bluuebunny/crossref_metadata_2025_split huggingface dataset:
Implementation of ironXS: a study of the acceptability and feasibility of genetic screening for hereditary hemochromatosis in high schools
Authors: Delatycki MB , Wolthuizen M , Collins V , Varley E , Craven J , Allen KJ , Aitken MA , Bond L , Lockhart PJ , Wilson GR , Macciocca I , Metcalfe SA 
Published: November 2009

Delatycki MB, Wolthuizen M, Collins V, Varley E, Craven J, Allen KJ, Aitken MA, Bond L, Lockhart PJ, Wilson GR, Macciocca I, Metcalfe SA. Implementation of ironXS: a study of the acceptability and feasibility of genetic screening for hereditary hemochromatosis in high schools.Hereditary hemochromatosis (HH), most often due to HFE C282Y homozygosity, is an iron overload disorder that can result in severe morbidity including hepatic cirrhosis. Predisposition to HH is easily diagnosed and morbidity is preventable by maintaining normal body iron and thus calls have been made to introduce community screening. The current study has been designed to assess the acceptability and feasibility of HH screening in high schools. Students (mostly 15–16 years of age) watched a purpose‐designed DVD for education about HH. Those with parental consent were then offered cheek‐brush screening for C282Y. Students completed a questionnaire prior to screening. The program was offered to 9187 students at 32 schools and 3489 (38%) had screening. Nineteen C282Y homozygotes (1 in 183) and 376 heterozygotes (1 in 9.3) were identified. More than 90% of students answered each of five knowledge questions correctly. Eight homozygotes (42%) had elevated transferrin saturation, but only two (10.5%) had marginally elevated serum ferritin (SF). We have shown that genetic screening for HH can successfully be offered in the high school setting. Ongoing research in this study will answer questions about the impact of high school students learning that they are at risk of HH.
Regional variation in infant hypoallergenic formula prescriptions in Australia
Authors: Mullins Raymond J. , Clark Sunday , Camargo Jr. Carlos A. 
Published: November 2009

Mullins RJ, Clark S, Camargo Jr CA. Regional variation in infant hypoallergenic formula prescriptions in Australia. Pediatr Allergy Immunol 2010: 21: e413–e420. © 2009 John Wiley & Sons A/SThere is little information on the regional distribution of food allergy in Australia. We examined the influence of latitude (a marker of sunlight/vitamin D status) on food allergy, as measured by 2007 infant hypoallergenic formula (IHF) prescription rates in children ages 0–2 yrs. Data were compiled from the 52 statistical divisions in mainland Australia plus the island of Tasmania (n = 53 observations). Data from the Australian Department of Health and Aging and the Australian Bureau of Statistics were analysed by statistical division. There was significant regional variability in hypoallergenic formula prescription rates (per 100,000 population/yr), with the highest rates in southern Australia (14,406) and the lowest in the north (721), compared with a national average of 4099. Geographical factors (decreasing latitude and increasing longitude) were associated with a higher rate of IHF prescriptions, such that rates were higher in southern vs. northern regions, and in eastern compared with western regions. Controlling for longitude, physician density and markers of socioeconomic status, southern latitudes were associated with higher hypoallergenic formulae prescription rates [β, −147.98; 95% confidence interval (CI) = −281.83 to −14.14; p = 0.03]. Controlling for latitude, physician density and markers of socioeconomic status, eastern longitudes were also associated with higher hypoallergenic formulae prescription rates (β, 89.69; 95% CI = 2.90–176.49; p = 0.04). Among young children, hypoallergenic formula prescription rates are more common in the southern and eastern regions of Australia. These data provide support for a possible role of sun exposure/vitamin D status (amongst other potential factors) in the pathogenesis of food allergy.
Impact of the post‐World War II generation on intensive care needs in Norway
Authors: LAAKE J. H. , DYBWIK K. , FLAATTEN H. K. , FONNELAND I.‐L. , KVÅLE R. , STRAND K. 
Published: November 2009

Background: A high birth rate during the first two decades following World War II has increased the proportion of elderly people in present‐day society and, consequently, the demand for health‐care services. The impact on intensive care services may become dramatic because the age distribution of critically ill patients is skewed towards the elderly. We have used registry data and population statistics to forecast the demand for intensive care services in Norway up until the year 2025.Methods: Data collected by the Norwegian intensive care registry (NIR), showing the age distribution in Norwegian intensive care units (ICU) during the years 2006 and 2007, were used with three different Norwegian prognostic models of population growth for the years 2008–2025 to compute the expected increase in intensive care unit bed‐days (ICU bed‐days).Results: The elderly were overrepresented in Norwegian ICUs in 2006–2007, with patients from 60 to 79 years of age occupying 44% of ICU bed‐days. Population growth from 2008 to 2025 was estimated to be from 11.1 to 26.4%, depending on the model used. Growth will be much larger in the age group 60–79 years. Other factors kept unchanged, this will result in an increase in the need for intensive care (ICU bed‐days) of between 26.1 and 36.9%.Conclusion: The demand for intensive care beds will increase markedly in Norwegian hospitals in the near future. This will have serious implications for the planning of infrastructure, education of health care personnel, as well as financing of our health care system.
Impact of chronic advanced aortic regurgitation on the perioperative outcome of noncardiac surgery
Authors: LAI H.‐C. , LAI H.‐C. , LEE W.‐L. , WANG K.‐Y. , TING C.‐T. , HUNG C.‐J. , LIU T.‐J. 
Published: November 2009

Background: Whether and how chronic advanced aortic regurgitation (AR) impacts the perioperative outcome of noncardiac surgery remains unclear.Methods: From November 1999 to December 2006, all patients undergoing noncardiac operations and ever examined by echocardiography within the last 6 months were screened. Those with chronic moderate–severe or severe AR were enrolled, provided they were not already trachea‐intubated or aortic valve operated, and the surgery was not performed under local anesthesia. Case‐matched subjects without significant AR served as controls. The perioperative outcomes of these patients were analyzed, and independent prognostic correlates were investigated by multivariate logistic regression analysis.Results: A total of 167 patients (male 131, mean age of 75 years) complying with the enrollment criteria were studied. Compared with the other 167 case‐matched control peers, patients with advanced AR risked potential hazards of serious hemodynamic instability (0.6%) and circulatory collapse (1.2%) during surgery despite the similar incidence of overall cardiac adverse events, and were further distressed with more cardiopulmonary complications (16.2% vs. 5.4%, P=0.003) and in‐hospital deaths (9% vs. 1.8%, P=0.008) post‐operatively. Multivariate regression analysis confirmed the correlation of advanced AR with perioperative mortality, and identified depressed left ventricular function, renal dysfunction, high surgical risk, and lack of cardiac medication as predictors of in‐hospital death.Conclusion: Chronic advanced AR complicates the perioperative outcome of noncardiac surgery as reflected by frequent cardiopulmonary morbidities and in‐hospital deaths, especially when coexisting with specified high‐risk clinical and surgical characteristics.
Ace gene dosage influences the development of renovascular hypertension
Authors: Ceroni Alexandre , Moreira Edson D , Mostarda Cristiano T , Silva Gustavo JJ , Krieger Eduardo M , Irigoyen Maria C 
Published: November 2009

Summary1. Clinical and experimental evidence highlights the importance of the renin–angiotensin system in renovascular hypertension. Furthermore, genetic factors affecting angiotensin‐converting enzyme (ACE) could influence the development of renovascular hypertension.2. To test the effect of small gene perturbations on the development of renovascular hypertension, mice harbouring two or three copies of the Ace gene were submitted to 4 weeks of two‐kidney, one‐clip (2K1C) hypertension. Blood pressure (BP), cardiac hypertrophy, baroreflex sensitivity and blood pressure and heart rate variability were assessed and compared between the different groups.3. The increase in BP induced by 2K1C was higher in mice with three copies of the Ace gene compared with mice with only two copies (46 vs 23 mmHg, respectively). Moreover, there was a 3.8‐fold increase in the slope of the left ventricle mass/BP relationship in mice with three copies of the Ace gene. Micewith three copies of the Ace gene exhibited greater increases in cardiac and serum ACE activity than mice with only two copies of the gene. Both baroreflex bradycardia and tachycardia were significantly depressed in mice with three copies of the Ace gene after induction of 2K1C hypertension. The variance in basal systolic BP was greater in mice with three copies of the Ace gene after 2K1C hypertension compared with those with only two copies of the gene (106 vs 54%, respectively). In addition, the low‐frequency component of the pulse interval was higher mice with three copies of the Ace gene after 2K1C hypertension compared with those with only two (168 vs 86%, respectively). Finally, in mice with three copies of the Ace gene, renovascular hypertension induced a 6.1‐fold increase in the sympathovagal balance compared with a 3.2‐fold increase in mice with only two copies of the gene.4. Collectively, these data provide direct evidence that small genetic disturbances in ACE levels per se have an influence on haemodynamic, cardiac mass and autonomic nervous system responses in mice under pathological perturbation.
Role of the renin–angiotensin–aldosterone system for control of arterial blood pressure following moderate deficit in total body sodium: Balance studies in freely moving dogs
Authors: Seeliger Erdmann , Lunenburg Till , Ladwig Mechthild , Reinhardt H Wolfgang 
Published: November 2009

Summary1. Total body sodium (TBS) is known as major determinant of arterial blood pressure (ABP) when TBS is increased, but little is known about ABP control following a deficit in TBS. The renin–angiotensin–aldosterone system (RAAS) controls ABP by controlling TBS via the Na‐retaining effects of angiotensin (Ang) II and aldosterone, as well as through the vasoconstrictor action of AngII. In the present study, we investigated the role of RAAS elements in ABP control following moderate TBS deficit.2. Balance studies of 4 days duration were performed in dogs. On Day 1, TBS was reduced by peritoneal dialysis (−3.5 mmol/kg bodyweight). On Days 1 and 2, dogs were on low Na intake (LSI; 0.5 mmol Na/kg bodyweight), whereas on Days 3 and 4 dogs were on high Na intake (HSI; 5.5 mmol Na/kg). In Protocol 1, the RAAS was left intact; in Protocol 2, angiotensin‐converting enzyme was inhibited by infusion of the angiotensin‐converting enzyme (ACE) inhibitor captopril (7 μg/kg per min) on Days 2–4; and in Protocol 3, in addition to ACE inhibition (ACE‐I), mineralocorticoid receptors (MR) were blocked using 300 mg, p.o., spironolactone twice daily on Days 2–4.3. During LSI, the TBS deficit could not be replenished and osmoregulation resulted in a deficit in total body water (TBW) of −12 to −15 mL/kg bodyweight. The RAAS was massively stimulated. In dogs with an intact RAAS, ABP did not decrease despite the TBW deficit. This was achieved by the vasoconstrictor action of AngII. At the same TBW deficit, ACE‐I significantly lowered ABP by approximately 17 mmHg. In dogs with an intact RAAS, the deficit in TBS and TBW was immediately replenished when enough Na was offered (HSI). Even during ACE‐I, the deficit was almost replenished. This was accomplished by AngII‐independent stimulation of aldosterone release. Arterial blood pressure increased in parallel with TBW. With additional blockade of MR, the deficit was not replenished and ABP remained reduced.4. These results indicate that with a moderate deficit in TBS and TBW, the RAAS is the major factor controlling ABP. First, the vasoconstrictive action of AngII fully compensates for the volume deficit. Second, stimulation of both renin release (and, thus, AngII and aldosterone) and aldosterone release independent of AngII is crucial for the restoration of TBS and TBW, thus controlling ABP.
Efficacy of butyrate analogues in HT‐29 cancer cells
Authors: Ooi Cheng C , Good Norm M , Williams Desmond B , Lewanowitsch Tanya , Cosgrove Leah J , Lockett Trevor J , Head Richard J 
Published: November 2009

Summary1. Butyrate is a well known product of starch fermentation by colonic bacteria and is of interest owing to its ability to induce in vitro apoptosis and cell differentiation, as well as to inhibit cell growth in colorectal and other cancer cells. Synthetic analogues of butyrate may also possess cellular activities in a variety of cultured cells. The aim of the present study was to evaluate the effects of butyrate analogues on apoptosis, proliferation and histone deacetylase (HDAC) activity in HT‐29 colorectal cancer cells. In addition, the effects of these analogues on lactate dehydrogenase leakage, as a measure of non‐specific cytotoxicity, were evaluated in HT‐29 cells.2. Of the 26 analogues examined, four (propionate, 4‐benzoylbutyrate, 4‐(4‐aminophenyl)butyrate and benzyloxyacetate) exhibited comparable effects to butyrate. Interestingly, no activity was noted for compounds carrying amino, hydroxyl or methyl substitutions at the 2‐, 3‐ or 4‐position of the aliphatic moiety of butyrate.3. In conclusion, chemical changes to the structure of butyrate can significantly modify the biological activity assayed in HT‐29 colorectal cancer cells in vitro.
Atorvastatin increases expression of low‐density lipoprotein receptor mRNA in human circulating mononuclear cells
Authors: Pocathikorn Anothai , Taylor Roger R , Mamotte Cyril DS 
Published: November 2009

Summary1. 3‐Hydroxy‐3‐methylglutaryl coenzyme A reductase (HMGCR) inhibitors, or statins, are commonly used to lower plasma cholesterol levels. HMGCR and the low‐density lipoprotein (LDL) receptor (LDLR) are of central importance to cholesterol homeostasis and yet there is a paucity of data on the effect of statins on the regulation of the LDLR and HMGCR in humans.2. In the present study, we examined the effect of atorvastatin on the expression of HMGCR, LDLR and LDLR‐related protein (LRP) mRNA in circulating mononuclear cells. Twelve human volunteers were treated with atorvastatin, 20 mg/day for 4 weeks.3. Atorvastatin decreased plasma total and LDL–cholesterol by 29% (P < 0.0001) and 41% (P < 0.001), respectively, and increased LDLR mRNA abundance, in absolute terms, by 35% (P < 0.001) and 31% (P < 0.0001) and 37% (P = 0.01) relative to reference GAPDH and β‐actin mRNA, respectively. In contrast, atorvastatin had no significant effect on LRP or HMGCR mRNA levels.4. The increase in LDLR mRNA in circulating mononuclear cells agrees with the few human studies conducted, as well as with in vitro and animal studies, whereas the unchanged HMGCR mRNA is consistent with the hepatic specificity of atorvastatin. The present study firmly documents an increase in LDLR mRNA levels in response to statin administration in normal humans.
High‐density lipoprotein: A potent inhibitor of inflammation
Authors: Murphy Andrew J , Woollard Kevin J 
Published: November 2009

Summary1. Inflammation is an important process, driving the progression of atherosclerosis. Stemming inflammation may be a mechanism to inhibit the progression of this disease.2. High‐density lipoprotein (HDL), a particle inversely related to cardiovascular disease, has been described as having a number of anti‐inflammatory functions. It has been shown that HDL inhibits endothelial inflammation in both in vitro and in vivo models, reducing the expression of key cell adhesion molecules. In addition, HDL has been shown to have an effect on the coagulation pathway by inhibiting platelet activation and reducing thrombus formation. Furthermore, by reducing the activation of leucocytes, HDL can inhibit leucocyte recruitment to the endothelium.3. High‐density lipoprotein infusion studies conducted in patients with inflammatory diseases have shown that acute treatment with HDL can effectively inhibit inflammation in vivo. Thus, HDL has been proven to be a potent inhibitor of inflammation, acting on a number of pathways, and this may suggest that HDL could be applied as an anti‐inflammatory molecule for a number of diseases.4. The present review highlights these important studies and reviews data on the anti‐inflammatory effects of HDL from in vitro and in vivo studies, in both humans and animal models of atherosclerosis and inflammatory‐related diseases.
Meta‐analysis of the role of high‐dose statins administered prior to percutaneous coronary intervention in reducing major adverse cardiac events in patients with coronary artery disease
Authors: Hao Pan‐Pan , Chen Yu‐Guo , Wang Jia‐Li , Ji Wen‐Qing , Xue Li , Liu Xiang‐Hong , Wang Xing‐Li , Zhang Yun 
Published: November 2009

Summary1. There is considerable evidence regarding the efficacy of statins for the primary and secondary prevention of coronary artery disease (CAD). However, due to lack of sufficient evidence, there is still doubt whether high‐dose statin therapy prior to percutaneous coronary intervention (PCI) is beneficial. In the present study, we performed a meta‐analysis to evaluate the effect of preoperative high‐dose statin therapy on the incidence of major adverse cardiac events (MACE) after successful PCI.2. Trials were retrieved through Medline (1980–2009) and the reference files limited to English‐language articles. Data were abstracted using a standardized protocol and a meta‐analysis was performed.3. Five studies of a total 1789 patients with CAD qualified for analysis. Administration of high‐dose statins in CAD patients before PCI was associated with a significant reduction in MACE 30 days after the procedure. The incidence of MACE in the high‐dose statin group (6.98%) was significantly lower than that in the placebo group (14.77%), with an odds ratio (OR) of 0.43 (95% confidence interval (CI) 0.31–0.59; P < 0.00001). The incidence of post‐PCI increases in creatine kinase MB in the high‐dose statin and placebo groups was 9.20%vs 18.83%, respectively (OR 0.43; 95% CI 0.33–0.58; P < 0.00001), whereas the incidence of increases in troponin I was 30.13%vs 44.53%, respectively (OR 0.53; 95% CI 0.43–0.67; P < 0.00001), respectively.4. In conclusion, high‐dose statin therapy before PCI provides a significant benefit over placebo in preventing post‐PCI MACE. Findings from the present analysis strongly support a strategy of routine loading of high‐dose statins before interventional therapy.
Prenatal alcohol exposure: Implications for cardiovascular function in the fetus and beyond
Authors: Parkington Helena C , Coleman Harold A , Wintour E Marelyn , Tare Marianne 
Published: November 2009

Summary1. The effects of heavy maternal alcohol consumption during pregnancy on cognitive and behavioural performance and craniofacial malformations in the offspring have been studied extensively. In contrast, the impact of maternal alcohol intake on the cardiovascular system of the offspring and the effects of more modest consumption have received very scant consideration.2. Adverse conditions in the pre‐ and neonatal periods can have a profound legacy on offspring health, including the risk of cardiovascular disease. Prenatal alcohol exposure can modulate vascular reactivity, including endothelial and smooth muscle function.3. Other effects of prenatal alcohol exposure are emerging, including impairment of nephrogenesis and kidney function and increased arterial stiffness. The impact of even modest prenatal alcohol exposure on cardiovascular health in the offspring remains to be determined.4. It is envisaged that the culmination of reduced renal and vascular capacity will render the offspring more vulnerable to cardiovascular disease with ageing and exposure to additional insults and lifestyle factors.
Rescue therapy with high‐dose oral phenobarbitone loading for refractory status epilepticus
Authors: Wilmshurst Jo M , Van Der Walt Jan‐Stefan , Ackermann Sally , Karlsson Mats O , Blockman Marc 
Published: November 2009

Aim:  Parenteral phenobarbitone was unavailable in South Africa from 2005 to 2006. This study aimed to establish the effectiveness of enteral phenobarbitone in the management of childhood status epilepticus.Method:  Patients in status epilepticus (December 2005–June 2006) received 20 mg/kg phenobarbitone via nasogastric tube in addition to standard status interventions (benzodiazepine boluses, phenytoin infusion). Phenobarbitone concentrations were taken post loading. Phenobarbitone population pharmacokinetics was analysed using non‐linear mixed effects modelling.Results:  Sixteen patients (7 female, 9 male) were assessed, median age 5 months (range 9 days–168 months). Nine patients received 20 mg/kg; the maximum total dosage administered was 80 mg/kg with a concentration of 283 µmol/L. The typical population value of the volume of distribution was 1.2 (95% confidence interval (CI): 0.8–1.6) L/kg with interindividual variability (as coefficient of variation) of 53% (95% CI, 9–74%). Seizure control was documented within 1 h (n= 8), 11/2 h (n= 1), 3 h (n= 1) and 4 h (n= 5) following enteral phenobarbitone loading. No adverse effects were apparent from the enteral phenobarbitone administration.Conclusion:  Patients tolerated enteral loading with phenobarbitone. A single enteral loading dose resulted in adequate phenobarbitone exposure. This practice was a safe intervention for centres lacking parenteral phenobarbitone. Therapeutic concentrations and seizure control after enteral loading suggested a role for enteral phenobarbitone in the management of acute status epilepticus as well as prophylaxis against seizure recurrence.
Treating infant sleep disturbance: Does maternal mood impact upon effectiveness?
Authors: Črnčec Rudi , Cooper Elizabeth , Matthey Stephen 
Published: November 2009

Aim:  To explore whether mild‐to‐moderate maternal depression affects the effectiveness of a behavioural approach to treating infant sleep disturbance (ISD).Methods:  The health records of 90 mothers attending an inpatient parenting service for management of their 5–12‐month‐old infant's sleep difficulties were examined. These records contained detailed, nurse‐completed, 24‐hour behaviour charts of infant sleeping and crying. Participants were allocated to the depression group based on Edinburgh Depression Scale score and/or review of mental health assessment notes.Results:  There were no differences between infants of mothers with (n= 39) or without (n= 51) depression on either (i) the severity of their initial sleeping difficulty, or (ii) their response to behavioural treatment. Both groups showed significant improvements over the 5‐day stay on all sleep variables observed, including number of night wakings, time to fall asleep, time spent crying at night and total time slept at night.Conclusions:  Mild‐to‐moderate maternal depression does not appear to attenuate ISD behavioural treatment outcomes. Given ISD treatment has been shown to improve maternal mood, the results of this study argue against recommendations initially to address maternal mood in isolation when managing ISD.