bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prognostication in severe acute respiratory syndrome: A retrospective time‐course analysis of 1312 laboratory‐confirmed patients in Hong Kong
Authors: CHAN Jane C.K. , TSUI Eva L.H. , WONG Vivian C.W. ,   The Hospital Authority SARS Collaborative Group
Published: June 2007

Background and objective:  The temporal importance of prognostic indicators for severe acute respiratory syndrome (SARS) has not been studied. This study identified the various clinical prognostic factors for SARS and described the temporal evolution of these factors in the course of the SARS illness in Hong Kong in 2003.Methods:  A retrospective analysis of the entire Hong Kong cohort of 1312 laboratory‐confirmed SARS patients aged 15–74 years was undertaken. Demographic, clinical and laboratory data at presentation and investigative data during the first 10 days of illness from the time of symptom onset were compiled. Two adverse outcomes were examined: hospital mortality and the development of oxygenation failure based on the estimated PaO2/FiO2 ratio of <200 mm Hg. Logistic regression was used to identify the association between these prognostic factors and outcomes.Results:  Based on adjusted odds ratios with a P‐value of <0.05, older age, male gender, elevated pulse rate and elevated neutrophil count were all predictive of oxygenation failure and death during the 10‐day illness. Raised serum albumin and creatinine phosphokinase (CPK) levels were predictive of hospital mortality during this period. The presenting ALT and CPK level and the day 7 and day 10 platelet counts were predictive of oxygenation failure while the day 7 LDH was predictive of death. Contact exposure outside health‐care institutions also appeared to carry higher risk of death.Conclusion:  This large‐scale analysis identified important discriminatory parameters related to the patients’ demographic profile (age and gender), severity of illness (pulse rate and neutrophil count), and multisystem derangement (platelet count, CPK, ALT and LDH), all of which prognosticated adverse outcomes during the SARS episode. While age, pulse rate and neutrophil count consistently remained significant prognosticators during the first 10 days of illness, the prognostic impact of other derangements was more time‐course dependent. Clinicians should be aware of the time‐course evolution of these prognosticators.
Prevalence of coronary artery abnormality in incomplete Kawasaki disease
Authors: SONOBE TOMOYOSHI , KIYOSAWA NOBUYUKI , TSUCHIYA KEIJI , ASO SEIJIRO , IMADA YOSHIO , IMAI YOKO , YASHIRO MAYUMI , NAKAMURA YOSHIKAZU , YANAGAWA HIROSHI 
Published: June 2007

AbstractBackground: The aim of the present study was to determine the prevalence of coronary artery abnormality (CAA) and other clinical features in patients with incomplete Kawasaki disease (iKD) using the data from the 17th Japanese nationwide survey of KD.Methods: iKD was defined as the presence of four or fewer of the principal symptoms of the Japanese diagnostic guidelines, regardless of whether the patient had CAA. A total of 15 857 cases were analyzed.Results: Among 15 857 cases, 83.9% of patients had five to six principal symptoms (complete KD: cKD), and 16.1% had iKD. The prevalence of CAA in cKD was 14.2%, and 18.4% in iKD. The prevalence of CAA in patients with four principal symptoms was 18.1%, which was higher than in cKD cases (14.2%). Although the reliability of the data has some limitations, the prevalence of CAA among patients with one to three symptoms was 19.3%. Among all CAA patients, 14% had four symptoms, and 6% had only one to three symptoms.Conclusion: Incomplete KD should not be equated with mild KD. Patients with four principal symptoms were comparable to cKD with respect to CAA occurrence. In patients with one to three symptoms also, especially in those under 1 year and older than 4 years of age, other significant symptoms and laboratory findings of the guidelines are very important in making a correct and early diagnosis of iKD so as to prevent CAA.
Is varicocelectomy indicated in subfertile men with clinical varicoceles who have asthenospermia or teratospermia and normal sperm density?
Authors: Okeke Linus , Ikuerowo Odunayo , Chiekwe Ifeanyi , Etukakpan Blessing , Shittu Olayiwola , Olapade‐Olaopa Olubunmi 
Published: June 2007

Objective:  Varicocele is the most common treatable cause of male infertility and is associated with progressive decline in testicular function. Varicocelectomy, a commonly performed operation, is indicated in infertile males with varicoceles who have oligospermia, asthenospermia, teratospermia or a combination of these factors. It is not clear if varicocelectomy is indicated if the patients have normal sperm density associated with asthenospermia or teratospermia.Methods:  We reviewed 167 patients with varicocele‐associated male infertility over a 7‐year period (December 1999–November 2005). Pre‐ and post‐varicocelectomy seminal fluid analyses, assessed using the World Health Organization criteria, were obtained at intervals of 4–6 months. Wilcoxon signed rank tests were used to evaluate for statistical significance and P ≤ 0.05 was considered significant.Results:  The mean age of the patients and their spouses were 35 and 28 years, respectively. The mean duration of infertility was 3.2 years (range, 1.5–7.5). Oligospermia, teratospermia, asthenospermia, oligospermia, asthenospermia and teratospermia (OAT) syndrome and azoospermia were found preoperatively in 106 (63.5%), 58 (34.7%), 154 (92%), 118 (71%) and 15 (9%) patients, respectively. Overall, significant improvements in semen volume (P < 0.001), sperm density (P < 0.001), sperm motility (P < 0.001) and sperm vitality (P < 0.001) were obtained after varicocelectomy. There was, however, no significant improvement in sperm morphology after varicocelectomy (P = 0.220). When patients with preoperative oligospermia (sperm density, <20 million/mL) were considered separately, varicocelectomy led to significant improvement in all the semen parameters except the sperm morphology (P = 0.183). Conversely, when varicocele patients with a sperm density of ≥20 million/mL (normospermia) associated with asthenospermia and/or teratospermia were considered separately, they did not show significant improvement in any of the semen parameters after varicocelectomy (P > 0.05). In addition, azoospermic patients did not show significant improvement in any of the semen parameters (P > 0.05)Conclusion:  No significant improvement in semen parameters may be obtained in patients with clinical varicocele and preoperative normospermia. It is possible that only patients with preoperative oligospermia may benefit from varicocelectomy. Larger multi‐institutional studies are needed to determine more definitively if asthenospermia or teratospermia in normospermic subfertile males with clinical varicoceles are in fact indications for varicocelectomy.
Reverse transcriptase‐polymerase chain reaction and immunohistochemical studies for detection of prostate stem cell antigen expression in prostate cancer: Potential value in molecular staging of prostate cancer
Authors: Joung Jae Young , Yang Seung Ok , Jeong In Gab , Han Kyung Suk , Seo Ho Kyung , Chung Jinsoo , Park Weon Seo , Lee Kang Hyun 
Published: June 2007

Objectives:  To determine whether detection of prostate stem cell antigen (PSCA) expression has potential for molecular staging in prostate cancer (PCa), we examined the relationship between established prognostic factors, biochemical recurrence (BCR) and PSCA expression.Methods:  This study was comprised of 66 patients who underwent radical prostatectomy for the treatment of PCa. We employed reverse transcriptase‐polymerase chain reaction (RT‐PCR) to detect PSCA mRNA‐bearing cells in peripheral blood, and used immunohistochemical (IHC) techniques to identify PSCA protein expression in microarrayed tissue.Results:  PSCA‐mRNA was detected in the peripheral blood of nine (13.6%) patients by RT‐PCR. Whereas 3.2% of patients with low‐grade disease were PSCA positive, 22.9% of patients with high‐grade disease were PSCA positive (P = 0.030). There was also a significant relationship of RT‐PCR PSCA positivity to whether or not the tumor was confined to the prostate. Whereas only 6.8% of patients with prostate‐confined disease were RT‐PCR PSCA positive, 27.3% of extraprostatic diseases were RT‐PCR PSCA positive (P = 0.022). IHC studies of tumor tissue microarrays demonstrated that PSCA expression intensity was related to both extraprostatic extension (P = 0.014) and positive surgical margin (P = 0.053). Whereas 23.8% of prostate‐confined diseases were high intensity, 54.5% of extraprostatic diseases were high intensity. BCR developed in seven patients (10.6%) during the follow‐up period (median, 16.2 months; range, 9–25 months). Prognostic factors increasing the risk of BCR included: seminal vesicle invasion (P = 0.004), extraprostatic disease (P = 0.019), lymphovascular emboli (P = 0.036) and RT‐PCR PSCA positivity (P = 0.004) in univariate analysis.Conclusions:  We were able to detect PSCA mRNA‐bearing cells in peripheral blood by RT‐PCR, and also identify PSCA protein expression in tumors by IHC analysis of tissue microarrays. RT‐PCR PSCA positivity in peripheral blood may be a potential modality for molecular staging of PCa.
Coupled elastoplasticity and viscoplasticity under thermomechanical loading
Authors: NAGODE M. , FAJDIGA M. 
Published: June 2007

ABSTRACTThis paper is a contribution to material behaviour modelling. Total strain is decomposed into elastoplastic and viscoplastic strains. Both parts are analysed separately and put together by the principle of superposition. The spring‐slider model controlled by either stress or strain enables elastoplasticity modelling under constant or variable temperature with the Prandtl operators. Viscoplasticity is taken into account, if temperature exceeds creep temperature, by adding a nonlinear damper to existing spring‐slider models, otherwise just elastoplasticity is considered. The material parameters result from isothermal strain‐controlled low cycle fatigue (LCF) tests. Hysteresis loops are assumed to be stabilized. The high speed of computation that is characteristic of Masing and memory rules is retained. Solving of differential equations is not required. The model developed so far is uniaxial, but a multiaxial extension is possible.
Brittle fracture of high‐strength steels at very low temperatures
Authors: RODRÍGUEZ‐MARTÍN R. , OCAÑA I. , MARTÍN‐MEIZOSO A. 
Published: June 2007

ABSTRACTHigh‐strength steels are used to increase the load carrying capacity of components. However, to guarantee a safe design, it is also necessary to combine high strength with adequate fracture toughness. In this paper, fracture toughness of three high‐strength steels with yield strengths ranging from 460 to 890 MPa has been studied at very low temperatures. Taking into account experimental evidence, a new mechanism of cleavage at very low temperatures is proposed. This mechanism considers the possibility of reaching the ideal strength (the stress at which the lattice of a single crystal losses its stability) in the immediate vicinity of the fatigue crack tip. Moreover, a computational model able to calculate the external load needed to produce a catastrophic failure of these steels has been developed.
Nigrostriatal cell firing action on the dopamine transporter
Authors: Rodriguez Manuel , Gonzalez Sergio , Morales Ingrid , Sabate Magdalena , Gonzalez‐Hernandez Tomas , Gonzalez‐Mora Jose Luis 
Published: June 2007

AbstractThe influence of nigrostriatal cell firing on the dopamine transporter (DAT) activity of the rat striatum was studiedin vivowith amperometric methods. Data were obtained after preventing dopamine (DA) release with α‐methyl‐l‐tyrosine and replenishing extracellular DA with local injections. The DA cell stimulation, which under basal conditions increased extracellular DA, decreased DA after this pre‐treatment, suggesting that firing activity facilitates the DA cell uptake of DA under these circumstances (drain response). Cocaine and GBR13069 markedly decreased the drain response, suggesting that it is dependent on DAT activation. Data obtained after haloperidol and apomorphine administration showed that the drain response was facilitated by pre‐synaptic DA receptor stimulation but that receptors are not a necessary requirement. Two components in the drain response were observed, one with a short latency and duration that needed high‐frequency stimuli, and the other with a long latency and duration that was even induced by low‐frequency stimuli. This is the first evidence showing that DAT can be activated by the firing activity in nigrostriatal cells in a direct way and without the participation of pre‐synaptic DA receptors.
Striatal dysfunction increases basal ganglia output during motor cortex activation in parkinsonian rats
Authors: Belluscio Mariano A. , Riquelme Luis A. , Murer M. Gustavo 
Published: June 2007

AbstractDuring movement, inhibitory neurons in the basal ganglia output nuclei show complex modulations of firing, which are presumptively driven by corticostriatal and corticosubthalamic input. Reductions in discharge should facilitate movement by disinhibiting thalamic and brain stem nuclei while increases would do the opposite. A proposal that nigrostriatal dopamine pathway degeneration disrupts trans‐striatal pathways' balance resulting in sustained overactivity of basal ganglia output nuclei neurons and Parkinson's disease clinical signs is not fully supported by experimental evidence, which instead shows abnormal synchronous oscillatory activity in animal models and patients. Yet, the possibility that variation in motor cortex activity drives transient overactivity in output nuclei neurons in parkinsonism has not been explored. In Sprague–Dawley rats with 6‐hydroxydopamine (6‐OHDA)‐induced nigrostriatal lesions, approximately 50% substantia nigra pars reticulata (SNpr) units show abnormal cortically driven slow oscillations of discharge. Moreover, these units selectively show abnormal responses to motor cortex stimulation consisting in augmented excitations of an odd latency, which overlapped that of inhibitory responses presumptively mediated by the trans‐striatal direct pathway in control rats. Delivering D1 or D2 dopamine agonists into the striatum of parkinsonian rats by reverse microdialysis reduced these abnormal excitations but had no effect on pathological oscillations. The present study establishes that dopamine‐deficiency related changes of striatal function contribute to producing abnormally augmented excitatory responses to motor cortex stimulation in the SNpr. If a similar transient overactivity of basal ganglia output were driven by motor cortex input during movement, it could contribute to impeding movement initiation or execution in Parkinson's disease.
Spontaneous glutamate release controls NT‐3‐dependent development of hippocampal calbindin–D28kphenotype through activation of sodium channelsex vivo
Authors: Pieraut Simon , Boukhaddaoui Hassan , Scamps Frédérique , Dayanithi Govindan , Sieso Victor , Valmier Jean 
Published: June 2007

AbstractFunctional NMDA and AMPA ionotropic glutamate receptors are expressed in embryonic hippocampal glutamatergic pyramidal neurons prior to synapse formation but their function and mechanisms of action are still unclear. At the same time, these neurons develop their calbindin–D28kphenotype through an activity‐dependent NT‐3 autocrine loop. Using single‐neuron microcultures, we show here that immature pyramidal neurons spontaneously secreted glutamate and that chronic blockade of either NMDA or AMPA receptors down‐regulated the number of calbindin–D28k‐positive pyramidal neurons without affecting neuronal survival. This antagonistic effect of glutamate ionotropic receptors was mimicked by anti‐TrkC antibodies and reversed by the application of NT‐3. Similar results were obtained inex vivoembryonic hippocampal slice cultures. Moreover, glutamate receptor blockade inhibited the generation of spontaneous sodium‐driven action potentials which, in turn, regulate both the endogenous secretion of NT‐3 and the calbindin–D28kphenotype acquisition. Altogether, these results suggest an unexpected role for glutamate in the development of the physiological and biochemical properties of hippocampal pyramidal neurons and support the idea that glutamate may underlie an activity‐dependent mode of differentiation prior to synapse formation.
Voluntary attention changes the speed of perceptual neural processing
Authors: Noguchi Yasuki , Tanabe Hiroki C. , Sadato Norihiro , Hoshiyama Minoru , Kakigi Ryusuke 
Published: June 2007

AbstractWhile previous studies in psychology demonstrated that humans can respond more quickly to the stimuli at attended than unattended locations, it remains unclear whether attention also accelerates the speed of perceptual neural activity in the human brain. One possible reason for this unclarity would be an insufficient spatial resolution of previous electroencephalography (EEG) and magnetoencephalography (MEG) techniques in which neural signals from multiple brain regions are merged with each other. Here, we addressed this issue by combining MEG with a novel stimulus‐presentation technique that can focus on neural signals from higher visual cortex where the magnitude of attentional modulation is prominent. Results revealed that the allocation of spatial attention induces both an increase in neural intensity (attentional enhancement) and a decrease in neural latency (attentional acceleration) to the attended compared to unattended visual stimuli (Experiment 1). Furthermore, an attention‐induced behavioural facilitation reported in previous psychological studies (Posner paradigm) was closely correlated with the neural ‘acceleration’ rather than ‘enhancement’ in the visual cortex (Experiment 2). In addition to bridging a gap between previous psychological and neurological findings, our results demonstrated a temporal dynamics of attentional modulation in the human brain.
The phagocytic capacity of neurones
Authors: Bowen Samantha , Ateh Davidson D. , Deinhardt Katrin , Bird Margaret M. , Price Karen M. , Baker Cathy S. , Robson Joanna C. , Swash Michael , Shamsuddin Wassim , Kawar Shalini , El‐Tawil Tariq , Roos Jesper , Hoyle Andrew , Nickols Carole D. , Knowles Charles H. , Pullen Anthony H. , Luthert Phillip J. , Weller Roy O. , Hafezparast Majid , Franklin Robin J. M. , Revesz Tamas , King Rosalind H. M. , Berninghausen Otto , Fisher Elizabeth M. C. , Schiavo Giampietro , Martin Joanne E. 
Published: June 2007

AbstractPhagocytosis is defined as the ingestion of particulates over 0.5 µm in diameter and is associated with cells of the immune system such as macrophages or monocytes. Neurones are not generally recognized to be phagocytic. Using light, confocal, time‐lapse and electron microscopy, we carried out a wide range of in‐vitro and in‐vivo experiments to examine the phagocytic capacity of different neuronal cell types. We demonstrated phagocytosis of material by neurones, including cell debris and synthetic particles up to 2.8 µm in diameter. We showed phagocytosis in different neuronal types, and demonstrated that debris can be transported from neurite extremities to cell bodies and persist within neurones. Flow cytometry analysis demonstrated the lack of certain complement receptors on neurones but the presence of others, including integrin receptors known to mediate macrophage phagocytosis, indicating that a restricted set of phagocytosis receptors may mediate this process. Neuronal phagocytosis occurs in vitro and in vivo, and we propose that this is a more widespread and significant process than previously recognized. Neuronal phagocytosis may explain certain inclusions in neurones during disease, cell‐to‐cell spread of disease, neuronal death during disease progression and provide a potential mechanism for therapeutic intervention through the delivery of particulate drug carriers.
Acute stress‐mediated increases in extracellular glutamate levels in the rat amygdala: differential effects of antidepressant treatment
Authors: Reznikov Leah R. , Grillo Claudia A. , Piroli Gerardo G. , Pasumarthi Ravi K. , Reagan Lawrence P. , Fadel Jim 
Published: June 2007

AbstractDepressive illness is associated with changes in amygdalar volume, and stressful life events are known to precipitate depressive episodes in this patient population. Stress affects amygdalar synaptic plasticity and several neurotransmitter systems have been implicated in stress‐mediated changes in the brain, including the glutamatergic system. However, the role of the glutamatergic system in stress‐mediated plasticity in the amygdala remains to be determined. Accordingly the current study examined the stress modulation of extracellular glutamate levels in the basolateral nucleus (BLA) and the central nucleus (CeA) of the amygdala byin vivomicrodialysis. Acute stress increased extracellular glutamate levels in the BLA and CeA, although the dynamics of these stress‐mediated changes were dramatically different in these amygdalar nuclei. Tetrodotoxin administration reduced basal, and completely eliminated stress‐mediated increases in glutamate efflux in the amygdala, demonstrating that stress effects are dependent on local axonal depolarization. Moreover, stress‐mediated increases in glutamate efflux in the BLA were inhibited by the antidepressant tianeptine but not by the selective serotonin‐reuptake inhibitor fluoxetine. Collectively, these data demonstrate that stress‐induced modulation of glutamate neurochemistry reflects a fundamental pathological change that may contribute to the aetiology and progression of depressive illness, and suggest that some antidepressants such as tianeptine may elicit their clinical effects by modulation of glutamatergic neurotransmission.
Testosterone decreases reactive astroglia and reactive microglia after brain injury in male rats: role of its metabolites, oestradiol and dihydrotestosterone
Authors: Barreto George , Veiga Sergio , Azcoitia Iñigo , Garcia‐Segura Luis M. , Garcia‐Ovejero Daniel 
Published: June 2007

AbstractPrevious studies have shown that the neuroprotective hormone, testosterone, administered immediately after neural injury, reduces reactive astrogliosis. In this study we have assessed the effect of early and late therapy with testosterone or its metabolites, oestradiol and dihydrotestosterone, on reactive astroglia and reactive microglia after a stab wound brain injury in orchidectomized Wistar rats. Animals received daily s.c. injections of testosterone, oestradiol or dihydrotestosterone on days 0–2 or on days 5–7 after injury. The number of vimentin immunoreactive astrocytes and the volume fraction of major histocompatibility complex‐II (MHC‐II) immunoreactive microglia were estimated in the hippocampus in the lateral border of the wound. Both early and delayed administration of testosterone or oestradiol, but not dihydrotestosterone, resulted in a significant decrease in the number of vimentin‐immunoreactive astrocytes. The volume fraction of MHC‐II immunoreactive microglia was significantly decreased in the animals that received testosterone or oestradiol in both early and delayed treatments and in animals that received early dihydrotestosterone administration. Thus, both early and delayed administration of testosterone reduces reactive astroglia and reactive microglia and these effects may be at least in part mediated by oestradiol, while dihydrotestosterone may mediate part of the early effects of testosterone on reactive microglia. In conclusion, testosterone controls reactive gliosis and its metabolites, oestradiol and dihydrotestosterone, may be involved in this hormonal effect. The regulation of gliosis may be part of the neuroprotective mechanism of testosterone.