bluuebunny/crossref_metadata_2025_split huggingface dataset:
Severe acute respiratory syndrome in surgical patients: a diagnostic dilemma
Authors: Tan Felicia Li Sher , Loo Wee Lim , Tan Seck Guan , Wong Chow Yin , Tan Yu‐Meng 
Published: March 2005

Background:  The diagnosis of severe acute respiratory syndrome (SARS) in surgical patients can potentially be missed based on current World Health Organization (WHO) case definitions.Method:  We report a retrospective case series of 10 surgical inpatients diagnosed with SARS following an outbreak in the surgical wards. Patients were included if they fulfilled the WHO case definition of probable SARS, had an active surgical problem and were admitted to the surgical wards during the outbreak period. Clinical histories, laboratory investigations and radiological findings were reviewed and analyzed.Results:  The mean age of the cohort was 57.6 years (range: 38−78 years). Nine patients had concomitant medical conditions. Three patients were in the early postoperative period, while the remaining seven were admitted for surgical related infections. All patients presented with fever, but only eight had accompanying respiratory symptoms. Lymphopenia and raised lactate dehydrogenase (LDH) was seen in seven patients. Eight patients had positive bacterial cultures. The primary abnormality on chest radiograph was air‐space opacification. Rapid progression of radiological changes was seen in seven patients. Mortality rate for our cohort is 20%.Conclusion:  The diagnosis of SARS in surgical patients differs from that previously described in normal patients. An apparent cause of fever and positive blood cultures cannot exclude a diagnosis of SARS. The current WHO case definition could result in delayed or even missed diagnosis. Early isolation of febrile patients with a positive contact history must be undertaken, even in the face of another identifiable cause.
Bilateral ankle blocks: A prospective audit
Authors: Rudkin Glenda E , Rudkin Adam K , Dracopoulos George C 
Published: March 2005

Background:  There are significant advantages to the practice of bilateral ankle block. However, clinicians are reluctant to employ this technique due to concerns over reliability, local anaesthetic longevity and toxicity, surgical efficiency, and patient comfort.Methods:  Sixty‐six patients undergoing bilateral ankle blocks during mid‐ and forefoot surgery were audited to determine success rate, local anaesthetic safety and efficacy, and patient acceptance. Intravenous sedation was administered both during insertion of ankle blocks and intraoperatively, as requested by the patient and as deemed necessary by the anaesthetist. The choice of local anaesthesia was either a 50/50 mixture of lignocaine 1.5% plain and ropivacaine 7.5 mg/mL, ropivacaine 7.5 mg/mL alone or ropivacaine 7.5 mg/mL and clonidine 1 µg/kg.Results:  A total of 89% of patients had a successful bilateral ankle block. Ropivacaine and clonidine combination, ropivacaine, and ropivacaine and lignocaine combination provided a mean length of action of 17 h, 14 h and 8 h, respectively. No adverse local anaesthetic events were reported. Sixty‐one per cent of patients remembered intraoperative events; only one patient would choose not to have the procedure performed again under ankle blocks.Conclusions:  The present audit demonstrates that bilateral ankle blocks are a safe and efficient technique. With appropriate doses of sedative drugs both during insertion of the ankle block and surgery, patients remain comfortable.
Laparoscopic live donor nephrectomy
Authors: Rao M. Mohan , Russell Christine H 
Published: March 2005

Background:  The demand for renal transplants is greater than the available kidneys. Live donation is one way of increasing the supply. Laparoscopic removal of the donor kidney appears to reduce morbidity for the donors. Some who are hesitant because of the morbidity associated with open nephrectomy are willing to consider the laparoscopic donor nephrectomy.Methods:  Laparoscopic donor nephrectomy was offered to all but three donors since the commencement of the programme in 1997. Data were collected both prospectively and retrospectively for the first 120 donors. Venous and arterial anatomy was assessed preoperatively by computed tomographic angiography.Results:  All but four donor procedures were completed laparoscopically. Three of these were for bleeding that could not be safely controlled laparoscopically and the fourth was a planned conversion to deal with the renal vessels, in the first right nephrectomy. Two kidneys were lost due to arterial thrombosis and two underwent segmental infarction after the loss of one of two or three separately anastomosed vessels. Three recipients had delayed function and two of them required dialysis postoperatively. Other minor complications occurred but were uncommon.Conclusions:  Laparoscopic live donor nephrectomy is safe for the donor and the transplant kidney. It offers the advantage of decreased morbidity for the donor, with a shorter hospital stay, earlier return to normal activity and, for some, early return to work.
Necrotizing fasciitis: analysis of 48 cases in South Auckland, New Zealand
Authors: Tiu Albert , Martin Richard , Vanniasingham Peter , MacCormick Andrew D. , Hill Andrew G. 
Published: March 2005

Background:  To assess the presentation, management and risk factors for mortality in necrotizing fasciitis at Middlemore Hospital in South Auckland, New Zealand.Methods:  A retrospective review of the medical records of patients presenting to Middlemore Hospital over a 6‐year period (1997−2002) with a diagnosis of necrotizing fasciitis.Results:  Forty eight patients were identified. There were 27 men and 21 women whose age ranged from 19 to 80 years (median 51 years) at presentation. Maori and Pacific Islanders accounted for 64% of total admissions despite making up only 31% of the referral population. Streptococcus Pyogenes was the most common bacterial isolate (54%). 31% of patients had polymicrobial infections. Sixty‐two per cent of cases involved extremities. The median number of operations and length of stay were 4 and 31 days, respectively. Overall mortality was 29%. In multivariate analysis, delay in surgical intervention (P = 0.015) and diabetes mellitus (P = 0.023) were found to be associated with increased mortality. Ethnicity, sex, type of pathogen, site of infection and increasing age did not affect mortality.Conclusion:  Necrotizing fasciitis remains a significant problem in our community especially in the Maori and Pacific population. Early surgical debridement decreases mortality rates.
Inguinal hernia repair with the Kugel patch
Authors: Reddy K. Marcus , Humphreys Wendy , Chew Andrew , Toouli James 
Published: March 2005

Background:  The Kugel hernia patch (Davol, Cranston, RI, USA) for treatment of inguinal hernias is a minimal access technique of inguinal herniorrhaphy, which aims to combine the utility of the open operation with the advantages of the laparoscopic procedures. The aim of the present study is to report an initial experience of a cohort of patients with inguinal hernias undergoing repair using this technique.Methods:  A prospective series of 107 inguinal hernia repairs performed between January 2000 and October 2003 in 96 patients, using the Bard Kugel hernia patch were entered into the study. Patient comfort, complications, activity levels postoperations and early recurrence were evaluated.Results:  The median age was 76 years (range 23−88 years). There were 107 inguinal hernias repaired. There were 11 bilateral, 39 left and 46 right sided hernias, 12 were recurrent. There were no major complications. There were no early recurrences. At 6 and 12 months there were one and two hernia recurrences, respectively. A further recurrence was noted at 2 years. There was no consistent relationship between having hernia surgery and loss of mobility. There was no difference in straight leg raising noted following surgery compared to the patients’ preoperative score. Ability to shower, dress, reach the toilet or perform housework by day 7 returned to normal. Shopping activities were resumed by day 30 in all patients.Conclusions:  The Kugel hernia operation is associated with minimal postoperative pain and rapid return to normal activity. There is a modest hernia recurrence rate, which needs to be addressed.
Microcrack initiation and growth in heat‐resistant 15Kh2MFA steel under cyclic deformation
Authors: YASNIY P. V. , HLADO V. B. , HUTSAYLYUK V. B. , VUHERER T. 
Published: March 2005

ABSTRACTThis paper presents the results of investigation of a nuclear reactor pressure vessel steel 15Kh2MFA of two strength levels under cyclic loading. The mechanism of microcrack formation on the surface and in the bulk of 15Kh2MFA steel under cyclic deformation was investigated. Analysis of the specimen surfaces has shown that microcracks are caused by cyclic sliding in grains most favourably oriented with respect to the direction of the maximum shear stresses. Transmission electron microscope investigations show that microcracks in the material inside the grains are formed mainly along the band‐type dislocation structure parallel to the dislocation subboundary. During cyclic deformation, the dislocation density on the subboundaries increases, in the local areas the dislocation density becomes limiting and it reaches the plasticity limit and causes microcrack formation. The interrelation of the average length of microcracks and their surface density with the energy density of inelastic deformation has been found.
Fatigue behaviour of tubular AlMgSi welded specimens subjected to bending–torsion loading
Authors: COSTA J. D. M. , ABREU L. M. P. , PINHO A. C. M. , FERREIRA J. A. M. 
Published: March 2005

ABSTRACTThis paper is concerned with an experimental and numerical study of the fatigue behaviour of tubular AlMgSi welded specimens subjected to biaxial loading. In‐phase torsion–bending fatigue tests under constant amplitude loading were performed in a standard servo‐hydraulic machine with a suitable gripping system. Some tests in pure rotating bending with and without steady torsion were also performed. The influence of stress ratio R and bending–torsion stress ratio were analysed. Correlation of the fatigue lives was done using the distortion energy hypothesis (DEH), based on the local stresses and strains. The applicability of the local strain approach method to the prediction of the fatigue life of the welded tubular specimens was also investigated. Static torsion has only a slight detrimental influence on fatigue strength. The DEH (von Mises criterion) based on local stresses in the weld toes was shown to satisfactorily correlate fatigue lives for in‐phase multiaxial stress–strain states. The stress–strain field intensity predictions were shown to have less scatter and are in better agreement with the experimental results than the equivalent strain energy density approach.
A fracture mechanics and mechanistic approach to the failure of cortical bone
Authors: RITCHIE R. O. , KINNEY J. H. , KRUZIC J. J. , NALLA R. K. 
Published: March 2005

ABSTRACTThe fracture of bone is a health concern of increasing significance as the population ages. It is therefore of importance to understand the mechanics and mechanisms of how bone fails, both from a perspective of outright (catastrophic) fracture and from delayed/time‐dependent (subcritical) cracking. To address this need, there have been many in vitro studies to date that have attempted to evaluate the relevant fracture and fatigue properties of human cortical bone; despite these efforts, however, a complete understanding of the mechanistic aspects of bone failure, which spans macroscopic to nanoscale dimensions, is still lacking. This paper seeks to provide an overview of the current state of knowledge of the fracture and fatigue of cortical bone, and to address these issues, whenever possible, in the context of the hierarchical structure of bone. One objective is thus to provide a mechanistic interpretation of how cortical bone fails. A second objective is to develop a framework by which fracture and fatigue results in bone can be presented. While most studies on bone fracture have relied on linear‐elastic fracture mechanics to determine a single‐value fracture toughness (e.g., Kc or Gc), more recently, it has become apparent that, as with many composites or toughened ceramics, the toughness of bone is best described in terms of a resistance‐curve (R‐curve), where the toughness is evaluated with increasing crack extension. Through the use of the R‐curve, the intrinsic and extrinsic factors affecting its toughness are separately addressed, where ‘intrinsic’ refers to the damage processes that are associated with crack growth ahead of the tip, and ‘extrinsic’ refers to the shielding mechanisms that primarily act in the crack wake. Furthermore, fatigue failure in bone is presented from both a classical fatigue life (S/N) and fatigue‐crack propagation (da/dN) perspective, the latter providing for an easier interpretation of fatigue micromechanisms. Finally, factors, such as age, species, orientation, and location, are discussed in terms of their effect on fracture and fatigue behaviour and the associated mechanisms of bone failure.
Resistance to fipronil in Drosophila simulans: influence of two point mutations in the RDL GABA receptor subunit
Authors: Le Goff Gaëlle , Hamon Alain , Bergé Jean‐Baptiste , Amichot Marcel 
Published: March 2005

AbstractThe Eyguières 42 strain of Drosophila simulans, obtained by laboratory selection, displayed ∼ 20 000‐fold resistance to the insecticide fipronil. Molecular cloning of the cDNA encoding the RDL GABA receptor subunit of this strain revealed the presence of two mutations: the Rdl mutation (A301G) and an additional mutation in the third transmembrane domain (T350M). In order to assess the individual and combined roles of the two mutations in fipronil resistance, the functional properties of wild‐type, A301G, T350M and A301G/T350M homomultimeric RDL receptors were compared by expression in Xenopus oocytes. In wild‐type receptors, the inhibition of GABA (EC30)‐induced currents by fipronil and picrotoxin was enhanced by repeated GABA applications. The A301G mutation nearly abolished this effect, decreased the sensitivity to fipronil and picrotoxin and increased the reversibility of inhibition. The T350M mutation also reduced the sensitivity to both antagonists. Of the four receptor variants tested, the double mutant showed the highest resistance to fipronil, following repeated GABA applications. In conclusion, the present study emphasizes new aspects of the pharmacological alterations induced by the Rdl mutation and shows that resistance to GABA receptor‐directed insecticides may implicate a mutation distinct from Rdl.
Pharmacological modulation of the endocannabinoid system in a viral model of multiple sclerosis
Authors: Mestre Leyre , Correa Fernando , Arévalo‐Martín Angel , Molina‐Holgado Eduardo , Valenti Marta , Ortar Giorgio , Di Marzo Vincenzo , Guaza Carmen 
Published: March 2005

AbstractTheiler's virus infection of the central nervous system (CNS) induces an immune‐mediated demyelinating disease in susceptible mouse strains and serves as a relevant infection model for human multiple sclerosis (MS). Cannabinoids have been shown to exert beneficial effects on animal models of MS and evidence suggests that the endocannabinoid system plays a role in the tonic control of spasticity. In this study we show that OMDM1 [(R)‐N‐oleoyl‐(1′‐hydroxybenzyl)‐2′‐ethanolamine] and OMDM2 [(S)‐N‐oleoyl‐(1′‐hydroxybenzyl)‐2′‐ethanolamine], two selective inhibitors of the putative endocannabinoid transporter and hence of endocannabinoid inactivation, provide an effective therapy for Theiler murine encephalomyelitis virus‐induced demyelinating disease (TMEV‐IDD). Treatment of TMEV‐infected mice with OMDM1 and OMDM2 enhanced anandamide levels in the spinal cord and ameliorated motor symptoms. This was associated with a down‐regulation of inflammatory responses in the spinal cord. In addition we show that OMDM1 and OMDM2 down‐regulate macrophage function by (i) decreasing the surface expression of major histocompatibility complex (MHC) class II molecules, (ii) inhibiting nitric oxide synthase‐2 (NOS‐2) expression and (iii) reducing the production of the pro‐inflammatory cytokines interleukin‐1beta (IL‐1β) and interleukin‐12 (IL‐12p40). Taken together, these results point to the manipulation of the endocannabinoid system as a possible strategy to develop future MS therapeutic drugs.
Neuroprotective effects of atorvastatin against glutamate‐induced excitotoxicity in primary cortical neurones
Authors: Bösel Julian , Gandor Florin , Harms Christoph , Synowitz Michael , Harms Ulrike , Djoufack Pierre Chryso , Megow Dirk , Dirnagl Ulrich , Hörtnagl Heide , Fink Klaus B. , Endres Matthias 
Published: March 2005

AbstractStatins [3‐hydroxy‐3‐methylglutaryl‐coenzyme A (HMG‐CoA) reductase inhibitors] exert cholesterol‐independent pleiotropic effects that include anti‐thrombotic, anti‐inflammatory, and anti‐oxidative properties. Here, we examined direct protective effects of atorvastatin on neurones in different cell damage models in vitro. Primary cortical neurones were pre‐treated with atorvastatin and then exposed to (i) glutamate, (ii) oxygen–glucose deprivation or (iii) several apoptosis‐inducing compounds. Atorvastatin significantly protected from glutamate‐induced excitotoxicity as evidenced by propidium iodide staining, nuclear morphology, release of lactate dehydrogenase, and mitochondrial tetrazolium metabolism, but not from oxygen–glucose deprivation or apoptotic cell death. This anti‐excitototoxic effect was evident with 2–4 days pre‐treatment but not with daily administration or shorter‐term pre‐treatment. The protective properties occurred independently of 3‐hydroxy‐3‐methylglutaryl‐CoA reductase inhibition because co‐treatment with mevalonate or other isoprenoids did not reverse or attenuate neuroprotection. Atorvastatin attenuated the glutamate‐induced increase of intracellular calcium, which was associated with a modulation of NMDA receptor function. Taken together, atorvastatin exerts specific anti‐excitotoxic effects independent of 3‐hydroxy‐3‐methylglutaryl‐CoA reductase inhibition, which has potential therapeutic implications.
Trophic factors attenuate nitric oxide mediated neuronal and axonal injuryin vitro: roles and interactions of mitogen‐activated protein kinase signalling pathways
Authors: Wilkins Alastair , Compston Alastair 
Published: March 2005

AbstractInflammation in the central nervous system occurs in diseases such as multiple sclerosis and leads to axon dysfunction and destruction. Bothin vitroandin vivoobservations have suggested an important role for nitric oxide (NO) in mediating inflammatory axonopathy. The purposes of this study were to model inflammatory axonopathyin vitroand identify modulators of the process. Rat cortical neurones were cultured and exposed to an NO‐donor plus potential protective factors. Cultures were then assessed for neuronal survival, axon survival and markers of intracellular signalling pathways. The NO‐donor produced dose‐dependent neuronal loss and a large degree of axon destruction. Oligodendrocyte conditioned medium (OCM) and insulin‐like growth factor type‐1 (IGF‐1), but not glial cell line‐derived neurotrophic factor (GDNF), improved survival of neurones exposed to NO donors. In addition p38 MAP kinase was activated by NO exposure and inhibition of p38 signalling led to neuronal and axonal survival effects. OCM and IGF‐1 (but not GDNF) reduced p38 activation in NO‐exposed cortical neurones. OCM, IGF‐1 and GDNF improved axon survival in cultures exposed to NO, a process dependent on mitogen‐activated protein kinase/extracellular signal‐related kinase signalling. This study emphasizes that different mechanisms may underlie neuronal/axonal destructive processes, and suggests that trophic factors may modulate NO‐mediated neurone/axon destruction via specific pathways.
Impaired proteasome activity and accumulation of ubiquitinated substrates in a hereditary neuropathy model
Authors: Fortun Jenny , Li Jie , Go Jocelyn , Fenstermaker Ali , Fletcher Bradley S. , Notterpek Lucia 
Published: March 2005

AbstractAccumulation of misfolded proteins and alterations in the ubiquitin–proteasome pathway are associated with various neurodegenerative conditions of the CNS and PNS. Aggregates containing ubiquitin and peripheral myelin protein 22 (PMP22) have been observed in the Trembler J mouse model of Charcot‐Marie‐Tooth disease type 1A demyelinating neuropathy. In these nerves, the turnover rate of the newly synthesized PMP22 is reduced, suggesting proteasome impairment. Here we show evidence of proteasome impairment in Trembler J neuropathy samples compared with wild‐type, as measured by reduced degradation of substrate reporters. Proteasome impairment correlates with increased levels of polyubiquitinated proteins, including PMP22, and the recruitment of E1, 20S and 11S to aggresomes formed either spontaneously due to the Trembler J mutation or upon proteasome inhibition. Furthermore, myelin basic protein, an endogenous Schwann cell proteasome substrate, associates with PMP22 aggregates in affected nerves. Together, our data show that in neuropathy nerves, reduced proteasome activity is coupled with the accumulation of ubiquitinated substrates, and the recruitment of proteasomal pathway constituents to aggregates. These results provide novel insights into the mechanism by which altered degradation of Schwann cell proteins may contribute to the pathogenesis of certain PMP22 neuropathies.
Inducers of oxidative stress block ciliary neurotrophic factor activation of Jak/STAT signaling in neurons
Authors: Kaur N. , Lu B. , R.K. Monroe  , Ward S.M. , Halvorsen S.W. 
Published: March 2005

AbstractGeneration of reactive oxygen species (ROS) with the accumulation of oxidative damage has been implicated in neurodegenerative disease and in the degradation of nervous system function with age. Here we report that ROS inhibit the activity of ciliary neurotrophic factor (CNTF) in nerve cells. Treatment with hydrogen peroxide (H2O2) as a generator of ROS inhibited CNTF‐mediated Jak/STAT signaling in all cultured nerve cells tested, including chick ciliary ganglion neurons, chick neural retina, HMN‐1 motor neuron hybrid cells, and SH‐SY5Y and BE(2)‐C human neuroblastoma cells. H2O2 treatment of non‐neuronal cells, chick skeletal muscle and HepG2 hepatoma cells, did not inhibit Jak/STAT signaling. The H2O2 block of CNTF activity was seen at concentrations as low as 0.1 mm and within 15 min, and was reversible upon removal of H2O2 from the medium. Also, two other mediators of oxidative stress, nitric oxide and rotenone, inhibited CNTF signaling. Treatment of neurons with H2O2 and rotenone also inhibited interferon‐γ‐mediated activation of Jak/STAT1. Depleting the intracellular stores of reduced glutathione by treatment of BE(2)‐C cells with nitrofurantoin inhibited CNTF activity, whereas addition of reduced glutathione protected cells from the effects of H2O2. These results suggest that disruption of neurotrophic factor signaling by mediators of oxidative stress may contribute to the neuronal damage observed in neurodegenerative diseases and significantly affect the utility of CNTF‐like factors as therapeutic agents in preventing nerve cell death.