bluuebunny/crossref_metadata_2025_split huggingface dataset:
Response to oral cyclosporine therapy and high sensitivity‐CRP level in chronic idiopathic urticaria
Authors: Ohtsuka Tsutomu 
Published: April 2010

AbstractBackground  Chronic idiopathic urticaria (CIU) is often resistant to common treatment of uriticaria.Objective To find out clinical and laboratory findings affecting the response of oral cyclosporine therapy in CIU.Subjects and methods  The response of oral cyclosporine therapy in 15 patients with CIU (male : female = 5 : 10, age 16–60 years old, mean 40.0 years old) was studied. Cyclosporine trough level was measured with an enzyme‐multiplied immunoassay, and high sensitivity‐CRP was measured with a nephelometric assay. The relation between high sensitivity‐CRP level and clinical and laboratory findings in CIU was also studied.Results  All the 15 CIU patients responded to oral cyclosporine therapy. High sensitivity‐CRP levels before the start of therapy were elevated in nine of 15 CIU patients. The distributions of treatment duration and basophile leukocytes counts in elevated high sensitivity‐CRP patients (8.7 ± 1.3 months, 0.20 ± 0.05%) were significantly shorter and elevated than those in patients showing no elevation (22.7 ± 1.7 months, 0.40 ± 0.05%) (P < 0.05, P < 0.05), respectively. No other clinical and laboratory findings between patients with elevated and not elevated high sensitivity‐CRP showed any significant differences.Conclusion  Chronic idiopathic urticaria patients with elevated high sensitivity‐CRP showed good response to oral cyclosporine therapy.
Antibody reactivity to Borrelia burgdorferi sensu stricto antigens in patients from the Brazilian Amazon region with skin diseases not related to Lyme disease
Authors: Santos Mônica , Ribeiro‐Rodrigues Rodrigo , Lobo Rogério , Talhari Sinésio 
Published: April 2010

AbstractIn the present study, we report the occurrence of borreliosis in patients from the Brazilian Amazonic region. Nineteen (7.2%) out of 270 dermatological patients with different skin diseases (no one with clinical Lyme disease), tested positive by ELISA for Borrelia burgdorferi. Serum samples from 15 out of the 19 ELISA‐positive patients were further evaluated by Western blot. Presence of Borrelia burgdorferi specific IgG was confirmed in eight (53.3%) out of the 15 patients. All eight patients with ELISA and Western blot positive reactions were treated with doxycycline, according to the Centers for Disease Control and Prevention guidelines. One of them had clinical manifestations of colagenosis and was sent to the Department of Internal Medicine for further investigation. Data presented here suggested that borreliosis “lato sensu” is in the Brazilian Amazon region.
The influence of childhood atopic dermatitis on health of mothers, and its impact on Asian families
Authors: Ho Roger C. M. , Giam Y. C. , Ng T. P. , Mak Anselm , Goh Daniel , Zhang Melvyn W. B. , Cheak Alicia , Van Bever Hugo P. 
Published: April 2010

Ho RCM, Giam YC, Ng TP, Mak A, Goh D, Zhang MWB, Cheak A, Van Bever HP. The influence of childhood atopic dermatitis on health of mothers, and its impact on Asian families. Pediatr Allergy Immunol 2010: 21: 501–507. © 2010 John Wiley & Sons A/SThis study examines maternal perceptions of paediatric atopic dermatitis (AD) on family and determines risk factors including severity of AD, maternal physical and mental health (MH), quality of life of patients and sociodemographics which predict a negative family impact. A cross‐sectional assessment using the Dermatitis Family Impact Questionnaire Scale to assess the impact of AD on family, Infant’s Dermatitis Quality of Life Index (<5‐yrs old) or Children’s Dermatitis Life Quality Index (5–17 yrs old) was used to measure health‐related quality of life (HRQOL) of paediatric patients with AD. A 12‐item Short‐Form Health Survey (SF‐12) was used to assess physical and MH of their mothers. Risk factors of adverse family impact were assessed using multiple regression analysis. One hundred and four patients with AD and their mothers were studied. Their mean ages (±s.d.) were respectively 6.4 ± 4.3 and 37.2 ± 6.6 yrs. In multiple regression analysis, Severity Scoring of Atopic Dermatitis (SCORAD) appeared to be associated with negative family impact and the association remained significant after adjustment for bio‐psycho‐social factors and HRQOL of patients. The association remained insignificant after adjustment for physical and MH of the mothers. Our results show that the severity of paediatric AD leads to negative family impact through reduction of physical and MH of the mothers, and is independent of patients’ HRQOL and sociodemographics. The current approach for managing paediatric AD in Asian society could include early multidisciplinary intervention, aiming at enhancing physical and MH of mothers while minimizing negative impact on family and social isolation. Further research will be welcomed as the results of this study mainly applied to Asian society which could be different to populations from other geographic areas.
Intravenous immunoglobulin preparation type: Association with outcomes for patients with acute Kawasaki disease
Authors: Manlhiot Cedric , Yeung Rae S. M. , Chahal Nita , McCrindle Brian W. 
Published: April 2010

Manlhiot C, Yeung RSM, Chahal N, McCrindle BW. Intravenous immunoglobulin preparation type: Association with outcomes for patients with acute Kawasaki disease. Pediatr Allergy Immunol 2010: 21: 515–521. © 2010 John Wiley & Sons A/STo determine whether two different intravenous immunoglobulin (IVIG) preparations were equally efficacious in the treatment of Kawasaki disease (KD). Single centre retrospective review of all patients treated with IVIG for KD between January 1990 and April 2007. Comparison of IVIG (dose 2 g/kg) from two commercial preparations; Iveegam® stabilized with sugar (lyophilized, 5 g/ml glucose, pH 6.4–7.2, IgA 10 μg/ml, 5% IgG/ml) and Gamimune® stabilized through acidification (no sugar, pH 4.0–4.5, IgA 270 μg/ml, 5% 1990–1999, 10% 1999–2007 IgG/ml). Propensity‐adjusted differences in duration of fever after treatment initiation, frequency of retreatment with IVIG, hospital stay and maximum coronary artery z‐score. A total of 954 patients were included, 862 (90%) were treated with Iveegam® and 92 (10%) were treated with Gamimune®. Patients’ demographic, clinical and laboratory characteristics were similar between the two groups. In propensity‐adjusted models, Iveegam® was found to be associated with higher probability of non‐response to IVIG (12% vs. 5%, p = 0.05) and longer median duration of fever after IVIG [1 (1–27) vs. 1 (1–8) days, p = 0.02] than Gamimune®. Nevertheless, Gamimune® was found to be associated with longer median duration of hospital stay [5 (2–49) vs. 4 (2–76) days, p < 0.0001] and higher median maximum coronary artery z‐score both at the end of the acute phase (+1.4 vs. +0.8, p < 0.0001) and 6–8 weeks after the acute phase (+0.7 vs. +0.4, p < 0.0001). IVIG preparations with lower IgA content and stabilized with glucose appear to be associated with improved coronary artery outcomes for patients with KD.
Association between serum levels of soluble CD40/CD40 ligand and organ damage in hypertensive patients
Authors: Yuan Ming , Ohishi Mitsuru , Wang Lin , Raguki Hiromi , Wang Haichang , Tao Ling , Ren Jun 
Published: April 2010

Summary1. CD40 and CD40 ligand (CD40L) have a critical role in the pathophysiology and risk prediction of coronary artery syndrome, including atherothrombosis and atherosclerosis. However, the contribution of the CD40/CD40L dyad, especially the soluble form of CD40L (sCD40L), to the pathophysiology of hypertension and associated organ damage remains unknown.2. In the present study, serum levels of CD40 and sCD40L were measured in 328 hypertensive patients with varying degrees of organ damage. The data revealed that serum levels of CD40 were significantly greater in patients with severe, but not mild, organ damage compared with patients without any organ damage. There were no significant differences in serum concentrations of sCD40L between patients with no, mild and severe organ damage. Concentrations of soluble CD40 were comparable in patients with mild organ damage that included left ventricular hypertrophy, retinal damage, renal dysfunction and proteinuria. In contrast, concentrations of soluble CD40 were increased significantly in patients with certain forms of severe organ damage, specifically stroke, but not coronary and peripheral artery disease.3. Collectively, our data indicate that upregulation of the CD40 system in hypertensive patients with certain forms of severe end‐organ damage may contribute to the pro‐inflammatory, pro‐atherogenic and prothrombotic milieu in hypertension.
Concomitant inactivation of the epidermal growth factor receptor, phosphatidylinositol 3‐kinase/Akt and Janus tyrosine kinase 2/signal transducer and activator of transcription 3 signalling pathways in cardiotoxin III‐treated A549 cells
Authors: Su Jung‐Chen , Lin Kuei‐Li , Chien Ching‐Ming , Chuang Pei‐Wen , Chang Long‐Sen , Lin Shinne‐Ren 
Published: April 2010

Summary1. Cardiotoxin (CTX) III, a basic polypeptide with 60 amino acid residues isolated from Naja naja atra venom, has potential anticancer therapeutic activity. The aim of the present study was to investigate the apoptotic effect (and the underlying mechanism of action) of CTX III in human adenocarcinoma A549 cells.2. It was found that CTX III induces apoptosis in A549 cells, as indicated by an increase in the sub‐G1 population, phosphatidylserine externalization, loss of mitochondrial membrane potential (Ψm) with cytochrome c release and activation of caspases 9 and 3. These actions were correlated with upregulation of Bax and Bad and downregulation of various anti‐apoptotic proteins, including Bcl‐2, Bcl‐XL, Mcl‐1, X‐linked inhibitor of apoptosis protein (XIAP) and p‐Bad in CTX III‐treated cells.3. The signal transduction pathways involved in the effects of CTX III in A549 cells were evaluated using 5 μmol/L AG1478, an inhibitor of the epidermal growth factor receptor (EGFR), and exposing cells to the drug for 8 h. The results indicated that CTX III suppresses phosphorylation of EGFR and activation of phosphatidylinositol 3‐kinase (PI3‐K)/Akt and Janus tyrosine kinase (JAK) 2/signal transducer and activator of transcription (STAT) 3, all of which are downstream molecules in the EGFR signalling pathway.4. Exposure of cells for 8 h to the PI3‐K inhibitor wortmannin (10 μmol/L) blocked JAK2 and STAT3 activation, whereas exposure of cells to the JAK2 inhibitor AG490 (5 μmol/L) decreased levels of phosphorylated (p‐) JAK2 and p‐STAT3 without affecting PI3‐K/Akt activation. These observations suggest that PI3‐K is an upstream activator of JAK2/STAT3. Furthermore, 5 μmol/L AG490 and 10 μmol/L wortmannin treatment of A549 cells for 8 h resulted in upregulation of Bax and Bad and downregulation of Bcl‐2, Bcl‐XL, XIAP and p‐Bad.5. Together, the results of the present study indicate that CTX III induces apoptosis in A549 cells by inactivating the EGFR, PI3‐K/Akt and JAK2/STAT3 signalling pathways.
Hypothesis: Multiple factors are associated with the lack of any beneficial effects of oestrogen‐replacement therapy in the late postmenopausal stage
Authors: Xiao Ming , Cao Guang‐Liang , Marshall Charles , Hu Gang 
Published: April 2010

Summary1. Epidemiological and clinical studies suggest that women may obtain cognitive benefits from oestrogen‐replacement therapy (ERT) during menopause transition rather than in the post‐menopausal stages. However, the underlying mechanisms remain to be determined.2. We propose that long‐term oestrogen deficiency may result in abnormal distribution and localization of brain oestrogen receptors, brain mitochondrial dysfunction, septohippocampal cholinergic degeneration and reactive gliosis. These multiple pathogenic factors may account for the lack of any beneficial effects of ERT in post‐menopausal women with or without Alzheimer’s disease.
Exercise training attenuates anaphylactic venoconstriction in rat perfused liver, but does not affect anaphylactic hypotension in conscious rats
Authors: Cui Sen , Shibamoto Toshishige , Zhang Wei , Kurata Yasutaka , Kashimura Osamu , Miyamae Shunichi 
Published: April 2010

Summary1. Exercise training attenuates circulatory shock due to haemorrhage, endotoxin or heatstroke. However, it remains unknown whether exercise training attenuates anaphylactic shock. Hepatic venoconstriction is involved in rat anaphylactic hypotension. In the present study, we determined the effects of exercise training on both anaphylaxis‐induced segmental venoconstriction in rat perfused livers and systemic anaphylaxis in conscious rats. The role of nitric oxide (NO) in the effect of exercise on the venoconstriction of perfused livers was also examined.2. Rats were subjected to running training on a motorized treadmill for 4 weeks. Two weeks prior to the anaphylaxis experiment, Sprague‐Dawley rats were actively sensitized with the antigen ovalbumin. In isolated livers perfused portally with blood, the portal venous pressure (Ppv) and sinusoidal pressure were measured to determine the pre‐ and post‐sinusoidal resistances (Rpre and Rpost, respectively). In conscious rats, systemic arterial pressure (SAP) and Ppv were determined.3. In the perfused livers of sedentary rats, antigen administration led to a predominant presinusoidal constriction, as evidenced by 4.6‐ and 1.7‐fold increases in Rpre and Rpost, respectively. The anaphylaxis‐induced increase in Rpre was significantly attenuated by 24% by exercise training. Inhibition of NO synthase with NG‐nitro‐l‐arginine methyl ester (100 μmol/L) 10 min prior to the injection of antigen enhanced anaphylactic venoconstriction, but did not alter the effect of exercise training on the increase in Rpre. In contrast, exercise training did not attenuate either anaphylactic hypotension or portal hypertension in conscious rats.4. In conclusion, exercise training attenuates the anaphylaxis‐induced presinusoidal constriction in rat isolated perfused livers, independent of NO production. However, this action is not evident in conscious rats and exercise training does not affect anaphylactic hypotension in conscious rats.
Nestin is a novel marker for renal tubulointerstitial injury in immunoglobulin A nephropathy
Authors: TOMIOKA MAI , HIROMURA KEIJU , SAKAIRI TORU , TAKEUCHI SHIGERU , MAESHIMA AKITO , KANEKO YORIAKI , KUROIWA TAKASHI , TAKEUCHI TOSHIYUKI , NOJIMA YOSHIHISA 
Published: April 2010

ABSTRACTAim:  Nestin, an intermediate filament originally identified as a marker of neural progenitor cells, is transiently expressed in endothelial cells and tubuloepithelial cells during kidney development. However, in adult kidneys, podocytes are the only cells that express nestin. In this study, we examined tubulointerstitial nestin expression in human glomerulonephritis.Methods:  Renal biopsy specimens obtained from 41 adult patients with immunoglobulin (Ig)A nephropathy were studied. Nestin expression was determined by immunohistochemical staining and estimated by digital image analysis. To identify the phenotype of nestin‐positive cells, a double immunofluorescent study was performed for nestin and CD34 (a marker for endothelial cells) or α‐smooth muscle actin (α‐SMA, a marker for myofibroblasts).Results:  In normal kidney, nestin expression was restricted to the podocytes and was not detected in tubular cells and tubulointerstitial cells. In contrast, increased nestin expression was observed at tubulointerstitial areas of IgA nephropathy. The degree of tubulointerstitial nestin expression was positively correlated with tubulointerstitial fibrosis (r = 0.546, P < 0.001). The double immunofluorescent study showed that most nestin‐positive cells in the interstitium were co‐stained with CD34 or α‐SMA, suggesting that peritubular endothelial cells and tubulointerstitial myofibroblasts express nestin during the progression of tubulointerstitial injury. In addition, strong nestin expression was associated with deterioration of renal function.Conclusion:  Nestin expression is associated with tubulointerstitial injury and predicts renal prognosis in IgA nephropathy. Nestin could be a new marker for peritubular endothelial cell injury and tubulointerstitial fibrosis.
The ultrastructural distribution of prestin in outer hair cells: a post‐embedding immunogold investigation of low‐frequency and high‐frequency regions of the rat cochlea
Authors: Mahendrasingam Shanthini , Beurg Maryline , Fettiplace Robert , Hackney Carole M. 
Published: April 2010

AbstractOuter hair cells (OHCs) of the mammalian cochlea besides being sensory receptors also generate force to amplify sound‐induced displacements of the basilar membrane thus enhancing auditory sensitivity and frequency selectivity. This force generation is attributable to the voltage‐dependent contractility of the OHCs underpinned by the motile protein, prestin. Prestin is located in the basolateral wall of OHCs and is thought to alter its conformation in response to changes in membrane potential. The precise ultrastructural distribution of prestin was determined using post‐embedding immunogold labelling and the density of the labelling was compared in low‐frequency and high‐frequency regions of the cochlea. The labelling was confined to the basolateral plasma membrane in hearing rats but declined towards the base of the cells below the nucleus. In pre‐hearing animals, prestin labelling was lower in the membrane and also occurred in the cytoplasm, presumably reflecting its production during development. The densities of labelling in low‐frequency and high‐frequency regions of the cochlea were similar. Non‐linear capacitance, thought to reflect charge movements during conformational changes in prestin, was measured in OHCs in isolated cochlear coils of hearing animals. The OHC non‐linear capacitance in the same regions assayed in the immunolabelling was also similar in both the apex and base, with charge densities of 10 000/μm2 expressed relative to the lateral membrane area. The results suggest that prestin density, and by implication force production, is similar in low‐frequency and high‐frequency OHCs.
Stem and progenitor cell compartments within adult mouse taste buds
Authors: Sullivan Jeremy M. , Borecki Alexander A. , Oleskevich Sharon 
Published: April 2010

AbstractAdult taste buds are maintained by the lifelong proliferation of epithelial stem and progenitor cells, the identities of which have remained elusive. It has been proposed that these cells reside either within the taste bud (intragemmal) or in the surrounding epithelium (perigemmal). Here, we apply three different in vivo approaches enabling single‐cell resolution of proliferative history to identify putative stem and progenitor cells associated with adult mouse taste buds. Experiments were performed across the circadian peak in oral epithelial proliferation (04:00 h), a time period in which mitotic activity in taste buds has not yet been detailed. Using double label pulse‐chase experiments, we show that defined intragemmal cells (taste and basal) and perigemmal cells undergo rapid, sequential cell divisions and thus represent potential progenitor cells. Strikingly, mitotic activity was observed in taste cells previously thought to be postmitotic (labelled cells occur in 30% of palatal taste buds after 1 h of BrdU exposure). Basal cells showed expression of the transcription factor p63, required for maintaining the self‐renewal potential of various epithelial stem cell types. Candidate taste stem cells were identified almost exclusively as basal cells using the label‐retaining cell approach to localize slow‐cycling cells (0.06 ± 0.01 cells per taste bud; n = 436 taste buds). Together, these results indicate that both stem‐ and progenitor‐like cells reside within the mammalian taste bud.
The effects of aging and chronic fluoxetine treatment on circadian rhythms and suprachiasmatic nucleus expression of neuropeptide genes and 5‐HT1Breceptors
Authors: Duncan Marilyn J. , Hester James M. , Hopper Jason A. , Franklin Kathleen M. 
Published: April 2010

AbstractAge‐related changes in circadian rhythms, including attenuation of photic phase shifts, are associated with changes in the central pacemaker in the suprachiasmatic nucleus (SCN). Aging decreases expression of mRNA for vasoactive intestinal peptide (VIP), a key neuropeptide for rhythm generation and photic phase shifts, and increases expression of serotonin transporters and 5‐HT1Breceptors, whose activation inhibits these phase shifts. Here we describe studies in hamsters showing that aging decreases SCN expression of mRNA for gastrin‐releasing peptide, which also modulates photic phase resetting. Because serotonin innervation trophically supports SCN VIP mRNA expression, and serotonin transporters decrease extracellular serotonin, we predicted that chronic administration of the serotonin‐selective reuptake inhibitor, fluoxetine, would attenuate the age‐related changes in SCN VIP mRNA expression and 5‐HT1Breceptors.In situhybridization studies showed that fluoxetine treatment does not alter SCN VIP mRNA expression, in either age group, at zeitgeber time (ZT)6 or 13 (ZT12 corresponds to lights off). However, receptor autoradiographic studies showed that fluoxetine prevents the age‐related increase in SCN 5‐HT1Breceptors at ZT6, and decreases SCN 5‐HT1Breceptors in both ages at ZT13. Therefore, aging effects on SCN VIP mRNA and SCN 5‐HT1Breceptors are differentially regulated; the age‐related increase in serotonin transporter sites mediates the latter but not the former. The studies also showed that aging and chronic fluoxetine treatment decrease total daily wheel running without altering the phase of the circadian wheel running rhythm, in contrast to previous reports of phase resetting by acute fluoxetine treatment.
GABAB receptor‐dependent modulation of network activity in the rat prefrontal cortex in vitro
Authors: Wang Ying , Neubauer Florian B. , Lüscher Hans‐Rudolf , Thurley Kay 
Published: April 2010

AbstractGABA (γ‐aminobutyric acid) can mediate inhibition via pre‐ and post/extrasynaptic GABA receptors. In this paper we demonstrate potentially post/extrasynaptic GABAB receptor‐dependent tonic inhibition in L2/3 pyramidal cells of rat medial prefrontal cortex (mPFC) in vitro. First, we show via voltage‐clamp experiments the presence of a tonic GABAB receptor‐dependent outward current in these neurons. This GABABergic current could be induced by ambient GABA when present at sufficient concentrations. To increase ambient GABA levels in the usually silent slice preparation, we amplified network activity and hence synaptic GABA release with a modified artificial cerebrospinal fluid. The amplitude of tonic GABAB current was similar at different temperatures. In addition to the tonic GABAB current, we found presynaptic GABAB effects, GABAB‐mediated inhibitory postsynaptic currents and tonic GABAA currents. Second, we performed current‐clamp experiments to evaluate the functional impact of GABAB receptor‐mediated inhibition in the mPFC. Activating or inactivating GABAB receptors led to rightward (reduction of excitability) or leftward (increase of excitability) shifts, respectively, of the input–output function of mPFC L2/3 pyramidal cells without effects on the slope. Finally, we showed in electrophysiological recordings and epifluorescence Ca2+‐imaging that GABAB receptor‐mediated tonic inhibition is capable of regulating network activity. Blocking GABAB receptors increased the frequency of excitatory postsynaptic currents impinging on a neuron and prolonged network upstates. These results show that ambient GABA via GABAB receptors is powerful enough to modulate neuronal excitability and the activity of neural networks.