bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparative Study of NonInvasive Vascular Imaging Techniques in the Evaluation of Chronic Venous Leg Ulcers
Authors: Yamaki Takashi , Nozaki Motohiro 
Published: January 2005

Aim:  To compare noninvasive vascular imaging techniques in the evaluation of chronic venous leg ulcers, and to detect the discriminating parameters between primary valvular incompetence (PVI) and postthrombotic syndrome (PTS).Methods:  A total of 61 limbs with chronic venous ulcers were included in this study. Of 61 limbs, 31 had PVI and remaining 30 had documented PTS. The distribution of venous reflux including superficial, deep, and perforating vein was determined by duplex ultrasound. The venous functions including venous volume (VV: ml), venous filling index (VFI: ml/sec), ejection fraction (EF: %), and residual volume fraction (RVF: %) were evaluated by air plethysmography (APG). The near–infrared spectroscopy (NIRS) was used to measure calf muscle total hemoglobin (tHb), oxygenated hemoglobin (O2Hb), and deoxygenated hemoglobin (HHb) levels using APG exercise protocol, and the changes in these parameters were divided into three patterns; Type I: The HHb does not increase beyond the O2Hb during the total procedure. Type II: The HHb increases beyond the O2Hb during the excise. Type III: The HHb increases beyond the O2Hb during the total procedure. Patients with Type III were considered to have most significant calf muscle dysfunction.Results:  Superficial venous incompetence was significantly predominant in the PVI (p = 0.031). The proportion of deep vein incompetence was significantly higher in the PTS (p = 0.023). Of these, patients with PTS had significantly higher proportion of femoral vein (FV) and popliteal vein (POPV) incompetence compared to these with PVI (p = 0.0006, 0.0015, respectively). There was no statistically significant difference in the proportion of perforator incompetence between the groups (p = 0.611). There were no significant differences in VV (94.8 ± 43.7, 84.7 ± 48.8, p > 0.999), VFI (5.04 ± 2.49, 5.19 ± 3.15, p = 0.236), EF (51.9 ± 19.2, 47.2 ± 25.3, p = 0.903), and RVF (54.8 ± 22.3, 66.1 ± 29.8, p = 0.378). In the NIRS examinations, Type I was found in 20 limbs (64.5%) in the PVI and 3 (10%) in the PTS, and this was a statistically significant (p < 0.0001). On the contrary, Type III was seen in 1 limb (3.2%) in the PVI and 19 (63.3%) in the PTS. The proportion of Type III was significantly higher in the PTS (p < 0.0001).Conclusions:  These data suggest that reflux in the FV and POPV might play more important role in the development of venous leg ulcers in patients with PTS. The APG–derived parameters did not improve the discrimination power between the two groups. The increased NIRS–derived HHb in the exercising calf muscle is profound in patients with PTS, suggestive of a promising parameter both in the discrimination of the patients with chronic venous leg ulcers and in the follow–up of the patients with deep vein thrombosis.
Dressing Effects on Cellular Proliferation and Assessment of Fibroblast's Adherence in Vitro
Authors: Bernard FX , Barrault C 
Published: January 2005

Introduction:  The aim of this study was to compare the effects of Urgotul® and other greasy dressings and interfaces on normal human dermal fibroblasts (NHDF) monolayers in vitro. The selected end points were the cell proliferation, the morphology of the extracellular matrix (ECM) upon dressing removal, and the structure of the underlying fibroblasts.Materials and methods:  Equivalent pieces of each dressing were applied on NHDF monolayers for different times. Cell proliferation was measured via [3H] thymidine incorporation. Identical cultures were used to assess the dressing impact on the morphology of cells in culture after MTT staining and micro‐photographing. ECM morphology was shown by immunoflorescence, using an anticollagen I antibody. Effects on cell ultrastructure were documented by confocal laser microscopy after tubulin/actin double labelling.Results:  Among the five tested greasy dressings and interfaces, only Urgotul® showed a stimulating effect on the proliferation of NHDF. Two dressings did not modify proliferation and two other had cytostatic effects.In addition, the lesions of the ECM upon dressing removal were clearly the lowest with Urgotul®(low adherence to cellular surface and/or to extracellular matrix). The ultrastructure of the NHDF in direct contact with Urgotul® was not significantly modified.Conclusion:  Fibroblasts are the key cells of wound healing. The use of nonaggressive greasy gauzes and/or interfaces promoting cell proliferation should be of interest. Clinical evaluations are required to confirm these in vitro results.
T cell repertoire in patients with stable scleroderma
Authors: Tiev K P , Abriol J , Burland M C , Antonelli D , Klatzmann D , Cabane J , Boyer O 
Published: January 2005

Summary
At onset of systemic sclerosis (SSc), T cells have been found to oligoclonally expand in the skin, presumably in response to auto-antigens, but the T cell repertoire has not been evaluated at a later stage. To determine whether a perpetuating immune response contributes to the pathogenesis of stable SSc, the T cell repertoire was analysed in patients with diffuse (d) or limited (l) SSc, and compared to patients with primary Raynaud's phenomenon (RP) or healthy volunteers (Ctrl). The T cell repertoire (total, CD4 or CD8 sorted blood T cells) was analysed by qualitative and quantitative immunoscope (14 BV families analysed) in 11 untreated dSSc and 11 untreated lSSc, 10 RP and 11 Ctrl. To better detect in vivo activated cells, repertoire analysis was also performed on sorted CD4 T cells after in vitro culture with IL-2. In parallel, 6 skin biopsies from SSc patients were analysed. After 7–8 years of disease evolution, SSc patients did not show detectable clonal T cell expansions in the skin, even after tentative expansion from the biopsy with IL-2. Total T cell, sorted CD4 and CD8 T cell repertoires from the blood of patients with SSc did not show significant perturbation as compared to patients with RP and Ctrl. After IL-2 culture for 7 days, blood CD4 T cells from the patients did not preferentially expand as compared to RP and Ctrl. These findings suggest that antigen-driven immune responses may play a lesser role in established SSc than at disease onset.
Elevated macrophage migration inhibitory factor (MIF) levels in the urine of patients with focal glomerular sclerosis
Authors: Matsumoto K , Maruyama N , Maruyama T , Ohnishi Y , Nonaka S , Inoshita A , Ito K , Kitajima S , Abe M , Satomura A , Fujita T 
Published: January 2005

Summary
The pathogenesis of focal glomerular sclerosis (FGS) is poorly understood. Macrophage migration inhibitory factor (MIF) is a potent pro-inflammatory cytokine released from T cells and macrophages, and is a key molecule in inflammation. To examine further the possible role of MIF in FGS, we measured MIF levels in the urine. The purpose of the present study was to evaluate the involvement of MIF in FGS. Urine samples were obtained from 20 FGS patients. The disease controls included 40 patients with minimal-change nephrotic syndrome (MCNS) and membranous nephropathy (MN). A group of healthy subjects also served as controls. Biopsies were performed in all patients prior to entry to the study. The samples were assayed for MIF protein by a sandwich enzyme-linked immunosorbent assay (ELISA). The levels of MIF in the urine of FGS patients were significantly higher than those of the normal controls and patients with MCNS and MN. In contrast, the levels of urinary MIF (uMIF) in patients with MCNS and MN did not differ significantly from normal values. In the present study, attention also focused on the relationship between uMIF levels and pathological features. Among the patients with FGS, uMIF levels were significantly correlated with the grade of mesangial matrix increase and that of interstitial fibrosis. There was also a significant correlation between uMIF levels and the number of both intraglomerular and interstitial macrophages. Although the underlying mechanisms remain to be determined, our study presents evidence that urinary excretion of MIF is increased in FGS patients with active renal lesions.
A new mouse model of lung allergy induced by the spores ofAlternaria alternataandCladosporium herbarummolds
Authors: Havaux X , Zeine A , Dits A , Denis O 
Published: January 2005

SummaryAsthma is a serious health problem and during the last decade various experimental models of asthma have been developed to study the pathogenesis of this disease. In this study we describe a new mouse model of asthma that uses the spores of Alternaria alternata and Cladosporium herbarum, two allergenic molds recognized as common inducers of rhinitis and asthma in humans. Here we demonstrate that A. alternata and C. herbarum spores are immunogenic when injected into BALB/c mice, and induce the production of specific IgM and IgG1 antibodies and strongly increase IgE serum levels. To induce the allergic response, mice were sensitized by two intraperitoneal (i.p.) injections and then intranasaly (i.n.) challenged with A. alternata and C. herbarum spores. Bronchoalveolar lavages (BALs) from these mice contained numerous macrophages, neutrophils, eosinophils and lymphocytes whereas neutrophils were the predominant BAL inflammatory cells in nonsensitized mice. Histological studies demonstrated an influx of eosinophils in peri-vascular and peri-bronchial areas and the presence of numerous epithelial goblet cells only in sensitized mice. Increased expression of mRNA specific for various chemokines (eotaxin, MIP-1α, MIP-2) and chemokine receptors (CCR-1, CCR-2 and CCR-5) was observed in the lungs of nonsensitized mice challenged with the spores. Expression of CCR-3 mRNA in the lungs and Th2 cytokine  (IL-4,  IL-5  and  IL-13)  secretion  in  the  BAL  was  additionally observed in sensitized and challenged mice. Finally we demonstrate through whole-body plethysmography that mold spore sensitization and challenge induce the development of an airway hyperreactivity in response to nebulized methacholine.
Mycophenolate mofetil and roscovitine decrease cyclin expression and increase p27kip1 expression in anti Thy1 mesangial proliferative nephritis
Authors: Chiara M , Menegatti E , Di Simone D , Davit A , Bellis D , Sferch D , De Rosa G , Giachino O , Sena L M , Roccatello D 
Published: January 2005

SummaryThe response of mesangial cells to a phlogistic challenge includes cell proliferation and mesangial matrix expansion. Cell proliferation is a highly regulated process which includes enhancing factors such as cyclins, cyclin dependent kinases, and inhibitory proteins, such as p27kip1. The aim of the study was to evaluate the effects of Mycophenolate mofetil (MMF), and roscovitine (R), on the cell cycle regulatory system when administered in the florid phase of the experimental model of mesangial proliferative nephritis induced by the anti Thy-1 antigen monoclonal antibody. Three days after nephritis induction, different groups were given MMF and R. Rats treated with MMF or R showed a slight decrease in mesangial proliferation and matrix expansion. Samples of cortical tissue were tested by ‘real time’ RT-PCR in order to study gene expression of cyclins B, D1, D2, D3, E, and the cyclin inhibitor p27kip1. Localization of mRNA was evaluated by in situ hybridization. Real time RT-PCR analysis showed a significant decrease in cyclins B, D1, D2, and D3 in rats treated with either MMF or R as compared to controls. Both MMF and R treatment induced a significant increase in p27kip1 mRNA expression. In situ hybridization showed a mesangial-endothelial expression pattern in glomeruli. The number of labelled cells per glomerulus, the number of positive glomeruli in each examined slide as well as cyclin D2 and D3 signal intensity was significantly lower in rats treated with MMF or R as compared to controls, whereas MMF or R treatment up-regulated p27kip1 mRNA expression. Immunohistochemical evaluation of p27kip1 aimed to examine the influence of MMF or R on protein expression confirmed up-regulation.
Involvement of Th1 cells and heat shock protein 60 in the pathogenesis of intestinal Behçet's disease
Authors: Imamura Y , Kurokawa M S , Yoshikawa H , Nara K , Takada E , Masuda C , Tsukikawa S , Ozaki S , Matsuda T , Suzuki N 
Published: January 2005

SummaryInvolvement of excessive Th1 cell functions and heat shock protein expression in the pathogenesis of Behçet's disease (BD) has been reported. In this study we have characterized immune responses in intestinal lesions of BD. Peripheral blood lymphocytes (PBL) of BD and healthy controls (HC) and tissue specimens of intestinal Behçet's disease (intestinal BD), Crohn's disease (CD) and ulcerative colitis (UC) were analysed for mRNA and protein expression by reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemistry, respectively. PBL of BD patients expressed the Th1-related chemokine receptor, CCR5 and CXCR3 preferentially compared with those of healthy controls. Intestinal lesions of BD expressed interferon (IFN)-γ, tumour necrosis factor (TNF)-α and interleukin (IL)-12 mRNA, indicating Th1 skewed responses in vivo. mRNA of Txk, a Tec family tyrosine kinase specific to Th1 cells, was expressed in the lesions, suggesting its contribution to the Th1-dominant responses. In the intestinal samples, CCR5 was detected in all the cases with BD, whereas Th2-related CCR3 and CCR4 were detected randomly, mainly in the cases with inactive BD and those receiving large amounts of prednisolone, indicating the Th1-dominant immune responses in the intestinal lesions. As the ligands of CCR5, MIP1α and MIP1β were detected, whereas RANTES was not. Heat shock protein (HSP) 60 was expressed in PBL and intestinal tissues of BD. Th1-dominant immune responses and HSP60 expression may induce the inflammatory responses and thus be associated with the pathogenesis of intestinal BD.
Generation of Th1 T cell responses directed to a HLA Class II restricted epitope from theAspergillusf16 allergen
Authors: Ramadan G , Davies B , Kurup V P , Keever-Taylor C A 
Published: January 2005

SummaryThe Aspergillus allergen Asp f16 has been shown to confer protective Th1 T cell-mediated immunity against infection with Aspergillus conidia in murine models. Here, we use overlapping (11-aa overlap with preceding peptide) pentadecapeptides spanning the entire 427-aa coding region of Asp f16 presented on autologous dendritic cells (DC) to evaluate the ability of this antigen to induce Th1 responses in humans. Proliferative responses were induced in five out of five donors, and one line with a high frequency of interferon (IFN)-γ-producing CD4+ T cells in response to the complete peptide pool was characterized. This line was cytotoxic to autologous pool-pulsed and Aspergillus culture extract-pulsed targets. Limitation of cytotoxicity to the CD4+ T cell subset was demonstrated by co-expression of the degranulation marker CD107a in response to peptide pool-pulsed targets. Cytotoxic T lymphocytes (CTL) killed Aspergillus hyphae and CTL culture supernatant killed Aspergillus conidia. By screening 21 smaller pools and individual peptides shared by positive pools we identified a single candidate sequence of TWSIDGAVVRT that elicited responses equal to the complete pool. The defined epitope was presented by human leucocyte antigen (HLA)-DRB1-0301. These data identify the first known Aspergillus-specific T cell epitope and support the use of Asp f16 in clinical immunotherapy protocols to prime protective immune responses to prevent or treat Aspergillus infection in immunocompromised patients.
The chemokine receptor CCR7 is expressed on epithelium of non-inflamed gastric mucosa, Helicobacter pylori gastritis, gastric carcinoma and its precursor lesions and up-regulated by H. pylori
Authors: Schmaußer B , Endrich S , Brändlein S , Schär J , Beier D , Müller-Hermelink H-K , Eck M 
Published: January 2005

Summary
CCR7 chemokine-receptor expression on tumour cells of gastric carcinoma has been associated with lymph-node metastasis and is thought to play an important role in metastasis. However, so far it is unknown whether CCR7 is newly up-regulated on gastric carcinoma or already expressed in non-neoplastic gastric epithelium. Therefore, epithelial CCR7 expression was investigated in the process of gastric carcinogenesis: non-inflamed mucosa –Helicobacter pylori gastritis – intestinal metaplasia/dysplasia – gastric carcinoma. CCR7 was expressed by gastric epithelium in non-inflamed gastric mucosa (n = 5), H. pylori gastritis (n = 17), intestinal metaplasia (n = 10), dysplasia (n = 3) and on tumour cells in 20 of 24 patients with gastric carcinoma (13/14 intestinal-type; 7/10 diffuse-type) as tested by immunohistochemistry. As CCR7 expression by gastric epithelium was significantly stronger in H. pylori gastritis than in non-infected mucosa, the influence of H. pylori on CCR7 receptor expression of gastric epithelial cells was investigated by fluorescence activated cell sorter analysis. H. pylori strains up-regulated the CCR7 chemokine-receptor in CCR7-positive cell lines. No difference in CCR7 up-regulation between cag+ and cag–H. pylori strains was found. Epithelial CCR7 up-regulation by H. pylori may alter the metastatic fate of gastric carcinoma. Additionally, CCR7 expression not only on gastric carcinoma, but also on non-neoplastic gastric epithelium, suggests a novel biological function.
Reasons for non‐treatment of hepatitis C in veterans in care
Authors: Butt A. A. , Wagener M. , Shakil A. O. , Ahmad J. 
Published: January 2005

Summary.  We prospectively studied 354 patients with hepatitis C virus (HCV) infection who were referred to a hepatology specialty clinic to find the reasons for non‐treatment of HCV. The median age was 48 years (range 27–77 years), 98.5% were male and 71% were white. Seventy per cent of the patients were not treated. The most common reasons for non‐treatment were non‐adherence to follow‐up visit (24%), normal liver enzymes (14%), concurrent medical problems (11%), alcohol and drug use (9%), psychiatric problems (7%), advanced liver disease (7%), referral for transplant evaluation (6.4%) and patient refusal, transfer of care to another facility and non‐detectable HCV RNA levels (5% each). The reason was not recorded for 5% of the patients and was treatment deferred in 2.4% while waiting for pegylated interferon approval. Non‐treatment was more likely in patients with less than 12 years of education and a history of incarceration. Patients who were lost to follow‐up and refused treatment were more likely to have current alcohol and drug use and a history of incarceration.
Conditions affecting hydrodynamics‐based gene delivery into mouse liver in vivo
Authors: Feng Deng‐Min , He Chen‐Xia , Miao Chao‐Yu , Lu Bin , Wu Wen‐Jun , Ding You‐Fa , Xue Jing‐Lun 
Published: January 2005

SUMMARY1. It has been demonstrated that the hydrodynamics‐based procedure has high efficiency to deliver foreign genes into the liver. The widespread use of this procedure in gene function studies and as a treatment option for liver and other organ diseases puts considerable importance on the investigation of various conditions that affect hydrodynamics‐based gene delivery into mouse liver in vivo.2. Various conditions, including the volume, speed and solution of the injection and the state, gender and strain of the animal were manipulated to evaluate their effect on the expression levels in mice of human factor IX (hFIX) 8 h after tail vein injection of the plasmid pCMV‐hFIX.3. It was found that an injection volume of 2–2.5 mL and an injection speed of 5–7 s were very effective in delivering DNA into the mouse liver. Using Ringer's solution as an injection fluid increased the efficiency of hFIX expression.4. Anaesthetized mice expressed higher hFIX than conscious mice. Males expressed higher hFIX than females. The ICR mouse strain demonstrated higher expression of the foreign gene than did the C57 strain.5. The effects of these specific factors on hFIX expression may be caused by variations in hydrostatic pressure, the degree of liver damage and liver size.6. It can be concluded that there are optimal conditions for hFIX expression in the liver. This information may be helpful for the application of hydrodynamics‐based procedures in the investigation of gene expression and gene therapy.
Anti‐infarct effect of magnesium is not mediated by adenosine A1 receptors in rat globally ischaemic isolated hearts
Authors: Ebrahimi S , Faghihi M , Keshavarz M , Kadkhodaee M , Mirershadi F , Asadi B 
Published: January 2005

SUMMARY1. The aim of present study was to investigate the effects of magnesium (Mg) on cardiac function and infarct size and to compare it effects with those of adenosine. The mechanism of Mg‐mediated cardioprotection was explored by combined use of Mg and a selective adenosine A1 receptor antagonist.2. Rat isolated hearts were used for Langendorff perfusion. Hearts were either non‐preconditioned or preconditioned with Mg (6 mmol/L) or adenosine (1 mmol/L) before 30 min sustained ischaemia followed by 120 min reperfusion. Within each of these protocols, hearts were divided into two groups; one group was exposed to the A1 receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX; 200 nmol/L). Infarct size was measured by the triphenyltetrazolium chloride method. Left ventricular function was assessed by left ventricular developed pressure (LVDP), the product of heart rate × LVDP and coronary flow (CF).3. The administration of Mg had an anti‐infarct effect independent of its effect on postischaemic functional recovery in rats. Both Mg and adenosine equipotently reduced infarct size, but this effect of Mg was not blocked by the simultaneous administration of DPCPX. Cardiac function was improved by both adenosine and Mg and blockade of adenosine A1 receptors attenuated these effects for both agents.4. In conclusion, the results of the present study indicate that stimulation of adenosine A1 receptors is not responsible for the anti‐infarct effect of Mg in ischaemic myocardium in rats, but that the Mg‐mediated protection of postischaemic functional recovery in rats is mediated by these receptors.
Splenogonadal fusion: Report of a case and review of the literature
Authors: ALIVIZATOS GERASIMOS , SKOLARIKOS ANDREAS , SOPILIDIS ODYSSEAS , FERAKIS NIKOLAOS , CHORTI MARIA 
Published: January 2005

Abstract We report a case of splenogonadal fusion masquerading as a testicular tumor and review the etiology, the pathogenesis and the management of this rare disease.A 20‐year‐old male patient presented with clinical and radiological findings of a left testicular mass for which he underwent a left radical inguinal orchidectomy. Histopathology of the removed testicle revealed no tumor. The gonad was fused to ectopic splenic tissue, the later forming a distinct encapsulated mass attached to the lower pole of the testicle inside the tunica vaginalis.Splenogonadal fusion, although a rare condition, may account for a non‐malignant testicular mass and should be suspected in young patients with other congenital anomalies.