bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surgical correction of unilateral and bilateral facial palsy
Authors: Harrison D H 
Published: September 2005

Abstract
Unilateral and bilateral facial palsies are debilitating and depressing conditions for the patient. For the past 30 years attempts have been made to improve the reanimation of these patients. The ability to transfer axons over significant distances with nerve grafts and the transfer of muscle that can be revascularised by microvascular surgery greatly improves results of this surgery. The revascularisation of muscle has been the important step forward but the re-focusing of interest in this condition has brought about a number of peripheral advances.
Gastrointestinal involvement in POEMS syndrome: a novel clinical manifestation
Authors: Dogan S , Beyazit Y , Shorbagi A , Köklü S , Ustunel S , Guler N , Uner A 
Published: September 2005

Abstract
POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) is characterised by a rare multisystem disorder of unknown pathogenesis. Although its pathophysiology is not well understood, overexpression of proinflammatory cytokines has been implicated. Gastrointestinal system disorders have not been reported among the components of the syndrome. A case is reported of POEMS syndrome with gastrointestinal involvement shown by gastrointestinal endoscopy.
Early diffusion weighted imaging and expression of heat shock protein 70 in newborn pigs with hypoxic ischaemic encephalopathy
Authors: Cheng Y , Liu G R , Guan J T , Guo Y L , Li Y K , Wu R H 
Published: September 2005

Abstract

Objective
To establish a cerebral hypoxia ischaemic model in piglets and to explore the early diffusion weighted imaging (DWI) as well as the expression of heat shock protein 70 (HSP70) with hypoxic ischaemic encephalopathy (HIE).

Methods
Twenty four 3 day old piglets were permanently ligated common carotid arteries bilaterally and ventilated with 3% oxygen for 30 minutes, and their brains were examined at three hours, six hours, and 24 hours after hypoxic ischaemia with T2 weighted images and diffusion weighted images. Apparent diffusion coefficient (ADC) values were measured and HSP70 expression was detected in the central and peripheral regions of lesions.

Results
Abnormal signal intensity was detected on DWI and ADC maps in three hypoxic ischaemic groups. ADC values in the central lesions rapidly decreased, whereas ADC values in the peripheral regions reduced prominently at 24 hours after hypoxic ischaemia. There were significant differences (p&lt;0.01) between ADC values of the central regions and the peripheral regions of lesions. The number of HSP70 positive cells was low at three hours, raised at the highest peak at six hours, and then rapidly decreased. There was statistical difference between HSP70 positive cells in the central regions and those in peripheral regions (p&lt;0.01).

Conclusion
DWI may identify more early lesions, and improve conspicuity in the acute setting. ADC values can be used as an objective measure for hypoxic ischaemic injury. Tissue reversibility can be further reflected according to the information of ADC values and HSP70 immunohistochemical staining.
Diagnosis and disease modifying treatments in multiple sclerosis
Authors: Zajicek J 
Published: September 2005

Abstract
Multiple sclerosis (MS) refers to scattered areas of hardening found on sectioning central nervous system tissue of affected people, usually after many years of illness. It rarely causes early death but is the commonest cause of neurological disability among young people. Overall results from controlled trials over the past 50 years have been rather disappointing but the comparatively recent licensing of drugs such as interferon beta and glatiramer acetate has led to a reappraisal of many aspects of MS. There are now new diagnostic criteria, which encompass developments in magnetic resonance imaging. Older clinical methods of measuring disease impact are now being re-evaluated to facilitate clinical trials of the approximate 150 new products currently being developed as potential disease modifying agents. The success and failure of agents that should be effective on theoretical grounds, together with advances in neuropathology, have led to fundamental questions regarding our basic understanding of disease pathogenesis being re-addressed.
Important cutaneous manifestations of inflammatory bowel disease
Authors: Trost L B , McDonnell J K 
Published: September 2005

AbstractInflammatory bowel disease (IBD) has many extraintestinal manifestations. Cutaneous manifestations are usually related to the activity of the bowel disease but may have an independent course. Anyone presenting with IBD should be examined for cutaneous manifestations. Pyoderma gangrenosum is a severe painful ulcerating disease that requires moist wound management and, in the absence of secondary infection, systemic corticosteroids, cyclosporine, or both. Infliximab may also be used. Erythema nodosum is a common cause of tender red nodules of the shins. Management includes leg elevation, NSAIDs, and potassium iodide. Oral manifestations of IBD include aphthous stomatitis, mucosal nodularity (cobblestoning), and pyostomatitis vegetans. Treatment should be directed both at the cutaneous lesions and at the underlying systemic condition.
Comparative study of enema retention and preference in ulcerative colitis
Authors: Ingram J R , Rhodes J , Evans B K , Newcombe R G , Thomas G A O 
Published: September 2005

Abstract

Background
Therapeutic enemas are often used to treat active colitis but their retention may be limited because of urgency to defecate. Some preparations may be better retained and tolerated than others because of their physical properties.

Aim
To compare patient preference and retention of four therapeutic enemas, including a nicotine enema, in patients with ulcerative colitis (UC).

Methods
Twenty four patients with active UC received the four trial enemas—corticosteroid, 5-amino salicylate (5-ASA), and nicotine liquid enemas and a corticosteroid foam, in a randomised order, taking one enema on each of four successive nights. Patients scored them 1 to 4 for ease of administration and retention, degree of abdominal bloating, and for their overall preference.

Results
Fifteen patients rated nicotine their overall favourite or second favourite, compared with 14 for corticosteroid foam and 11 for 5-ASA and corticosteroid liquids, but this was not significant (p = 0.302). Overall, there was no significant difference in overnight retention. However, the nicotine enema tended to be less well retained in patients with milder urgency but a higher proportion retained it overnight with more severe urgency (p = 0.031 compared with 5-ASA enema).

Conclusion
There was no significant difference in patient preference or overall duration of retention for the four enemas.
Implications of the new definition of myocardial infarction
Authors: Wong C-K , White H D 
Published: September 2005

Abstract
The new definition of acute myocardial infarction is based primarily on raised troponin levels because of the sensitivity and specificity of these markers and their correlation with the pathophysiology of acute coronary syndromes with plaque fissuring or rupture and embolisation of platelets causing myocyte necrosis. Raised troponin levels are associated with increased risks of death and recurrent myocardial infarction. Greater treatment benefit with low molecular weight heparin, IIb/IIIa antagonists and revascularisation is seen when troponin levels are raised. There are many implications for patients and society of the new definition including changes in insurability and ability to continue certain occupations. Many more patients, who would previously been diagnosed as having unstable angina, will now be diagnosed as having had an acute myocardial infarction. In addition case fatality rates will fall and comparison with previous epidemiological studies using the old definition will be problematic. However, the new definition may result in greater use of evidence based therapies with improved patient outcomes and decreased community death rates.
Impact of Short-Term Administration of High-Density Lipoproteins and Atorvastatin on Atherosclerosis in Rabbits
Authors: Nicholls Stephen J. , Cutri Belinda , Worthley Stephen G. , Kee Patrick , Rye Kerry-Anne , Bao Shisan , Barter Philip J. 
Published: September 2005

Objective—This study investigates effects of short-term administration of high-density lipoproteins (HDL) and a statin on atherosclerosis in cholesterol-fed rabbits. Effects of HDL apolipoprotein and phospholipid composition have also been investigated.Methods and Results—Aortic atherosclerosis was established over 17 weeks in 46 rabbits by balloon denudation and cholesterol feeding. During the past 5 days of the cholesterol-feeding period, animals received: (1) no treatment; (2) oral atorvastatin 5 mg/kg on each of the 5 days; or (3) infusions of HDL (8 mg/kg apolipoprotein A-I) on days 1 and 3 of the treatment phase. After euthanization, lesion size and composition were assessed by histological and immunohistochemical analysis. HDL (but not atorvastatin) reduced lesion size by 36% (P<0.05). The ratio of smooth muscle cells to macrophages in the lesions increased 2.6-fold in animals infused with HDL (P<0.05) and 4-fold in those receiving atorvastatin (P<0.01). HDL and atorvastatin reduced matrix metalloproteinase (MMP)-9 expression by 42% (P<0.05) and 45% (P<0.03), respectively. HDL increased thrombomodulin expression 2-fold (P<0.03). The beneficial effects on lesion area and plaque cellular composition were influenced by HDL phospholipid and apolipoprotein composition.Conclusion—Infusing small amounts of HDL rapidly reduces lesion size and is comparable to atorvastatin in promoting a stable plaque phenotype.
Transcranial Ultrasound Brain Perfusion Assessment With a Contrast Agent-Specific Imaging Mode
Authors: Hölscher Thilo , Wilkening Wilko , Draganski Bogdan , Meves Saskia H. , Eyding Jens , Voit Heinz , Bogdahn Ulrich , Przuntek Horst , Postert Thomas 
Published: September 2005

Background and Purpose—The purpose of this study was to assess brain perfusion with an ultrasound contrast-specific imaging mode and to prove if the results are comparable between 2 centers using a standardized study protocol.Methods—A total of 32 individuals without known cerebrovascular disease were included in the study. Perfusion studies were performed ipsilaterally in an axial diencephalic plane after intravenous administration of 0.75 mL of Optison. Offline time intensity curves (TIC) were generated in different anatomic regions. Both centers used identical study protocols, ultrasound machines, and contrast agent.Results—In both centers, the comparison of the parameter time to peak intensity (TPI) revealed significantly shorter TPIs in the main vessel structures compared with any parenchymal region of interest (ROI), whereas no significant differences were seen between the parenchymal ROIs. The parameter peak intensity (PI) varied widely interindividually in both centers, whereas theinter-ROI comparison revealed statistical significance (P<0.05) in most of the cases according to the following pattern: (1) lentiforme nucleus > thalamus and white matter region, (2) thalamus > white matter region, and (3) main vessel > any parenchymal structure. Similar results were achieved in both centers independently.Conclusion—The study demonstrates that brain perfusion assessment with an ultrasound contrast-specific imaging mode is comparable between different centers using the same study protocol.
SHPS-1 promotes the survival of circulating erythrocytes through inhibition of phagocytosis by splenic macrophages
Authors: Ishikawa-Sekigami Tomomi , Kaneko Yoriaki , Okazawa Hideki , Tomizawa Takeshi , Okajo Jun , Saito Yasuyuki , Okuzawa Chie , Sugawara-Yokoo Minako , Nishiyama Uichi , Ohnishi Hiroshi , Matozaki Takashi , Nojima Yoshihisa 
Published: September 2005

AbstractThe lifespan of circulating red blood cells (RBCs) produced in bone marrow is determined by their elimination through phagocytosis by splenic macrophages. The mechanism by which RBC elimination is regulated has remained unclear, however. The surface glycoprotein SHPS-1, a member of the immunoglobulin superfamily, is abundant in macrophages. We have now examined the regulation of RBC turnover with the use of mice that express a mutant form of SHPS-1 lacking most of its cytoplasmic region. The mutant mice manifested mild anemia as well as splenomegaly characterized by expansion of the red pulp. The numbers of erythroid precursor cells in the spleen and of circulating reticulocytes were also increased in the mutant mice. In contrast, the half-life of circulating RBCs was reduced in these animals, and the rate of clearance of injected opsonized RBCs from the peripheral circulation was increased in association with their incorporation into splenic macrophages. Phagocytosis of opsonized RBCs by splenic macrophages from mutant mice in vitro was also increased compared with that observed with wild-type macrophages. These results suggest that SHPS-1 negatively regulates the phagocytosis of RBCs by splenic macrophages, thereby determining both the lifespan of individual RBCs and the number of circulating erythrocytes.
Hierarchy of molecular-pathway usage in bone marrow homing and its shift by cytokines
Authors: Bonig Halvard , Priestley Gregory V. , Papayannopoulou Thalia 
Published: September 2005

AbstractEfficient bone marrow (BM) homing is a prerequisite for successful engraftment of transplanted hematopoietic cells (HPCs). Contradictory conclusions about the contribution of SDF-1/CXCR4 have clouded our understanding of its role within the molecular pathway cooperation needed for BM homing, particularly with the well-defined hierarchic network of adhesion molecules. In the present study we sought to unravel cooperative and compensatory molecular pathways guiding BM homing. Fresh BM-HPCs, rendered either SDF-1 unresponsive or Gi-signaling refractory, homed quite efficiently, because of compensation by α4-integrin interacting with VCAM-1. The contribution of SDF-1/CXCR4- or Gi-protein-mediated signals to BM homing became apparent after their blockade was combined with deletion of α4-integrin, leading to dramatic reduction in BM homing. Similar conclusions were revealed when VCAM-1-deficient hosts were used. Cytokine incubation changed the functional properties of BM-HPCs and hierarchy of molecular pathway usage in homing, by shifting the dominance among the homing mediators: loss of CXCR4 or Gi-signaling now significantly reduced BM homing, with only partial compensation through α4/VCAM-1 and endothelial selectins. These studies depict a flexible hierarchy of cooperating homing pathways, in which dominant players are repositioned with changing cytokine milieu, and possibly source of HPCs.
The N-terminus of hepcidin is essential for its interaction with ferroportin: structure-function study
Authors: Nemeth Elizabeta , Preza Gloria C. , Jung Chun-Ling , Kaplan Jerry , Waring Alan J. , Ganz Tomas 
Published: September 2005

Abstract
Hepcidin is the principal iron-regulatory hormone. It acts by binding to the iron exporter ferroportin, inducing its internalization and degradation, thereby blocking cellular iron efflux. The bioactive 25 amino acid (aa) peptide has a hairpin structure stabilized by 4 disulfide bonds. We synthesized a series of hepcidin derivatives and determined their bioactivity in a cell line expressing ferroportin-GFP fusion protein, by measuring the degradation of ferroportin-GFP and the accumulation of ferritin after peptide treatment. Bioactivity was also assayed in mice by the induction of hypoferremia. Serial deletion of N-terminal amino acids caused progressive decrease in activity which was completely lost when 5 N-terminal aa's were deleted. Synthetic 3-aa and 6-aa N-terminal peptides alone, however, did not internalize ferroportin and did not interfere with ferroportin internalization by native hepcidin. Deletion of 2 C-terminal aa's did not affect peptide activity. Removal of individual disulfide bonds by pairwise substitution of cysteines with alanines also did not affect peptide activity in vitro. However, these peptides were less active in vivo, likely because of their decreased stability in circulation. G71D and K83R, substitutions previously described in humans, did not affect hepcidin activity. Apart from the essential nature of the N-terminus, hepcidin structure appears permissive for mutations.
Synergistic antileukemic interactions between 2-medroxyestradiol (2-ME) and histone deacetylase inhibitors involve Akt down-regulation and oxidative stress
Authors: Gao Ning , Rahmani Mohamed , Shi Xianglin , Dent Paul , Grant Steven 
Published: September 2005

Abstract
Interactions between the endogenous estradiol metabolite 2-medroxyestradiol (2-ME) and histone deacetylase inhibitors (HDACIs) have been investigated in human leukemia cells. Coadministration of subtoxic or marginally toxic concentrations of 2-ME and SAHA or sodium butyrate in diverse human leukemia-cell types resulted in a marked increase in oxidative damage (eg, generation of reactive oxygen species [ROSs]), mitochondrial injury (eg, cytochrome c release and Bax translocation), caspase activation, and apoptosis. These interactions were also noted in primary human leukemia cells but not in normal bone marrow CD34+ cells. Synergistic interactions between these agents were associated with inactivation of Akt and activation of c-Jun N-terminal kinase (JNK). Essentially all of these events were reversed by free radical scavengers such as the manganese superoxide dismutase (MnSOD) mimetic TBAP and catalase. Notably, treatment with 2-ME/HDACIs resulted in down-regulation of thioredoxin, MnSOD, and glutathione peroxidase. Enforced activation of Akt blocked 2-ME/HDACI-mediated mitochondrial injury, caspase activation, and JNK up-regulation, but not generation of ROSs. Pharmacologic or genetic (siRNA) interruption of the JNK pathway also significantly attenuated the lethality of this regimen. Together, these findings support a model in which antileukemic synergism between 2-ME and HDACIs stems primarily from induction of oxidative damage, leading in turn to Akt inactivation and JNK activation, culminating in mitochondrial injury and apoptosis. They also raise the possibility that these events may preferentially occur in leukemic versus normal hematopoietic cells.
Human mesenchymal stem cells modulate B-cell functions
Authors: Corcione Anna , Benvenuto Federica , Ferretti Elisa , Giunti Debora , Cappiello Valentina , Cazzanti Francesco , Risso Marco , Gualandi Francesca , Mancardi Giovanni Luigi , Pistoia Vito , Uccelli Antonio 
Published: September 2005

AbstractHuman mesenchymal stem cells (hMSCs) suppress T-cell and dendritic-cell function and represent a promising strategy for cell therapy of autoimmune diseases. Nevertheless, no information is currently available on the effects of hMSCs on B cells, which may have a large impact on the clinical use of these cells. hMSCs isolated from the bone marrow and B cells purified from the peripheral blood of healthy donors were cocultured with different B-cell tropic stimuli. B-cell proliferation was inhibited by hMSCs through an arrest in the G0/G1 phase of the cell cycle and not through the induction of apoptosis. A major mechanism of B-cell suppression was hMSC production of soluble factors, as indicated by transwell experiments. hMSCs inhibited B-cell differentiation because IgM, IgG, and IgA production was significantly impaired. CXCR4, CXCR5, and CCR7 B-cell expression, as well as chemotaxis to CXCL12, the CXCR4 ligand, and CXCL13, the CXCR5 ligand, were significantly down-regulated by hMSCs, suggesting that these cells affect chemotactic properties of B cells. B-cell costimulatory molecule expression and cytokine production were unaffected by hMSCs. These results further support the potential therapeutic use of hMSCs in immune-mediated disorders, including those in which B cells play a major role.
Tourette syndrome and learning disabilities
Authors: Burd Larry , Freeman Roger D , Klug Marilyn G , Kerbeshian Jacob 
Published: September 2005

Abstract
Background
Tourette Syndrome (TS) is a neurodevelopmental disorder of childhood. Learning disabilities are frequently comorbid with TS. Using the largest sample of TS patients ever reported, we sought to identify differences between subjects with TS only and subjects with TS and a comorbid learning disability.

Methods
We used the Tourette Syndrome International Consortium database (TIC) to compare subjects with comorbid Tourette Syndrome and learning disabilities (TS + LD) to subjects who did not have a comorbid learning disability (TS - LD). The TIC database contained 5,500 subjects. We had usable data on 5,450 subjects.

Results
We found 1,235 subjects with TS + LD. Significant differences between the TS + LD group and the TS - LD group were found for gender (.001), age onset (.030), age first seen (.001), age at diagnosis (.001), prenatal problems (.001), sibling or other family member with tics (.024), two or more affected family members (.009), and severe tics (.046). We used logistic modeling to identify the optimal prediction model of group membership. This resulted in a five variable model with the epidemiologic performance characteristics of accuracy 65.2% (model correctly classified 4,406 of 5,450 subjects), sensitivity 66.1%, and specificity 62.2%.

Conclusion
Subjects with TS have high prevalence rates of comorbid learning disabilities. We identified phenotype differences between the TS - LD group compared to TS + LD group. In the evaluation of subjects with TS, the presence of a learning disability should always be a consideration. ADHD may be an important comorbid condition in the diagnosis of LD or may also be a potential confounder. Further research on etiology, course and response to intervention for subjects with TS only and TS with learning disabilities is needed.