tbuckley/cabot-search huggingface dataset:
Health benefits of Nordic walking; a systematic review
Authors: Stephanie Mathieson, Chung-Wei Christine Lin
Journal: British Journal of Sports Medicine (2014)

▸ Tschentscher M, Niederseer D, Niederseer J Health benefits of Nordic Walking; a systematic review. Am J Prev Med , 2013;44:76–84.

Physical activity is essential for good health. Physical inactivity is a leading risk factor for non-communicable diseases, accounting for more than three million preventable deaths.1 A recent physical activity trend is Nordic walking, which is a form of brisk walking utilising walking poles that actively engages the arms and upper body. It is promoted as a safe, efficient, biodynamic exercise with numerous health benefits, suitable for all ages.

To examine the health benefits of Nordic walking.

Database searches of Web of Knowledge, PubMed, CENTRAL, CINAHL and PEDro, from 1950 to the present (date not specified) were conducted to identify randomised controlled trials (RCTs) and observational studies, written in English and German, using the main search terms of ‘Nordic walking,’ ‘pole walking,’ ‘pole striding’ and ‘exerstriders’. Excluded studies included ‘improper’ Nordic walking technique or if Nordic walking poles were not used. Two independent reviewers performed …
Psychopathology in Young People With Intellectual Disability
Authors: Stewart L. Einfeld, Andrea M. Piccinin, Andrew Mackinnon, Scott M. Hofer, John Taffe, Kylie M. Gray, Daniel E. Bontempo, Lesa R. Hoffman, Trevor Parmenter, Bruce J. Tonge
Journal: JAMA (2006)

Comorbid severe mental health problems complicating intellectual disability are a common and costly public health problem. Although these problems are known to begin in early childhood, little is known of how they evolve over time or whether they continue into adulthood.To study the course of psychopathology in a representative population of children and adolescents with intellectual disability.The participants of the Australian Child to Adult Development Study, an epidemiological cohort of 578 children and adolescents recruited in 1991 from health, education, and family agencies that provided services to children with intellectual disability aged 5 to 19.5 years in 6 rural and urban census regions in Australia, were followed up for 14 years with 4 time waves of data collection. Data were obtained from 507 participants, with 84% of wave 1 (1991-1992) participants being followed up at wave 4 (2002-2003).The Developmental Behaviour Checklist (DBC), a validated measure of psychopathology in young people with intellectual disability, completed by parents or other caregivers. Changes over time in the Total Behaviour Problem Score and 5 subscale scores of the DBC scores were modeled using growth curve analysis.High initial levels of behavioral and emotional disturbance decreased only slowly over time, remaining high into young adulthood, declining by 1.05 per year on the DBC Total Behaviour Problem Score. Overall severity of psychopathology was similar across mild to severe ranges of intellectual disability (with mean Total Behaviour Problem Scores of approximately 44). Psychopathology decreased more in boys than girls over time (boys starting with scores 2.61 points higher at baseline and ending with scores 2.57 points lower at wave 4), and more so in participants with mild intellectual disability compared with those with severe or profound intellectual disability who diverged from having scores 0.53 points lower at study commencement increasing to a difference of 6.98 points below severely affected children by wave 4. This trend was observed in each of the subscales, except the social-relating disturbance subscale, which increased over time. Prevalence of participants meeting criteria for major psychopathology or definite psychiatric disorder decreased from 41% at wave 1 to 31% at wave 4. Few of the participants (10%) with psychopathology received mental health interventions during the study period.These results provide evidence that the problem of psychopathology comorbid with intellectual disability is both substantial and persistent and suggest the need for effective mental health interventions.
Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression
Authors: Darrell D. Belke, Sandrine Betuing, Martin J. Tuttle, Christophe Graveleau, Martin E. Young, Mark Pham, Dongfang Zhang, Robert C. Cooksey, Donald A. McClain, Sheldon E. Litwin, Heinrich Taegtmeyer, David Severson, C. Ronald Kahn, E. Dale Abel
Journal: Journal of Clinical Investigation (2002)

To investigate the role of insulin signaling on postnatal cardiac development, physiology, and cardiac metabolism, we generated mice with a cardiomyocyte-selective insulin receptor knockout (CIRKO) using cre/loxP recombination. Hearts of CIRKO mice were reduced in size by 20-30% due to reduced cardiomyocyte size and had persistent expression of the fetal beta-myosin heavy chain isoform. In CIRKO hearts, glucose transporter 1 (GLUT1) expression was reduced by about 50%, but there was a twofold increase in GLUT4 expression as well as increased rates of cardiac glucose uptake in vivo and increased glycolysis in isolated working hearts. Fatty acid oxidation rates were diminished as a result of reduced expression of enzymes that catalyze mitochondrial beta-oxidation. Although basal rates of glucose oxidation were reduced, insulin unexpectedly stimulated glucose oxidation and glycogenolysis in CIRKO hearts. Cardiac performance in vivo and in isolated hearts was mildly impaired. Thus, insulin signaling plays an important developmental role in regulating postnatal cardiac size, myosin isoform expression, and the switching of cardiac substrate utilization from glucose to fatty acids. Insulin may also modulate cardiac myocyte metabolism through paracrine mechanisms by activating insulin receptors in other cell types within the heart.
The Changing Face of the Na<sup>+</sup>/H<sup>+</sup> Exchanger, NHE1: Structure, Regulation, and Cellular Actions
Authors: L. K. Putney, S. P. Denker, D. L. Barber
Journal: The Annual Review of Pharmacology and Toxicology (2002)

The NHE family of ion exchangers includes six isoforms (NHE1–NHE6) that function in an electroneutral exchange of intracellular H + for extracellular Na + . This review focuses on the only ubiquitously expressed isoform, NHE1, which is localized at the plasma membrane where it plays a critical role in intracellular pH (pH i ) and cell volume homeostasis. All NHE isoforms share a similar topology: an N-terminus of 12 transmembrane (TM) α-helices that collectively function in ion exchange, and a C-terminal cytoplasmic regulatory domain that modulates transport activity by the TM domain. Extracellular signals, mediated by diverse classes of cell-surface receptors, regulate NHE1 activity through distinct signaling networks that converge to directly modify the C-terminal regulatory domain. Modifications in the C-terminus, including phosphorylation and the binding of regulatory proteins, control transport activity by altering the affinity of the TM domain for intracellular H + . Recently, it was determined that NHE1 also functions as a membrane anchor for the actin-based cytoskeleton, independently of its role in ion translocation. Through its effects on pH i homeostasis, cell volume, and the actin cortical network, NHE1 regulates a number of cell behaviors, including adhesion, shape determination, migration, and proliferation.
Association of proinflammatory cytokines and chemotherapy-associated cognitive impairment in breast cancer patients: a multi-centered, prospective, cohort study
Authors: Y.T. Cheung, T. Ng, M. Shwe, H.K. Ho, K.M. Foo, M.T. Cham, J.A. Lee, G. Fan, Y.P. Tan, W.S. Yong, P. Madhukumar, S.K. Loo, S.F. Ang, M. Wong, W.Y. Chay, W.S. Ooi, R.A. Dent, Y.S. Yap, R. Ng, A. Chan
Journal: Annals of Oncology (2015)

Existing evidence suggests that proinflammatory cytokines play an intermediary role in postchemotherapy cognitive impairment. This is one of the largest multicentered, cohort studies conducted in Singapore to evaluate the prevalence and proinflammatory biomarkers associated with cognitive impairment in breast cancer patients.Chemotherapy-receiving breast cancer patients (stages I-III) were recruited. Proinflammatory plasma cytokines concentrations [interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, granulocyte-macrophage colony-stimulating factor, interferon-γ and tumor necrosis factor-α] were evaluated at 3 time points (before chemotherapy, 6 and 12 weeks after chemotherapy initiation). The FACT-Cog (version 3) was utilized to evaluate patients' self-perceived cognitive disturbances and a computerized neuropsychological assessment (Headminder) was administered to evaluate patients' memory, attention, response speed and processing speed. Changes of cognition throughout chemotherapy treatment were compared against the baseline. Linear mixed-effects models were applied to test the relationships of clinical variables and cytokine concentrations on self-perceived cognitive disturbances and each objective cognitive domain.Ninety-nine patients were included (age 50.5 ± 8.4 years; 81.8% Chinese; mean duration of education = 10.8 ± 3.3 years). Higher plasma IL-1β was associated with poorer response speed performance (estimate: -0.78; 95% confidence interval (CI) -1.34 to -0.03; P = 0.023), and a higher concentration of IL-4 was associated with better response speed performance (P = 0.022). Higher concentrations of IL-1β and IL-6 were associated with more severe self-perceived cognitive disturbances (P = 0.018 and 0.001, respectively). Patients with higher concentrations of IL-4 also reported less severe cognitive disturbances (P = 0.022).While elevated concentrations of IL-6 and IL-1β were observed in patients with poorer response speed performance and perceived cognitive disturbances, IL-4 may be protective against chemotherapy-associated cognitive impairment. This study is important because cytokines would potentially be mechanistic mediators of chemotherapy-associated cognitive changes.
CSF Eosinophilia Following Myelography
Authors: H. Preston Holley
Journal: JAMA (1979)

WE recently encountered a patient in whom eosinophilic meningitis developed following myelography with iophendylate (Pantopaque). This unusual reaction has been described previously in only two patients<sup>1</sup>and, to our knowledge, never in the English language literature. <h3>Report of a Case</h3> A 56-year-old man was admitted to the Baltimore Veterans Administration Hospital with a history of increasing weakness on the left side and neck pain exacerbated by motion over the previous six weeks. The patient had a long history of left otitis media and alcohol abuse; he had also noted a recent decrease in the force of micturition. Abnormal findings on physical examination were a perforated left tympanic membrane and a moderately enlarged prostate. Neurological examination demonstrated diminished hearing on the left, which was confirmed by audiometry. There were hypesthesia, hypalgesia, and a deficit of vibratory sensation involving the entire left leg to the groin. Weakness and decreased deep tendon
Aflibercept/Folfiri vs Placebo/Folfiri in Metastatic Colorectal Cancer: A Post-Hoc Analysis of Median Overall Survival in Velour from the Retrospectively Assessed Time of Starting First-Line Treatment
Authors: Tabernero Josep, Macarulla Teresa, Humblet Yves, ten Tije Albert, Kroening Hendrik, Grávalos Cristina, Le-Guennec Solenn, Dochy Emmanuelle, Van Cutsem Eric
Journal: Annals of Oncology (2014)
Vascular Cell Senescence
Authors: Tohru Minamino, Issei Komuro
Journal: Circulation Research (2007)

Cardiologists and most physicians believe that aging is an independent risk factor for human atherosclerosis, whereas atherosclerosis is thought to be a characteristic feature of aging in humans by many gerontologists. Because atherosclerosis is among the age-associated changes that almost always escape the influence of natural selection in humans, it might be reasonable to regard atherosclerosis as a feature of aging. Accordingly, when we investigate the pathogenesis of human atherosclerosis, it may be more important to answer the question of how we age than what specifically promotes atherosclerosis. Recently, genetic analyses using various animal models have identified molecules that are crucial for aging. These include components of the DNA-repair system, the tumor suppressor pathway, the telomere maintenance system, the insulin/Akt pathway, and other metabolic pathways. Interestingly, most of the molecules that influence the phenotypic changes of aging also regulate cellular senescence, suggesting a causative link between cellular senescence and aging. For example, DNA-repair defects can cause phenotypic changes that resemble premature aging, and senescent cells that show DNA damage accumulate in the elderly. Excessive calorie intake can cause diabetes and hyperinsulinemia, whereas dysregulation of the insulin pathway has been shown to induce cellular senescence in vitro. Calorie restriction or a reduction of insulin signals extends the lifespan of various species and decreases biomarkers of cellular senescence in vivo. There is emerging evidence that cellular senescence contributes to the pathogenesis of human atherosclerosis. Senescent vascular cells accumulate in human atheroma tissues and exhibit various features of dysfunction. In this review, we examine the hypothesis that cellular senescence might contribute to atherosclerosis, which is a characteristic of aging in humans.
An Evolutionary Space-Time Model with Varying Among-Site Dependencies
Authors: Adi Stern, Tal Pupko
Journal: Molecular Biology and Evolution (2005)

It is now widely accepted that sites in a protein do not undergo independent evolutionary processes. The underlying assumption is that proteins are composed of conserved and variable linear domains, and thus rates at neighboring sites are correlated. In this paper, we comprehensively examine the performance of an autocorrelation model of evolutionary rates in protein sequences. We further develop a model in which the level of correlation between rates at adjacent sites is not equal at all sites of the protein. High correlation is expected, for example, in linear functional domains. On the other hand, when we consider nonlinear functional regions (e.g., active sites), low correlation is expected because the interaction between distant sites imposes independence of rates in the linear sequence. Our model is based on a hidden Markov model, which accounts for autocorrelation at certain regions of the protein and rate independence at others. We study the differences between the novel model and models which assume either independence or a fixed level of dependence throughout the protein. Using a diverse set of protein data sets we show that the novel model better fits most data sets. We further analyze the potassium-channel protein family and illustrate the relationship between the dependence of rates at adjacent sites and the tertiary structure of the protein.
Influence of psychological coping on survival and recurrence in people with cancer: systematic review
Authors: M. Petticrew
Journal: BMJ (2002)

<h3>Abstract</h3> <b>Objective:</b> To summarise the evidence on the effect of psychological coping styles (including fighting spirit, helplessness/hopelessness, denial, and avoidance) on survival and recurrence in patients with cancer. <b>Design:</b> Systematic review of published and unpublished prospective observational studies. <b>Main outcome measures:</b> Survival from or recurrence of cancer. <b>Results:</b> 26 studies investigated the association between psychological coping styles and survival from cancer, and 11 studies investigated recurrence. Most of the studies that investigated fighting spirit (10 studies) or helplessness/hopelessness (12 studies) found no significant associations with survival or recurrence. The evidence that other coping styles play an important part was also weak. Positive findings tended to be confined to small or methodologically flawed studies; lack of adjustment for potential confounding variables was common. Positive conclusions seemed to be more commonly reported by smaller studies, indicating potential publication bias. <b>Conclusion:</b> There is little consistent evidence that psychological coping styles play an important part in survival from or recurrence of cancer. People with cancer should not feel pressured into adopting particular coping styles to improve survival or reduce the risk of recurrence. <h3>What is already known on this topic</h3> Survival from cancer is commonly thought to be influenced by a person9s psychological coping style Some studies have shown that a coping style involving fighting spirit rather than helplessness/hopelessness is associated with survival and recurrence, though the evidence is inconsistent <h3>What this study adds</h3> This systematic review suggests that there is no consistent association between psychological coping and outcome of cancer Publication bias and methodological flaws in some of the primary studies may explain some of the previous positive findings There is no good evidence to support the development of psychological interventions to promote particular types of coping in an attempt to prolong survival
Muscarinic Control of Histamine Release from Airways
Authors: TORSTEN REINHEIMER, THORSTEN MÖHLIG, SACHA ZIMMERMANN, KARL-DIETER HÖHLE, IGNAZ WESSLER
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Isolated human bronchi and rat tracheae were incubated in organ baths to measure histamine release. The calcium ionophore A23187, 3 micromol/L in rat trachea and 10 micromol/L in human bronchi, stimulated histamine release by 145 +/- 50% (n = 6) and 270 +/- 48% (n = 7) above the prestimulation level, respectively. Acetylcholine (100 pmol/L; human bronchi) or oxotremorine (1, 100, 10,000 nmol/L; rat trachea) did not affect the spontaneous histamine release. In rat tracheae neither acetylcholine nor oxotremorine inhibited A23187-evoked histamine release, whereas 100 pmol/L acetylcholine significantly suppressed the evoked histamine release in human bronchi by 86%. For receptor characterization the following subtype-specific muscarinic receptor antagonists were applied: pirenzepine (M1 subtype), para-fluorohexahydrosiladifendiol (pFHHSiD; similar affinities at human cloned M1-, M3-, and M4-receptors), AF-DX 116 (M2 subtype), and clozapine (antagonist at cloned M1-, M2-, M3-receptors; agonist at cloned M4-receptors). Pirenzepine, pFHHSiD, AF-DX 116, and clozapine (100 nmol/L each) antagonized the inhibitory effect of 100 pmol/L acetylcholine by 83 +/- 20% (n = 6), 83 +/- 9% (n = 8), 50 +/- 14% (n = 6), and 35 +/- 7% (6). In conclusion, a species difference exists in the cholinergic control of histamine release between human and rat airways. In human airways muscarinic receptors most likely of the M1 subtype are involved in the inhibitory control of mast cell function, whereas such an inhibitory pathway does not exist in the rat trachea.
PANCREAS TRANSPLANTATION FOR DIABETES MELLITUS
Authors: Robert J. Stratta, M.D, Jennifer L. Larsen, M.D, Kathleen Cushing, R.N., B.S.N
Journal: Annual Review of Medicine (1995)

▪ Abstract Vascularized pancreas transplantation has assumed an increasing role in the treatment of diabetes mellitus. Through 1993, over 5500 pancreas transplants have been performed worldwide, with over 80% being combined pancreas-kidney transplants. Overall one-year patient survival exceeds 90% and graft survival (complete insulin independence) exceeds 70%. Although successful pancreas transplantation achieves euglycemia and complete insulin independence, this occurs at the expense of hyperinsulinemia and chronic immunosuppression. The net result of these changes on diabetic complications in the long term remains to be determined. In the short term, improvement in the quality of life and possible prevention of further morbidity associated with diabetes makes pancreas transplantation an important therapeutic option, particularly when combined with a kidney transplant, in appropriately selected diabetic patients.
Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in <i>Mycobacterium tuberculosis</i> infection
Authors: Diana Di Liberto, Massimo Locati, Nadia Caccamo, Annunciata Vecchi, Serena Meraviglia, Alfredo Salerno, Guido Sireci, Manuela Nebuloni, Neus Caceres, Pere-Joan Cardona, Francesco Dieli, Alberto Mantovani
Journal: The Journal of Experimental Medicine (2008)

D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6(-/-) mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor alpha, interleukin 1beta, and interferon gamma) in bronchoalveolar lavage and serum. High levels of inflammatory cytokines in D6(-/-) infected mice were associated with liver and kidney damage, resulting in both liver and renal failure. Blocking inflammatory CC chemokines with a cocktail of antibodies reversed the inflammatory phenotype of D6(-/-) mice but led to less controlled growth of M. tuberculosis. Thus, the D6 decoy receptor plays a key role in setting the balance between antimicrobial resistance, immune activation, and inflammation in M. tuberculosis infection.
Dermoscopic findings of haemosiderotic and aneurysmal dermatofibroma: report of six patients
Authors: P. Zaballos, Á. Llambrich, M. Ara, Z. Olazarán, J. Malvehy, S. Puig
Journal: British Journal of Dermatology (2005)

Background The clinical diagnosis of dermatofibroma is commonly easy. However, the differentiation of dermatofibroma from other cutaneous tumours is difficult in some instances, primarily in atypical cases and rare variants. Haemosiderotic dermatofibroma is a variant composed of numerous small vessels, extravasated erythrocytes and intra- and extracellular haemosiderin deposits. Aneurysmal dermatofibroma is a variant composed of large, blood-filled spaces without endothelial lining. Some authors consider that haemosiderotic dermatofibroma is an early stage in the development of aneurysmal dermatofibroma. The clinical differential diagnosis of haemosiderotic or aneurysmal dermatofibroma must include melanoma and other melanocytic tumours, vascular neoplasms, adnexal tumours and nonspecific cysts. Dermoscopy improves the diagnostic accuracy in pigmented and nonpigmented skin lesions. Objectives To evaluate specific dermoscopic criteria. Methods Dermoscopic examination (using the DermLite Foto; 3Gen, LLC, Dana Point, CA, U.S.A.) of six patients with haemosiderotic or aneurysmal dermatofibromas was performed to evaluate specific dermoscopic criteria. Results A multicomponent pattern with a central bluish or reddish homogeneous area in combination with white structures and a peripheral delicate pigment network along with vascular structures was noted in five of six lesions. Conclusions This dermoscopic pattern yielded the diagnosis of haemosiderotic or aneurysmal dermatofibroma in most cases. However, this multicomponent pattern may present in some melanomas and although it is useful in determining a clinical diagnosis of aneurysmal dermatofibroma, it may not be specific to this entity.