on field survey data. We conclude that pumas probably were a minor factor in the decline of the deer population in our area and did not suppress deer recovery. We propose that winter snowfall was the primary ultimate and proximate factor in the deer decline and suppression of their recovery.