tbuckley/cabot-search huggingface dataset:
Subthalamic nucleus deep brain stimulation for Parkinson’s disease: 8 years of follow-up
Authors: Dianyou Li, Chunyan Cao, Jing Zhang, Shikun Zhan, Shengdi Chen, Bomin Sun
Journal: Translational Neurodegeneration (2013)

The short-term benefits of bilateral stimulation of the subthalamic nucleus (STN) in patients with advanced Parkinson's disease (PD) are well documented, but long-term benefits are still uncertain. The aim of this study is to evaluate the outcome of 8 years of bilateral STN stimulation to PD patients.In this study, 31 consecutive PD patients were treated with bilateral STN stimulation. Their functional status was measured using the Activities of Daily Living section of the Unified Parkinson's Disease Rating Scale (UPDRS-ADL) at drug on (with medication) and drug off (without medication) states preoperatively and at 1, 5, and 8 years postoperatively. In addition, Levodopa equivalent doses and stimulation parameters were also assessed.After 8 years of STN stimulation, the UPDRS-ADL scores were improved by 4% at drug off status (P > 0.05) and 22% at drug on status (P < 0.05) compared with baseline; the levodopa daily doses were reduced by 28% (P < 0.05) compared with baseline; the stimulation voltage and pulse width were not changed, but the stimulation frequency was decreased remarkably compared with the 5 years of follow-up. Adverse events were observed in 6 patients, including misplacement of the electrode and skin erosion requiring further surgery. All events were resolved without permanent sequelae. 2 patients died of aspiration pneumonia 6 and 7 years after surgery.The marked improvement in UPDRS-ADL scores were still observed after 8 years of bilateral STN stimulation with medication.
Effect of cholecystokinin-pancreozymin and secretin on the volume, composition, and enzymatic activity of hepatic bile in rabbits
Authors: S. Kirchmayer, A. Tarnawski, H. Drozdz, K. Cichecka
Journal: Gut (1972)

In rabbits given cholecystokinin-pancreozymin intravenously a statistically significant increase in bile volume and alkaline phosphatase (AP) activity was observed. There was also an increase in the total amount of protein, cholesterol, bicarbonates Na, K, Ca, Mg, and the total activity of alkaline phosphatase and leucineaminopeptidase (LAP) secreted in bile within 90 minutes after pancreozymin injection. Pancreozymin had no effect on the concentration and output of taurocholates and the activity of gammaglutamyltranspeptidase (GGTP) and alanineaminotransferase (ALAT) in bile. Secretin neither changes the volume nor the concentration of any of the investigated components in rabbit bile.
Relative power of linkage and transmission disequilibrium test strategies to detect non-HLA linked coeliac disease susceptibility genes
Authors: S Bevan, S Popat, R S Houlston
Journal: Gut (1999)

<h3>BACKGROUND</h3> Susceptibility to coeliac disease is genetically determined by possession of specific HLA DQ alleles, acting in concert with one or more non-HLA linked genes. The pattern of familial risk is most parsimonious with a multiplicative model for the interaction between these two classes of genes. Haplotype sharing probabilities across the HLA region in affected sibling pairs suggest that genes within the MHC complex contribute no more than 40% of the sibling familial risk of coeliac disease, making the non-HLA linked gene (or genes) the stronger determinant of coeliac disease susceptibility. Attempts to localise these non-HLA linked genes have been carried out using both linkage and association tests. <h3>AIMS</h3> To review the evidence for the involvement of non-HLA linked genes in coeliac disease, and to compare the relative merits of linkage and transmission disequilibrium tests (TDT) to detect the non-HLA linked gene (or genes) contributing to the development of coeliac disease. <h3>METHODS</h3> Under a range of genetic models the number of affected sibling pairs needed to detect linkage was compared with the number of families required to show a relation between marker and disease, adopting the TDT strategy. <h3>RESULTS AND CONCLUSIONS</h3> Power calculations show that, if there is a single major non-HLA linked susceptibility locus, a non-parametric linkage approach may well prove effective. However, if there are a number of non-HLA susceptibility genes, each with small effect, the sample size necessary for linkage studies will be prohibitive and a systematic search for allelic association should be a more effective strategy.
Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen.
Authors: J S Stamler, J A Osborne, O Jaraki, L E Rabbani, M Mullins, D Singel, J Loscalzo
Journal: Journal of Clinical Investigation (1993)

Elevated levels of homocysteine are associated with an increased risk of atherosclerosis and thrombosis. The reactivity of the sulfhydryl group of homocysteine has been implicated in molecular mechanisms underlying this increased risk. There is also increasingly compelling evidence that thiols react in the presence of nitric oxide (NO) and endothelium-derived relaxing factor (EDRF) to form S-nitrosothiols, compounds with potent vasodilatory and antiplatelet effects. We, therefore, hypothesized that S-nitrosation of homocysteine would confer these beneficial bioactivities to the thiol, and at the same time attenuate its pathogenicity. We found that prolonged (> 3 h) exposure of endothelial cells to homocysteine results in impaired EDRF responses. By contrast, brief (15 min) exposure of endothelial cells, stimulated to secrete EDRF, to homocysteine results in the formation of S-NO-homocysteine, a potent antiplatelet agent and vasodilator. In contrast to homocysteine, S-NO-homocysteine does not support H2O2 generation and does not undergo conversion to homocysteine thiolactone, reaction products believed to contribute to endothelial toxicity. These results suggest that the normal endothelium modulates the potential, adverse effects of homocysteine by releasing EDRF and forming the adduct S-NO-homocysteine. The adverse vascular properties of homocysteine may result from an inability to sustain S-NO formation owing to a progressive imbalance between the production of NO by progressively dysfunctional endothelial cells and the levels of homocysteine.
LINE-1 (L1) Lineages in the Mouse
Authors: Stephen C. Hardies, Liping Wang, Lanxin Zhou, Yingping Zhao, N. Carol Casavant, Shijun Huang
Journal: Molecular Biology and Evolution (2000)

Recently, a rapidly amplifying family of mouse LINE-1 (L1) has been identified and named TF. The evolutionary context surrounding the derivation of the TF family was examined through phylogenetic analysis of sequences in the 3′ portion of the repeat. The Mus musculus domesticus TF family was found to be the terminal subfamily of the previously identified L1Md4 lineage. The L1Md4 lineage joins the other prototypical mouse LINE-1 lineage (the L1MdA2 lineage) approximately 1 MYA at about the time of the common ancestor of M. m. domesticus, Mus spicilegus, and Mus spretus. However, the TF family from M. m. domesticus was found to join to the previously reported M. spretus Ms475 and Ms7024 LINE-1 families at just 0.5 MYA, indicating horizontal transfer. The TF family from M. m. domesticus was then found to be even more recently related to LINE-1's from another species, M. spicilegus. A separate spretus A2 lineage was found through a directed search of a PCR library. This lineage, in contrast to the spretus TF lineage, does join domesticus at about 1 MYA, as would be expected in the absence of horizontal transfer. A third major family was also found that splits off from the L1Md4 lineage shortly after its departure from the L1MdA2 lineage. The new family, named the Z family, was found to contain the de novo LINE-1 inserts causing the beige and med mutations. Whether the split with the Z family was before or after the recombination that introduced the F-type promoters and defined the inception of TF as a lineage is unclear. In enumerating copies of the various LINE-1 families, we found that TF 3′ ends were not much more numerous than the reported number of 5′ ends, suggesting that TF may not be subjected to the 90% truncation pattern typical of LINE-1 as a whole.
99mTc HMDP bone scanning in generalised nodal osteoarthritis. II. The four hour bone scan image predicts radiographic change.
Authors: C W Hutton, E R Higgs, P C Jackson, I Watt, P A Dieppe
Journal: Annals of the Rheumatic Diseases (1986)

In 14 patients with generalised nodal osteoarthritis a four hour bone scan image was found to predict the changes that occur on the radiograph at follow up between three and five years later. The scan abnormality appeared to precede the development of radiographic signs, and joints abnormal on scintigraphy showed most progression. Normal joints and joints abnormal on x ray alone showed little progression, and those that did subsequently alter became abnormal on scan. Scanning may provide a sensitive technique for monitoring osteoarthritis, it may enable a greater understanding of the underlying disease process, and allow evaluation of modifying therapeutic procedures.
Felty's syndrome associated with high levels of IgA rheumatoid factor.
Authors: R H Withrington, I Teitsson, M H Seifert, H Valdimarsson
Journal: Annals of the Rheumatic Diseases (1984)

A 64-year-old woman with rheumatoid arthritis developed Felty9s syndrome. Her serum contained large amounts of IgA rheumatoid factor (RF) but insignificant levels of IgM-RF and IgG-RF. It is postulated that the high levels of IgA-RF may have contributed to the neutropenia.
Follow-up on Metabolic Markers in Children Treated for Obstructive Sleep Apnea
Authors: Karen A. Waters, Sinthu Sitha, Louise M. O'Brien, Sherryn Bibby, Carina de Torres, Silvano Vella, Roland de la Eva
Journal: American Journal of Respiratory and Critical Care Medicine (2006)

Rationale: In adults, obstructive sleep apnea (OSA) is associated with metabolic dysfunction that improves with treatment of OSA. No equivalent studies exist in children.Objective: To examine the relationship between metabolic markers and OSA with time and treatment in children.Methods: Metabolic markers measured on a fasting morning blood sample at diagnostic polysomnography and follow-up 1.3 ± 0.6 yr later.Measurements and Main Results: Forty-five children (34 males), aged 6.9 ± 3.5 yr, and including 12 obese subjects, were in the final analysis. There were no differences in metabolic markers between children with and without OSA at initial study; however, obese children had significantly higher insulin (106.1 ± 72.1 vs. 66.7 ± 37.6 pmol/L; p = 0.028), insulin/glucose ratio (23.7 ± 14.3 vs. 14.7 ± 8.0; p = 0.02), and significantly lower high-density lipoprotein cholesterol (1.3 ± 0.2 vs. 1.6 ± 0.4 nmol/L; p = 0.005) than nonobese children. Twenty children underwent surgical removal of adenotonsillar tissue, whereas 12 children with OSA elected not to have treatment. OSA persisted after treatment in five children, and resolved in 27. Thirteen children did not have OSA on initial or follow-up studies. At follow-up, there was a small but significant improvement in total cholesterol in those children whose OSA was resolved (4.8 ± 0.8 to 4.7 ± 0.6 nmol/L; p = 0.005) and a trend for obese children with persisting OSA to have elevated insulin levels compared with obese children without OSA (p = 0.07).Conclusion: Obesity appears to be the major influence on metabolic dysfunction in children with OSA, but these preliminary data also suggest that resolution or persistence of OSA may affect changes in metabolic function over time.
Shear Stress Is Differentially Regulated Among Inbred Rat Strains
Authors: Jamila Ibrahim, Jody K. Miyashiro, Bradford C. Berk
Journal: Circulation Research (2003)

An important compensatory response to atherosclerosis is vascular remodeling, with maintenance of vessel lumen diameter and shear stress. Both hemodynamic and environmental factors contribute to vascular remodeling and shear stress regulation, and the process is probably also influenced by genetic factors. To establish an animal model for genetic analysis of shear stress regulation and vascular remodeling, we studied the effects of chronic flow alteration in four inbred rat strains. By ligating the left internal and external carotid arteries, we caused a ≈90% decrease in left common carotid blood flow and a ≈50% increase in right (contralateral) common carotid flow. After 4 weeks of altered flow, there were significant interstrain differences with respect to the change in carotid outer diameter (OD), the relationship between flow and shear stress, and the extent to which shear stress was normalized. Genetically hypertensive rats (GH) exhibited the greatest reduction in shear stress in response to increased flow, stroke-prone spontaneously hypertensive rats (SHR-SP) exhibited a smaller response, and Brown Norway (BN) rats exhibited the smallest response. SHR-SP and GH also differed significantly in outward remodeling (defined as an increase in lumen and vessel diameter) in increased flow arteries. In response to decreased flow, BN rats exhibited the smallest reduction in shear stress. These findings demonstrate significant strain-dependent differences in shear stress regulation and vascular remodeling in response to altered flow. This study emphasizes the important role of genetic factors in vascular remodeling and suggests that genetic analysis of these strains will provide novel insights into the underlying mechanisms.
Effects of aging, gender, and physical training on peripheral vascular function.
Authors: W H Martin, T Ogawa, W M Kohrt, M T Malley, E Korte, P S Kieffer, K B Schechtman
Journal: Circulation (1991)

Blood pressure and total peripheral resistance increase with age. However, the effect of age on vasodilatory capacity has not been characterized.To delineate the effects of aging, gender, and physical training on peripheral vascular function, we measured blood pressure during submaximal and maximal treadmill exercise and measured blood pressure, calf blood flow, and calf conductance (blood flow/mean blood pressure) at rest and during maximal hyperemia in 58 healthy sedentary subjects (men aged 25 +/- 5 and 65 +/- 3 years and women aged 27 +/- 5 and 65 +/- 4 years) and in 52 endurance exercise-trained subjects (men aged 30 +/- 3 and 65 +/- 4 years and women aged 27 +/- 3 and 65 +/- 3 years). Systolic and mean blood pressures were higher at rest, during maximal calf hyperemia, and during submaximal exercise of the same intensity in the older than in the younger subjects of the same gender and exercise training status (p less than 0.01). The magnitude of the age-related effect on blood pressure during exercise was greater in women than in men (p less than 0.01). Diastolic blood pressure during submaximal exercise was also higher in the older than in the younger subjects (p less than 0.05) but not in women treated with estrogen replacement. In contrast, systolic and mean blood pressures during submaximal work were lower in physically conditioned subjects than in sedentary age- and gender-matched subjects (p less than 0.05) but not in older women. Increased age was associated with reduced maximal calf conductance in women (p less than 0.01) but not in men. However, calf vasodilatory capacity was higher in trained than in untrained subjects (p less than 0.01), regardless of age and gender. There was a significant inverse relation between maximal calf conductance and systolic, diastolic, and mean blood pressures during submaximal exercise (r = -0.31 to -0.53, p less than 0.01) and a direct relation between maximal calf conductance and maximal oxygen uptake (r = 0.66, p less than 0.0001).Thus, for healthy subjects between the ages of 25 and 65 years, there is an interactive effect between age and gender and an independent effect of physical training on peripheral vascular function.
Revised TN Categorization for Colon Cancer Based on National Survival Outcomes Data
Authors: Leonard L. Gunderson, John Milburn Jessup, Daniel J. Sargent, Frederick L. Greene, Andrew K. Stewart
Journal: Journal of Clinical Oncology (2009)

Purpose The sixth edition of American Joint Committee on Cancer (AJCC) Cancer Staging Manual for colon cancer subdivided stage II into IIA (T3N0) and IIB (T4N0) and stage III into IIIA (T1-2N1M0), IIIB (T3-4N1M0), and IIIC (anyTN2M0). Subsequent analyses supported revised substaging of stage III because of improved survival for T1-2N2 versus T3-4N2 and T4N1 survival was more similar to T3-4N2 than to T3N1. The AJCC Hindgut Taskforce sought population-based validation that depth of invasion and nodal status interact to affect survival. Patients and Methods Surveillance, Epidemiology, and End Results (SEER) population-based data from January 1992 to December 2004 for 109,953 colon cancer patients were compared with National Cancer Data Base (NCDB) data on 134,206 patients. T4N0 cancers were stratified by tumors that perforate visceral peritoneum (T4a) versus tumors that invade or are adherent to adjacent organs or structures (T4b). N1 and N2 were stratified by number of involved positive lymph nodes (N+): N1a/N1b (1 v 2-3), N2a/N2b (4 to 6 v ≥ 7). Five-year observed and relative survival data were obtained for each TN category. Results SEER colon cancer analyses confirm that patients with T1-2N0 cancers have better survival than T3N0, T3N0 better than T4N0, T1-2N2 better than T3-4N2, and T4bN1 similar to T4N2. Patients with T4a lesions have better survival than T4b by N category. The number of positive nodes affects survival for each T category. Conclusion This SEER population-based colon cancer analysis is highly consistent with rectal cancer pooled analysis and SEER rectal cancer analyses, supporting the shift of T1-2N2 lesions from IIIC to IIIA/IIIB, shifting T4bN1 from IIIB to IIIC, subdividing T4/N1/N2, and revising substaging of stages II/III. Survival outcomes by TN category for colon and rectal cancer are strikingly similar.
Use of Different Postmenopausal Hormone Therapies and Risk of Histology- and Hormone Receptor–Defined Invasive Breast Cancer
Authors: Agnès Fournier, Alban Fabre, Sylvie Mesrine, Marie-Christine Boutron-Ruault, Franco Berrino, Françoise Clavel-Chapelon
Journal: Journal of Clinical Oncology (2008)

Purpose We previously found that the risk of invasive breast cancer varied according to the progestagen component of combined postmenopausal hormone therapy (CHT): progesterone, dydrogesterone, or other progestagens. We conducted the present study to assess how these CHTs were associated with histology- and hormone receptor-defined breast cancer. Patients and Methods We used data from the French E3N cohort study, with 80,391 postmenopausal women followed for a mean duration of 8.1 years; 2,265 histologically confirmed invasive breast cancers were identified through biennial self-administered questionnaires completed from 1990 to 2002. The relative risks (RRs) were estimated using Cox proportional hazards models. Results Compared with postmenopausal hormone therapy (HT) never-use, ever-use of estrogen+progesterone was not significantly associated with the risk of any breast cancer subtype, but increasing duration of estrogen+progesterone was associated with increasing risks of lobular (P = .06) and estrogen receptor–positive/progesterone receptor–negative (ER+/PR−; P = .02). Estrogen+dydrogesterone was associated with a significant increase in risk of lobular carcinoma (RR, 1.7; 95% CI, 1.1 to 2.6). Estrogen+other progestagens was associated with significant increases in risk of ductal and lobular carcinomas (RR, 1.6; 95% CI, 1.3 to 1.8; and 2.0; 95% CI, 1.5 to 2.7, respectively), of ER+/PR+ and ER+/PR− carcinomas (RR, 1.8; 95% CI, 1.5 to 2.1; and 2.6; 95% CI, 1.9 to 3.5, respectively), but not of ER−/PR+ or ER−/PR− carcinomas (RR, 1.0; 95% CI, 0.5 to 2.1; and 1.4; 95% CI, 0.9 to 2.0, respectively). Conclusion The increase in risk of breast cancer observed with the use of CHTs other than estrogen+progesterone and estrogen+dydrogesterone seems to apply preferentially to ER+ carcinomas, especially those ER+/PR−, and to affect both ductal and lobular carcinomas.
Iodine-123 metaiodobenzylguanidine scintigraphic assessment of the transplanted human heart: Evidence for late reinnervation
Authors: Teresa de Marco, Michael Dae, Monita S.F. Yuen-Green, Shantha Kumar, Krishnankutty Sudhir, Fraser Keith, Thomas M. Amidon, Celia Rifkin, Cindy Klinski, Debra Lau, Elias H. Botvinick, Kanu Chatterjee
Journal: Journal of the American College of Cardiology (1995)
Salivary secretion and connective tissue disease in man.
Authors: R W Matthews, K D Bhoola, J J Rasker, M I Jayson
Journal: Annals of the Rheumatic Diseases (1985)

Parotid and submandibular gland secretions collected from patients with rheumatoid arthritis or systemic sclerosis have been analysed and the results compared with those obtained from a matched group of healthy individuals. Flow rates were measured and the saliva samples assayed for amylase, kallikrein, protein, and salivary IgA concentration. The results showed that only patients with rheumatoid arthritis had a reduced salivary flow, especially parotid flow, with a significantly increased concentration of salivary IgA in both parotid and submandibular saliva. Patients with systemic sclerosis did not show significantly altered salivary flow rates, but there was a marked depletion of salivary IgA content in both parotid and submandibular saliva. Neither disease states appeared to alter the kallikrein or amylase content of saliva. The possible clinical value of these findings is discussed.
Differential diagnosis of calf pain with musculoskeletal ultrasound imaging
Authors: D Kane, P V Balint, R Gibney, B Bresnihan, R D Sturrock
Journal: Annals of the Rheumatic Diseases (2003)

Alport syndrome is a hereditary, progressive, hematuric nephropathy characterized by glomerular basement membrane abnormalities with frequent hearing defects and ocular anomalies. The disease is associated with mutations in genes encoding the α3, α4, or α5 chains of type IV collagen, <i>COL4A3</i>, or <i>COL4A4</i> in the autosomal forms of the disease, <i>COL4A5</i> in the more frequent X-linked variety. Ultrastructural changes in the glomerular basement membrane and frequent abnormal expression of type IV collagen chains in renal and skin basement membranes are crucial elements for the diagnosis of Alport syndrome, determination of the mode of inheritance, and genetic counseling. Animal models have provided invaluable tools to study the mechanisms leading to progressive deterioration of the glomerular basement membrane and ultimately to renal failure, and to evaluate benefits of potential targeted therapies.
Assessment of gender differences in health status with the Leicester Cough Questionnaire (LCQ)
Authors: S S Birring, I D Pavord
Journal: Thorax (2009)

completely.Rather we assume that a MCPyV prevalence of 7.5% represents the MCPyV prevalence in the general population.We found almost identical numbers for the MCPyV prevalence in non-MCC tumours of sun-exposed skin. 7More data will be needed to prove this assumption.Nevertheless, the morphological similarities of both tumours are striking and will keep the intriguing idea of a possibly (polyoma-) virus-associated pathogenesis in mind.