tbuckley/cabot-search huggingface dataset:
Population-Based Study of Diabetes and Risk Characteristics in Turkey
Authors: Ilhan Satman, Temel Yilmaz, Ahmet Sengül, Serpil Salman, Fatih Salman, Sevil Uygur, Irfan Bastar, Yildiz Tütüncü, Mehmet Sargin, Nevin Dinççag, Kubilay Karsidag, Sibel Kalaça, Cihangir Özcan, Hilary King
Journal: Diabetes Care (2002)

OBJECTIVES—To investigate for the first time the prevalence of diabetes and impaired glucose tolerance (IGT) nationwide in Turkey; to assess regional variations and relationships between glucose intolerance and lifestyle and physical risk factors. RESEARCH DESIGN AND METHODS—The Turkish Diabetes Epidemiology Study (TURDEP) is a cross-sectional, population-based survey that included 24,788 subjects (age ≥20 years, women 55%, response 85%). Glucose tolerance was classified according to World Health Organization recommendations on the basis of 2-h blood glucose values. RESULTS—Crude prevalence of diabetes was 7.2% (previously undiagnosed, 2.3%) and of IGT, 6.7% (age-standardized to world and European populations, 7.9 and 7.0%). Both were more frequent in women than men (P &amp;lt; 0.0001) and in those living in urban rather than rural communities (P &amp;lt; 0.001). Prevalence rates of hypertension and obesity were 29 and 22%, respectively. Both were more common among women than men (P &amp;lt; 0.0001). Prevalence of diabetes and IGT increased with rising BMI, waist-to-hip ratio (WHR), and waist girth (P &amp;lt; 0.0001). Multiple logistic regression analysis revealed that age, BMI, WHR, familial diabetes, and hypertension were independently associated with diabetes, age, BMI, WHR, familial diabetes, and hypertension with IGT (except for familial diabetes in women with IGT). Education was related to diabetes in men but was protective for diabetes and IGT in women. Socioeconomic status appeared to decrease the risk of IGT in men while it increased the risk in women. Smoking had a protective effect for IGT in both sexes. CONCLUSIONS—Diabetes and IGT are moderately common in Turkey by international standards. Associations with obesity and hypertension have been confirmed. Other lifestyle factors had a variable relationship with glucose tolerance.
Standard tobacco packaging still being considered but is not a "silver bullet," says health department
Authors: A. O'Dowd
Journal: BMJ (2013)

Proposals for England to introduce standardised packaging of tobacco products are still under “active consideration” by the government but are not the only possible solution to reduce smoking, MPs have been told.

During a passionate two and a half hour debate on standardised packaging of tobacco products, held in the House of Commons on 7 November, MPs argued about the imperative for and the possible overestimated benefits from such packaging being adopted.

The Department of Health held a consultation on standardised packaging between April and August of 2012,1 and in July this year it announced that it wanted to wait for more evidence on the effects of such packaging on tobacco consumption before deciding whether to adopt the policy.2

Bob Blackman, the Conservative MP for Harrow East and secretary of the all party group on smoking and health, opening the debate, said, “At the moment there is still an attractive promotional aspect of tobacco, which …
Oedemerid blister beetle dermatosis
Authors: D. Nicholls, Deborah Greig
Journal: British Journal of Dermatology (1988)

Journal Article Oedemerid blister beetle dermatosis Get access D. Nicholls, D. Nicholls St. John's Hospital for Diseases of the Skin, London Search for other works by this author on: Oxford Academic Google Scholar Deborah Greig Deborah Greig Auckland Hospital, Auckland, New Zealand Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 119, Issue s33, 1 July 1988, Pages 20–21, https://doi.org/10.1111/j.1365-2133.1988.tb05345.x Published: 01 July 1988
c-Jun NH2-terminal kinase-dependent upregulation of DR5 mediates cooperative induction of apoptosis by perifosine and TRAIL
Authors: Lei Fu, Yi-Dan Lin, Heath A Elrod, Ping Yue, Youtake Oh, Bo Li, Hui Tao, Georgia Z Chen, Dong M Shin, Fadlo R Khuri, Shi-Yong Sun
Journal: Molecular Cancer (2010)

Abstract Background Perifosine, an alkylphospholipid tested in phase II clinical trials, modulates the extrinsic apoptotic pathway and cooperates with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to augment apoptosis. The current study focuses on revealing the mechanisms by which perifosine enhances TRAIL-induced apoptosis. Results The combination of perifosine and TRAIL was more active than each single agent alone in inducing apoptosis of head and neck squamous cell carcinoma cells and inhibiting the growth of xenografts. Interestingly, perifosine primarily increased cell surface levels of DR5 although it elevated the expression of both DR4 and DR5. Blockade of DR5, but not DR4 upregulation, via small interfering RNA (siRNA) inhibited perifosine/TRAIL-induced apoptosis. Perifosine increased phosphorylated c-Jun NH 2 -terminal kinase (JNK) and c-Jun levels, which were paralleled with DR4 and DR5 induction. However, only DR5 upregulaiton induced by perifosine could be abrogated by both the JNK inhibitor SP600125 and JNK siRNA. The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5. Moreover, no increased production of reactive oxygen species was detected in perifosine-treated cells although reduced levels of intracellular GSH were measured. Conclusions DR5 induction plays a critical role in mediating perifosine/TRAIL-induced apoptosis. Perifosine induces DR5 expression through a JNK-dependent mechanism independent of reactive oxygen species.
ABSENCE OF THE GLOXYLATE SHUNT IN THE SKIN OF MOUSE AND RAT
Authors: Paul D. Mier, Jose J. M. A. Hurk
Journal: British Journal of Dermatology (1973)

Journal Article ABSENCE OF THE GLOXYLATE SHUNT IN THE SKIN OF MOUSE AND RAT Get access Paul D. Mier, Paul D. Mier Department of Dermatology University of Nijmegan The Netherlands Search for other works by this author on: Oxford Academic Google Scholar José J. M. A. van den Hurk José J. M. A. van den Hurk Department of Dermatology University of Nijmegan The Netherlands Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 88, Issue 3, 1 March 1973, Pages 308–309, https://doi.org/10.1111/j.1365-2133.1973.tb07555.x Published: 01 March 1973
Expression of endothelial nitric oxide synthase in human eccrine clear cells
Authors: Y. SIIIMIZU, M. SAKAI, Y. UMEMURA, H. UEDA
Journal: British Journal of Dermatology (1997)

Nitric oxide is generated from L-arginine by nitric oxide synthase (NOS), which has at least three isoforms; endothelial-type NOS (eNOS) and brain-type NOS (bNOS) are constitutive enzymes, and inducible-type NOS (iNOS) is expressed after stimulation. Studies by the avidin-biotin immunocomplex method, revealed eNOS immunoreactivity exclusively in the human eccrine clear cells. No eNOS immunoreactivity was observed in the eccrine dark cells or myoepithelial cells. No staining of iNOS or bNOS was observed in the eccrine gland. These findings indicate that NO plays a physiological part in the production and/or excretion of sweat in the human skin eccrine gland.
Interleukin-10 Deficiency Impairs Bone Marrow–Derived Endothelial Progenitor Cell Survival and Function in Ischemic Myocardium
Authors: Prasanna Krishnamurthy, Melissa Thal, Suresh Verma, Eneda Hoxha, Erin Lambers, Veronica Ramirez, Gangjian Qin, Douglas Losordo, Raj Kishore
Journal: Circulation Research (2011)

Endothelial progenitor cell (EPC) survival and function in the injured myocardium is adversely influenced by hostile microenvironment such as ischemia, hypoxia, and inflammatory response, thereby compromising full benefits of EPC-mediated myocardial repair.We hypothesized that interleukin-10 (IL-10) modulates EPC biology leading to enhanced survival and function after transplantation in the ischemic myocardium.Myocardial infarction (MI)-induced mobilization of bone marrow EPC (Sca-1+Flk1+cells) into the circulation was significantly impaired in IL-10 knockout (KO) mice. Bone marrow transplantation to replace IL-10 KO marrow with wild-type (WT) marrow attenuated these effects. Impaired mobilization was associated with lower stromal cell-derived factor (SDF)-1 expression levels in the myocardium of KO mice. Interestingly, SDF-1 administration reversed mobilization defect in KO mice. In vitro, hypoxia-mediated increases in CXCR4 expression and cell survival were lower in IL-10-deficient EPCs. Furthermore, SDF-1-induced migration of WT EPCs was inhibited by AMD3100, an inhibitor of CXCR4. To further study the effect of IL-10 on in vivo EPC survival and engraftment into vascular structures, GFP-labeled EPC were injected intramyocardially after induction of MI, and the mice were treated with either saline or recombinant IL-10. The IL-10-treated group showed increased retention of transplanted EPCs in the myocardium and was associated with significantly reduced EPC apoptosis after MI. Interestingly, increased EPC retention and their association with the vascular structures was observed in IL-10-treated mice. Increased EPC survival and angiogenesis in the myocardium of IL-10-treated mice corroborated with improved left ventricular function, reduced infarct size, and fibrosis in the myocardium. In vitro, IL-10-induced increase in VEGF expression in WT EPC was abrogated by STAT3 inhibitor, suggesting IL-10 signals through STAT3 activation.Taken together, our studies demonstrate that MI-induced EPC mobilization was impaired in IL-10 KO mice and that IL-10 increases EPC survival and function possibly through activation of STAT3/VEGF signaling cascades, leading to attenuation of MI-induced left ventricular dysfunction and remodeling.
Strategies to Prevent and Control the Emergence and Spread of Antimicrobial-Resistant Microorganisms in Hospitals
Authors: D A Goldmann, R A Weinstein, R P Wenzel, O C Tablan, R J Duma, R P Gaynes, J Schlosser, W J Martone
Journal: JAMA (1996)

<h3>Objective.</h3> —To provide hospital leaders with strategic goals or actions likely to have a significant impact on antimicrobial resistance, outline outcome and process measures for evaluating progress toward each goal, describe potential barriers to success, and suggest countermeasures and novel improvement strategies. <h3>Participants.</h3> —A multidisciplinary group of experts was drawn from the following areas: hospital epidemiology and infection control, infectious diseases (including graduate training programs), clinical practice (including nursing, surgery, internal medicine, and pediatrics), pharmacy, administration, quality improvement, appropriateness evaluation, behavior modification, practice guideline development, medical informatics, and outcomes research. Representatives from appropriate federal agencies, the Joint Commission on Accreditation of Healthcare Organizations, and the pharmaceutical industry also participated. <h3>Evidence.</h3> —Published literature, guidelines, expert opinion, and practical experience regarding efforts to improve antibiotic utilization and prevent and control the emergence and dissemination of antimicrobial-resistant microorganisms in hospitals. <h3>Consensus Process.</h3> —Participants were divided into two quality improvement teams: one focusing on improving antimicrobial usage and the other on preventing and controlling transmission of resistant microorganisms. The teams modeled the process a hospital might use to develop and implement a strategic plan to combat antimicrobial resistance. <h3>Conclusions.</h3> —Ten strategic goals and related process and outcome measures were agreed on. The five strategic goals to optimize antimicrobial use were as follows: optimizing antimicrobial prophylaxis for operative procedures; optimizing choice and duration of empiric therapy; improving antimicrobial prescribing by educational and administrative means; monitoring and providing feedback regarding antibiotic resistance; and defining and implementing health care delivery system guidelines for important types of antimicrobial use. The five strategic goals to detect, report, and prevent transmission of antimicrobial resistant organisms were as follows: to develop a system to recognize and report trends in antimicrobial resistance within the institution; develop a system to rapidly detect and report resistant microorganisms in individual patients and ensure a rapid response by caregivers; increase adherence to basic infection control policies and procedures; incorporate the detection, prevention, and control of antimicrobial resistance into institutional strategic goals and provide the required resources; and develop a plan for identifying, transferring, discharging, and readmitting patients colonized with specific antimicrobial-resistant pathogens. (<i>JAMA</i>. 1996;275:234-240)
Roentgenographic Identification of Human Remains
Authors: Leonard Atkins
Journal: JAMA (1978)

BONE roentgenograms as a means of identifying human remains can be of great value to medical examiners. This is especially true when there is need to identify an unknown decomposed body of an adult without fingerprints. Teeth, as landmarks, may be of help, but they may be absent (as in the case presented) or antemortem dental records may not be available for comparison. Since bone roentgenograms are common diagnostic examinations, an antemortem study may be available for comparison. The following case illustrates this point, and in the Comment legal points are made about using this kind of evidence. <h3>Report of a Case</h3> On July 6, 1977, a human skull with a missing mandible was found on the shore of Deer Island in Boston Harbor. Only one upper molar tooth was present, and the remaining tooth sockets were empty. One month later skeletal remains consisting of a torso and limbs with
INFECTIVITY OF BLOOD DURING THE COURSE OF EXPERIMENTAL YELLOW FEVER
Authors: N. Paul Hudson, Cornelius B. Philip
Journal: The Journal of Experimental Medicine (1929)

Five M. rhesus fatally infected with yellow fever virus ran varied and typical courses, death occurring from 82 hours to 10 days after infecting. Batches of A. aegypti were fed daily on each monkey and specimens of blood injected into other animals. By mosquito transfer, the virus was found to be circulating in the peripheral blood 1 or 2 days after the infecting and the same interval before the onset of fever; in one instance, mosquitoes became infectious by feeding on a monkey 12 hours after its inoculation. Mosquitoes continued to acquire infectivity during the febrile period and for 1 day thereafter, except in one instance when death occurred during fever which prevented post-febrile testing. By subinoculation of blood, the disease was transferred before and after, as well as during the same interval as in mosquito transmission. In one of two attempts, the virus was carried by this means as early as 12 hours after the donor animal was infected. Following the first day of the post-febrile period, blood transmissions were irregularly fatal beyond the period infective for mosquitoes. These results point to a remarkably rapid multiplication of the virus in the animal host, in one case a blood subinoculation (0.5 cc.) being successful at the first test 24 hours after the donor monkey was bitten by only 2 A. aegypti. The regular acquisition of infectivity by mosquitoes fed during the incubation period is of especial interest in indicating the infectivity of human cases for mosquitoes before the appearance of clinical symptoms. This offers one explanation for the insidious propagation of epidemics of yellow fever and should be useful in the institution of control activities during an outbreak of this disease.
Corrigendum to “Corticosteroids stimulate selectively transforming growth factor (TGF)-β receptor type III expression in transdifferentiating hepatic stellate cells”[J Hepatol 40 (2004) 69–76]
Authors: Lucia Wickert, Muna Abiaka, Ursula Bolkenius, Axel M. Gressner
Journal: Journal of Hepatology (2004)
AIDS in Paradise
Authors: R E Koenig
Journal: JAMA (1999)

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American Society of Clinical Oncology Clinical Practice Guideline on Uses of Serum Tumor Markers in Adult Males With Germ Cell Tumors
Authors: Timothy D. Gilligan, Jerome Seidenfeld, Ethan M. Basch, Lawrence H. Einhorn, Timothy Fancher, David C. Smith, Andrew J. Stephenson, David J. Vaughn, Roxanne Cosby, Daniel F. Hayes
Journal: Journal of Clinical Oncology (2010)

Purpose To provide recommendations on appropriate uses for serum markers of germ cell tumors (GCTs). Methods Searches of MEDLINE and EMBASE identified relevant studies published in English. Primary outcomes included marker accuracy to predict the impact of decisions on outcomes. Secondary outcomes included proportions of patients with elevated markers and statistical tests of elevations as prognostic factors. An expert panel developed consensus guidelines based on data from 82 reports. Results No studies directly compared outcomes of decisions with versus without marker assays. The search identified few prospective studies and no randomized controlled trials; most were retrospective series. Lacking data on primary outcomes, most Panel recommendations are based on secondary outcomes (relapse rates and time to relapse). Recommendations The Panel recommended against using markers to screen for GCTs, to decide whether orchiectomy is indicated, or to select treatment for patients with cancer of unknown primary. To stage patients with testicular nonseminomas, the Panel recommended measuring three markers (α-fetoprotein [AFP], human chorionic gonadotropin [hCG], and lactate dehydrogenase [LDH]) before and after orchiectomy and before chemotherapy for those with extragonadal nonseminomas. They also recommended measuring AFP and hCG shortly before retroperitoneal lymph node dissection and at the start of each chemotherapy cycle for nonseminoma, and periodically to monitor for relapse. The Panel recommended measuring postorchiectomy hCG and LDH for patients with seminoma and preorchiectomy elevations. They recommended against using markers to guide or monitor treatment for seminoma or to detect relapse in those treated for stage I. However, they recommended measuring hCG and AFP to monitor for relapse in patients treated for advanced seminoma.
p73 or p53 Directly Regulates Human <i>p53</i> Transcription to Maintain Cell Cycle Checkpoints
Authors: Shulin Wang, Wafik S. El-Deiry
Journal: Cancer Research (2006)

Abstract Whereas the p53 tumor suppressor protein plays a central role in cellular checkpoints that respond to damage or stress to prevent tumorigenesis, the transcriptional control of the p53 gene has remained unclear. We show that chemotherapeutic agents induce p53 transcription and that p73 or p53 transactivates endogenous p53 expression through direct binding to the p53 promoter. Silencing of p53 or p73 by RNA interference significantly suppresses p53 transcription under physiologic conditions or in response to cellular stress. Mutational analysis of the human p53 promoter localized a p53 DNA-binding site, which confers p53- or p73-dependent p53 promoter activation. Importantly, impaired p53-mediated autoregulation of p53 transcription by inducible-interfering RNA results in aberrant cell cycle regulation and suppression of p53-mediated apoptosis. Thus, a positive feedback loop regulates human p53 expression and involves p73 and p53. Disruption of p53 transcription contributes to defective checkpoint control. (Cancer Res 2006; 66(14): 6982-9)
TGF-β1/ALK5-induced monocyte migration involves PI3K and p38 pathways and is not negatively affected by diabetes mellitus
Authors: Servé Olieslagers, Evangelia Pardali, Vadim Tchaikovski, Peter ten Dijke, Johannes Waltenberger
Journal: Cardiovascular Research (2011)

Monocytes contribute to arteriogenesis by infiltration to sites of collateral growth and subsequent production and release of growth factors. Transforming growth factor β1 (TGF-β1) mediates monocyte motility and stimulates arteriogenesis. TGF-β1 signalling mechanisms mediating monocyte motility are unknown so far. Moreover, the influence of cardiovascular risk factor diabetes on TGF-β1-induced monocyte migration remains to be elucidated. Stimulation of primary human monocytes with TGF-β1 endorsed phosphorylation of v-Akt murine thymoma viral oncogene analogues protein (AKT), p38, and extracellular signal-related kinase 1/2 (ERK1/2), besides the activation of the SMA/MAD homologues protein (SMAD) pathway. Inhibition of the TGF-βtype 1 receptor, alias activin receptor-like kinase 5 (ALK5), hindered monocyte chemotaxis towards TGF-β1 and TGF-β1-activated downstream signalling cascades. Individual genetic knock-downs for receptor-regulated SMAD2 and SMAD3 did not affect monocyte migration to TGF-β1. Inhibition of phosphoinositide 3 kinase (PI3K) activity, but not AKT, diminished both basal and TGF-β1-mediated monocyte motility. TGF-β1-induced monocyte chemotaxis did not rely on ERK1/2, but rather on p38. Remarkably, TGF-β1 was able to stimulate chemotaxis of diabetic monocytes. The current study provides novel insights into the molecular mechanisms of TGF-β1-induced monocyte migration, requiring ALK5 kinase activity and signalling via PI3K and p38. TGF-β1-driven monocyte motogenicity is fully functional in diabetic conditions, which is in sharp contrast to the impaired chemotactic responses to certain other arteriogenic cytokines. Therefore, TGF-β1 may be a promising candidate for endogenously and exogenously stimulating collateral growth in diabetic patients.