tbuckley/cabot-search huggingface dataset:
Coping Style in Relation to the Consumption of Factor Concentrate in HIV-Infected Hemophiliacs during the Years after Their Infection Became Known
Authors: Vanja Blomkvist, Töres Theorell, Hans Jonsson, Sam Schulman, Erik Berntorp, Lennart Stiegendal
Journal: Psychotherapy and Psychosomatics (1994)

A psychosocial investigation offered to all HIV-infected men with moderately severe or severe hemophilia in Sweden was made in 1986. Most of these men had been infected in the years 1980-1984 and told about their own infection in 1985. A noninfected group of hemophiliacs was used as a reference group in the psychosocial investigation. A psychosocial prognosis was made on the basis of the coping style observed by means of the Coping Wheel. Among subjects who showed evidence of a passive-pessimistic coping style, there was a significant decrease in the number of factor concentrate units received in 1987 and 1988. Among subjects in the group with a more active-optimistic coping style, there was a tendency of increasing the use of factor concentrate during the years after the HIV-infection became known. This result indicates that awareness of HIV-infection may influence specific hemophilia behavior among subjects with passive-depressed coping style.
Scintigraphic Visualization of Human Malignant Melanoma with N-isopropyl-P-[l-123] lodoamphetamine
Authors: MAKOTO WADA, YUICHI ICHIYA, MAKOTO KATSURAG, YASUO KUWABARA, ZENJI AYABE, KEIICH MATSUURA, YASUZO TAKESHITA
Journal: Clinical Nuclear Medicine (1985)

Marked accumulation of I-123 IMP was noted in a patient with malignant melanoma. This preliminary finding suggests the potential role of I-123 IMP for detection and evaluation of the disease.
The Problems Presented by School Preventive Medicine in Rural Areas
Authors: A. C. T. Perkins
Journal: BMJ (1929)

th'e jwvicardial sac were 19 oz. of straw-coloured fluid(l.'I'lR P)arietal hiver of p)ericardium was adhllerent to th( let lulln, and(l the -visceral layer was covered withi organized fib)int, especiallv at the base of the lheart.The uwo- cat-dittra was pale and slightly softened.Three eavitje.s, or aneurysmal dilatations (Fig. 2), occupied the posterior j)ait of tihe b)ase of the left ventricle; their diameters were 1'-, 1/2, ald(l 1/2 ii.Theil ventri(ular surface was covetred R ittl rouigh injected( giaiinilation tissite:
Type I interferon system activation and association with disease manifestations in systemic sclerosis
Authors: M.-L. Eloranta, K. Franck-Larsson, T. Lovgren, S. Kalamajski, A. Ronnblom, K. Rubin, G. V. Alm, L. Ronnblom
Journal: Annals of the Rheumatic Diseases (2010)

<h3>Objectives</h3> To study the presence of interferogenic autoantibodies in systemic sclerosis (SSc) and their correlation with clinical manifestations, serum levels of interferon α (IFNα) and chemokines of importance in the disease process. <h3>Methods</h3> Peripheral blood mononuclear cells (PBMCs) or purified plasmacytoid dendritic cells (pDCs) from healthy donors were stimulated with sera from patients with SSc (n=70) or healthy individuals (n=30), together with necrotic or apoptotic cell material. The IFNα produced and serum levels of IFNα, IFN-inducible protein-10 (IP-10)/chemokine (C-X-C motif) ligand 10, monocyte chemoattractant protein-1 (MCP-1)/(C-C motif) ligand-2 (CCL-2), macrophage inflammatory protein-1α (MIP-1α)<b>/</b>CCL-3 and RANTES/CCL-5 were measured and correlated with the presence of autoantibodies and clinical manifestations in the patients with SSc. <h3>Results</h3> Sera from both diffuse SSc and limited SSc contained interferogenic antibodies, which correlated with the presence of anti-ribonucleoprotein and anti-Sjögren syndrome antigen autoantibodies. The pDCs were responsible for the IFNα production which required interaction with FcγRII and endocytosis. Increased serum levels of IP-10 were associated with vascular manifestations such as cardiac involvement (p=0.027) and pulmonary arterial hypertension (p=0.036). Increased MCP-1 or IFNα serum levels were associated with lung fibrosis (p=0.019 and 0.048, respectively). Digital ulcers including digital loss were associated with increased serum levels of IFNα (p=0.029). <h3>Conclusion</h3> An activated type I IFN system previously seen in several other systemic autoimmune diseases is also present in SSc and may contribute to the vascular pathology and affect the profibrotic process.
Abstract 688: Promoter methylation of death receptor decoy genes in blood and risk of melanoma in melanoma-prone families .
Authors: Paula L. Hyland, Laura S. Burke, Ruth M. Pfeiffer, Margaret A. Tucker, Alisa M. Goldstein, Xiaohong R. Yang
Journal: Cancer Research (2013)

Abstract Background: Cutaneous malignant melanoma (CMM) is an etiologically heterogeneous disease with genetic, environmental, and host characteristics and their interactions contributing to risk. Recently, gene-specific promoter methylation in blood has been associated with the risk of several cancers including breast, lung and pancreatic. We thus examined whether gene-specific promoter methylation was associated with risk of CMM in individuals from melanoma-prone families. Methods: We measured the promoter methylation status of 15 genes (CDH1, COL1A2, DAPK, DDIT4L, HSPB6, LOX, MT1G, NPM2, p14, p16, PTEN, RASSF1, MAGEA3, TNFRSF10C and TNFRSF10D) previously shown to be aberrantly methylated in melanoma tumors using bisulfite pyrosequencing at 65 CpGs in peripheral blood mononuclear cells (PBMCs) from 236 individuals (114 melanoma cases and 122 unaffected individuals) in 64 melanoma-prone families. For functional validation we obtained gene expression data for 14 out of the 15 genes through independent expression profiling analysis. We also compared the values from each methylated promoter to mRNA expression. We used logistic regression to evaluate the association between CMM status and average promoter methylation controlling for age, sex and adjusting variance for familial correlation. Results: In unaffected individuals, overall promoter methylation levels were low for most of these genes in blood. Only TNFRSF10C (P=0.009) and TNFRSF10D (P=0.010) showed the expected negative correlation between promoter methylation and gene expression. Therefore, we focused on these two genes in subsequent analyses. Compared to controls, CMM cases had significantly lower promoter methylation at TNFRSF10C (P= 0.002) and TNFRSF10D (P=0.045). This difference remained significant after further adjusting for CDKN2A, dysplastic nevi and pigmentation characteristics. Significance: TNFRSF10C and TNFRSF10D encode separate decoy death receptors, whose overexpression in both normal and malignant cells can inhibit apoptosis. Our findings support a potential association between reduced promoter methylation of TNFRSF10C and TNFRSF10D in blood and risk of CMM in our melanoma-prone families. Citation Format: Paula L. Hyland, Laura S. Burke, Ruth M. Pfeiffer, Margaret A. Tucker, Alisa M. Goldstein, Xiaohong R. Yang. Promoter methylation of death receptor decoy genes in blood and risk of melanoma in melanoma-prone families . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 688. doi:10.1158/1538-7445.AM2013-688
Association of diabetes mellitus and chronic hepatitis C virus infection
Authors: Andrew L. Mason, Johnson Y. Lau, Nicole Hoang, KePing Qian, Graeme J. Alexander, Lizhe Xu, Linsheng Guo, Sheraj Jacob, Fredric G. Regenstein, Robert Zimmerman, James E. Everhart, Clive Wasserfall, Noel K. Maclaren, Robert P. Perrillo
Journal: Hepatology (1999)

While patients with liver disease are known to have a higher prevalence of glucose intolerance, preliminary studies suggest that hepatitis C virus (HCV) infection may be an additional risk factor for the development of diabetes mellitus. To further study the correlation of HCV infection and diabetes, we performed a retrospective analysis of 1,117 patients with chronic viral hepatitis and analyzed whether age, sex, race, hepatitis B virus (HBV) infection, HCV infection, and cirrhosis were independently associated with diabetes. In addition, a case-control study was conducted to determine the seroprevalence of HCV infection in a cohort of 594 diabetics and 377 clinic patients assessed for thyroid disease. In the former study after the exclusion of patients with conditions predisposing to hyperglycemia, diabetes was observed in 21% of HCV-infected patients compared with 12% of HBV-infected subjects (P =.0004). Multivariate analysis revealed that HCV infection (P =.02) and age (P =.01) were independent predictors of diabetes. In the diabetes cohort, 4.2% of patients were found to be infected with HCV compared with 1.6% of control patients (P =.02). HCV genotype 2a was observed in 29% of HCV-RNA-positive diabetic patients versus 3% of local HCV-infected controls (P <.005). In conclusion, the data suggest a relatively strong association between HCV infection and diabetes, because diabetics have an increased frequency of HCV infection, particularly with genotype 2a. Furthermore, it is possible that HCV infection may serve as an additional risk factor for the development of diabetes, beyond that attributable to chronic liver disease alone.
Abstract 5458: GADD45α nickel induction inhibits JNKs/p38 activity by promoting PP2Cα expression
Authors: Yonghui Yu, Jingxia Li, Yu Wan, Jimin Gao, Chuanshu Huang
Journal: Cancer Research (2012)

Abstract Growth arrest and DNA damage (GADD) 45α is a member of GADD inducible gene family, which can be induced in cell response to oxidative stresses. GADD45α upregulation is able to induce MKK4/JNK activation in some published experimental systems. However, we demonstrated here that the depletion of GADD45α in mouse embryonic fibroblasts (MEFs) (GADD45α-/-) resulted in an increase in the phosphorylation of MKK4/7, MKK3/6 and consequently specific up-regulated the activation of JNK/p38 and their downstream transcription factors, such as c-Jun and ATF2, in comparison to those in GADD45α+/+ MEFs due to nickel exposure. This up-regulation of MKK-JNK/p38 pathway in GADD45α-/- could be rescued by the re-constitutional expression of HA-GADD45α in GADD45α-/-, GADD45α-/- (HA-GADD45α). Subsequent studies indicated that GADD45α deletion repressed expression of PP2Cα, the phosphotase of MKK3/6 and MKK4/7. Collectively, our results demonstrate a novel function and mechanisms responsible for GADD45α regulation of MKK/MAPK pathway, further provides insight into understanding the big picture of GADD45α in the regulation of cellular responses to oxidative stress and environmental carcinogens. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5458. doi:1538-7445.AM2012-5458
The Teaching of Proctology and the Role and Associations of the Specialty
Authors: Raymond J. Jackman
Journal: JAMA (1965)

In<i>Origin of Species</i>, Charles Darwin wrote about "how plants and animals remote in the scale of nature are bound together by a web of complex relations." His example of the red clover and its relationship to the bumblebees which pollinate it is a classic in descriptive ecology. He discovered that bumblebees, which have exceptionally long tongues, are the only insects which can effectively pollinate the deep-red clover flowers. From this he argued that the success of red clover in England can be attributed to the fact that bumblebees are so prevalent there. He then proceeded to quote an authority who had found that there were more bumblebee nests in the vicinity of towns and villages than elsewhere because field mice, which eat bumblebee combs and larvae, are scarce around towns. Field mice are scarce around towns because towns usually have a large number of cats which prey on field
Technology for minimal access surgery
Authors: A. Cuschieri
Journal: BMJ (1999)

One of the important changes in medical practice over the past two decades has been the reduction in traumatic insult inherent in surgical interventions. The new surgical and interventional approaches are usually referred to as minimally invasive. However, this terminology is inappropriate for two reasons. Firstly, it carries connotations of increased safety, which is not the case. Secondly, it is semantically incorrect since to invade is absolute, and indeed such interventions are as invasive as open surgery in terms of reach of the various organs and tissues. The hallmark of the new approaches is the reduction in the trauma of access. Hence, a more appropriate generic term is minimal access therapy.1 

#### Summary points

Minimal access therapy comprises minimal access surgery, interventional flexible endoscopy, and percutaneous interventional radiology

The main advantage is reduced trauma of access, which allows more rapid recovery

Imaging systems which allow surgeons to look down on the operating field help overcome mapping problems and improve performance

New instruments are being developed that give surgeons greater freedom of movement

Operating theatres need to be specially designed to cope with the new equipment

Minimal access therapy comprises several approaches, involves various disciplines, and cuts across the various specialties within these disciplines. In essence, however, it has three arms: minimal access surgery, interventional flexible endoscopy, and percutaneous interventional radiology. These therapeutic approaches are largely complementary, and increasingly they are used together to treat individual cases. The advent of minimal access therapy has emphasised the need to regroup existing specialists from different disciplines to form multidisciplinary disease related treatment groups—for example, gastrointestinal, cardiovascular, or musculoskeletal groups. Such groups would facilitate real progress and efficiency in management and treatment of many diseases.

Minimal access therapy aims to minimise the traumatic insult to the patient without compromising the safety and efficacy of the treatment …
Referral patterns and diagnoses in women attending a urodynamic unit.
Authors: D. P. Keane, S. D. Eckford, A. M. Shepherd, P. Abrams
Journal: BMJ (1992)

Although it is recognised that the prevalence of urinary incontinence increases with age,' it is not known whether this is mirrored by a similar increase in referral for urodynamic studies.The aim of this study was to determine the association with age of referral patterns and urodynamic diagnoses in women with urinary incontinence.
t(5;12)(q23–31;p13) with ETV6-ACSL6 gene fusion in polycythemia vera
Authors: A Murati, J Adélaïde, V Gelsi-Boyer, A Etienne, V Rémy, H Fezoui, D Sainty, L Xerri, N Vey, S Olschwang, D Birnbaum, M Chaffanet, M J Mozziconacci
Journal: Leukemia (2006)
787 BMS-766, A NOVEL HCV NS5A INHIBITOR WITH ENHANCED RESISTANCE COVERAGE
Authors: M. Gao, R. Fridell, C. Wang, J.-H. Sun, D. O'boyle, L. Valera, P. Nower, A. Monikowski, M. Kirk, H. Huang, C. Ngo, H. Fang, R. Knox, Y.-K. Wang, V. Nguyen, F. Wang, L. Snyder, R. Lavoie, J. Bender, J. Kadow, M. Cockett, N. Meanwell, M. Belema
Journal: Journal of Hepatology (2011)
Serotonin Transporter Inhibition Prevents and Reverses Monocrotaline-Induced Pulmonary Hypertension in Rats
Authors: Christophe Guignabert, Bernadette Raffestin, Rima Benferhat, William Raoul, Patricia Zadigue, Dominique Rideau, Michel Hamon, Serge Adnot, Saadia Eddahibi
Journal: Circulation (2005)

Background— Progression of pulmonary hypertension (PH) is associated with increased lung expression of the serotonin transporter (5-HTT), which leads to hyperplasia of the pulmonary artery smooth muscle cells (PA-SMCs). Given the postulated causal relation between 5-HTT overexpression and PH, we herein investigated whether the highly selective 5-HTT inhibitor fluoxetine prevented and/or reversed PH induced by monocrotaline (MCT) in rats. Selective 5-HT 1B/1D , 5-HT 2A , and 5-HT 2B receptor antagonists were used for comparative testing. Methods and Results— MCT injection (60 mg/kg SC) was followed by an early peak in lung 5-HTT expression on day 1, which preceded the onset of PH. Established PH on day 15 was associated with a sustained 5-HTT increase. Continued fluoxetine treatment completely prevented PA-SMC proliferation and PH development and also suppressed the late 5-HTT increase, without affecting the early peak. The 5-HT receptor antagonists did not affect PH. Fluoxetine (10 mg · kg −1 · d −1 PO) started 3 weeks after MCT injection completely reversed established PH, normalizing PA pressure and structure. MCT-induced PH was also associated with increased expression of various cytokines, but only interleukin-1β and monocyte chemotactic protein-1 increased at the early phase and stimulated 5-HTT expression by cultured PA-SMCs. Conclusion— Upregulation of lung 5-HTT induced by MCT appears necessary to initiate the development of pulmonary vascular remodeling, whereas a sustained increase in 5-HTT expression may underlie both the progression and the maintenance of MCT-induced PH. Complete reversal of established PH by fluoxetine provides a rationale for new therapeutic strategies in human PH.
Direct Activation of Emmprin and Associated Pathogenesis by an Oncogenic Herpesvirus
Authors: Zhiqiang Qin, Lu Dai, Mark G. Slomiany, Bryan P. Toole, Chris Parsons
Journal: Cancer Research (2010)

Emmprin (extracellular matrix metalloproteinase inducer) is a multifunctional glycoprotein expressed by cancer cells and stromal cells in the tumor microenvironment. Through both direct effects within tumor cells and promotion of tumor-stroma interactions, emmprin induces tumor cell invasiveness and regional angiogenesis. The Kaposi's sarcoma-associated herpesvirus (KSHV) is a common etiology for cancers arising in the setting of immune suppression, including Kaposi's sarcoma and primary effusion lymphoma. However, whether emmprin expression and function are regulated by KSHV or other oncogenic viruses in the tumor microenvironment to promote viral cancer pathogenesis remains unknown. Fibroblasts and endothelial cells support latent KSHV infection and represent cellular components of Kaposi's sarcoma lesions. Therefore, we used primary human fibroblasts and endothelial cells to determine whether KSHV itself regulates emmprin expression, and whether KSHV-emmprin interactions mediate cell invasiveness. We found that KSHV promotes fibroblast and endothelial cell invasiveness following de novo infection through the upregulation of emmprin, and that this effect is mediated by the KSHV-encoded latency-associated nuclear antigen. We also found that emmprin promotes invasiveness, as well as colony formation, by primary effusion lymphoma cells derived from human tumors. Collectively, these data implicate KSHV activation of emmprin as an important mechanism for cancer progression and support the potential utility of targeting emmprin as a novel therapeutic approach for KSHV-associated tumors.
Serum Interleukin-6 Level but not Genotype Predicts Survival after Resection in Stages II and III Gastric Carcinoma
Authors: Wei-Chih Liao, Jaw-Town Lin, Chun-Ying Wu, Shih-Pei Huang, Ming-Tsan Lin, Ariel Sing-Huei Wu, Yu-Jie Huang, Ming-Shiang Wu
Journal: Clinical Cancer Research (2008)

Abstract Purpose: It has been suggested that interleukin-6 (IL-6) is a prognostic indicator for survival in patients with gastric carcinoma, but this has not been proved using survival analysis. In Asians, the −634G allele is associated with increased IL-6 production. The objective of this study was to evaluate the association between serum IL-6 levels, −634G/C polymorphism, and overall survival after resection for gastric carcinoma. Experimental Design: A total of 155 consecutive patients with gastric carcinoma were evaluated. Serum IL-6 levels were analyzed using an enzyme-linked immunoabsorbent assay. Genotype was determined by PCR and restriction fragment length polymorphism. Serum levels and survival were correlated with genotype and clinicopathologic factors. Results: Age and stage, but not −634G/C genotype, were associated with serum IL-6 levels. The median survival for patients with stage II or stage III gastric carcinoma was 1,418 days in patients with low (≤13 pg/mL) versus 618 days in patients with high (&amp;gt;13 pg/mL) serum IL-6 levels (P = 0.038). Results of a multivariate analysis showed that serum IL-6 level of &amp;gt;13 pg/mL was a significant predictor of poor survival (hazard ratio, 1.77; 95% confidence interval, 1.07-2.92; P = 0.026). Conclusions: Serum IL-6 level of &amp;gt;13 pg/mL correlates with tumor progression and is an independent predictor of poor survival after resection. In patients with stage II and III gastric carcinoma, serum IL-6 level is more effective than stage as a prognostic indicator. By measuring IL-6, these patients can be divided into two groups with significant differences in survival. The −634G/C polymorphism is not associated with serum IL-6 level or survival.
Loss of p21 Permits Carcinogenesis from Chronically Damaged Liver and Kidney Epithelial Cells despite Unchecked Apoptosis
Authors: Holger Willenbring, Amar Deep Sharma, Arndt Vogel, Andrew Y. Lee, Andreas Rothfuss, Zhongya Wang, Milton Finegold, Markus Grompe
Journal: Cancer Cell (2008)
Factories of Death: Japanese Biological Warfare, 1932-45, and the American Cover-up
Authors: Robert N. Proctor
Journal: JAMA (1996)

The Nazi medical crimes against humanity are familiar. Much less familiar are the medical crimes inflicted by Japanese army physicians in Manchuria during much of this same period—crimes that match, both in scope and brutality, anything performed by the Nazi physicians in Europe. In<i>Factories of Death</i>, Sheldon Harris, emeritus professor of history at California State University at Northridge, provides the most comprehensive account to date of the Japanese medical experiments, an impressive piece of scholarship that tells how doctors abused human bodies to test biowarfare agents and how US government authorities after the war refused to prosecute, choosing instead to exploit the information gathered for the American biowarfare effort at Fort Detrick. The story begins in 1932, when the Japanese army gave 200 000 yen and a command of 300 men to Ishii Shiro, a young professor of immunology with the rank of major in the medical corps, to
Farm accidents in children.
Authors: D. Cameron, C. Bishop, J. R. Sibert
Journal: BMJ (1992)

OBJECTIVE--To examine the problem of accidental injury to children on farms. DESIGN--Prospective county based study of children presenting to accident and emergency departments over 12 months with injuries sustained in a farm setting and nationwide review of fatal childhood farm accidents over the four years April 1986 to March 1990. SETTING--Accident and emergency departments in Aberystwyth, Carmarthen, Haverfordwest, and Llanelli and fatal accidents in England, Scotland, and Wales notified to the Health and Safety Executive register. SUBJECTS--Children aged under 16. MAIN OUTCOME MEASURE--Death or injury after farm related accidents. RESULTS--65 accidents were recorded, including 18 fractures. Nine accidents necessitated admission to hospital for a mean of two (range one to four) days. 13 incidents were related to tractors and other machinery; 24 were due to falls. None of these incidents were reported under the statutory notification scheme. 33 deaths were notified, eight related to tractors and allied machinery and 10 related to falling objects. CONCLUSIONS--Although safety is improving, the farm remains a dangerous environment for children. Enforcement of existing safety legislation with significant penalties and targeting of safety education will help reduce accident rates further.