bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diet prescription for non‐alcoholic fatty liver disease: Is it worth the effort? A systematic review
Authors: ROSSI Megan , HICKMAN Ingrid J. 
Published: February 2011

AbstractAim:  The objective of this review was to assess the effectiveness of diet interventions for improving disease severity in non‐alcoholic fatty liver disease. A secondary aim was to identify the effectiveness of different methods of dietetic service delivery for achieving weight reduction in this patient group.Methods:  A review of studies from 1999 to 2009 was conducted. Studies were included if they reported non‐alcoholic fatty liver disease diagnosis by either liver histology analysis, imaging or by persistent hypertransaminasaemia, were English language studies of human adults, ≥18 years, that had implemented a dietary component in the intervention.Results:  From the 102 papers identified, 20 met inclusion criteria: two randomised controlled trials, two controlled trials (allocation method not disclosed), two non‐randomised experimental studies and 14 case series. Methods of diet prescription differed substantially among studies. Weight reduction appeared to be associated with a reduction in steatosis; however, improvements in other features of liver disease remain unclear. There appeared to be a relationship between the intensity of dietetic contact and weight loss.Conclusion:  There is limited evidence available to assess the effectiveness of diet interventions on histological severity of non‐alcoholic fatty liver disease. There is good evidence that clinically significant weight reduction can improve steatosis and risk factors for non‐alcoholic fatty liver disease. A relationship may exist between the frequency of dietetic consultations and amount of weight reduction achieved in patients with non‐alcoholic fatty liver disease. Fortnightly intervention for a minimum of three months to achieve at least 5% weight loss is recommended.
The views from the hills: fatal accidents, child safety and licensing adventure activities
Authors: McArdle David 
Published: February 2011

Two recent fatal accident inquiries (FAIs) in Scotland have potentially far-reaching ramifications for educational provision across the whole of the UK. The deaths of two teenage children during the course of outdoor adventure activities led the sheriff in one of those inquiries to recommend a review of the regulatory framework which governs those activities. This call for an across-the-board review means the outdoor education sector – which includes organisations which provide outdoor education for schools groups as well as those offering more adventurous experiences for children outside term time – is now likely to face a degree of scrutiny greater than any it has experienced since the 1993 Lyme Bay disaster.This paper draws upon research interviews with those who work in outdoor education in some of the more remote areas of Scotland. The data from those interviews indicate that some of the issues that ought to be considered in any such review will not be immediately apparent from reading either the fatal accident inquiries' determinations or the literature which is available either on the Heath and Safety Executive's website or otherwise in the public domain. In particular, it appears that some issues which have only reached a wider audience by virtue of these FAIs have actually been the source of longstanding concerns among the stakeholders, dating back to the mid-1990s when the regulatory framework that came into being in the wake of Lyme Bay was still under discussion. This paper therefore uses the interviewees' responses to help develop a greater understanding of the issues that exist in this particular sector and to illustrate the legal and logistical challenges that it faces.
Current understanding of increased insulin sensitivity after exercise – emerging candidates
Authors: Maarbjerg S. J. , Sylow L. , Richter E. A. 
Published: February 2011

AbstractExercise counteracts insulin resistance and improves glucose homeostasis in many ways. Apart from increasing muscle glucose uptake quickly, exercise also clearly increases muscle insulin sensitivity in the post‐exercise period. This review will focus on the mechanisms responsible for this increased insulin sensitivity. It is believed that increased sarcolemmal content of the glucose transporter GLUT4 can explain the phenomenon to some extent. Surprisingly no improvement in the proximal insulin signalling pathway is observed at the level of the insulin receptor, IRS1, PI3K or Akt. Recently more distal signalling component in the insulin signalling pathway such as aPKC, Rac1, TBC1D4 and TBC1D1 have been described. These are all affected by both insulin and exercise which means that they are likely converging points in promoting GLUT4 translocation and therefore possible candidates for regulating insulin sensitivity after exercise. Whereas TBC1D1 does not appear to regulate insulin sensitivity after exercise, correlative evidence in contrast suggests TBC1D4 to be a relevant candidate. Little is known about aPKC and Rac1 in relation to insulin sensitivity after exercise. Besides mechanisms involved in signalling to GLUT4 translocation, factors influencing the trans‐sarcolemmal glucose concentration gradient might also be important. With regard to the interstitial glucose concentration microvascular perfusion is particular relevant as correlative evidence supports a connection between insulin sensitivity and microvascular perfusion. Thus, there are new candidates at several levels which collectively might explain the phenomenon.
Old Chromophores, New Photoactivation Paradigms, Trendy Applications: Flavins in Blue Light‐Sensing Photoreceptors†
Authors: Losi Aba , Gärtner Wolfgang 
Published: February 2011

AbstractThe knowledge on the mechanisms by which blue light (BL) is sensed by diverse and numerous organisms, and of the physiological responses elicited by the BL photoreceptors, has grown remarkably during the last two decades. The basis for this “blue revival” was set by the identification and molecular characterization of long sought plant BL sensors, employing flavins as chromophores, chiefly cryptochromes and phototropins. The latter photosensors are the foundation members of the so‐called light, oxygen, voltage (LOV)‐protein family, largely spread among archaea, bacteria, fungi and plants. The accumulation of sequenced microbial genomes during the last years has added the BLUF (Blue Light sensing Using FAD) family to the BL photoreceptors and yielded the opportunity for intense “genome mining,” which has presented to us the intriguing wealth of BL sensing in prokaryotes. In this contribution we provide an update of flavin‐based BL sensors of the LOV and BLUF type, from prokaryotic microorganisms, with special emphasis to their light‐activation pathways and molecular signal‐transduction mechanisms. Rather than being a fully comprehensive review, this research collects the most recent discoveries and aims to unveil and compare signaling pathways and mechanisms of BL sensors.
Blue and Red Light‐Induced Germination of Resting Spores in the Red‐Tide Diatom Leptocylindrus danicus†
Authors: Shikata Tomoyuki , Iseki Mineo , Matsunaga Shigeru , Higashi Sho‐ichi , Kamei Yasuhiro , Watanabe Masakatsu 
Published: February 2011

AbstractPhotophysiological and pharmacological approaches were used to examine light‐induced germination of resting spores in the red‐tide diatom Leptocylindrus danicus. The equal‐quantum action spectrum for photogermination had peaks at about 440 nm (blue light) and 680 nm (red light), which matched the absorption spectrum of the resting spore chloroplast, as well as photosynthetic action spectra reported for other diatoms. DCMU, an inhibitor of photosynthetic electron flow near photosystem II, completely blocked photogermination. These results suggest that the photosynthetic system is involved in the photoreception process of light‐induced germination. Results of pharmacological studies of the downstream signal transduction pathway suggested that Ca2+ influx is the closest downstream neighbor, followed by steps involving calmodulin, nitric oxide synthase, guanylyl cyclase, protein‐tyrosine‐phosphatase, protein kinase C and actin polymerization and translation.
An assessment of three noncommercial DNA extraction methods from dried blood spots for beta‐thalassaemia mutation identification
Authors: KARTHIPAN S. N. , GEORGE E. , JAMEELA S. , LIM W. F. , TEH L. K. , LEE T. Y. , CHIN V. K. , LAI M. I. 
Published: February 2011

SummaryIntroduction:  Dried blood spots (DBS) are currently the recommended sample collection method for newborn screening programmes in America. Early diagnosis of beta‐thalassaemia screening is essential as it provides an added advantage especially in sickle cell disease. Beta‐thalassaemia frequency is high in many poor countries, and the cost of using commercial DNA extraction kits can be prohibitive. Our study assessed three methods that use minimal reagents and materials to extract DNA from DBS for beta‐thalassaemia identification.Methods:  The methods assessed in this study were Tris–EDTA (TE) buffer‐based method by Bereczky et al. (American Journal of Tropical Medicine and Hygiene 72, 2005, 249), NaCL/NaOH/Sodium dodecyl sulphate (SDS) method by Huang et al. (Human Genetics 84, 1990, 129) and NaOH method by Zhou et al. (Analytical Biochemistry 354, 2006, 159). Extracted DNA was amplified for three common beta‐thalassaemia mutations in Malaysia.Results:  Amplicons derived from TE buffer‐based method were very faint and almost nonexistent while the NaCl/NaOH/SDS method did not produce any visible amplicons. The extraction using NaOH method produced visible bands that were comparable to the standard method using extraction kit.Conclusion:  The NaOH method is a simple method that uses minimal equipment and reagents that make it labour‐ and cost‐effective. This method could be adopted by poorer countries to extract DNA for beta‐thalassaemia mutation characterization.
ABCB1 identifies a subpopulation of uveal melanoma cells with high metastatic propensity
Authors: Landreville Solange , Agapova Olga A. , Kneass Zachary T. , Salesse Christian , William Harbour J. 
Published: February 2011

SummaryMetastasis of tumor cells to distant organs is the leading cause of death in melanoma. Yet, the mechanisms of metastasis remain poorly understood. One key question is whether all cells in a primary tumor are equally likely to metastasize or whether subpopulations of cells preferentially give rise to metastases. Here, we identified a subpopulation of uveal melanoma cells expressing the multidrug resistance transporter ABCB1 that are highly metastatic compared to ABCB1− bulk tumor cells. ABCB1+ cells also exhibited enhanced clonogenicity, anchorage‐independent growth, tumorigenicity and mitochondrial activity compared to ABCB1− cells. A375 cutaneous melanoma cells contained a similar subpopulation of highly metastatic ABCB1+ cells. These findings suggest that some uveal melanoma cells have greater potential for metastasis than others and that a better understanding of such cells may be necessary for more successful therapies for metastatic melanoma.
Ultrastructure of anterior lens capsule of intumescent white cataract
Authors: Hawlina Marko , Stunf Spela , Hvala Anastazija 
Published: February 2011

Abstract.Purpose:  To analyse the anterior lens capsule thickness and ultrastructure changes of intumescent white cataracts in comparison with nuclear cataracts to prove possible structural reasons for surgical difficulties with the intumescent white cataract.Methods:  Anterior lens capsules from 35 eyes with intumescent white and 35 eyes with nuclear cataracts were analysed for their thickness by semithin sections technique and for morphological characteristics by transmission electron microscopy.Results:  Capsule thickness was not significantly different in intumescent white compared to nuclear cataracts (mean values 17.5 and 18.5 μm, respectively, p = 0.369). The main morphological features of capsules were extrusions of capsule at the basement membrane‐epithelial border embedding cellular material which were significantly more frequent in intumescent cataracts. Filaments in the basement membrane as well as rarefication of its structure and lamellae were often concomitant with the extrusions.Conclusions:  Anterior capsules of white intumescent cataracts do not differ in thickness but have different ultrastructure morphology compared to nuclear cataracts. The extrusions of basement membrane at the basement membrane‐epithelial border towards epithelium, the filamentary inclusions within basement membrane and its rarefication could be the structural causes of tensile weakness and hence additional reason to surgical problems.
Toxoplasma gondii protects against H2O2‐induced apoptosis in ARPE‐19 cells through the transcriptional regulation of apoptotic elements and downregulation of the p38 MAPK pathway
Authors: Choi Si‐Hwan , Park Sung Jun , Cha Guang‐Ho , Quan Juan Hua , Chang Nam‐Sik , Ahn Myoung‐Hee , Shin Dae‐Whan , Lee Young‐Ha 
Published: February 2011

Abstract.Purpose:  Toxoplasmosis, which is caused by the protozoan parasite Toxoplasma gondii, can lead to severe visual impairment. T. gondii inhibits or delays programmed cell death caused by various apoptotic triggers; however, the mechanisms involved in the T. gondii‐induced suppression of apoptosis in retinal cells have not been analysed in detail.Methods:  We investigated the role of T. gondii infection in H2O2‐induced apoptosis in human retinal pigment epithelial cells (ARPE‐19) by monitoring the activities of apoptosis‐regulating molecules and mitogen‐activated protein kinases (MAPKs), including p38 MAPK. We also examined the gene downstream from p38 MAPK.Results:  T. gondii infection significantly inhibited the cellular toxicity of H2O2 (500 μm) and increased cell viability in a multiplicity of infection (MOI)‐dependent manner by reducing DNA fragmentation and reactive oxygen species (ROS) generation in ARPE‐19 cells. Western blot analysis also showed that T. gondii infection prevented the host cell expression of pro‐apoptotic factors, such as Bad and Bax, and the activation of caspase‐3. Infection with T. gondii increased the expression of the anti‐apoptotic factor Bcl‐2 in ARPE‐19 cells under oxidative stress. In accordance with these findings, Toxoplasma infection was protective enough to suppress the phosphorylation of p38 MAPK following H2O2 treatment. Exposure to H2O2 increased the expression of heme oxygenase‐1 (HO‐1) in ARPE‐19 cells, and its expression was significantly inhibited in H2O2‐treated infected cells.Conclusion:  The protective function of T. gondii infection against ROS‐induced apoptosis results from changes in the expression of apoptotic molecules and the downregulation of stress‐induced intracellular signalling.
Clinical Efficacy of Aniracetam, Either as Monotherapy or Combined with Cholinesterase Inhibitors, in Patients with Cognitive Impairment: A Comparative Open Study*
Authors: Koliaki Chrysi C. , Messini Chaido , Tsolaki Magda 
Published: February 2011

SUMMARYIntroduction: Dementia constitutes an increasingly prevalent cognitive disorder with serious socioeconomic implications. Aims: In the present study, we aimed to evaluate the efficacy of aniracetam, either as monotherapy or combined with cholinesterase inhibitors (ChEIs), in terms of several neuropsychological parameters, in a considerable number of patients with dementia. Results: In our prospective, open‐label study, we enrolled a total of 276 patients (mean age 71 ± 8 years, 95 males) with cognitive disorders. Our study population comprised four groups: no treatment group (n = 75), aniracetam monotherapy group (n = 58), ChEIs monotherapy group (n = 68), and group of combined treatment (n = 68). Patients were examined with validated neuropsychological tests at baseline, 3, 6, and 12 months of treatment. In patients treated with aniracetam, all studied parameters were adequately maintained at 6 and 12 months, while emotional state was significantly improved at 3 months. In patients treated with ChEIs, we observed a significant cognitive deterioration at 12 months. The comparison between aniracetam and ChEIs in patients with relatively mild dementia (15 ≤ MMSE ≤ 25) revealed a significantly better cognitive performance with aniracetam at 6 months and improved functionality at 3 months. Comparing aniracetam monotherapy with combined treatment in the same population, aniracetam performed better in the cognitive scale at 6 months, and displayed a notable tendency for enhanced mood at 12 months and improved functionality at 6 months. Conclusions: Our findings indicate that aniracetam (a nootropic compound with glutamatergic activity and neuroprotective potential) is a promising option for patients with cognitive deficit of mild severity. It preserved all neuropsychological parameters for at least 12 months, and seemed to exert a favorable effect on emotional stability of demented patients.
Stem Cell Challenges in the Treatment of Neurodegenerative Disease
Authors: Feng Zhongling , Gao Feng 
Published: February 2011

SUMMARYNeurodegenerative diseases result from the gradual and progressive loss of neural cells and lead to nervous system dysfunction. The rapidly advancing stem cell field is providing attractive alternative options for fighting these diseases. Results have provided proof of principle that cell replacement can work in humans with Parkinson's disease (PD). However, three clinical studies of cell transplantation were published that found no net benefit, while patients in two of the studies developed dyskinesias that persisted despite reductions in treatment. Induced pluripotent stem cells (iPSC) have major potential advantages because patient‐specific neuroblasts are suitable for transplantation, avoid immune reactions, and can be produced without the use of human ES cells (hESC). Although iPSCs have not been successfully used in clinical trials for PD, patients with amyotrophic lateral sclerosis (ALS) were treated with autologous stem cells and, though they had some degree of decline one year after treatment, they were still improved compared with the preoperative period or without any drug therapy. In addition, neural stem cells (NSCs), via brain‐derived neurotrophic factor (BDNF), have been shown to ameliorate complex behavioral deficits associated with widespread Alzheimer's disease (AD) pathology in a transgenic mouse model of AD. So far, the FDA lists 18 clinical trials treating multiple sclerosis (MS), but most are in preliminary stages. This article serves as an overview of recent studies in stem cell and regenerative approaches to the above chronic neurodegenerative disorders. There are still many obstacles to the use of stem cells as a cure for neurodegenerative disease, especially because we still don't fully understand the true mechanisms of these diseases. However, there is hope in the potential of stem cells to help us learn and understand a great deal more about the mechanisms underlying these devastating neurodegenerative diseases.
Metabolic Syndrome and Bipolar Disorder: What Should Psychiatrists Know?
Authors: de Almeida Karla M. , Moreira Camila L. R. L. , Lafer Beny 
Published: February 2011

SUMMARYThis paper reviews the association between bipolar disorder (BD) and metabolic syndrome (MetS), focusing on the etiopathogenetic and pathophysiological aspects of this association and on the recommendations for preventing and managing MetS in patients with BD. We conducted a nonsystematic literature review by means of a MEDLINE search. The exact causal relationship between MetS and BD is still uncertain. The side effects of psychotropic medications may be a major contributor to the increased rates of MetS in patients with BD. Other factors such as unhealthy lifestyles, common neuroendocrine and immuno‐inflammatory abnormalities, and genetic vulnerability may also play a role in explaining the high rates of MetS in BD. Strategies to prevent and treat the MetS and its cardiovascular consequences in patients with BD include accurate screening and monitoring of the patient and appropriate psychoeducation on weight control, healthy nutrition, and increased physical activity. When deciding on pharmacological therapy for the treatment of the components of the MetS, drug interactions and the effects of the medications on mood must be taken into account.
Acupuncture for Posttraumatic Stress Disorder: Conceptual, Clinical, and Biological Data Support Further Research
Authors: Hollifield Michael 
Published: February 2011

SUMMARYPosttraumatic stress disorder (PTSD) is common, debilitating, and has highly heterogeneous clinical and biological features. With the exception of one published preliminary clinical trial, rationale in support of the efficacy of acupuncture, a modality of Chinese medicine (CM), for PTSD has not been well described. This is a focused review of conceptual and clinical features of PTSD shared by modern western medicine (MWM) and CM, and of biological mechanisms of acupuncture that parallel known PTSD pathology. MWM and CM both recognize individual developmental variables and interactions between external conditions and internal responses in the genesis of PTSD. There is one published and one unpublished clinical trial that preliminarily support the efficacy of acupuncture for PTSD. Although there have been no mechanistic studies of acupuncture in human PTSD, extant research shows that acupuncture has biological effects that are relevant to PTSD pathology. Conceptual, clinical, and biological data support possible efficacy of acupuncture for PTSD. However, further definitive research about simultaneous clinical and biological effects is needed to support the use of acupuncture for PTSD in health care systems.
VLED and formula LED in the management of type 2 diabetes: defining the clinical need and research requirements
Authors: Lean M. 
Published: February 2011

SummaryIt has been known for many years that substantial weight loss, achieved by bariatric surgery or non‐surgical means can mean normalize glucose tolerance. Recent randomized controlled trial evidence indicates that >15 kg weight loss is necessary, to this and it may lead to near normalization (doubling) of life expectancy. Less than 5% of patients achieve this through even the best, evidence‐based medical weight management programme (Counterweight http://www.counterweight.org).A weight loss of >15 kg is easily achievable by 8 weeks very low‐energy diet (VLED)/LELD (Low energy Liquid‐formula Diet) in compliant patients, with little difference between 400 and 800 kcal day−1, but weight maintenance after VLED has until recently been so poor that VLED is not, at present, recommended in clinical guidelines. However, mean weight loss close to >15 kg can be maintained 18–24 months using a variety of maintenance strategies. These include a structured reintroduction of foods linked to an education programme with behavioural strategies, intermittent VLED use and prescribable anti‐obesity drugs (dexfenfluramine, orlistat, sibutramine). Most of these studies have been in non‐diabetic subjects.A new ‘curative’ paradigm in type 2 diabetes mellitus management, aiming to normalize glucose tolerance and health risks by achieving and maintaining >15 kg loss, as soon as possible after diagnosis, should be highly acceptable to patients, generating many additional Quality Adjusted Life Years (QALYs). It is likely to be highly cost‐effective by avoiding the current recommended, mainly palliative, model, using polypharmacy which provides an overall risk reduction of only 5–10%.Clinical trials are on‐going to establish the feasibility of delivering formula (LELD) and a maintenance programme to large numbers of patients within routine primary care. There is urgent need, to run similar studies in diabetic patients. New approaches to long‐term (lifelong) maintenance of weight loss and a non‐diabetic state may include anti‐obesity drugs.