bluuebunny/crossref_metadata_2025_split huggingface dataset:
Islet transplant – a secure future for cellular replacement therapy in diabetes
Authors: Shapiro AMJ , Lakey JRT 
Published: July 2003

AbstractOutcomes in clinical islet transplantation have recently been transformed, following the introduction of steroid‐free, sirolimus based immunosuppression and the development of more refined methods for islet isolation from the donor pancreas. With the ‘Edmonton Protocol’, currently 85% of patients (28 completed transplants) remain free of insulin at the one year time‐point, and three in four patients remain free beyond three years. Variants of this protocol have now been successfully replicated in over 150 patients worldwide. Complete normalisation of glycated haemoglobin suggests that this therapy is likely to prevent, stabilise and possibly reverse early complications of diabetes. Progress with single donor islet transplant will allow many more patients with type 1 diabetes to be treated, but will fail to meet the enormous demand for this type of therapy.Development of safer, low‐dose anti‐rejection therapies with very low risk of cancer or infectious complications is likely to further broaden the indications for islet transplant therapy in diabetes. If tolerance (or near‐tolerance) could be safely induced, protecting against both autoimmune and alloimmune rejection, then islet transplantation could possibly be applied in children, possibly allowing the use of laparoscopic live donor distal pancreatectomy to expand the available donor source. Recent progress both in stem cell biology and in xenotransplantation suggests that ultimately a limitless source of insulin secreting tissues will be found. The light at the end of the tunnel for patients with type 1 diabetes just got brighter. Copyright © 2003 John Wiley & Sons, Ltd.
Advances in islet transplantation and the UK islet transplant consortium
Authors: Paget MB , Downing R 
Published: July 2003

AbstractIslet transplantation has surpassed whole pancreas transplantation as a cure for diabetes mellitus since the success of the Edmonton group. It is a safer procedure and requires minimal surgical intervention, yet offers excellent results in terms of achieving insulin independence. It also offers a more physiological insulin profile than current insulin replacement therapy. The UK Islet Transplant Consortium, founded by Diabetes UK, is in the process of establishing a programme of clinical islet transplantation in the UK.The immunosuppression required to protect islet grafts remains a threat to the long‐term health of transplant recipients and research into the possibility of circumventing the need for immunosuppression continues. The main areas under investigation include immunoisolation of islet grafts, HLA class II mismatching between donor and recipient, destruction of immune‐reactive dendritic cells in culture, in vitro pre‐treatment of islets to reduce their immunogenicity and genetic modification of islets to produce localised immunosuppression and prevent the release of MHC molecules.Because of the shortage of donors, researchers are looking toward alternative sources of glucose‐responsive insulin‐secreting tissue. Xenotransplantation would offer an attractive solution if the risk of transferring animal endogenous retroviruses can be eliminated. The expansion of mature beta‐cells, beta‐cell progenitors in pancreatic ducts or embryonic stem cells into viable tissue for transplant is also being researched in the hope of finding a solution for the tissue shortage issue. Encouraging advances have been made in many of these areas, creating a sense of anticipation and excitement for the future. Copyright © 2003 John Wiley & Sons, Ltd.
The low carbohydrate diet—personal experience in type 2 diabetes
Authors: Arnold Michael 
Published: July 2003

AbstractFollowing the low‐carbohydrate diet, defined by Drs Berstein, Eades and Atkins, I have lost 23% of my body weight and my blood sugar, total cholesterol and HbA1chave all fallen. I have also been able to taper off my diabetes medication. This article summarises my experience with this dietary approach. Copyright © 2003 John Wiley & Sons, Ltd.
The low carbohydrate/low insulin regimen – personal experience in type 1 diabetes
Authors: Raab Ron 
Published: July 2003

AbstractIn this article, I describe my before and after experience in adopting a low carbohydrate/low insulin/moderate protein/appropriate fat approach to the management of my type 1 diabetes. The Diabetes Centre in New York specialises in this approach and this article is based on what I learnt there and have applied since June 1998. I outline the rationale for and advantages of this approach and the contradictions inherent in the high carbohydrate/high insulin approach. These are my personal views and do not represent the position of organisations with which I work. Copyright © 2003 Ron Raab.
Carbohydrate intake in diabetes: how much is optimal?
Authors: Troughton Jacqui 
Published: July 2003

AbstractNutritional advice that has little or no supporting evidence is still being given to people with diabetes. Advice pertaining to carbohydrate can be misleading. People with diabetes need evidence‐based information about carbohydrates and to be given the knowledge and skills necessary to adjust their lifestyle, medication and/or insulin around the choices they wish to make. Copyright © 2003 John Wiley & Sons, Ltd.
Parallel clinical course of diabetes in a husband and wife with type 2 diabetes
Authors: Chowdhury TA , Lasker SS 
Published: July 2003

AbstractA 50‐year‐old South Asian man was diagnosed with type 2 diabetes on a routine test. He found his wife to have diabetes shortly afterwards. Baseline clinical findings at diagnosis were similar in the husband and wife. Over the course of the next seven years, there was a remarkable similarity in the clinical course of the spouses' glycaemic control, blood pressure control, weight and, most recently, the onset of microvascular complications. This is the first report of such marked similarity in the clinical course of diabetes in spouses, and suggests that environmental factors may be important in the progression of type 2 diabetes. Copyright © 2003 John Wiley & Sons, Ltd.
Thermal and electrical effects caused by outdoor hot‐spot testing in associations of photovoltaic cells
Authors: García M. C. Alonso , Herrmann W. , Böhmer W. , Proisy B. 
Published: July 2003

AbstractAn outdoor test facility has been prepared for the evaluation of the thermal and electrical effects caused by outdoor hot‐spot testing in crystalline silicon modules. Five module types have been subjected to an outdoor test programme with the purpose of analysing their hot‐spot endurance. The worst‐case cell in each module type has been detected by laboratory characterisation under reverse‐bias operation of all the individual cells included in the module. These cells, encapsulated within the module, have been operated at different shading fractions with bypass diodes around 18 or 24 cells. A data acquisition system has monitored temperatures and current flows during the day, completing the tests via infrared characterisation during the hours of maximum irradiance. The influence of the type of module, the number of cells per bypass diode, the position and amount of shading and the leakage current of the cell is presented. This information is useful for cell and module manufacturers and system installers who must select the necessary protection criteria to guarantee long lifetimes for PV systems; it also helps to clarify hot‐spot testing procedures in international standards. Copyright © 2003 John Wiley & Sons, Ltd.
Local series resistance mapping of silicon solar cells by microwave photoconductivity decay measurements
Authors: Ballif C. , Peters S. , Borchert D. 
Published: July 2003

AbstractWe present a new non‐destructive mapping technique which yields information on the local series resistance in Si solar cells. The technique is based on microwave photoconductivity decay measurements performed on reverse‐biased Si solar cells. For reverse‐biased devices, the initial decay time measured after a high‐intensity laser pulse is shown to be directly proportional to the local series resistances between the excited area and the cell metallisation. We illustrate how high contact resistance between the fingers and the emitter, resistive back‐surface contacts or finger interruptions lead to an increase of the microwave detected decay time. Copyright © 2003 John Wiley & Sons, Ltd.
Cu(In,Ga)Se2thin films grown with a Cu‐poor/rich/poor sequence: growth model and structural considerations
Authors: Kessler J. , Chityuttakan C. , Lu J. , Schöldström J. , Stolt L. 
Published: July 2003

AbstractThin films of Cu(In,Ga)Se2are grown by a co‐evaporation process in which the In, Ga, and Se fluxes, as well as the substrate temperature, are constant and the only variable is the Cu flux. This Cu flux varies in three steps in such a way that the growing film evolves from Cu‐poor to Cu‐rich and then back to Cu‐poor. The film growth is monitored by the ‘end point detection’ method, and film thicknesses of the order of 2 μm are deposited in less than 20 min. Quality devices (efficiencies above 15%) are produced in our baseline processes for all of the other synthesis steps. The Cu(In,Ga)Se2layers are studied from a (112) versus (220) (204) orientation and recrystallization point of view. Including the results from a previous study on the influence of the substrate temperature to the present X‐ray diffraction and scanning as well as tunneling electron microscopy data, a five‐stage growth model for the films is described. The specific features of these films are that they are weakly (220) (204) oriented and exhibit crevices in their top fractions. The growth model hypothesizes about the origins of these crevices and on how to avoid them. Copyright © 2003 John Wiley & Sons, Ltd.
General temperature dependence of solar cell performance and implications for device modelling
Authors: Green Martin A. 
Published: July 2003

AbstractSolar cell performance generally decreases with increasing temperature, fundamentally owing to increased internal carrier recombination rates, caused by increased carrier concentrations. The temperature dependence of a general solar cell is investigated on the basis of internal device physics, producing general results for the temperature dependence of open‐circuit voltage and short‐circuit current, as well as recommendations for generic modelling. Copyright © 2003 John Wiley & Sons, Ltd.
Record efficiencies for EFG and string ribbon solar cells
Authors: Hahn G. , Geiger P. 
Published: July 2003

AbstractSolar cells have been processed on Edge‐defined Film‐fed Growth and String Ribbon silicon. Based on a standard process developed for different types of multicrystalline materials including evaporation of contacts and photolithography for front‐contact formation, optimisations have been implemented to deal with the special needs of these low‐cost ribbon materials. Especially a remote plasma hydrogenation step and a change from evaporated to screen‐printed aluminium back‐surface‐field improved cell parameters drastically. Independently confirmed stable efficiencies of 16.7% (EFG) and 17.7% (String Ribbon) have been achieved on 4 cm2cells (full area). These values represent the highest stable efficiencies obtained for multicrystalline silicon ribbons so far. Copyright © 2003 John Wiley & Sons, Ltd.
Solar cell efficiency tables (version 22)
Authors: Green Martin A. , Emery Keith , King David L. , Igari Sanekazu , Warta Wilhelm 
Published: July 2003

AbstractConsolidated tables showing an extensive listing of the highest independently confirmed efficiencies for solar cells and modules are presented. Guidelines for inclusion of results into these tables are outlined and new entries since January 2003 are reviewed. Copyright © 2003 John Wiley & Sons, Ltd.
Familial aggregation of prostate cancer in African‐Americans and white Americans
Authors: Cunningham Glenn R. , Ashton Carol M. , Annegers John F. , Souchek Julianne , Klima Marcella , Miles Brian 
Published: July 2003

AbstractBACKGROUNDWe compared the incidence of prostate cancer in first‐degree family members of African‐Americans with that in white Americans.METHODSA historical cohort design was used to enroll 330 incident cases <80 years of age that were diagnosed at the Houston VA Medical Center between June 9, 1993 and June 8, 1996. We compared incidence rates in the probands' families with the incidence rates found in contemporaneous data from the national and regional Surveillance, Epidemiology, and End‐Results (SEER) program.RESULTSThree‐hundred five probands (41% African‐American) had evaluable first‐degree relatives (394 African‐American, 527 non‐African‐American). The standardized incidence ratio was 1.61 overall (95% confidence interval (CI): 1.22–2.13) and did not differ between African‐American and non‐African‐American families: 1.58 (1.05–2.29) and 1.65 (1.06–2.45) in African‐Americans and non‐African‐Americans, respectively.CONCLUSIONSThe similar level of familial aggregation is evidence that the higher incidence of prostate cancer in African‐Americans is not attributable to a higher prevalence of germline mutations predisposing to the disease. Prostate 56: 256–262, 2003. © 2003 Wiley‐Liss, Inc.
Quantitative PSA RT‐PCR for preoperative staging of prostate cancer
Authors: Kurek Ralf , Ylikoski Alice , Renneberg Heiner , Konrad Lutz , Aumüller Gerd , Roddiger Sandra J. , Zamboglou Nikolaos , Tunn Ulf W. , Lilja Hans 
Published: July 2003

AbstractBACKGROUNDThe clinical value of detecting prostate specific antigen (PSA) mRNA in the peripheral blood mononuclear cell fraction of patients (pts) by standard RT‐PCR assays with localized prostate cancer remains controversial. We used a quantitative RT‐PCR assay to measure the PSA mRNA copy number in addition to the qualitative PSA RT‐PCR and correlated the results with clinical parameters.METHODSTotal RNA was extracted from the peripheral blood mononuclear cell fraction of 115 prostate cancer pts prior to radical retropubic prostatectomy (RP) who received 3 months of neoadjuvant androgen deprivation. For quantitative RT‐PCR, a PSA‐like internal standard (IS) was added to each sample prior to reverse transcription and the PCR products for PSA and IS were selectively detected with fluorescent europium chelates after hybridization. Corresponding qualitative PSA–RT‐PCR was performed for all samples.RESULTSThe median PSA copy number was 126 (range: 0–37988). There were no significant correlations established between qualitative or quantitative RT‐PCR results and given clinical parameters. Corresponding quantitative and qualitative RT‐PCR results were significantly associated (P = 0.01).CONCLUSIONSWe were unable to show any additional value of quantitative as well as qualitative PSA RT‐PCR for preoperative staging of prostate cancer so far. Nevertheless, the long‐term follow up of the patients has to be awaited. Prostate 56: 263–269, 2003. © 2003 Wiley‐Liss, Inc.
Mitogen‐activated protein kinase pathway is involved in androgen‐independent PSA gene expression in LNCaP cells
Authors: Franco Omar E. , Onishi Takehisa , Yamakawa Kensuke , Arima Kiminobu , Yanagawa Makoto , Sugimura Yoshiki , Kawamura Juichi 
Published: July 2003

AbstractBACKGROUNDProstate specific antigen (PSA) is regulated by growth factors and hormones through functional androgen responsive elements in the promoter region of the PSA gene. However, the molecular basis for androgen independent PSA elevation in hormone refractory prostate cancer is unknown. The purpose of this study was to investigate the role of MAP kinase activation in androgen independent regulation of PSA expression.METHODSLNCaP cells transfected with MEK1 expression vector with or without the MAP kinase inhibitor U0126 under low androgen conditions were analyzed by luciferase assay and electrophoretic mobility shift assay (EMSA).RESULTSTransfection experiments of the proximal PSA promoter linked to Luc‐reporter identified one region designated as “B” motif centered at −60 bp to be essential for basal activation. Co‐transfection with the MEK1 activated vector enhanced PSA expression, while mutation of the “B” motif totally abrogated this induction. EMSA showed a specific DNA–protein complex, but Sp1 family members and AR do not interact with the “B” region by supershift analysis.CONCLUSIONSOur data suggest that enhanced androgen‐independent PSA gene expression in MAP kinase‐induced LNCaP cells is mediated, at least in part, by the “B” motif of the PSA promoter. Prostate 56: 319–325, 2003. © 2003 Wiley‐Liss, Inc.
Human prostate cancer cells and xenografts are targeted and destroyed through luteinizing hormone releasing hormone receptors
Authors: Leuschner Carola , Enright Frederick M. , Gawronska–Kozak Barbara , Hansel William 
Published: July 2003

AbstractBACKGROUNDA conjugate of a lytic peptide, hecate, and a 15‐amino acid segment of the β‐chain of chorionic gonadotropin (CG) destroyed human prostate xenografts in nude mice by targeting LH receptors. Since these xenografts also express LHRH receptors, we prepared a LHRH–hecate conjugate and tested its ability to destroy PC‐3 cells in vitro and in vivo.MATERIALS AND METHODSLHRH–hecate was added to cultures of PC‐3, BRF 41 T, DU145, and LNCaP cells in the presence and absence of steroids. PC‐3 xenografts were established in nude male mice, which were treated with LHRH–hecate.RESULTSInjections of LHRH–hecate resulted in tumor growth arrest and marked reduction of tumor burden (62.2 mg/g body weight in saline controls vs. 10.5 mg/g body weight in treated mice;P < 0.0001); unconjugated LHRH and hecate had no effect on tumor burden and tumor viability (48.5 mg/g body weight in LHRH treated animals vs. 63.2 mg/g body weight in hecate treated mice). Marked tumor necrosis occurred in conjugate treated mice. Removal of steroids from the culture media decreased the sensitivity of LNCaP and PC‐3 cells to the LHRH–hecate; adding estrogen restored the sensitivity.CONCLUSIONSLHRH–hecate may be effective in treating hormone dependent and independent prostate cancers. Prostate 56: 239–249, 2003. © 2003 Wiley‐Liss, Inc.
Elevated serum progastrin‐releasing peptide (31–98) level is a predictor of short response duration after hormonal therapy in metastatic prostate cancer
Authors: Yashi Masahiro , Nukui Akinori , Kurokawa Shinsuke , Ochi Masanori , Ishikawa Shinya , Goto Kentaro , Kobayashi Yutaka , Muraishi Osamu , Tokue Akihiko 
Published: July 2003

AbstractBACKGROUNDThe neuroendocrine (NE) pathway has been attracting attention as a mechanism for the androgen‐independent progression because the neuropeptide provokes tumor growth and inhibits apoptosis under androgen‐deprived milieu in prostate cancer cells. On the basis that serum progastrin‐releasing peptide (ProGRP) is elevated in patients with advanced disease stage, we examined the prognostic value of the neuropeptide.METHODSSerum ProGRP status was determined with an enzyme‐linked immunosorbent assay (ELISA) in 460 men with benign and malignant prostatic diseases, chronic renal failure, and healthy controls. Seventy patients with metastatic prostate cancer including four patients (5.7%) with NE carcinoma who underwent hormonal therapy were enrolled in the prognostic analyses by Cox proportional hazards model.RESULTSThe serum status steadily shifted toward predominant expression of ProGRP with the progression of prostate cancer into metastatic and androgen‐independent stages. Univariate analysis revealed that the deteriorated performance status (PS) and extent of bony disease (EOD), and high serum alkaline phosphatase (ALP), serum ProGRP, and nadir prostate‐specific antigen (PSA) levels were associated with a lower progression‐free survival (PFS) rate (P < 0.005). Multivariate analysis demonstrated that PS, serum ProGRP, and nadir PSA held an independent predictive value for PFS (P < 0.05), and all correlated with bone‐related factors. Serum ProGRP was the most significant predictor among pre‐treatment factors in this model (P = 0.0094).CONCLUSIONSThe neuropeptide precursor ProGRP is a distinct serum marker that is useful to know the NE milieu and provides prognostic information in patients with advanced prostate cancer. Standard therapy for metastatic prostate cancer may make progress when further studies will clarify the causative link between serum ProGRP level and androgen‐independent disease progression. Prostate 56: 305–312, 2003. © 2003 Wiley‐Liss, Inc.
Stable expression of full length human androgen receptor in PC‐3 prostate cancer cells enhances sensitivity to retinoic acid but not to 1α,25‐dihydroxyvitamin D3
Authors: Murthy Shalini , Marcelli Marco , Weigel Nancy L. 
Published: July 2003

AbstractBACKGROUNDPC‐3 prostate cancer cell growth is inhibited by 1α,25‐dihydroxyvitamin D3 (1,25 D) and retinoids, but not to the same extent as the androgen receptor (AR) positive LNCaP prostate cancer cells. Previous reports suggest a role for AR in growth inhibition of LNCaP cells by 1,25 D and retinoids. PC‐3 cells do not express AR. We therefore asked whether re‐expression of AR would enhance the response of PC‐3 cells to 1,25 D and retinoids.METHODSPC‐3 cells were stably transfected with wild type human AR cDNA. Pooled cells expressing AR protein at levels comparable to LNCaP cells were used to analyze response to 1,25 D, retinoids, androgens, and anti‐androgens.RESULTSAR re‐expression in PC‐3 cells restored response to androgens and anti‐androgens, but growth inhibition by 1,25 D was not significantly altered. However, cells were sensitized to low levels of retinoids, and, in contrast to the parental PC‐3 cells, sub‐optimal levels of 1,25 D and retinoids caused additive growth inhibition.CONCLUSIONSRestoring AR expression and activity in PC‐3 cells results in enhanced sensitivity to low levels of retinoids while the response to 1,25 D remains unaltered. Thus, the involvement of AR in prostate cancer growth inhibition by 1,25 D appears to be cell line specific. Prostate 56: 293–304, 2003. © 2003 Wiley‐Liss, Inc.