bluuebunny/crossref_metadata_2025_split huggingface dataset:
ANATOMICAL VARIATIONS OF THE COMMON CAROTID ARTERY BIFURCATION
Authors: Lo Albert , Oehley Michael , Bartlett Adam , Adams Dave , Blyth Phil , Al‐Ali Saad 
Published: October 2006

Background:  The correlation of the common carotid artery (CCA) bifurcation and its surrounding structures is poorly described. The aim of this study was to describe the anatomy of the CCA bifurcation relative to its surrounding structures.Method:  We dissected a total of 67 carotid specimens from 36 embalmed cadavers. CCA bifurcation occurred at the superior border of thyroid cartilage in 39% and at the body of hyoid bone in 40% of specimens.Results:  The superior thyroid artery arose more commonly from the CCA (52.3%) than the external carotid artery (46.2%). The vagus nerve was posterior to the carotid bifurcation in 40 (60%), posterior–lateral in 24 (36%), posterior–medial in 2 (3%) and anterior–lateral in 1 specimen (1.5%). The hypoglossal nerve was closer to the CCA bifurcation when the CCA bifurcated at the level of the hyoid bone than when it bifurcated at the superior border of the thyroid cartilage (P < 0.05). The correlation of the common facial vein and the carotid artery was highly variable.Conclusion:  The presence of a high CCA bifurcation should caution surgeons that the hypoglossal nerve lies in closer proximity and is more vulnerable. Preoperatively documenting the level of the CCA bifurcation may be helpful in identifying those patients at increased risk of iatrogenic injury.
TUMOUR SIZE AS A PREDICTOR OF AXILLARY NODE METASTASES IN PATIENTS WITH BREAST CANCER
Authors: Laura Sharon , Coombs Nathan J. , Ung Owen , Boyages John 
Published: October 2006

Background:  The ability to predict the behaviour of breast cancer from its dimensions allows the clinician to inform a woman about the absolute benefits of adjuvant therapies or further surgery to control her disease. Tumour size and grade are independent predictors of nodal disease. This study aims to generate a tool, using Australian data, allowing surgeons to calculate the probability of axillary lymph node involvement in a preoperative setting.Methods:  The histological reports of patients with breast cancer treated in 1995 in New South Wales were examined and tumour size, grade and nodal status recorded. Univariate and multivariate analyses identified predictors of node positivity and, using linear regression analysis, a simple formula to predict nodal involvement was derived.Results:  In a 6‐month period, 754 women had non‐metastatic, unifocal breast cancer treated with surgery and complete axillary dissection and 283 (37.5%) had positive nodes. Tumour size remained an independent predictor of node positivity and the probability (%), y, of nodal involvement may be predicted by the formula y = 1.5 × tumour size (mm) + 7, r = 0.939 and P = 0.001.Conclusions:  This paper shows the need to assess the axilla in every patient because even patients with small tumours (0–5 mm) have the possibility of axillary involvement (7–14.5%). Use of this simple formula allows clinicians and patients to make informed decisions about the possible need for a full axillary dissection to reduce the chance of understaging and potentially undertreating a woman’s breast cancer.
XANTHOGRANULOMATOUS PYELONEPHRITIS: OUR EXPERIENCE WITH REVIEW OF PUBLISHED REPORTS
Authors: Dwivedi Udai S. , Goyal Neeraj K. , Saxena Vaibhav , Acharya Rajiba L. , Trivedi Sameer , Singh Pratap B. , Vyas Nachiket , Datta Biswajeet , Kumar Abhay , Das Suren 
Published: October 2006

Background:  The aim of this study was to analyse the cases of xanthogranulomatous pyelonephritis with review of published reports.Methods:  We retrospectively reviewed all nephrectomy specimens during February 1995 to January 2006. We found 26 cases of xanthogranulomatous pyelonephritis. We prepared a chart of these cases consisting of preoperative symptoms, laboratory findings, radiological imaging results and preoperative diagnosis. Open nephrectomy was carried out in all cases.Results:  Age group of the patients was 6–65 years and male : female ratio was 1.6:1. Twenty‐two patients presented to us with intermittent high‐grade fever, 21 with flank pain, 18 with loin mass, 2 with haematuria and 1 was detected during screening of vague gastrointestinal symptoms. Twenty‐five patients had pyuria and only 10 had sterile urine culture. In all patients, only one kidney was affected. All patients had renal calculi 10–42 mm in size with bilaterally enlarged kidneys. Ipsilateral kidney was enlarged because of hydronephrosis or pyonephrosis in all cases and contralateral kidney was enlarged because of compensatory hypertrophy in 13 cases. Ipsilateral kidney had severely compromised renal function in all cases. Associated psoas abscess was present in one and tuberculosis in another.Conclusion:  Xanthogranulomatous pyelonephritis is a relatively rare entity that is associated with obstruction, stones and infection of the urinary tract. Late presentation leads to loss of renal parenchyma. It cannot be differentiated preoperatively with renal tumours (renal cell carcinoma and Wilms’ tumour), pyonephrosis, infected hydronephrosis and renal lymphoma. Nephrectomy and antibiotics are the treatment of choice.
PIP3EA and PD‐168077, two selective dopamine D4 receptor agonists, induce penile erection in male rats: site and mechanism of action in the brain
Authors: Melis Maria Rosaria , Succu Salvatora , Sanna Fabrizio , Melis Tiziana , Mascia Maria Stefania , Enguehard‐Gueiffier Cécile , Hubner Harald , Gmeiner Peter , Gueiffier Alain , Argiolas Antonio 
Published: October 2006

AbstractPIP3EA (2‐[4‐(2‐methoxyphenyl)piperazin‐1‐yl‐methyl]imidazo[1,2‐a]pyridine) and PD‐168077 (N‐[4‐2‐cyanophenylpiperazin‐1‐ylmethyl]‐3‐methylbenzamide maleate), two selective dopamine D4 agonists, administered systemically, intracerebroventricularly or into the paraventricular nucleus of the hypothalamus induce penile erection in male Sprague–Dawley rats. A U‐inverted dose–response curve was found with either compound when given subcutaneously (1–100 µg/kg) or intracerebroventricularly (0.1–20 µg/rat), but not into the paraventricular nucleus (10–200 ng/rat). The pro‐erectile effect of PIP3EA and of PD‐168077 occurs concomitantly with an increased nitric oxide (NO) production in the paraventricular nucleus, as measured by the increased concentration of nitrites and nitrates found in the dialysate obtained from the paraventricular nucleus by intracerebral microdialysis. These effects of PIP3EA and PD‐168077 were reduced by L‐745,870 (3‐[4‐(4‐chlorophenyl)piperazin‐1‐ylmethyl]‐1H‐pyrrolo[2,3‐b]pyridine trihydrochloride), a selective dopamine D4 receptors antagonist, by ω‐conotoxin, a blocker of voltage‐dependent Ca2+channels of the N‐type, byS‐methyl‐thiocitrulline, a neuronal nitric oxide synthase inhibitor, and byd(CH2)5Tyr(Me)2‐Orn8‐vasotocin, an oxytocin receptor antagonist, given into the lateral ventricles, but not into the paraventricular nucleus. Comparison of the dose–response curves of PIP3EA and PD‐168077 revealed that PIP3EA is as potent as PD‐168077 when given into the paraventricular nucleus, but more potent when given systemically. However, both compounds are less efficacious (e.g. induce a lower number of penile erection episodes) than apomorphine, a classical mixed dopamine receptor agonist, irrespective of the route of administration. These results confirm previous findings showing that central D4 receptors mediate penile erection and show that dopamine D4 receptor agonists act in the paraventricular nucleus to facilitate penile erection by increasing central oxytocinergic neurotransmission.
Endocannabinoids modulate stress‐induced suppression of hippocampal cell proliferation and activation of defensive behaviours
Authors: Hill Matthew N. , Kambo Jaspreet S. , Sun Jane C. , Gorzalka Boris B. , Galea Liisa A. M. 
Published: October 2006

AbstractThe endocannabinoid system has been shown to regulate both the hypothalamic–pituitary–adrenal (HPA) axis and emotionality. The present experiment was designed to examine whether pharmacological modulation of the endocannabinoid system would affect the suppression of hippocampal cell proliferation and increase in defensive behaviours seen following exposure to predator odour (trimethylthiazoline; TMT) stress. Rats were administered either an endocannabinoid uptake inhibitor (AM404; 2 mg/kg) or a cannabinoid CB1 receptor antagonist (AM251; 5 mg/kg) 30 min prior to exposure to TMT. Exposure to TMT reduced cell proliferation in the dentate gyrus and increased the expression of defensive burying. Administration of AM404 significantly inhibited defensive burying, and attenuated the reduction in cell proliferation in response to TMT exposure. Administration of AM251 alone significantly increased cell proliferation; however, pretreatment with AM251 prevented neither the stress‐induced suppression of cell proliferation nor the stress‐induced increase in behavioural responses. These results support previous research demonstrating that augmentation of endocannabinoid signalling can suppress stress‐responsive systems. They also suggest that endocannabinoids may play a complex role in the regulation of neurogenesis via cell proliferation in the hippocampus.
Viral‐induced inflammation is accompanied by β‐amyloid plaque reduction in brains of amyloid precursor protein transgenic Tg2576 mice
Authors: Stahl Tobias , Reimers Christine , Johne Reimar , Schliebs Reinhard , Seeger Johannes 
Published: October 2006

AbstractAmyloid plaques, one of the neuropathological hallmarks of Alzheimer's disease, and their main constituent, the amyloid β‐peptide (Aβ), are triggers of the activation of innate inflammatory mechanisms involving the activation of microglia. To dissect the effects of a non‐Aβ‐specific microglial activation on the Aβ metabolism, we employed a viral infection‐based model. Transgenic mice expressing a mutated form of the human amyloid precursor protein (Tg2576) were used. In preceding experiments, 2‐week‐old transgenic mice and non‐transgenic littermates were infected intracerebrally with the neurotropic Borna disease virus and investigated at 2, 4 and 14 weeks post‐infection. The Borna disease virus‐inoculated mice showed a persisting, subclinical infection of cortical and limbic brain areas characterized by slight T‐cell infiltrates, expression of cytokines and a massive microglial activation in the hippocampus and neocortex. Viral‐induced effects reached their peak at 4 weeks post‐infection. In 14‐month‐old Tg2576 mice, characterized by the deposition of diffuse and dense‐core amyloid plaques in cortical brain regions, Borna disease virus‐induced microglial activation in the vicinity of Aβ deposits was used to investigate the influence of a local inflammatory response on these deposits. At 4 weeks post‐infection, histometric analyses employing Aβ immunohistochemistry revealed a decrease of the cortical and hippocampal Aβ‐immunopositive area. This overall decrease was accompanied by a decrease of parenchymal thioflavin‐S‐positive amyloid deposits and an increase of such deposits in the walls of cerebral vessels, which indicates that the elicitation of a non‐Aβ‐specific microglial activation may contribute to a reduction of Aβ in the brain parenchyma.
Altered cortico‐striatal synaptic plasticity and related behavioural impairments in reeler mice
Authors: Marrone Maria Cristina , Marinelli Silvia , Biamonte Filippo , Keller Flavio , Sgobio Carmelo Alessio , Ammassari‐Teule Martine , Bernardi Giorgio , Mercuri Nicola B. 
Published: October 2006

AbstractReelin‐deficient mice have been used to investigate the role of this extracellular protein in cortico‐striatal plasticity and striatum‐related behaviours. Here we show that a repetitive electrical stimulation of the cortico‐striatal pathway elicited long‐term potentiation (LTP) in homozygous reeler (rl/rl) mice, while causing long‐term depression in their wild‐type (+/+) littermates. The N‐methyl‐d‐aspartic acid (NMDA) receptor antagonist d‐(–)‐2 amino‐5‐phosphonopentanoic acid prevented the induction of LTP in (rl/rl) mice, thus confirming that this form of synaptic plasticity was NMDA receptor‐dependent. Interestingly, in the presence of tiagabine, a blocker of γ‐aminobutyric acid (GABA) re‐uptake system, the probability that (rl/rl) mice showed LTP decreased significantly, thus suggesting an impaired GABAergic transmission in reeler mutants. Consistent with this view, a decreased density of parvalbumin‐positive GABAergic striatal interneurons was found in (rl/rl) mice in comparison to (+/+) mice. Finally, compatible with their abnormal striatal function (rl/rl) mice exhibited procedural learning deficits. Our data, showing alterations in cortico‐striatal plasticity largely depending on a depressed GABAergic tone, delineate a mechanism whereby the lack of reelin may affect cognitive functions.
An in vivo analysis of Schwann cell programmed cell death in embryonic mice: the role of axons, glial growth factor, and the pro‐apoptotic gene Bax
Authors: Winseck Adam K. , Oppenheim Ronald W. 
Published: October 2006

AbstractBuilding upon previous in vitro studies, the present investigation involves an in vivo examination of Schwann cell programmed cell death (PCD) and development in the brachial spinal ventral roots of embryonic mice. The period of Schwann cell PCD was found to occur between embryonic days (E) 11.5 and 18.5, which is in close coincidence with the PCD period of associated brachial motoneurons (E13.5–E18.5). Additionally, Schwann cells exhibited a peak in proliferation at E11.5, and differentiation from the precursor to the immature Schwann cell stage between E12.5 and E14.5. Axon‐mediated Schwann cell survival was demonstrated in vivo by excitotoxic elimination of motoneurons and their axons, via NMDA treatment in utero. This treatment increased apoptotic Schwann cell death within degenerating ventral roots. Conversely, in utero co‐treatment of glial growth factor (GGF) with NMDA resulted in decreased Schwann cell death, a finding which supports previous reports of the promotion of Schwann cell survival by GGF. Analysis of mice lacking Bax, a pro‐apoptotic Bcl‐2 protein, revealed that Schwann cell PCD occurred independently of Bax. However, owing to the lack of motoneuron PCD in Bax‐knockout mice, and the corresponding increase in the number of ventral root axons, a decrease in Schwann cell PCD was observed during the normal period of motoneuron PCD. In conclusion, our findings regarding the regulation of Schwann cell development in vivo are consistent with the conclusions from in vitro studies, including a dependency on axons for survival and proliferation signals, timing of differentiation, and a dependency on GGF.
Differential disinhibition of the neonatal hypothalamic– pituitary–adrenal axis in brain‐specific CRH receptor 1‐knockout mice
Authors: Schmidt M. V. , Deussing J. M. , Oitzl M. S. , Ohl F. , Levine S. , Wurst W. , Holsboer F. , Müller M. B. , De Kloet E. R. 
Published: October 2006

AbstractIn the adult, corticotropin‐releasing hormone (CRH) is the key mediator for the behavioural and neuroendocrine response to stress. It has also been hypothesized that, during postnatal development of the stress system, CRH controls the activity of the HPA axis and mediates the effects of early disturbances, e.g. 24 h of maternal deprivation. In the current study we investigated the function of specific brain corticotropin‐releasing hormone receptor type 1 (CRHR1) subpopulations in the control of the HPA axis during postnatal development under basal conditions as well as after 24 h of maternal deprivation. We used two conditional CRHR1‐deficient mouse lines which lack this receptor, either specifically in forebrain and limbic structures (Cam‐CRHR1) or in all neurons (Nes‐CRHR1). Basal circulating corticosterone was increased in Nes‐CRHR1 mice compared to controls. Corticosterone response to maternal deprivation was significantly increased in both CRHR1‐deficient lines. In the paraventricular nucleus, Cam‐CRHR1 animals displayed enhanced CRH and decreased vasopressin expression levels. In contrast, gene expression in Nes‐CRHR1 pups was strikingly similar to that in maternally deprived control pups. Furthermore, maternal deprivation resulted in an enhanced response of Cam‐CRHR1 pups in the brain, while expression levels in Nes‐CRHR1 mouse pups were mostly unchanged. Our results demonstrate that brainstem and/or hypothalamic CRHR1 contribute to the suppression of basal corticosterone secretion in the neonate, while limbic and/or forebrain CRHR1 dampen the activation of the neonatal HPA axis induced by maternal deprivation.
Beyond macronutrients: element variability and multielement stoichiometry in freshwater invertebrates
Authors: Karimi Roxanne , Folt Carol L. 
Published: October 2006

AbstractWe contrasted concentrations of macronutrients (C, N and P), essential (As, Cu, Zn and Se) and non‐essential metals (Pb, Hg and Cd) in invertebrates across five lakes and June to October in one lake. We predicted that somatic concentrations of tightly regulated elements would be less variable than weakly and unregulated elements. Within each taxon, variation was lowest in macronutrients, intermediate in essential micronutrients, and highest in non‐essential metals, which corresponded in rank to homeostatic regulation strength for the same elements calculated from the literature. Hence, homeostatic regulation may strongly influence variation in element concentrations of biotain situ. Of the individual elements, only taxonomic differences in C and N were consistent across lakes and over a season. Nevertheless, canonical discriminant analyses successfully discriminated among taxa based on taxonomic multielement composition. Thus, relative taxonomic differences in multielement composition appear more informative than absolute stoichiometric formulae when considering the role of inherently variable trace elements in ecological investigations.
Community maturity, species saturation and the variant diversity–productivity relationships in grasslands
Authors: Guo Qinfeng , Shaffer Terry , Buhl Thomas 
Published: October 2006

AbstractDetailed knowledge of the relationship between plant diversity and productivity is critical for advancing our understanding of ecosystem functioning and for achieving success in habitat restoration efforts. However, effects and interactions of diversity, succession and biotic invasions on productivity remain elusive. We studied newly established communities in relation to preexisting homogeneous vegetation invaded by exotic plants in the northern Great Plains, USA, at four study sites for 3 years. We observed variant diversity–productivity relationships for the seeded communities (generally positive monotonic at three sites and non‐monotonic at the other site) but no relationships for the resident community or the seeded and resident communities combined at all sites and all years. Community richness was enhanced by seeding additional species but productivity was not. The optimal diversity (as indicated by maximum productivity) changed among sites and as the community developed. The findings shed new light on ecosystem functioning of biodiversity under different conditions and have important implications for restoration.
Diabetes care in rest homes in Christchurch, New Zealand
Authors: Gill E. A. , Corwin P. A. , Mangin D. A. , Sutherland M. G. 
Published: October 2006

AbstractAim  To determine the prevalence and describe the management of known diabetes in a group of New Zealand rest homes.Methods  A random sample of 54 rest homes in Christchurch were studied. Residents with known diabetes were identified by rest home staff and interviewed. Selected staff members of all rest homes were also interviewed using structured questionnaires. The medical and nursing records and laboratory results of all residents with known diabetes were reviewed and all information pertaining to diabetes management recorded.Results  The prevalence of known diabetes in Christchurch rest homes was 11.7%. Residents with known diabetes had a mean of five other comorbidities and were prescribed a mean of 7.5 medications. Of residents with diabetes, 45% were taking oral glucose‐lowering agents, 28% were on a diet alone and 27% on insulin treatment. The mean blood pressure was 134/73 mmHg. The mean HbA1c was 7.3%. Routine blood glucose monitoring was performed often but residents with possible hypoglycaemic episodes frequently did not have their blood glucose level checked.Conclusions  The prevalence of known diabetes in Christchurch rest homes is similar to that found in British studies but less than that found in studies from the USA. Indicators of quality of care in residents with diabetes in this study appeared to be satisfactory, in contrast to other studies. There was poor recognition by staff of the necessity of checking acutely blood glucose levels in residents with diabetes who became unwell.
Mother to child transmission of diabetes mellitus: does gestational diabetes program Type 2 diabetes in the next generation?
Authors: McLean M. , Chipps D. , Cheung N. Wah 
Published: October 2006

AbstractAim  Type 2 diabetes is frequently familial. Hyperglycaemia in pregnancy might act in addition to genetic factors to cause diabetes in the children of mothers with gestational diabetes mellitus (GDM). The first manifestation of this in female offspring is likely to be GDM in their own pregnancies. We compared the incidence of GDM in daughters of diabetic mothers and diabetic fathers to determine if in utero exposure to hyperglycaemia increased the risk of a diabetes‐prone phenotype in offspring.Methods  We analysed the outcome of a GDM screening programme in women with a family history of diabetes in their mother (n = 535), father (n = 566), both parents (n = 77) or neither (n = 4672).Results  GDM was twice as common in the daughters of diabetic mothers (11%) than diabetic fathers (5%, P = 0.002). Women with two diabetic parents were no more likely to have GDM than women with only a diabetic mother.Conclusions  Genetic predisposition to GDM should be equally shared by daughters of diabetic mothers and fathers. An excess of maternal transmission of diabetes is consistent with an epigenetic effect of hyperglycaemia in pregnancy acting in addition to genetic factors to produce diabetes in the next generation.