bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Tai Chi and resistance training on cardiovascular risk factors in elderly Chinese subjects: a 12‐month longitudinal, randomized, controlled intervention study
Authors: Thomas G. Neil , Hong Athena W. L. , Tomlinson Brian , Lau Edith , Lam Chris W. K. , Sanderson John E. , Woo Jean 
Published: November 2005

SummaryBackground   Tai Chi is rapidly gaining in popularity, worldwide. This study was performed to assess its impact on cardiovascular risk factors in comparison with resistance training exercises in elderly Chinese subjects.Methods  A total of 207 healthy elderly participants (65–74 years, 113/207 (55%) men) were randomly assigned to one of three intervention groups: (1) Tai Chi, three times/week for 1 h/session (n = 64); (2) resistance training exercise, three times/week for 1 h/session (n = 65); (3) usual level of physical activity control group (n = 78). Anthropometric measures, dual X‐ray densitometry body composition, blood pressure, lipids, glycaemic and insulin sensitivity indices were measured at baseline and 12 months. Repeated‐measures analysis of variance (anova) was used to assess the between‐group changes using a last‐observation‐carried‐forward intention‐to‐treat approach.Results  A total of 180 (87·0%) subjects completed the study. No significant changes were identified in the Tai Chi group compared to the resistance training or control group. Of the primary outcomes, only the improvement in the insulin sensitivity index differed, being significantly greater in the resistance training than in the control group [mean difference 0·018 (95% confidence interval ( CI) 0·000–0·037) mmol glucose/min, P = 0·02), and tending to be greater than in the Tai Chi group (mean difference 0·019 (95% CI 0·000–0·038) mmol glucose/min, P < 0·06).Conclusion  Tai Chi had no significant effect on any measure compared to the controls, whereas resistance training improved the insulin sensitivity index in this 12‐month study.
Thyroid dysfunction and serum lipids: a community‐based study
Authors: Walsh John P. , Bremner Alexandra P. , Bulsara Max K. , O'Leary Peter , Leedman Peter J. , Feddema Peter , Michelangeli Valdo 
Published: November 2005

SummaryObjective  It is uncertain whether subclinical hypothyroidism (SCH) is associated with hypercholesterolaemia, particularly in subjects with SCH and serum TSH ≤ 10 mU/l.Design, patients and measurements  Cross‐sectional study of 2108 participants in a 1981 community health survey in Busselton, Western Australia. Serum total cholesterol and triglycerides were measured in all subjects and high density lipoprotein cholesterol (HDL‐C) measured (and low density lipoprotein cholesterol (LDL‐C) calculated) in a subgroup of 631 subjects at the time of the survey. In 2001, TSH and free T4 concentrations were measured on archived sera stored at −70 °C. Serum lipid concentrations in subjects with thyroid dysfunction and euthyroid subjects were compared using linear regression models.Results  In the group as a whole, serum total cholesterol was higher in subjects with SCH (N = 119) than in euthyroid subjects (N = 1906) (mean ± SD 6·3 ± 1·3 mmol/l vs. 5·8 ± 1·2 mmol/l, P < 0·001 unadjusted, P = 0·061 adjusted for age, age2 and sex). Serum total cholesterol was similarly elevated in subjects with SCH and TSH ≤ 10 mU/l (N = 89) (6·3 ± 1·3 mmol/l, P < 0·001 unadjusted, P = 0·055 adjusted for age, age2 and sex). In the subgroup analysis, LDL‐C was higher in subjects with SCH (N = 30) than in euthyroid subjects (N = 580) (4·1 ± 1·2 mmol/l vs. 3·5 ± 1·0 mmol/l, P < 0·01 unadjusted, P = 0·024 adjusted for age, age2 and sex). LDL‐C was significantly increased in subjects with SCH and TSH ≤ 10 mU/l (N = 23) (4·3 ± 1·3 mmol/l, P < 0·001 unadjusted, P = 0·002 adjusted for age, age2 and sex).Conclusion  SCH is associated with increased serum LDL‐C concentrations, which is significant after adjustment for age, age2 and sex.
Multiple endocrine neoplasia 2A due to a unique C609S RET mutation presents with pheochromocytoma and reduced penetrance of medullary thyroid carcinoma
Authors: Kinlaw William B. , Scott Sarah M. , Maue Robert A. , Memoli Vincent A. , Harris Robert D. , Daniels Gilbert H. , Porter Donna M. , Belloni Dorothy R. , Spooner Edward T. , Ernesti Manfred M. , Noll Walter W. 
Published: November 2005

SummaryObjective   We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature. We characterized the clinical phenotype of the kindred and the biochemical mechanism of this new mutation.Patients and design   The index case, a 42‐year‐old woman, presented with pheochromocytoma. We screened 29 family members for the presence of the mutation. Of the 15 mutation‐positive family members, 11 agreed to undergo further evaluation by physical examination, calcium and pentagastrin‐stimulated calcitonin levels, measurement of urinary metanephrines, adrenal imaging and serum calcium levels. Biochemical characterization of the mutation was by transient transfection of human neuroblastoma cells and Western blot analysis.Results   This kindred demonstrated an inheritance pattern consistent with autosomal dominant pheochromocytoma. Strikingly, no clinically evident case of medullary thyroid cancer (MTC) was observed among mutation‐positive family members. Thyroidectomy in six cases revealed C‐cell hyperplasia in all and microscopic MTC in two cases. Transfection experiments using human neuroblastoma cells showed that the mutant RET, unlike the wild‐type receptor, is constitutively phosphorylated in the absence of ligand, and thus resembles other previously characterized MEN 2A mutations.Conclusions   The identification of a new mutation causing a MEN 2A phenotype that features pheochromocytoma and the surprising absence of clinically apparent MTC has significant implications for carriers of this mutation and provides further insights into the genotype–phenotype correlation in MEN 2A.
Genotyping of an Italian papillary thyroid carcinoma cohort revealed high prevalence of BRAF mutations, absence of RAS mutations and allowed the detection of a new mutation of BRAF oncoprotein (BRAFV599Ins)
Authors: Carta Claudio , Moretti Sonia , Passeri Lucia , Barbi Flavia , Avenia Nicola , Cavaliere Antonio , Monacelli Massimo , Macchiarulo Antonio , Santeusanio Fausto , Tartaglia Marco , Puxeddu Efisio 
Published: November 2005

SummaryObjectives  The genes RET and RAS, and more recently BRAF, have been shown to be frequently mutated in human papillary thyroid carcinomas (PTC). The aim of this study was to genotype for these mutations a cohort of thyroid tumours collected at our institutions.Design and patients  Thyroid tumours removed from 51 subjects were analysed, including 43 PTC and 8 non‐PTC tumours [3 follicular adenomas (FA), 4 follicular carcinomas (FTC) and 1 anaplastic carcinoma (AC)].Measurements  RET/PTC1 and RET/PTC3 expression was evaluated by reverse transcriptase‐polymerase chain reaction, whereas screening of BRAF (exon 15) and RAS (HRAS, KRAS2 and NRAS) mutations were performed, respectively, by single strand conformation polymorphism and denaturing high‐pressure liquid chromatography.Results  RET/PTC expressions was positive in 5/43 (11·6%) PTC and in none of the non‐PTC tumour. Similarly, BRAF mutations were positive only in PTC, but with a higher prevalence (24/43 positives, 55·8%). All but one BRAF mutation resulted in the prototypic substitution of valine 600 with a glutamic acid. In one case, a somatic in‐frame insertion of three bases at codon 599 resulted in the insertion of an additional valine. RET/PTC expression and BRAF mutations were mutually exclusive. Screening of the RAS gene allowed identification of oncogenic mutations in 1/3 (33·3%) FA and 3/4 (75%) FTC. None of the PTCs was positive for RAS.Conclusions  These data indicate that BRAF mutations are the most frequent genetic event in PTC and that RAS mutations, besides being a genetic hallmark of follicular tumours, are rare or completely absent in PTC from our area. Together, BRAF mutations and rarer RET rearrangements accounted for a genetic event in two‐thirds of PTCs. This study showed a novel and presumably oncogenic mutation of BRAF, which is BRAFV599Ins.
Does growth hormone cause cancer?
Authors: Jenkins P. J. , Mukherjee A. , Shalet S. M. 
Published: November 2005

SummaryThe ability of GH, via its mediator peptide IGF‐1, to influence regulation of cellular growth has been the focus of much interest in recent years. In this review, we will explore the association between GH and cancer. Available experimental data support the suggestion that GH/IGF‐1 status may influence neoplastic tissue growth. Extensive epidemiological data exist that also support a link between GH/IGF‐1 status and cancer risk. Epidemiological studies of patients with acromegaly indicate an increased risk of colorectal cancer, although risk of other cancers is unproven, and a long‐term follow‐up study of children deficient in GH treated with pituitary‐derived GH has indicated an increased risk of colorectal cancer. Conversely, extensive studies of the outcome of GH replacement in childhood cancer survivors show no evidence of an excess of de novo cancers, and more recent surveillance of children and adults treated with GH has revealed no increase in observed cancer risk. However, given the experimental evidence that indicates GH/IGF‐1 provides an antiapoptotic environment that may favour survival of genetically damaged cells, longer‐term surveillance is necessary; over many years, even a subtle alteration in the environmental milieu in this direction, although not inducing cancer, could result in acceleration of carcinogenesis. Finally, even if GH/IGF‐1 therapy does result in a small increase in cancer risk compared to untreated patients with GH deficiency, it is likely that the eventual risk will be the same as the general population. Such a restoration to normality will need to be balanced against the known morbidity of untreated GH deficiency.
Apoptosis is reduced in the colonic mucosa of patients with acromegaly
Authors: Bogazzi Fausto , Russo Dania , Locci Maria Teresa , Chifenti Barbara , Ultimieri Federica , Raggi Francesco , Cosci Chiara , Sardella Chiara , Costa Aurelio , Gasperi Maurizio , Bartalena Luigi , Martino Enio 
Published: November 2005

SummaryBackground  Patients with acromegaly have an increased risk of developing colonic tumours; reduced apoptosis is considered a leading mechanism in tumorigenesis. GH and IGF‐1 decrease apoptosis in several cell lines including human colonic adenocarcinoma, but it is unknown whether epithelial cells of colonic mucosa of patients with acromegaly have reduced apoptosis.Aim  The aim of the study was to evaluate the degree of apoptosis in a cross‐sectional study, in biopsy samples of colonic mucosa obtained from patients with acromegaly.Patients and methods  Eleven patients with active, untreated acromegaly (AcroUntr), 16 patients with acromegaly in remission (AcroRem) and 23 controls were enrolled in the study. Samples of colonic mucosa were obtained during colonoscopy; apoptosis was evaluated by either DNA fragmentation or terminal deoxynucleotidyl transferase assay.Results  Apoptotic cells were 60·0 ± 2·5% in samples of colonic mucosa of controls, 62·0 ± 3·4% in those from patients with AcroRem (P = ns vs. controls), and 39·0 ± 4·1% in those from patients with AcroUntr (P < 0·0001 vs. the other groups). Apoptosis was inversely related to serum IGF‐I (r = 0·771, P < 0·001) or GH (r = 0·404, P = 0·05) levels and less to the estimated duration of disease (r = 0·384, P = 0·07). PPARγ is considered to be a tumour suppressor gene the expression of which might be involved in colonic tumorigenesis. The expression of PPARγ was lower in the colonic mucosa of patients with AcroUntr (2845 ± 947 transcripts) than in that of controls (35 200 ± 2450 transcripts) or AcroRem (29 547 ± 3650 transcripts) (P < 0·005). The recovery of PPARγ expression was associated with apoptosis in most cells. The lower degree of apoptosis in patients with AcroUntr was associated with a reduced expression of the antiapoptotic Bax protein.Conclusion  In conclusion, patients with AcroUntr have reduced apoptosis in colonic mucosa that is apparently reversed after acromegaly is cured. It is conceivable that reduced apoptosis may represent an early event in colonic tumorigenesis of patients with acromegaly.
Is the anteroposterior and transverse diameter ratio of nonpalpable thyroid nodules a sonographic criteria for recommending fine‐needle aspiration cytology?
Authors: Cappelli Carlo , Pirola Ilenia , Cumetti Davide , Micheletti Linda , Tironi Andrea , Gandossi Elena , De Martino Elvira , Cherubini Laura , Agosti Barbara , Castellano Maurizio , Mattanza Chiara , Rosei E. Agabiti 
Published: November 2005

SummaryBackground  As a consequence of the increasing application of ultrasound (US) technology, the detection of asymptomatic nonpalpable thyroid nodules has generally increased. The aim of our study was to assess if the anteroposterior and transverse diameter ratio of nonpalpable thyroid nodules (A/T) ≥ 1 could be a sonographic criterion for recommending fine‐needle aspiration cytology (FNAC).Methods  From January 2002 to January 2004, 828 consecutive solid nonpalpable thyroid nodules were evaluated by ultrasonography, colour‐Doppler and FNAC in our department. Cases were selected from 2217 patients, referred to our thyroid unit for US‐guided FNAC from the greater Brescia area, an endemic zone for goitre. Entry criteria included the presence at US of a solid thyroid nodule that was nonpalpable at physical examination, euthyroid condition and no previous diagnosis of thyroid malignancy. All patients with suspicious or malignant cytology underwent surgery.Results  One hundred and twenty‐seven nodules with inadequate cytology were excluded from the study. Thyroid malignancy was observed in 67 (9·6%) nodules. At US, cancers presented a solid hypoechoic appearance in 79·1% of cases, blurred margins in 47·8%, microcalcification in 73·1%, intranodular vascular pattern in 56·7% and A/T ≥ 1 in 83·6%. A hypoechoic appearance (OR 4·3), blurred margins (OR 2·6), microcalcification (OR 6·1), intranodular vascular pattern (OR 10·2) and A/T ≥ 1 (OR 22·4) were independent risk factors of malignancy.Conclusions  A/T ≥ 1 in conjunction with at least one other sonographic risk factor is able to detect the majority of carcinoma and, moreover, it limits the FNAC procedures to only 15·9% of all the nodules.
Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance
Authors: Makino Shinya , Handa Hiroshi , Suzukawa Koji , Fujiwara Masayoshi , Nakamura Masaharu , Muraoka Shogo , Takasago Ikumi , Tanaka Yasushi , Hashimoto Kozo , Sugimoto Tamotsu 
Published: November 2005

SummaryObjective  To investigate whether sleep‐disordered breathing and/or plasma adiponectin levels are associated with insulin resistance independent of obesity or fat distribution in obstructive sleep apnoea syndrome (OSAS).Design  Cross‐sectional clinical study.Patients  Two‐hundred and thirteen Japanese patients with OSAS aged 27–80 years were divided into three groups: 30 with mild OSAS [apnoea–hypopnoea index (AHI) = 10·3 ± 0·9 episodes/h, minimum oxygen saturation (min SpO2) = 87·3 ± 0·9%], 98 with moderate OSAS (AHI = 28·9 ± 0·6 episodes/h, min SpO2 = 82·1 ± 0·7%), and 85 with severe OSAS (AHI = 68·1 ± 2·8 episodes/h, min SpO2 = 72·3 ± 1·6%). Twenty‐one patients undergoing diabetic treatments (two mild, nine moderate and 10 severe) were excluded from the assessment of insulin resistance and plasma adiponectin measurements.Measurements  Fat distribution [evaluated according to visceral (V) and subcutaneous (S) fat areas using computed tomography scanning at the umbilical level], blood pressure, metabolic parameters and hormones including insulin and adiponectin were measured. After full polysomnography, venous blood was collected between 0600 and 0700 h.Results  Severe OSAS patients were more hypertensive than mild and moderate OSAS. Fasting plasma glucose (FPG) and fasting plasma insulin and homeostasis model assessment of insulin resistance (HOMA‐IR) levels were all higher in severe OSAS than mild and moderate OSAS patients. HOMA‐IR was correlated not only with obesity [body mass index (BMI), V and S areas] but also with apnoea (AHI, min SpO2 and desaturation time). Additionally, HOMA‐IR was correlated positively with haemoglobin (Hb)A1c, systolic (SBP) and diastolic blood pressure (DBP), triglycerides and free fatty acids (FFA), and negatively with high density lipoprotein (HDL)‐cholesterol, suggesting that insulin resistance is a key component of the metabolic syndrome in OSAS. Plasma adiponectin levels were not different between mild, moderate and severe OSAS groups. Plasma adiponectin levels were correlated with HOMA‐IR and V area, but not AHI or min SpO2. Stepwise multiple regression analysis, however, revealed that BMI, AHI and plasma adiponectin were independently associated with HOMA‐IR.Conclusion  Sleep‐disordered breathing was associated with insulin resistance independent of obesity. Although plasma adiponectin was also an independent determinant of HOMA‐IR in OSAS patients, plasma adiponectin was more closely related to obesity than to sleep apnoea. Although treatment of sleep‐disordered breathing with nasal continuous positive airway pressure reportedly improves insulin sensitivity, our findings suggest that treatment of obesity is also essential in ameliorating insulin resistance at least through increased plasma adiponectin levels in OSAS.
Breast cyst fluids increase the proliferation of breast cell lines in correlation with their hormone and growth factor concentration
Authors: Enriori Pablo J. , Vázquez Stella Maris , Chiauzzi Violeta , Pérez Cecilia , Fischer Carlos R. , Gori Jorge R. , Etkin Alberto E. , Charreau Eduardo , Calandra Ricardo S. , Lüthy Isabel A. 
Published: November 2005

SummaryObjective and design  Gross cystic disease (GCD) of the breast is reported to occur in 7% of women in the developed world and, although not premalignant, is thought to be associated with an increased risk of breast cancer. Hormone and growth factor concentration levels were measured in breast cyst fluid (BCF) to correlate them with their mitogenic activity in tumour (MCF‐7) or nontransformed (MCF‐10A) cells.Results  Oestradiol (E2), oestrone (E1), E2‐sulfate (E2‐S), E1‐sulfate (E1‐S) and epidermal growth factor (EGF) concentrations were, as expected, significantly higher in type I than in type II cysts, while transforming growth factor‐beta 2 (TGF‐β2) showed higher levels in type II cysts. Fifty per cent of the BCF samples stimulated [3H]‐thymidine incorporation into MCF‐7 cells while 34·5% inhibited this parameter. In MCF‐10A cells, most BCF samples were stimulatory (85%). E2, E1 and EGF concentrations in BCF samples correlated significantly and positively with cell proliferation in MCF‐7 cells, whereas a significant negative correlation was found for TGF‐β2. In MCF‐10A cells, only E2‐S and E1‐S exhibited significant positive correlation, whereas a significant negative correlation was found for TGF‐β2. Progesterone (Pg), E2 and EGF incubated under the same conditions had a stimulatory effect on [3H]‐thymidine incorporation into MCF‐7 cells, whereas TGF‐β2 inhibited this parameter. Pg, E2, E1 and EGF significantly stimulated this parameter in MCF‐10A cells.Conclusions  The stimulatory action of BCF on cell proliferation in a model of human breast epithelial cells could partly explain the increased incidence of breast cancer in cyst‐bearing women.
Comprehensive study of urinary cortisol metabolites in hyperthyroid and hypothyroid patients
Authors: Hoshiro M. , Ohno Y. , Masaki H. , Iwase H. , Aoki N. 
Published: November 2005

SummaryObjective To further analyse the significance and mutual relationship of thyroid function‐linked alterations in cortisol metabolism that have been separately and variously reported.Patients and measurements Twenty‐four‐hour urine samples from 21 patients with hyperthyroidism (Graves’ disease), 16 patients with hypothyroidism (Hashimoto's thyroiditis), 21 healthy age‐ and sex‐matched controls for hyperthyroidism, and 16 healthy age‐ and sex‐matched controls for hypothyroidism were evaluated for 6β‐hydroxycortisol (6β‐OHF), tetrahydrocortisol (THF), tetrahydrocortisone (THE), allo‐tetrahydrocortisol (allo‐THF), urinary free cortisol (UFF), urinary free cortisone (UFE) and 17‐hydroxycorticosteroid (17‐OHCS).Results Urinary 17‐OHCS, THE and allo‐THF levels increased considerably in hyperthyroid patients compared to the controls, while UFF and THF showed no difference between the two groups. Urinary 6β‐OHF was significantly lower in the hyperthyroid patients than in the controls. Both the urinary allo‐THF + THF/THE and the UFF/UFE ratios were significantly lower in the hyperthyroid patients than in the controls, whereas only the former was significantly higher in the hypothyroid patients than in the controls. The urinary allo‐THF/THF ratio was significantly higher in the hyperthyroid patients and significantly lower in the hypothyroid patients than in the controls. In an analysis of pooled subjects including all groups (n = 64), free T4 levels correlated negatively (P < 0·0001) with the urinary allo‐THF + THF/THE ratio but not with the UFF/UFE ratio. The serum levels of free T4 correlated positively (P < 0·0001) with the urinary allo‐THF/THF ratio.Conclusion The thyroid hormones seem to affect the total 11β‐HSD activity (allo‐THF + THF/THE) more strongly than the renal 11β‐HSD2 activity (UFF/UFE). 5α‐reductase activity (allo‐THF/THF) is also enhanced in hyperthyroidism, while the reduction of urinary 6β‐OHF in hyperthyroidism might be a secondary effect of the altered activity of the total 11β‐HSD and 5α‐reductase.
Low total normal motile count values are associated with increased sperm disomy and diploidy rates in infertile patients
Authors: BERNARDINI LUCA M. , CALOGERO ALDO E. , BOTTAZZI CRISTINA , LANTERI SILVIA , VENTURINI PIER LUIGI , BURRELLO NUNZIATINA , PALMA ADELE DE , CONTE NORY , RAGNI NICOLA 
Published: November 2005

SummaryThis study was undertaken to evaluate the possibility of identifying men at increased risk of sperm aneuploidy and diploidy on the bases of specific cut‐off values of the total normal motile count (TNMC). Twenty‐seven consecutive, unselected male patients referred to our Unit were studied: 11 patients with normal sperm parameters (group A) suffering from unexplained infertility and 16 infertile patients with abnormal sperm parameters (group B). Disomy rates for chromosomes 1, 4, 8, 12, 18, X and Y were ascertained for each patient by means of triple and double fluorescence in situ hybridization (FISH) experiments. Both univariate and multivariate statistical analyses by principal component analysis (PCA) were performed for comparisons between sperm aneuploidy rates and semen quality (TNMC). TNMC scores in the two groups were significantly different (23.5 × 106 and 1.52 × 106, in groups A and B, respectively, p = 0.00002). In general, higher sperm disomy rates were noted for all chromosomes in group B compared with group A. Statistical significance was observed for disomy 1, total disomy rate (3.36% vs. 1.38%), and diploidy (0.49% vs. 0.19%) (p < 0.01). For disomy 4 and 8, differences resulted close to significance. PCA clearly showed how independent variables were inter‐related. Infertile men with TNMC <2 × 106 (male factor) were found to be at increased risk for sperm aneuploidy and diploidy. Multivariate analysis by PCA resulted as a useful method to visualize the information of the data sets on a bi‐dimensional plot considering all the patients and all the variables at the same time.