tbuckley/cabot-search huggingface dataset:
Epidemiology of scabies prevalence in the U.K. from general practice records
Authors: S. Lassa, M.J. Campbell, C.E. Bennett
Journal: British Journal of Dermatology (2011)

Scabies is a contagious parasitic infestation which causes an allergic reaction to just a few mites.To examine the epidemiology of scabies consultations in the U.K. by age, sex, region of the country and time.Data were obtained from the THIN (The Health Information Network) database provided by EPIC U.K. in which each consultation episode is coded according to a 'READ' code. Data were available for 1997-2005 inclusive (9 years) for approximately 8·5% of the U.K. population from 12 regions of the U.K. We used harmonic analysis to model the data over time and derived cycle amplitudes and phases for each region in the U.K.There was a significantly greater infestation rate among females with a relative risk of 1·24 (P < 0·001) relative to males. The age group 10-19 years had the highest infestation rates (with rates of 4·55 per 1000 and 5·92 per 1000 for males and females, respectively). The middle age groups had the smallest infestation rates. A cycle with length of between 15 and 17 years was derived, and the phase times of the cycles for each region suggested a progression of the disease originating from the North East, spreading to Northern parts of the U.K. and then to the Midlands and the South.The study confirms earlier studies with regard to the age/sex distribution of scabies. We suggest a contagious pattern of spread of scabies infestation in the U.K. with an epidemic cycle length of 15-17 years.
Cognitive assessment in preschool children with sleep-disordered breathing
Authors: Nicoletta Pietroapoli, Jole Rabasco, Ottiavio Vitelli, Maria Chiara Supino, Alessandra Tabarrini, Chiara Romano, Marco Del Pozzo, Maria Pia Villa
Journal: European Respiratory Journal (2014)

Introduction 

Sleep-disordered breathing (SDB) has been associated with impaired cognitive and behavioural function in school children; little is known about younger children, although the age of 3 to 5 years is more affected and it is particularly important to further neurobehavioral development.

Aim and objectives 

To assess cognitive functions in preschool children affected by SDB.

Methods 

We enrolled 58 preschool children (age ranged 3-6 years; mean age 4.36 ± 0.97; 50% male) attending our Paediatric Sleep Centre and receiving a polysomnographic diagnosis of Primary Snoring (PS) or Obstructive Sleep Apnea Syndrome (OSA). Children with psychiatric disorders, EEG abnormalities, epilepsy, genetic syndromes and unable to speak fluent Italian were excluded. All children underwent a neurocognitive assessment using the Wechsler Preschool and Primary Scale of Intelligence- Third Edition (WPPSI-III).

Results 

28 children received diagnosis of PS or mild OSA (mean Apnea-Hypopnea Index (AHI) 2.56 ± 1.21) and 30 moderate-severe OSA (mean AHI 14.49 ± 11.7). In both groups, the cognitive assessment showed high scores on Verbal IQ (109.24 ± 11.78 vs 111.55 ± 12.25), Performance IQ (111.2 ± 10.75 vs 111.38 ± 11.01), and Full IQ (111.68 ± 11.06 vs 113.55 ± 12.88), without any statistical differences.

Conclusions 

SDB of any severity in preschool children is not associated with poorer cognitive performance; therefore it could be argued that short duration of SDB don't cause neurocognitive damage. Further studies on larger series of children are warranted to confirm our preliminary data and to compare our results with cognitive assessment in a control group.
Predictors of changes in health status between and within patients 12 months post left ventricular assist device implantation
Authors: Corline Brouwers, Nicolaas de Jonge, Kadir Caliskan, Olivier Manintveld, Quincy‐Robyn Young, Annemarie Kaan, Jennifer Kealy, Johan Denollet, Susanne S. Pedersen
Journal: European Journal of Heart Failure (2014)
Redefining leadership in health care
Authors: T. Treasure
Journal: BMJ (2001)

> O wad some power the giftie gie us, To see oursels as others see us! It would frae monie a blunder free us, And foolish notion. Robert Burns, To a Louse 

Arecent workshop run by the Royal College of Surgeons and the NHS Confederation on the leadership role of consultants took as “a given” that the medical staff of a hospital are a central resource and that without them there would be nothing worth calling a health service to manage or administer. This struck a chord with the consultants. It was also recognised that the consultant workforce is riven with disaffection.1 Less overtly stated but evident in group discussions was the perception of hospital managers that consultants are inclined to be headstrong and do not always use their influence and abilities in the best overall interests of the organisation that employs them. This prompted various versions of the “doctors know best” gambit and the ploy which runs “I can go to the private sector where they will provide the facilities my patients need.” When this current of righteous indignation runs hottest it is worth asking for Robert Burns's “giftie” to see ourselves as other see us. This workshop, with its mix of eloquent and knowledgeable surgeons and managers, was an opportunity for consultants to glimpse how others see them—as leaders or otherwise—rather than merely ruminate on their disgruntlement.

The personality types of qualifying doctors include the range found in the working population, but after qualification those who become consultants in acute clinical specialties—who traditionally take the …
Ustekinumab in the treatment of palmoplantar pustulosis
Authors: S. Gerdes, J. Franke, S. Domm, U. Mrowietz
Journal: British Journal of Dermatology (2010)

Journal Article Ustekinumab in the treatment of palmoplantar pustulosis Get access S. Gerdes, S. Gerdes Psoriasis‐Center at the Department of Dermatology, University Clinic of Schleswig‐Holstein, Campus Kiel, Schittenhelmstr. 7, Kiel 24105, Germany E‐mail: sgerdes@dermatology.uni‐kiel.de Search for other works by this author on: Oxford Academic Google Scholar J. Franke, J. Franke Psoriasis‐Center at the Department of Dermatology, University Clinic of Schleswig‐Holstein, Campus Kiel, Schittenhelmstr. 7, Kiel 24105, Germany E‐mail: sgerdes@dermatology.uni‐kiel.de Search for other works by this author on: Oxford Academic Google Scholar S. Domm, S. Domm Psoriasis‐Center at the Department of Dermatology, University Clinic of Schleswig‐Holstein, Campus Kiel, Schittenhelmstr. 7, Kiel 24105, Germany E‐mail: sgerdes@dermatology.uni‐kiel.de Search for other works by this author on: Oxford Academic Google Scholar U. Mrowietz U. Mrowietz Psoriasis‐Center at the Department of Dermatology, University Clinic of Schleswig‐Holstein, Campus Kiel, Schittenhelmstr. 7, Kiel 24105, Germany E‐mail: sgerdes@dermatology.uni‐kiel.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 163, Issue 5, 1 November 2010, Pages 1116–1118, https://doi.org/10.1111/j.1365-2133.2010.09897.x Published: 01 November 2010
Abstract 19647: The Evolution of Cardiac Output and Cerebral Blood Flow in the Perinatal Transition in Hypoplastic Left Heart Syndrome: a Longitudinal Study
Authors: Lindsay Mills, Akiko Hirose, Santokh Dhillon, Etienne Fortin-Pellerin, Winnie Savard, Po-Yin Cheung, Deborah Fruitman, Nee S Khoo, Lisa K Hornberger
Journal: Circulation (2014)

Background:  Cardiovascular adaptation through the perinatal transition has not been previously explored in fetuses with hypoplastic left heart syndrome (HLHS). We sought to investigate the evolution of cardiac output in HLHS from late gestation through the perinatal period with comparison to healthy fetuses. As fetal HLHS has progressive middle cerebral arterial (MCA) Doppler changes suggestive of brain sparing, we further examined the impact of the transition on MCA blood flow. We hypothesized ductal patency with falling pulmonary vascular resistance after birth in HLHS could lead to cerebral steal.   Methods:  We prospectively recruited 9 healthy and 11 pregnancies complicated by fetal HLHS. Echocardiograms were performed before birth at ≥37 weeks gestation and after birth at 4-6, 20-24, and 40-48 hours (all newborns), and 3-5 days (HLHS neonates only). Ventricular stroke volumes (SV) were determined using pulse Doppler and semilunar valve diameters, and combined cardiac output (CCO) was calculated (SV x heart rate (HR)). MCA pulsatility index (PI) was determined using the peak systolic, end diastolic and mean velocities.   Results:  In late gestation, the CCO was similar between groups (HLHS mean 404 ± 91 vs. control 373 ± 96cc/kg/min). After birth, there was a trend towards higher CCO in HLHS at 4-6 and 20-24 hours (p= 0.06), which reached significance at 48 hours (587±155 vs controls 402±73 cc/kg/min, p=0.03). The CCO was highest in HLHS at 3-5 days (672 ± 117cc/kg/min, p   Conclusions:  HLHS newborns significantly increase their cardiac output in the perinatal transition, particularly from 48 hours onward, through both increased HR and SV. While just prior to birth the MCA PI in HLHS suggests brain sparing, a reverse finding is observed after birth, which could reflect increased CCO and/or cerebral steal. This could be a period of cerebral vulnerability.
Abstract 13792: Inhibitory Effects of Eicosapentaenoic Acid on Arterial Calcification in Klotho Mutant Mice
Authors: Kazufumi Nakamura, Daijii Miura, Kei Yunoki, Yasushi Koyama, Yukihiro Saito, Minoru Satoh, Kazuhiro Osawa, Toru Miyoshi, Kunihisa Kohno, Hiroshi Morita, Hiroshi Ito
Journal: Circulation (2014)

Background:  The klotho gene was identified as an “aging-suppressor” gene in mice that accelerates arterial calcification when disrupted. Expression levels of serum and local vascular klotho are reduced in patients with chronic kidney disease (CKD) and that the decrease in expression level of klotho is associated with arterial calcification. Intake of eicosapentaenoic acid (EPA), an n-3 fatty acid, reduces the risk of fatal coronary artery disease. However, the effects of EPA on arterial calcification have not been fully elucidated.   Purpose:  The aim of this study was to evaluate the effect of EPA on arterial calcification in klotho mutant mice.   Methods:  Four-week-old klotho mutant mice (n=24, 12 males & 12 females) and wild-type (WT) mice (n=24, 12 males & 12 females) were given a diet containing 5% EPA (EPA food, klotho and WT: n=12, each) or not containing EPA (control food, klotho and WT: n=12, each) for 4 weeks. Calcium volume score (CVS) of the thoracic and abdominal aorta was assessed by multi-detector computed tomography.   Results:  CVS were significantly elevated in klotho mice after 4 weeks of control food (before vs after feeding, P   Conclusions:  Administration of EPA prevents arterial calcification together with reduction of expression levels of the NOX4 gene and NOX activity via GPR120 in klotho mutant mice.
The microwell-mesh: A novel device and protocol for the high throughput manufacturing of cartilage microtissues
Authors: Kathryn Futrega, James S Palmer, Mackenzie Kinney, William B Lott, Mark D Ungrin, Peter W Zandstra, Michael R Doran
Journal: Biomaterials (2015)

Microwell platforms are frequently described for the efficient and uniform manufacture of 3-dimensional (3D) multicellular microtissues. Multiple partial or complete medium exchanges can displace microtissues from discrete microwells, and this can result in either the loss of microtissues from culture, or microtissue amalgamation when displaced microtissues fall into common microwells. Herein we describe the first microwell platform that incorporates a mesh to retain microtissues within discrete microwells; the microwell-mesh. We show that bonding a nylon mesh with an appropriate pore size over the microwell openings allows single cells to pass through the mesh into the microwells during the seeding process, but subsequently retains assembled microtissues within discrete microwells. To demonstrate the utility of this platform, we used the microwell-mesh to manufacture hundreds of cartilage microtissues, each formed from 5 × 10(3) bone marrow-derived mesenchymal stem/stromal cells (MSC). The microwell-mesh enabled reliable microtissue retention over 21-day cultures that included multiple full medium exchanges. Cartilage-like matrix formation was more rapid and homogeneous in microtissues than in conventional large diameter control cartilage pellets formed from 2 × 10(5) MSC each. The microwell-mesh platform offers an elegant mechanism to retain microtissues in microwells, and we believe that this improvement will make this platform useful in 3D culture protocols that require multiple medium exchanges, such as those that mimic specific developmental processes or complex sequential drug exposures.
Abstract 5785: A Novel Function of Regulator of G-protein Signaling 2: Stabilization of Signal Transducer and Activator of Transcription 3 Phosphorylation
Authors: Hong Yue, Russell Desnoyer, Wei Li, Sadashiva Karnik
Journal: Circulation (2009)

Background: Regulator of G protein signaling proteins (RGS) are known to regulate G protein coupled receptor (GPCR) signaling at the plasma membrane through their GTPase-activating protein activity. We have previously identified RGS2 as a downstream target of unphosphorylated Signal Transducer and Activator of Transcription 3 (U-STAT3). U-STAT3 mediated Angiotensin II (AngII) type 1 receptor (AT1R), a GPCR, induced cardiac hypertrophy but the mechanism is unclear. Hypothesis: RGS2 is the mediator of U-STAT3 regulated Ang II/AT1R signaling. Methods and Results: In AT1R overexpressing HEK293 cells and HL-1 cells (a mouse cardiomyocyte cell line), Ang II stimulation induced RGS2 expression in parallel with U-STAT3. The localization, distribution and expression of RGS2 were changed upon Ang II stimulation. RGS2 was mainly localized in the nucleus, which was also confirmed in human vascular smooth muscle cells. Gene transfection of RGS2 dose-dependently increased phosphorylated STAT3 (P-STAT3), and maintained a high level of P-STAT3 up to 24 hrs. Co-immunoprecipitation assay identified a complex formed between RGS2 and P-STAT3, suggesting that RGS2 plays a role in maintaining P-STAT3 stability. Treatment with AT1R antagonist, losartan, decreased RGS2/P-STAT3 interaction, suggesting that this interaction is dependent on AT1R activation. On the other hand, in cells overexpressing AT1R and Y705F mutant STAT3, which cannot be phosphorylated on residue 705 (U-STAT3), chromatin immunoprecipitation assay demonstrated that Y705F mutant STAT3 binds to a consensus GAS motif located in the RGS2 promoter, providing direct evidence that RGS2 is a downstream target of U-STAT3. siRNA-mediated gene knockdown of STAT3 consistently caused decreased RGS2 expression in AT1R overexpressing cells. Conclusions: Chronic activation of AT1R induced U-STAT3 overexpression and subsequently induced overexpression of RGS2, which interacted with and stabilized P-STAT3. P-STAT3 further increases the transcription of stat3 gene, forming a positive feedback loop. We reported for the first time a novel function of RGS2, stabilization of P-STAT3, in mediating U-STAT3 regulated Ang II/AT1R signaling. Further studies are now underway utilizing engineered mice model. This research has received full or partial funding support from the American Heart Association, Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania &amp; West Virginia).
Transcriptional activation of urokinase by the Krüppel-like factor Zf9/COPEB activates latent TGF-β1 in vascular endothelial cells
Authors: Soichi Kojima, Shinichi Hayashi, Kentaro Shimokado, Yasuhiro Suzuki, Jun Shimada, Massimo P. Crippa, Scott L. Friedman
Journal: Blood (2000)
Abstract 19179: Prognostic Value of Combined Coronary Computed Tomography Angiography and Positron Emission Tomography Perfusion Imaging in Patients With Suspected Coronary Artery Disease
Authors: Teemu Maaniitty, Iida Soukka, Antti Saraste, Valtteri Uusitalo, Heikki Ukkonen, Sami Kajander, Maija Mäki, Jeroen Bax, Juhani Knuuti
Journal: Circulation (2014)

Objectives: Hybrid imaging using coronary computed tomography angiography (CTA) and positron emission tomography (PET) perfusion imaging accurately detects functionally significant coronary artery disease (CAD), but its optimal clinical use remains unknown. We studied the prognostic significance of strategy utilizing sequential CTA for exclusion of CAD followed by PET perfusion imaging for evaluating functional significance of any suspected obstructive lesions with a hybrid PET-CT device in symptomatic patients with suspected intermediate probability of CAD. Methods: We identified a cohort of 864 consecutive patients undergone hybrid PET-CT for the detection of suspected CAD. All patients had CTA and based on CTA findings, haemodynamic significance of any suspected stenoses was evaluated by PET perfusion imaging using H 2 15 O during adenosine-induced stress. Major adverse cardiac events (MACE) including death, myocardial infarction (MI) and unstable angina pectoris (UAP), were collected from the national healthcare statistics. Results: After exclusion of 97 patients undergone early (&lt; 6 months) revascularization, 767 patients with age of 61 ± 10 years (41% males) were followed-up for a median time of 2.5 years. During the follow-up 6 deaths, 5 MIs and 3 UAPs occurred. In 462 patients, obstructive CAD was excluded based on CTA alone and the remaining patients with suspected stenoses (n=305, 39.8%) underwent PET perfusion imaging. In patients with normal or non-obstructive CTA annual incidence of MACE was only 0.16%, whereas in patients with suspected stenosis based on CTA it was 1.36% (p&lt;0.05 vs. no stenosis). In patients with suspected obstructive lesion based on CTA, patients with normal PET perfusion had significantly lower event rate than patients with ischemia (0.54 vs. 2.78%, p&lt;0.05). Conclusion: In patients with suspected obstructive CAD PET perfusion imaging after CT angiography is able to accurately identify those patients with high risk of future MACE. Sequential use of CTA and PET perfusion imaging appears powerful and safe strategy for targeting therapeutic procedures in high risk individuals.
Localization of human BRCA1 and its loss in high-grade, non-inherited breast carcinomas
Authors: Cindy A. Wilson, Lillian Ramos, Maria R. Villaseñor, Karl H. Anders, Michael F. Press, Kathy Clarke, Beth Karlan, Jun-Jie Chen, Ralph Scully, David Livingston, Robert H. Zuch, Michael H. Kanter, Sylvan Cohen, Frank J. Calzone, Dennis J. Slamon
Journal: Nature Genetics (1999)
Press: Smear tests and seat belts
Authors: N. W Goodman
Journal: BMJ (2001)

Will cervical cancer screening survive media misunderstanding?

The Times editorial (4 May) got it right: “A collective panic over cervical cancer screening errors will achieve nothing.” The headline writers did not quite see it that way. If they had, the Times ' front page headline would have read: “Cervical tests successful for two thirds of cancers.” Instead, they went for “Cervical tests fail to detect cancer in a third of cases.” By not including the words “shock” or “fears,” the Times ' coverage of the audit of the Leicestershire cervical screening programme was slightly less alarmist than that of other broadsheets.

In an unfortunate coincidence, the report into the locum work of the retired pathologist James Elwood—“who misread the cancer tests of more than 250 patients” ( Daily Mail , 4 May)—was published on the same day as the Leicestershire audit. The Elwood case seems less one of mistaken pathological diagnosis—when his …
Abstract MP48: Genetic Variation, Human Metabolome and Incident Heart Failure among African-Americans in the Atherosclerosis Risk in Communities (ARIC) Study
Authors: Bing Yu, Alanna C Morrison, Thomas H Mosley, Amil M Shah, Scott D Solomon, Calum Macrae, Patricia P Chang, Richard A Gibbs, Eric Boerwinkle
Journal: Circulation (2015)

Introduction: Heart failure (HF) results from the interaction of multiple genes and environmental factors. The human metabolome reflects multiple cellular and physiologic processes and forms a bridge between the genome and HF. Hypothesis: We assessed the hypothesis that the human metabolome is associated with and may mediate the first hospitalization for HF. Methods: We examined the association between the human serum metabolome, measured by GC-MS and LC-MS, and incident hospitalized HF with median 22 years of follow-up among 1850 African-Americans in the Atherosclerosis Risk in Communities (ARIC) Study (HF events = 355). We next tested the relationship of identified metabolites with LV ejection fraction, mass and wall thickness measured by echocardiography. We genotyped a candidate metabolomics-influencing variant, rs77271279, in the entire ARIC cohort (10,263 European-Americans and 3,543 African-Americans) to evaluate its effect on incident HF. Results: Six out of 308 analyzed named metabolites were sig...
Abstract 3661: Crucial roles of cytokine-signaling for alteration in functions of myeloid-derived suppressor cells
Authors: Kentaro Sumida, Yosuke Ono, Junya Ohtake, Kazutaka Masuko, Satoshi Terada, Shun Kaneumi, Takuto Kishikawa, Toshiyuki Kita, Hidemitsu Kitamura
Journal: Cancer Research (2014)

Abstract Various types of myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) were generated from immature myeloid cells (ImCs) according to the state of tumor microenvironments. In human cancer patients, MDSCs are generally defined as monocytic (CD11b+, CD14+, and HLA-DR-/low) or granulocytic (CD11b+ and CD15+) myeloid cells with antitumor and immunosuppressive activities. In order to develop the effective cancer immunotherapy, these immune suppressor populations should be restrictlly controlled in tumor bearing hosts. In the present research, we evaluated the immunological functions of monocytic or granulocytic myeloid cells, which were collected from tumor tissues of colorectal cancer patients. We found here that myeloid populations in tumor tissues significantly induced immuno-modulating factors such as IL-6, IL-10, VEGF, iNOS, ARG1, IDO1, and IDO2. In addition, we confirmed that tumor-infiltrating myeloid-populations exhibited a significant immunosuppressive activity than those prepared from peripheral blood mononuclear cells (PBMCs). To investigate how tumor-infiltrating MDSCs acquired the immunosuppressive activity, we focused on the effect of tumor-derived factors (TDFs) on immunosuppressive activity. PBMCs from healthy volunteers were cultured in the presence of IL-6, TGF-β, and granulocyte macrophage colony-stimulating factor (GM-CSF) for 6 days, and then differentiated into Mo-MDSCs (CD11b+CD14+CD33+)-like phenotype cells. The generated Mo-MDSCs were further isolated by using cell sorter system and cultured with donor matched T cells and stimulated with anti-CD3/CD28 beads for 3 days. As a result, we confirmed that T cell proliferation was significantly inhibited by the addition of Mo-MDSCs generated with IL-6, TGF-β and GM-CSF. On the other hand, these populations showed immunostimulating ability in the presence of IFN-g in vitro, suggesting the Mo-MDSCs might have multi-differencing potentials. These results indicated that tumor-infiltrating MDSCs acquired stronger immunosuppressive activity by tumor-derived IL-6 and TGF-β, however the function might be altered in response to cytokine conditions. Thus, we concluded that IL-6 and TGF-β induced functional maturation of MDSCs in tumor microenvironments, suggesting promising targets to improve the immunological responses by immunotherapy for cancer patients. Citation Format: Kentaro Sumida, Yosuke Ono, Junya Ohtake, Kazutaka Masuko, Satoshi Terada, Shun Kaneumi, Takuto Kishikawa, Toshiyuki Kita, Hidemitsu Kitamura. Crucial roles of cytokine-signaling for alteration in functions of myeloid-derived suppressor cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3661. doi:10.1158/1538-7445.AM2014-3661