bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modified scar grade
Authors: Maeshima Akiko M. , Niki Toshiro , Maeshima Arafumi , Yamada Tesshi , Kondo Haruhiko , Matsuno Yoshihiro 
Published: December 2002

AbstractBACKGROUNDSeveral studies have shown the prognostic value of desmoplasia for lung adenocarcinomas. The authors evaluated the density and extent of desmoplasia by modifying the scar grade, as well as the prognostic impact on patient survival.METHODSModified scar grade was defined as follows: Grade 1, no desmoplasia; Grade 2, sparse desmoplastic reaction; Grade 3, dense desmoplastic reaction with diameter of 10 mm or less; Grade 4, dense desmoplastic reaction with diameter exceeding 10 mm. In addition, the prognostic impact of conventional histologic factors and modified scar grade was analyzed in 239 cases of small peripheral lung adenocarcinoma (maximum dimension, ≤ 30 mm) for which long‐term follow‐up data were available.RESULTSThe 5 and 10‐year survival rates according to the modified scar grade were 100% and 100% for Grade 1 lung adenocarcinoma (n = 29); 91.7% and 83.7% for Grade 2 (n = 61); 67.6% and 52.7% for Grade 3 (n = 78); and 50.0% and 37.5% for Grade 4 (n = 71), respectively. A significant difference in patient survival was found between Grade 1 or 2 versus Grade 3 or 4 (P < 0.0001, by log rank test). Multivariate analysis showed that modified scar grade was an independent prognostic factor (P = 0.0176), as were pathologic stage (P = 0.0293), lymph node metastasis (P = 0.0191), lymphatic permeation (P = 0.0022), and pleural involvement (P = 0.0452). Modified scar grade also had a significant impact on survival in various subsets of patients, including those with pathologic Stage IA disease, patients with tumors of diameter 20 mm or less, or patients with mixed subtype tumors with a bronchioloalveolar component.CONCLUSIONSModified scar grade is a useful prognostic factor in patients with small lung adenocarcinomas. Tumors with a sparse fibroblastic reaction (modified scar Grade 2) may represent early invasive cancers or invasive cancers with low malignant potential, which should be distinguished from frankly invasive cancers (modified scar Grade 3 or 4). Cancer 2002;95:2546–54. © 2002 American Cancer Society.DOI 10.1002/cncr.11006
p53 codon 72 polymorphism (C/G) and the risk of human papillomavirus‐associated carcinomas in China
Authors: Li Tao , Lu Zhe‐Ming , Guo Mei , Wu Qin‐Jiao , Chen Ke‐Neng , Xing Hai‐Ping , Mei Qiang , Ke Yang 
Published: December 2002

AbstractBACKGROUNDHuman papillomavirus (HPV) plays an important role in the development of carcinomas at various body sites. It was found previously that the p53 codon 72 polymorphism (C/G) is a high‐risk factor for the development HPV‐associated cervical carcinoma. However, it still was considered controversial in several studies of cervical and esophageal carcinoma.METHODSIn the current study, the authors used an allele specific polymerase chain reaction (PCR) method to analyze correlation between the p53 codon 72 (C/G) polymorphism and HPV‐associated, noncancerous esophageal epithelium as well as esophageal, ovarian, and breast carcinoma in the Chinese population. Esophageal balloon cytology examination samples were obtained from high‐incidence and low‐incidence populations for esophageal carcinoma in Anyang (Henan Province).RESULTSThirty‐six of 48 esophageal balloon samples from the high‐incidence population were HPV positive, and 13 of 33 esophageal balloon samples from the low‐incidence population were HPV positive. Thirty‐nine of 62 esophageal carcinoma samples from Anyang Tumor Hospital were HPV positive. Twenty‐six of 39 ovarian carcinoma samples from the Second Affiliated Hospital of Inner Mongolia Medical College were HPV positive. Nineteen of 82 breast carcinoma samples from Beijing Cancer Hospital were HPV positive. It is noteworthy that the distribution of the p53 codon 72 Arg homozygous genotype in HPV positive samples of esophageal epithelium, ovarian carcinoma, and breast carcinoma was significantly higher compared with HPV negative tumor samples. (P < 0.05).CONCLUSIONSThe current results suggest that the p53 codon 72 Arg homozygous genotype is one of the high‐risk genetic factors for HPV‐associated malignancies among the Chinese population. Cancer 2002;95:2571–6. © 2002 American Cancer Society.DOI 10.1002/cncr.11008
A multicenter Phase II study of the intravenous administration of liposomal tretinoin in patients with acquired immunodeficiency syndrome‐associated Kaposi's sarcoma
Authors: Bernstein Zale P. , Chanan‐Khan Asher , Miller Kena C. , Northfelt Donald W. , Lopez‐Berestein Gabriel , Gill Parkash S. 
Published: December 2002

AbstractBACKGROUNDA multicenter trial was conducted to determine the efficacy and toxicity of escalating dosages of liposomal tretinoin (all‐trans‐retinoic acid) administered once or three times weekly in patients with acquired immunodeficiency syndrome (AIDS)‐associated Kaposi sarcoma.METHODSSeventy‐six patients with acquired immunodeficiency syndrome (AIDS)‐associated Kaposi sarcoma were randomized to receive the study drug either once (n = 30) or 3 times weekly (n = 46). The starting dosage was 60 mg/m2, which was escalated to 90 mg/m2 and then 120 mg/m2 if the drug was well tolerated (≤ Grade 2 toxicities [according to the Southwest Oncology Group toxicity scale]). Four weeks of therapy constituted 1 cycle; patients could receive up to 8 cycles and those who completed 8 cycles were given the option of receiving extended therapy. Clinical response was defined as complete response (CR), partial response (PR), or stable disease (SD).RESULTSEfficacy was assessed after the completion of 3 treatment cycles; 28.9% of patients (22 of 76 patients) responded (no CRs, 1 PR, and 21 SDs). Among the patients receiving treatment 3 times weekly, 16 of 49 patients (32.7%) achieved a clinical response at the end of the third treatment cycle (no CRs, 1 PR, and 15 SDs). Concomitant or prior use of protease inhibitors did not appear to affect the patient's response to treatment (P = 0.183).CONCLUSIONSLiposomal tretinoin is a new therapeutic agent that has been reported to have some clinical activity in patients with AIDS‐associated Kaposi sarcoma. A three‐times‐per‐week dosing schedule was noted to be more effective compared with a once‐a‐week schedule without any significant difference in toxicity reported. Cancer 2002;95:2555–61. © 2002 American Cancer Society.DOI 10.1002/cncr.11009
Study of transport properties co – evaporated lead telluride (PbTe) thin films
Authors: Khairnar U.P. , Pawar P.H. , Bhavsar G.P. 
Published: December 2002

AbstractThin films of lead telluride (PbTe) of thicknesses ranging from 1000 Å to 2500 Å have been prepared by co‐evaporation (three temperature) technique, onto precleaned amorphous glass substrates at various temperatures. The deposited samples were annealed and annealed samples were used for characterization. Resistivity of these samples was measured by four‐probe technique as a function of thickness and temperature. Activation energy for charge transport have been evaluated and found in the range of 0.09 to 0.106 eV. Thermoelectric power has been measured and found to be positive indicating that the samples are p‐type semiconducting material. Mobility variation with temperature has been estimated (evaluated) and correlated with scattering mechanism in the entire range of temperature studied. The X‐ray diffraction analysis confirmed that films are polycrystalline having cubic structure cell and lattice parameters are reported.
Effects of nateglinide and glibenclamide on postprandial lipid and glucose metabolism in type 2 diabetes
Authors: Vakkilainen Juha , Mero Niina , Schweizer Anja , Foley James E. , Taskinen Marja‐Riitta 
Published: December 2002

AbstractBackgroundPostprandial hyperlipemia and small, dense LDL particles are features of dyslipidemia in type 2 diabetes. The purpose of this study was (1) to determine whether the oral insulinotropic drugs, nateglinide and glibenclamide, can overcome the defect of insulin action to suppress the hepatic VLDL release after a meal and decrease the postprandial lipemia and (2) to evaluate the acute effect of postprandial hypertriglyceridemia on LDL particle size in subjects with type 2 diabetes.MethodsForty‐three subjects with type 2 diabetes and mean baseline HbA1c 7.6% (95% CI 7.3 to 7.9) were treated with nateglinide 120 mg three times daily or glibenclamide 5 mg once or twice daily for 12 weeks in a double‐blind randomised trial. Insulin, glucose, and lipoprotein responses to a mixed fat‐rich meal were determined for 8 h postprandially at baseline and at 12 weeks on‐trial.ResultsNateglinide and glibenclamide significantly augmented the maximal response in serum insulin at 60 min postprandially compared with the response without the drug [additional increase 25.0 mU/l (95% CI 11.2–38.8) p = 0.001 and 12.5 mU/l (95% CI 4.6–20.3) p = 0.003, respectively] and reduced hyperglycemia. Neither drug affected fasting or postprandial lipid or lipoprotein levels. LDL size did not significantly change in the 8‐h postprandial period.ConclusionsAlthough nateglinide and glibenclamide increase postprandial insulin secretion and attenuate hyperglycemia, they do not alleviate postprandial lipemia in subjects with type 2 diabetes and good glycemic control. Although small LDL particle size is associated with chronic hypertriglyceridemia, LDL size does not change during acute postprandial hypertriglyceridemia. Copyright © 2002 John Wiley & Sons, Ltd.
Normal renal function 8 to 13 years after Cyclosporin A therapy in 285 diabetic patients
Authors: Assan Roger , Blanchet Françoise , Feutren Gilles , Timsit José , Larger Etienne , Boitard Christian , Amiel Claude , Bach Jean‐François 
Published: December 2002

AbstractBackgroundCyclosporin A (CyA) may induce acute nephrotoxicity. The question has been raised of the possible long‐term unfavorable course of CyA‐induced lesions. Advantage was taken of a large cohort of diabetic patients treated for several months using moderate CyA dosage to evaluate the long‐term evolution of renal function in such patients.MethodsTwo hundred and eighty five recently diagnosed type 1 diabetic patients having received CyA for a mean of 19.9 months were monitored for 13 years, in parallel with 100 similar patients treated with insulin alone.ResultsIn the CyA‐treated group, a transient increase in creatininemia levels occurred during the first 18 months of treatment associated with a transient increase in renal vascular resistance. Both effects disappeared later on: creatininemia levels then remained normal. Inulin and p‐aminohippurate (PAH) clearances remained normal throughout follow‐up. Neither permanent renal failure nor progressive deterioration of renal function occurred in either group or in individual patients. A 10 to 12% increase in inulin and PAH clearance was elicited by IV amino acid infusion at 7 to 10 years, a finding consistent with a normal renal functional reserve. Patients with moderate kidney lesions on biopsy at 1 year had normal and stable clearance values at 7 to 13 years. The prevalence of arterial hypertension and retinopathy was lower in the CyA‐treated group than in the control group, possibly because of the tighter metabolic control obtained in the CyA group.ConclusionThese results suggest that low‐dose CyA treatment combined with thorough monitoring does not result in long‐term renal dysfunction. Copyright © 2002 John Wiley & Sons, Ltd.
Impaired glucose tolerance and insulinopenia in the GK‐rat causes peripheral neuropathy
Authors: Murakawa Yuichi , Zhang Weixian , Pierson Christopher R , Brismar Tom , Östenson Claes‐Göran , Efendic Suad , Sima Anders A. F. 
Published: December 2002

AbstractBackgroundRecent studies indicate that impaired glucose tolerance (IGT) in man is a causative factor in idiopathic sensory neuropathy, and that insulinopenia may contribute substantially to the severity of diabetic peripheral neuropathy. The effect of sustained IGT and progressive insulinopenia in the absence of overt hyperglycemia on peripheral nerve abnormalities was examined in the Goto–Kakizaki (GK)‐rat.MethodsTwo and eighteen‐month‐old GK rats with decreased glucose tolerance and overt insulinopenia, respectively, were examined with respect to nerve function, structure, morphometry and molecular integrity, and were compared to age‐matched control rats.ResultsBoth 2‐(p < 0.001) and 18‐month‐old (p < 0.001) GK rats showed reduced body weight. Blood glucose levels following glucose tolerance tests were elevated in both the 2‐month and the 18‐month‐old GK rats. Fasting plasma insulin levels in the 2‐month GK rats were increased threefold (p < 0.05) but decreased by 71% (p < 0.001) in the 18‐month GK rats. The two‐month GK rats showed a normal nerve conduction velocity, whereas in the 18‐month GK rats it was reduced to 76% (p < 0.001) of control values. No morphometric abnormalities were found in the 2‐month GK rats, whereas the 18‐month GK rats showed loss of small myelinated fibers (p < 0.001), atrophy and loss of unmyelinated axons (p < 0.05) and an increased (p < 0.01) frequency of regenerating fibers. In the older GK rats, both mRNA and protein expression of nerve growth factor (NGF) in the sciatic nerve were significantly reduced (p < 0.001 and p < 0.05), and NGFR TrkA (high affinity NGF receptor) and NGFRp75 (low affinity NGF‐receptor) protein expression was reduced in dorsal root ganglia (DRG) (both p < 0.05). These changes were accompanied by significantly reduced protein expressions of substance P (SP) and calcitonin gene–related protein (CGRP) in DRG's (both p < 0.001) as well as a 40% (p < 0.001) decrease in SP and a 62% (p < 0.001) decrease in CGRP‐positive DRG neurons. In the sciatic nerve, SP and CGRP protein expression was decreased by 71% (p < 0.01) and 79% (p < 0.01), respectively.ConclusionIGT combined with hyperinsulinemia for 2 months have no detectable effect on peripheral nerve function or structure. In contrast, IGT and subsequent insulinopenia result in a functional and structural neuropathy associated with impaired NGF support and neuropeptide synthesis. We suggest that these abnormalities are mainly due to insulinopenia rather than hyperglycemia. Copyright © 2002 John Wiley & Sons, Ltd.
Therapy of type 2 diabetes mellitus based on the actions of glucagon‐like peptide‐1
Authors: Holst Jens Juul 
Published: December 2002

AbstractGLP‐1 is a peptide hormone from the intestinal mucosa. It is secreted in response to meal ingestion and normally functions in the so‐called ileal brake, that is, inhibition of upper gastrointestinal motility and secretion when nutrients are present in the distal small intestine. It also induces satiety and promotes tissue deposition of ingested glucose by stimulating insulin secretion. Thus, it is an essential incretin hormone. In addition, the hormone has been demonstrated to promote insulin biosynthesis and insulin gene expression and to have trophic effects on the beta cells. The trophic effects include proliferation of existing beta cells, maturation of new cells from duct progenitor cells and inhibition of apoptosis. Furthermore, glucagon secretion is inhibited. Because of these effects, the hormone effectively improves metabolism in patients with type 2 diabetes mellitus. Thus, continuous subcutaneous administration of the peptide for six weeks in patients with rather advanced disease greatly improved glucose profiles and lowered body weight, haemoglobin A1C, and free fatty acids (FFA). In addition, insulin sensitivity doubled and insulin responses to glucose were greatly improved. There were no side effects. Continuous administration is necessary because of rapid degradation by the enzyme dipeptidyl peptidase‐IV. Alternative approaches include the use of analogues that are resistant to the actions of the enzyme, as well as inhibitors of the enzyme. Both approaches have shown remarkable efficacy in both experimental and clinical studies. The GLP‐1‐based therapy of type 2 diabetes, therefore, represents a new and attractive alternative. Copyright © 2002 John Wiley & Sons, Ltd.
Glucose‐stimulated signaling pathways in biphasic insulin secretion
Authors: Straub Susanne G. , Sharp Geoffrey W. G. 
Published: December 2002

AbstractGlucose‐stimulated biphasic insulin secretion involves at least two signaling pathways, the KATP channel‐dependent and KATP channel‐independent pathways, respectively. In the former, enhanced glucose metabolism increases the cellular adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio, closes KATP channels and depolarizes the cell. Activation of voltage‐dependent Ca2+ channels increases Ca2+ entry and [Ca2+]i and stimulates insulin release. The KATP channel‐independent pathways augment the response to increased [Ca2+]i by mechanisms that are currently unknown. However, they affect different pools of insulin‐containing granules in a highly coordinated manner. The β‐cell granule pools can be minimally described as reserve, morphologically docked, readily and immediately releasable. Activation of the KATP channel‐dependent pathway results in exocytosis of an immediately releasable pool that is responsible for the first phase of glucose‐stimulated insulin release. Following glucose metabolism, the rate‐limiting step for the first phase lies in the rate of signal transduction between sensing the rise in [Ca2+]i and exocytosis of the immediately releasable granules. The immediately releasable pool of granules can be enlarged by previous exposure to glucose (by time‐dependent potentiation, TDP), and by second messengers such as cyclic adenosine monophosphate (cyclic AMP) and diacylglycerol (DAG). The second phase of glucose‐stimulated insulin secretion is due mainly to the KATP channel‐independent pathways acting in synergy with the KATP channel‐dependent pathway. The rate‐limiting step here is the conversion of readily releasable granules to the state of immediate releasability, following which, in an activated cell they will undergo exocytosis. In the rat and human β‐cell the KATP channel‐independent pathways induce a time‐dependent increase in the rate of this step that results in the typical rising second‐phase response. In the mouse β‐cell the rate appears not to be changed much by glucose. Potential intermediates involved in controlling the rate‐limiting step include increases in cytosolic long‐chain acyl‐CoA levels, adenosine triphosphate (ATP) and guanosine triphosphate (GTP), DAG binding proteins, including some isoforms of protein kinase (PKC), and protein acyl transferases. Agonists that can change the rate‐limiting steps for both phases of insulin release include those like glucagon‐like peptide 1 (GLP‐1) that raise cyclic AMP levels and those like acetylcholine that act via DAG. Copyright © 2002 John Wiley & Sons, Ltd.
Glucose‐responsive insulin‐producing cells from stem cells
Authors: Kaczorowski David J. , Patterson Ethan S. , Jastromb William E. , Shamblott Michael J. 
Published: December 2002

AbstractRecent success with immunosuppression following islet cell transplantation offers hope that a cell transplantation treatment for type 1 (juvenile) diabetes may be possible if sufficient quantities of safe and effective cells can be produced. For the treatment of type 1 diabetes, the two therapeutically essential functions are the ability to monitor blood glucose levels and the production of corresponding and sufficient levels of mature insulin to maintain glycemic control. Stem cells can replicate themselves and produce cells that take on more specialized functions. If a source of stem cells capable of yielding glucose‐responsive insulin‐producing (GRIP) cells can be identified, then transplantation‐based treatment for type 1 diabetes may become widely available. Currently, stem cells from embryonic and adult sources are being investigated for their ability to proliferate and differentiate into cells with GRIP function. Human embryonic pluripotent stem cells, commonly referred to as embryonic stem (ES) cells and embryonic germ (EG) cells, have received significant attention owing to their broad capacity to differentiate and ability to proliferate well in culture. Their application to diabetes research is of particular promise, as it has been demonstrated that mouse ES cells are capable of producing cells able to normalize glucose levels of diabetic mice, and human ES cells can differentiate into cells capable of insulin production. Cells with GRIP function have also been derived from stem cells residing in adult organisms, here referred to as endogenous stem cell sources. Independent of source, stem cells capable of producing cells with GRIP function may provide a widely available cell transplantation treatment for type 1 diabetes. Copyright © 2002 John Wiley & Sons, Ltd.
Laxative misuse and behavioral disinhibition in bulimia nervosa
Authors: Bruce Kenneth R. , Koerner Naomi M. , Steiger Howard , Young Simon N. 
Published: December 2002

AbstractObjectiveVarious reports suggest that purging with laxatives is associated with greater behavioral impulsivity in bulimia nervosa (BN) patients. We investigated the extent to which laxative misuse corresponds to specific impulse‐control problems.MethodParticipants included bulimic women who misuse laxatives (BNL+; n = 12), bulimic women who do not misuse laxatives (BNL−; n = 33), and healthy normal eaters (NE; n = 26). Participants completed the Go/No‐Go discrimination task (a well‐validated computerized measure of response disinhibition), as well as self‐report questionnaires of impulsivity, eating symptoms, and general psychopathology.ResultsCompared with the other groups, the BNL+ group made more commission errors on the Go/No‐Go under cues for punishment, indicating they were more disinhibited when faced with possible negative outcomes. Compared with the BNL− group, the BNL+ group was also more likely to differ from the NE group on self‐reported impulsivity. There were no differences between the two bulimic groups on eating symptoms and the three groups did not differ in terms of general psychopathology.DiscussionFindings suggest that, controlling for eating symptoms and psychopathology, laxative misuse among BN patients is associated with difficulty inhibiting incorrect responses in the face of perceived threats. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 33: 92–97, 2003.
A T‐LCLC type immittance converter
Authors: Irie Hisaichi , Kisimoto Haruki 
Published: December 2002

Abstract“Immittance converter” is short for “impedance–admittance converter.” The immittance converter has an input impedance that is proportional to the admittance of the load connected across output terminals. In this converter, the output current is proportional to the input voltage and the input current is proportional to the output voltage. Consequently, it converts a constant voltage source into a constant current source and a constant current source into a constant voltage source.It is well known that the quarter‐wavelength transmission line shows immittance conversion characteristics. However, it has very long line length for the switching frequency, and is not suitable for power electronics application. Thus, we proposed immittance converters that consist of lumped elements L, C and show improved immittance conversion characteristics at a resonant frequency. In this paper, we propose a T‐LCLC‐type immittance converter, which has the transitive configuration and both advantages of T‐LCL‐ and π‐CLC‐type immittance converters. We show voltage–current transformation characteristics and frequency characteristics and efficiency characteristics of the T‐LCLC immittance converter. These characteristics were determined analytically and experimentally. © 2002 Wiley Periodicals, Inc. Electr Eng Jpn, 142(3): 57–63, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/eej.10095