bluuebunny/crossref_metadata_2025_split huggingface dataset:
Seamounts, knolls and petit‐spot monogenetic volcanoes on the subducting Pacific Plate
Authors: Hirano Naoto , Koppers Anthony A. P. , Takahashi Ayu , Fujiwara Toshiya , Nakanishi Masao 
Published: June 2008

ABSTRACTOn the western part of the Pacific Plate most seamounts formed during the Cretaceous period in the so‐called West Pacific Seamount Province (WPSP). On the northwestern part of the same plate, the Joban and Japanese Seamount Trail (JJST) are also composed of Early Cretaceous seamounts. However, two new groups of knolls were recently discovered during multibeam surveys on the Pacific Plate along the Japan Trench. One group consists of circular knolls that are flat‐topped in shape and correspond to eruptive ages of approximately 75 Ma. The other group consists of irregularly shaped knolls, also called petit‐spot volcanoes, that are found on the outer‐rise systems of the subducting Pacific Plate. These petit‐spots seem much younger and available age data suggest that they only formed in the last few million years. Acoustic reflective data, which are simultaneously obtained with bathymetrical data, are a most powerful tool to distinguish the petit‐spots from the Cretaceous edifices in the WPSP and JJST. In this paper, we present the results of an exploratory search for these new kind of petit‐spot volcanoes along the trenches in the Pacific Ocean, with an emphasis on the Japan and Tonga trenches. The sizes of these irregularly shaped petit‐spot volcanoes are several orders of magnitude less than the Cretaceous seamounts and circular knolls, yet they appear to be ubiquitous on the ocean floor, in particular, where incipient melts in the asthenosphere can be squeezed out by tectonic forces.
Insulin, adiponectin, IGFBP‐1 levels and body composition in small for gestational age born non‐obese children during prepubertal ages
Authors: Sancakli Ozlem , Darendeliler Feyza , Bas Firdevs , Gokcay Gulbin , Disci Rian , Aki Semih , Eskiyurt Nurten 
Published: June 2008

SummaryBackground  Being small for gestational age (SGA) at birth and postnatal growth pattern may have an impact on insulin resistance and body composition in later life. Adiponectin is a strong determinant of insulin sensitivity.Objective  The aim of this study was to evaluate insulin resistance and adiponectin levels in SGA born children with catch‐up growth (CUG) in the absence of obesity in prepubertal ages and relations with body composition and insulin‐like growth factor binding protein (IGFBP)‐1.Methods  Twenty‐four (15F, 9M) SGA born children with CUG but without obesity were evaluated at age 6·3 ± 0·5 years with respect to glucose, insulin, IGFBP‐1, leptin and adiponectin levels, and body composition by dual‐energy X‐ray absorptiometry (DEXA). Their data were compared to that of 62 (27F, 35M) appropriate for gestational age (AGA) children.Results  SGA and AGA children had similar height standard deviation score (SDS) corrected for parental height and body mass index (BMI) SDS. Homeostasis model for insulin resistance (HOMA‐IR) was significantly high in SGA (0·7 ± 0·6) than in AGA children (0·4 ± 0·2) (P = 0·029). There were no significant differences in leptin, IGFBP‐1, adiponectin, and total and truncal fat between SGA and AGA children. However, being born SGA and having higher BMI in the upper half for the distribution in the sample, although within normal ranges, was associated with lower adiponectin levels (estimated means of log adiponectin levels 3·8 ± 0·3 vs. 4·4 ± 0·1 µg/ml, P = 0·040).Conclusions  SGA children with CUG and with no obesity have higher insulin levels compared to AGA children. Both SGA birth and recent size seem to have an effect on serum adiponectin levels in childhood.
The G/G genotype of a single nucleotide polymorphism at –1066 of c‐Jun N‐terminal kinase 1 gene (MAPK8) does not affect type 2 diabetes susceptibility despite the specific binding of AP2α
Authors: Osawa Haruhiko , Yamada Kazuya , Tabara Yasuharu , Ochi Masaaki , Onuma Hiroshi , Nishida Wataru , Shimizu Ikki , Kawamoto Ryuichi , Fujii Yasuhisa , Miki Tetsuro , Ohashi Jun , Makino Hideichi 
Published: June 2008

SummaryObjective  The c‐Jun N‐terminal kinase 1 (JNK1, mitogen‐activated kinase 8; MAPK8) phosphorylates insulin receptor substrate‐1 (IRS‐1) at serine 307, which induces insulin resistance. MAPK8 activity is increased in obese insulin‐resistant mice, whereas mapk8 (–/–) mice show decreased adiposity and improved insulin sensitivity. The aim of this study was to determine the relationship between single nucleotide polymorphisms (SNPs) of MAPK8 and type 2 diabetes (T2DM).Design, patients and measurements  Approximately 2 kb of 5′ flanking and the coding regions were initially sequenced in 24 Japanese T2DM subjects. Identified SNPs were genotyped in 204 T2DM cases and 201 nondiabetic controls. The function of promoter SNP–1066 (g.–1066G > A, rs10857561) was analysed by electrophoretic mobility shift assay (EMSA) and luciferase assay. SNP–1066 was further genotyped in a total of 498 cases and 407 controls, and in 2075 subjects in the general population.Results  In 204 cases and 201 controls, 11 identified SNPs were not associated with T2DM. These SNPs were in the same linkage disequilibrium (LD) block. The tag SNP–1066 was not associated with T2DM in a total of 498 cases and 407 controls with the power > 80% when the relative risk is > 1·31. Functionally, transcription factor AP2α specifically recognized G but not A at –1066. MAPK8 promoter activity was unchanged between G and A. In 2075 subjects, neither body mass index (BMI), fasting plasma glucose (FPG), homeostasis model assessment insulin resistance index (HOMA‐IR), nor β cell function index (HOMA‐β) was associated with SNP–1066.Conclusions  The G/G genotype of MAPK8 SNP–1066 did not affect T2DM susceptibility despite specific binding of AP2α.
Variation in Niemann–Pick C1‐like 1 gene as a determinant of apolipoprotein B‐100 kinetics and response to statin therapy in centrally obese men
Authors: Chan Dick C. , Watts Gerald F. , Wang Jian , Hegele Robert A. , Van Bockxmeer Frank M. , Barrett P. Hugh R. 
Published: June 2008

SummaryObjective  Niemann–Pick C1‐like 1 protein (NPC1L1) plays a key role in lipoprotein metabolism. We examined the association of common genetic polymorphisms in NPC1L1 on apolipoprotein (apo) B‐100 metabolism and the response to statin treatment in 37 men with central obesity.Research methods and procedure  Very‐low density lipoprotein (VLDL) and low‐density lipoprotein (LDL)–apoB kinetics were determined using stable isotope method. NPC1L1 genotypes (1735G > C, 25432A > C and 27677T > C) were determined by allele‐specific methods. These three polymorphisms are defined as haplotype, namely 1735C‐25432A‐27677T, and was designated as ‘haplotype 2’.Results  Relative to non‐2/2 haplotype (n = 23), subjects with the 2/2 haplotype (n = 14) had significantly increased plasma concentrations of total, LDL‐cholesterol, and total apoB (P < 0·05). The fractional catabolic rate (FCR) of LDL‐apoB was significantly lower in 2/2 subjects compared with non‐2/2 subjects (P < 0·05), with an associated increase in LDL‐apoB pool size in the former group. Sixteen subjects were then treated with 40 mg atorvastatin (6 weeks): 2/2 subjects (n = 8) had a significantly greater reduction in plasma concentrations of cholesterol and total apoB and in LDL‐apoB pool size, as well as a greater increase in LDL‐apoB FCR compared with non‐2/2 subjects. There were no significant treatment‐related between‐haplotype differences in VLDL‐apoB kinetics or in plasma concentrations of lathosterol and campesterol.Conclusion  Our data demonstrate that NPC1L1 2/2 haplotype was associated with variation in LDL‐apoB metabolism and its response to statin therapy in centrally obese men, by a mechanism that did not involve changes in VLDL‐apoB kinetics, nor cholesterol synthesis or absorption.
The evaluation of metabolic parameters and insulin sensitivity for a more robust diagnosis of the polycystic ovary syndrome
Authors: Amato Marco Calogero , Galluzzo Aldo , Finocchiaro Sara , Criscimanna Angela , Giordano Carla 
Published: June 2008

SummaryBackground  Polycystic ovary syndrome (PCOS) is considered predominantly as a hyperandrogenetic syndrome and the evaluation of metabolic parameters and insulin sensitivity is not mandatory.Context  PCOS diagnostic criteria [National Institute of Health (NIH), Rotterdam Consensus (ROT), Androgen Excess Society (AES)] are unanimous recognized. We aimed to assess in women with suspected PCOS whether the application of the three diagnostic criteria differently characterizes the metabolic profile and insulin sensitivity.Design  Retrospective study in a cohort of women admitted to our Outpatient Clinic for suspected PCOS.Patients  Two hundred and four women with suspected PCOS in comparison to a group of normal, age‐matched Sicilian women (N = 34) without signs of metabolic syndrome.Measurements  We evaluated hyperandrogenaemia and clinical hyperandrogenism, ovarian morphology, hypothalamo–hypophyseal axis and metabolic syndrome parameters. An oral glucose tolerance test (OGTT; 75 g glucose) measured areas under the curve (AUC) for insulin, C peptide and homeostasis model assessment of insulin‐resistance (HOMA‐IR) were performed.Results  The prevalence of PCOS was 51% according to NIH, 83% to ROT and 70·6% to AES, and only 100 patients were qualified simultaneously under these three criteria. The prevalence of the metabolic syndrome in PCOS women was 26·92% (NIH), 21·77% (ROT) and 23·61% (AES), respectively. In comparison to healthy women, PCOS women showed increased fasting insulinaemia (PCOS/ROT: P = 0·028; PCOS/NIH: P = 0·007; PCOS/EAS: P = 0·023), 120 min insulin after OGTT insulinaemia (for the three criteria: P < 0·001), AUC2h insulin (for the three criteria: P < 0·001) and AUC2h C peptide (for the three criteria: P < 0·001).Conclusions  Our study highlights the fact that regardless of the diagnostic criteria used, evaluation of the metabolic parameters and insulin sensitivity is important for a correct diagnosis of PCOS and a therapeutic approach.
A novel phenotypic expression associated with a new mutation in LMNA gene, characterized by partial lipodystrophy, insulin resistance, aortic stenosis and hypertrophic cardiomyopathy
Authors: Araújo‐Vilar David , Lado‐Abeal Joaquin , Palos‐Paz Fernando , Lattanzi Giovanna , Bandín Manuel A. , Bellido Diego , Domínguez‐Gerpe Lourdes , Calvo Carlos , Pérez Oscar , Ramazanova Alia , Martínez‐Sánchez Noelia , Victoria Berta , Costa‐Freitas Ana Teresa 
Published: June 2008

SummaryBackground  Lipodystrophies are a heterogeneous group of diseases characterized by abnormal fat distribution. Familial partial lipodystrophy 2 (FPLD2) is due to mutations in the LMNA gene. Previous studies have suggested that LMNA mutations 5′ to the nuclear localization signal (NLS) are more likely to underlie laminopathies with cardiac or skeletal muscle involvement, while mutations 3′ to the NLS are more likely to underlie lipodystrophy and progeroid syndromes.Objective  To study the clinical and molecular features of a subject with FPLD.Subjects and methods  We carried out mutational analysis of LMNA gene in a woman with FPLD phenotype and in her relatives. Insulin resistance was evaluated by minimal model. Body composition was evaluated by dual‐energy X‐ray absorptiometry (DEXA). Echocardiography was done in affected subjects. 3T3‐L1 preadipocytes were transfected with wild‐type or mutant prelamin A constructs. In transfected cells, lamin A was detected using a Cy3‐conjugated monoclonal anti‐FLAG antibody.Results  The patient showed atypical fat distribution, insulin resistance, severe aortic stenosis and hypertrophic cardiomyopathy. She has an affected 11‐year‐old son, not yet lipodystrophic but with an incipient aortic disease. LMNA sequencing showed that mother and son were both heterozygous for a novel c.1772G > T missense mutation in exon 11, which causes the substitution of the cysteine at residue 591 by a phenylalanine (C591F). In mouse preadipocytes transfected with the mutant human LMNA gene, the mutant lamin A isoform was mislocated in the nucleus.Conclusions  This patient shows a novel clinical form of FPLD2, due to a mutation affecting lamin A only, with cardiac involvement.
Serum levels of the adipokine visfatin are increased in pre‐eclampsia
Authors: Fasshauer Mathias , Waldeyer Theresa , Seeger Jeannette , Schrey Susanne , Ebert Thomas , Kratzsch Jurgen , Lossner Ulrike , Bluher Matthias , Stumvoll Michael , Faber Renaldo , Stepan Holger 
Published: June 2008

SummaryObjective  Pre‐eclampsia (PE) is a serious cardiovascular complication in pregnancy which shares risk factors with the metabolic syndrome including insulin resistance and obesity. Recently, visfatin was introduced as a novel insulin‐mimetic adipokine which is up‐regulated when weight is gained. In the current study, we investigated visfatin serum levels in pre‐eclamptic patients as compared to healthy gestational age‐matched controls.Patients and measurements  Visfatin was quantified by ELISA in control (n = 20) and PE (n = 15) patients. Furthermore, visfatin was correlated to clinical and biochemical measures of renal function, glucose and lipid metabolism, as well as inflammation.Results  Mean maternal visfatin serum levels adjusted for maternal age were about twofold up‐regulated in PE (31·1 ± 23·4 µg/l) as compared to controls (15·7 ± 23·1 µg/l). Furthermore, visfatin concentrations correlated positively with age, blood pressure, creatinine, free fatty acids (FFA), IL‐6 and C reactive protein (CRP), whereas a negative correlation was found with fasting insulin and the HOMA‐insulin resistance index (HOMA‐IR). In multivariate analyses, HOMA‐IR and CRP remained independently associated with visfatin serum levels and explained 58% of the variation in visfatin concentrations.Conclusions  We show that maternal visfatin levels are significantly increased in PE patients. Furthermore, insulin sensitivity and inflammatory status independently predict serum visfatin levels.
Sizes of abdominal organs in adults with severe short stature due to severe, untreated, congenital GH deficiency caused by a homozygous mutation in the GHRH receptor gene
Authors: Oliveira Carla R. P. , Salvatori Roberto , Nóbrega Luciana M. A. , Carvalho Erick O. M. , Menezes Menilson , Farias Catarine T. , Britto Allan V. O. , Pereira Rossana M. C. , Aguiar‐Oliveira Manuel H. 
Published: June 2008

SummaryObjective  To assess the sizes of intra‐abdominal organs of adult subjects with untreated severe congenital isolated GH deficiency (IGHD) due to lack of functional GHRH receptor (GHRH‐R), and to verify whether there is proportionality between size of organ and adult stature and body surface area (BSA).Subjects and methods  By using ultrasound, we studied the sizes (absolute and corrected by height, weight and BSA) of the intra‐abdominal organs of 18 adult subjects with IGHD (eight females, IGHD group) who have never received GH replacement therapy. They were all homozygous for the same null mutation (IVS1 + 1G → A) in the GHRH receptor gene (GHRH‐R). They were compared with normal controls from the same region.Results  After correction for BSA, subjects lacking a functional GHRH‐R have normal prostate and ovaries size, small spleen and uterus, and large liver, pancreas and kidney.Conclusions  Size of individual abdominal organs is influenced in different ways by severe and congenital lack of GH due to a GHRH‐R mutation.
Assessment of the efficacy and safety of intravenous conivaptan in patients with euvolaemic hyponatraemia: subgroup analysis of a randomized, controlled study
Authors: Verbalis Joseph G. , Zeltser David , Smith Neila , Barve Abhijit , Andoh Masakazu 
Published: June 2008

SummaryObjective and design Most cases of euvolaemic hyponatraemia are associated with elevated plasma levels of AVP. Conivaptan is a high‐affinity, nonpeptide vasopressin V1A/V2‐receptor antagonist. We performed a subgroup analysis of a multicentre, randomized, placebo‐controlled, double‐blind, parallel‐group study to evaluate the efficacy and safety of intravenous (i.v.) conivaptan for the treatment of euvolaemic hyponatraemia.Patients Fifty‐six euvolaemic patients with serum [Na+] of 115 to < 130 mmol/l received conivaptan 40 or 80 mg/day or placebo via continuous i.v. infusion for 4 days. A 20‐mg loading dose was administered intravenously over 30 min in the conivaptan groups; the placebo group received a placebo loading dose.Measurements Change in serum [Na+], measured by the baseline‐adjusted area under the serum [Na+]–time curve (AUC), was the primary efficacy parameter. Secondary efficacy measures included the time from the first dose to a confirmed ≥ 4 mmol/l increase in serum [Na+], total time with serum [Na+] ≥ 4 mmol/l above baseline, change in serum [Na+] from baseline, and number of patients with a confirmed ≥ 6 mmol/l increase in serum [Na+] or normal [Na+]. Safety assessments included adverse events (AE), incidence of overly rapid correction of serum [Na+], and changes in vital signs and electrocardiographic and clinical laboratory parameters.Results During the first 2 days of treatment, and over the entire 4‐day treatment period, both conivaptan doses significantly increased the serum [Na+] AUC more than placebo (P < 0·01). Conivaptan 40 and 80 mg/day significantly improved all secondary efficacy measures. Conivaptan was generally well tolerated; infusion‐site reaction was the most common AE.Conclusions In hospitalized patients with euvolaemic hyponatraemia, i.v. conivaptan significantly increased serum [Na+] promptly and was well tolerated.
Influence of iodine on the reference interval of TSH and the optimal interval of TSH: results of a follow‐up study in areas with different iodine intakes
Authors: Guan Haixia , Shan Zhongyan , Teng Xiaochun , Li Yushu , Teng Di , Jin Ying , Yu Xiaohui , Fan Chenling , Chong Wei , Yang Fan , Dai Hong , Yu Yang , Li Jia , Chen Yanyan , Zhao Dong , Shi Xiaoguang , Hu Fengnan , Mao Jinyuan , Gu Xiaolan , Yang Rong , Chen Wei , Tong Yajie , Wang Weibo , Gao Tianshu , Li Chenyang , Teng Weiping 
Published: June 2008

SummaryObjective  The aim of the present study was to evaluate whether the status of iodine nutrition influences the TSH concentration in a selected Chinese reference population according to the criteria proposed by National Academy of Clinical Biochemistry (NACB) and regular thyroid ultrasonography, to establish a new reference interval of TSH based on the wide variation of iodine nutrition in populations, and to identify an optimal interval of TSH by following up the cohort with normal TSH concentrations at baseline.Design  The study was conducted in Panshan, Zhangwu and Huanghua, the regions with mildly deficient, more than adequate and excessive iodine intake, respectively. Of the 3761 unselected subjects who were enrolled at baseline, 2237 met the criteria for a reference population. Of 3048 subjects with normal serum TSH at baseline, 2727 (80·0%) participated in the 5‐year follow‐up study. TSH and thyroid autoantibodies in serum and iodine in urine were measured, and B‐mode ultrasonography of the thyroid was performed.Results  In the reference population, there was a urinary iodine‐related increment of serum TSH levels (r = 0·21, P = 0·000), and the mean levels of TSH in Panshan, Zhangwu and Huanghua were 1·15, 1·28 and 1·93 mIU/l, respectively (P = 0·000), corresponding to the rising regional iodine intake. Based on the overall data, we obtained a reference interval of 0·3–4·8 mIU/l. TSH concentrations obtained in the follow‐up study correlated well with those at baseline (r = 0·58, P = 0·000). A baseline serum TSH > 1·9 mIU/l was associated with an increased incidence of development of supranormal TSH and a baseline serum TSH < 1·0 mIU/l was associated with an increased incidence of subnormal TSH development.Conclusions  Iodine nutrition is an important factor associated with TSH concentration even in the rigorously selected reference population. Baseline TSH of 1·0–1·9 mIU/l is an optimal interval with the lowest incidence of abnormal TSH in 5 years.
Familial prevalence and age of RET germline mutations: implications for screening
Authors: Machens Andreas , Dralle Henning 
Published: June 2008

SummaryObjective  No comprehensive information exists nationwide about the familial prevalence and age of rearranged during transfection (RET) germline mutations. The current investigation was undertaken to provide such natural history data which are urgently needed to enable factual decision‐making about DNA‐based screening programmes for RET germline mutations.Design  Descriptive study drawn on countrywide referrals to a specialist surgical centre.Patients  Included were 452 patients from 141 German RET families: 277 carriers referred for pre‐emptive or therapeutic surgery, and 175 additional carriers or relatives with endocrine tumours associated with multiple endocrine neoplasia type 2 (MEN2).Measurements  Key variables included familial prevalence, phenotype and latest year of birth of RET germline mutations.Results  A total of 26 different RET germline mutations were identified among the 141 RET families: C634R (21%); M918T (15%); C634Y (9%); L790F/TTG→TTT (8%), Y791F (7%), V804M (6%); C620R and C634F (5% each); L790F/TTG→TTC and C634S/TGC→TCC (4% each); C618S/TGC→AGC, C634G and S891A (2% each); C618F and E768D (1% each); and in < 1% each: C609G, C611F, C611Y, C618G, C618Y, C620S/TGC→AGC, C620S/TGC→TCC, C620Y, C630R, D631Y and V804L. Most of these differences in prevalence rates, seemingly, were caused by recent spontaneous mutations in the germline. With rare exceptions, longstanding transmission was noted in at least one RET family per affected codon. Many germline mutations were traceable back to the early 20th, and a few even to the 19th century.Conclusions  These data reveal the potential of DNA‐based screening of all relevant RET exons, especially for index patients with solitary, seemingly sporadic disease.
Serum resistin is positively correlated with the accumulation of metabolic syndrome factors in type 2 diabetes
Authors: Osawa Haruhiko , Ochi Masaaki , Tabara Yasuharu , Kato Kenichi , Yamauchi Junko , Takata Yasunori , Nishida Wataru , Onuma Hiroshi , Shimizu Ikki , Fujii Yasuhisa , Miki Tetsuro , Ohashi Jun , Makino Hideichi 
Published: June 2008

SummaryObjective  Resistin, secreted from adipocytes, causes insulin resistance in rodents. We reported that the G/G genotype of a resistin gene promoter single nucleotide polymorphism (SNP) at −420 increases type 2 diabetes (T2DM) susceptibility by enhancing promoter activity. We also showed that serum resistin was positively correlated with G at SNP‐420, the duration of T2DM, and HbA1c in T2DM. The aim of this study was to determine the relation between serum resistin and factors related to the metabolic syndrome (MetS) in T2DM.Design, patients and measurements  We analysed 238 Japanese T2DM subjects (124 males and 114 females, age 60·2 ± 11·3 years, body mass index (BMI) 24·1 ± 3·9) whose overnight fasting sera were available. Serum resistin was measured using ELISA.Results  Serum resistin was higher in subjects with either obesity (P = 0·041), low HDL (P = 0·004), high triglycerides (TG) (P = 0·019), hypertension (HT) (P = 0·001) or atherosclerosis (P = 0·012). Simple regression analysis revealed that serum resistin was correlated with lower HDL, TG and high‐sensitivity C‐reactive protein (hsCRP). Multiple regression analysis (or logistic regression analysis for HT), adjusted for age, gender, BMI and the duration of T2DM, revealed that serum resistin was correlated with lower HDL (P = 0·008), TG (P = 0·041), HT (P = 0·031) and hsCRP (P = 0·004). Serum resistin was positively correlated with the number of MetS factors, independent of age, gender and the duration of T2DM (P < 0·001). Adjustment by either thiazolidinedione (TZD) treatment or hsCRP had no effects on these findings.Conclusions  Serum resistin was positively correlated with the accumulation of MetS factors in T2DM.