tbuckley/cabot-search huggingface dataset:
Environmental Lead after Hurricane Katrina: Implications for Future Populations
Authors: Felicia A. Rabito, Shahed Iqbal, Sara Perry, Whitney Arroyave, Janet C. Rice
Journal: Environmental Health Perspectives (2011)

As a result of Hurricane Katrina, > 100,000 homes were destroyed or damaged and a significant amount of sediment was deposited throughout the city of New Orleans, Louisiana. Researchers have identified the potential for increased lead hazards from environmental lead contamination of soils.We assessed the distribution of residential soil and dust lead 2 years poststorm and compared soil lead before and after the storm.We conducted a cross-sectional study in New Orleans in which households were selected by stratified random sampling. A standard residential questionnaire was administered, and lead testing was performed for both the interior and exterior of homes. Logistic regression was used to identify significant predictors of interior and exterior lead levels in excess of allowable levels.One hundred nine households were enrolled; 61% had at least one lead measurement above federal standards. Of homes with bare soil, 47% had elevated lead and 27% had levels exceeding 1,200 ppm. Housing age was associated with soil lead, and housing age and soil lead were associated with interior lead. Race, income, and ownership status were not significantly associated with either interior or exterior lead levels. The median soil lead level of 560 ppm was significantly higher than the median level of samples collected before Hurricane Katrina.The high prevalence (61%) of lead above recommended levels in soil and dust samples in and around residences raises concern about potential health risks to the New Orleans population, most notably children. Steps should be taken to mitigate the risk of exposure to lead-contaminated soil and dust. Further research is needed to quantify the possible contribution of reconstruction activities to environmental lead levels.
BET bromodomain inhibition suppresses TH17-mediated pathology
Authors: Deanna A. Mele, Andres Salmeron, Srimoyee Ghosh, Hon-Ren Huang, Barbara M. Bryant, Jose M. Lora
Journal: The Journal of Experimental Medicine (2013)

Interleukin (IL) 17-producing T helper (T(H)17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine T(H)17 differentiation from naive CD4(+) T cells, as well as in the activation of previously differentiated T(H)17 cells. We provide evidence that BET controls T(H)17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector T(H)17-associated cytokines, including IL17, IL21, and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in T(H)17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in T(H)17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and T(H)17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions.
DNA Damage Binding Protein Component DDB1 Participates in Nucleotide Excision Repair through DDB2 DNA-binding and Cullin 4A Ubiquitin Ligase Activity
Authors: Jinyou Li, Qi-En Wang, Qianzheng Zhu, Mohamed A. El-Mahdy, Gulzar Wani, Mette Prætorius-Ibba, Altaf A. Wani
Journal: Cancer Research (2006)

Abstract Functional defect in DNA damage binding (DDB) activity has a direct relationship to decreased nucleotide excision repair (NER) and increased susceptibility to cancer. DDB forms a complex with cullin 4A (Cul4A), which is now known to ubiquitylate DDB2, XPC, and histone H2A. However, the exact role of DDB1 in NER is unclear. In this study, we show that DDB1 knockdown in human cells impaired their ability to efficiently repair UV-induced cyclobutane pyrimidine dimers (CPD) but not 6-4 photoproducts (6-4PP). Extensive nuclear protein fractionation and chromatin association analysis revealed that upon irradiation, DDB1 protein is translocated from a loosely bound to a tightly bound in vivo chromatin fraction and the DDB1 translocation required the participation of functional DDB2 protein. DDB1 knockdown also affected the translocation of Cul4A component to the tightly bound form in UV-damaged chromatin in vivo as well as its recruitment to the locally damaged nuclear foci in situ. However, DDB1 knockdown had no effect on DNA damage binding capacity of DDB2. The data indicated that DDB2 can bind to damaged DNA in vivo as a monomer, whereas Cul4A recruitment to damage sites depends on the fully assembled complex. Our data also showed that DDB1 is required for the UV-induced DDB2 ubiquitylation and degradation. In summary, the results suggest that (a) DDB1 is critical for efficient NER of CPD; (b) DDB1 acts in bridging DDB2 and ubiquitin ligase Cul4A; and (c) DDB1 aids in recruiting the ubiquitin ligase activity to the damaged sites for successful commencement of lesion processing by NER. (Cancer Res 2006; 66(17): 8590-7)
Rukn Uddin Haider
Authors: A. Z Faruqi
Journal: BMJ (2009)

After qualifying, Rukn Uddin Haider (known to friends and family as “Arif”) set forth on an adventurous journey—by train across India, via ship to Europe, and finally to London in 1960. He completed a diploma in tropical medicine and worked for some time in Liverpool, Southport, and Preston. In 1974 he became the first Asian …
The evolving role of Alemtuzumab in management of patients with CLL
Authors: S Faderl, S Coutré, J C Byrd, C Dearden, A Denes, M J S Dyer, S A Gregory, J G Gribben, P Hillmen, M Keating, S Rosen, P Venugopal, K Rai
Journal: Leukemia (2005)
Severe Hypertriglyceridemia With Pancreatitis
Authors: Frank M. Sacks, Maxine Stanesa, Robert A. Hegele
Journal: JAMA Internal Medicine (2013)

<h3>Importance</h3> Recurrent pancreatitis is a potentially fatal complication of severe hypertriglyceridemia. Genetic defects and lifestyle risk factors may render this condition unresponsive to current treatments. <h3>Observations</h3> We report this first case of long-term management of intractable near-fatal recurrent pancreatitis secondary to severe hypertriglyceridemia by a novel use of lomitapide, an inhibitor of microsomal triglyceride transfer protein, recently approved for treatment of familial homozygous hypercholesterolemia. The patient had been hospitalized many times for pancreatitis since age 15 years. Her serum triglyceride level averaged 3900 mg/dL while she received therapy with approved lipid drugs. She is homozygous for a coding mutation (P234L) in lipoprotein lipase, leaving her unable to metabolize triglycerides in chylomicrons and very low density lipoproteins (VLDL). Lomitapide reduces the secretion of chylomicrons and VLDL. Lomitapide, which was started when she was 44 years old after near-fatal pancreatitis, lowered her fasting triglyceride level from greater than 3000 mg/dL to a mean (SD) of 903 (870) mg/dL while she received 30 mg/d and to 524 (265) mg/dL while she received 40 mg/d; eliminated chronic abdominal pain; and prevented pancreatitis. However, fatty liver, present before treatment, progressed to steatohepatitis and fibrosis after 12 to 13 years. <h3>Conclusions and Relevance</h3> Lomitapide prevented pancreatitis in severe intractable hypertriglyceridemia but at a potential long-term cost of hepatotoxicity.
Acute massive pulmonary embolism following pulmonary resection
Authors: H. M. Singh, S. Mudbidri, R. M. E. Seal
Journal: Thorax (1970)

Eighteen cases of acute massive and fatal pulmonary embolism following pulmonary resection are summarized. Clinical presentation is distinct in this group of patients. In one-third of the cases there was radiological evidence of major embolism several hours before the acute dramatic episode. At necropsy there seemed to be no correlation between the vascular area obstructed and the acute clinical deterioration. Longest survival occurred in those patients with (<i>a</i>) the best pre-operative respiratory function, and (<i>b</i>) the least operative and post-operative complications.
Potential funding crisis for the Radiation Effects Research Foundation
Authors: Mark P Little, Maria Blettner, John D Boice, Bryn A Bridges, Elisabeth Cardis, Monty W Charles, Florent de Vathaire, Richard Doll, Kenzo Fujimoto, Dudley Goodhead, Bernd Grosche, Per Hall, Wolfgang F Heidenreich, Peter Jacob, Suresh H Moolgavkar, Colin R Muirhead, Ohtsura Niwa, Herwig G Paretzke, Richard B Richardson, Jonathan M Samet, Roy E Shore, Tore Straume, Richard Wakeford, Yasuhito Sasaki
Journal: The Lancet (2004)
641 Efficient replication of hepatitis C virus genotype 2A subgenomic replicon isolated from fulminant hepatitis patients
Authors: T KATO, T DATE, M MIYAMOTO, T WAKITA
Journal: Hepatology (2003)

Recently, the intriguing possibility has been raised that heart failure may be mediated by the biological effects of cytokines. Indeed, we found elevation of plasma concentrations of various cytokines in patients with myocardial disease. We also detected positive tumor necrosis factor (TNF-alpha) immunoreactivity in right atrial tissues obtained during surgery from patients with severe heart failure. Therefore, we postulated that some aspects of heart failure may be related to non-lethal down-modulation of cardiac function by immune cells and their cytokines. Testing this hypothesis in an experimental model of murine myocarditis, we found that injection of recombinant human TNF-alpha increased mortality of the animals infected with myocarditis virus. The anti-TNF-alpha monoclonal antibody improved survival and attenuated the myocardial lesions. Whereas, administration of recombinant human IL-2 in the acute viremic stage increased survival rate, and resulted in less intense pathological changes in the myocardium while in the subacute aviremic stage, the same amount of IL-2 reduced survival rate and exacerbated severity of the disease. Therefore, cytokine release may initiate a beneficial inflammatory and immune response in the acute phase of the disease process, but the continued induction of cytokines and the enhanced natural killer (NK) cell activity in the later stage are no longer protective. Vesnarinone, a recently synthesized inotropic agent which has proved to benefit patients with congestive heart failure by improving prognosis, also increased the survival of individual subjects in the above-mentioned murine model of heart failure. Cytotoxicity of NK cells obtained from the virus infected animals was substantially reduced when treated with vesnarinone. Vesnarinone also inhibited production of TNF-alpha and other cytokines from stimulated human lymphocytes and cultured murine splenocytes. We conclude, therefore, that inhibition of NK cell activity and suppression of cytokine production appear to be important immunological defense mechanisms which could contribute to the observed salutary effects of vesnarinone in the treatment of chronic heart failure. More broadly, immunomodulation could pave the way for a new frontier in the management of heart failure.
SPECT Hepatic Scintigraphy
Authors: STEPHEN R. BUNKER, ROBERT D. KARL, WILLIAM H. HOWARD, MICHAEL F. HARTSHORNE, WILLIAM P. SCHMIDT, MICHAEL A. CAWTHON, JOHN M. BAUMAN
Journal: Clinical Nuclear Medicine (1984)

The authors report a case of “hot spot” localization on SPECT hepatic scintigraphy secondary to IVC obstruction. The tomographic slices demonstrated the location of the focal increase in radiotracer activity as anterior, within the medial segment of the left lobe of the liver. Radionuclide angiography confirmed the extensive collateral vasculature of IVC obstruction.
Meningococcal Disease in Los Angeles County, California, and among Men in the County Jails
Authors: Jordan W. Tappero, Roshan Reporter, Jay D. Wenger, Bridget A. Ward, Michael W. Reeves, Timm S. Missbach, Brian D. Plikaytis, Laurene Mascola, Anne Schuchat
Journal: New England Journal of Medicine (1996)

From January through March 1993, there were 54 cases of meningococcal disease in Los Angeles County, California, of which 9 occurred among men incarcerated in the county's jail system, which was 40 percent above capacity at the time. Several of the 45 patients from the community had had contact with men recently released from a county jail.We interviewed patients from the community (n=42) and neighborhood controls matched with the patients for age, race, and ethnic group (n=84) about potential exposures. We collected and cultured pharyngeal swabs for Neisseria meningitidis from men entering the central jail (n=162), men leaving the central jail (n=379), members of the jail staff (n=121), and patients at a community health center (n=214). Meningococcal isolates were identified by serotyping and multilocus enzyme electrophoresis.The presence of community-acquired meningococcal disease was strongly associated with exposure to a person who had been in or worked at one of the county jails (multivariate matched odds ratio, 18.5; 95 percent confidence interval, 3.8 to 90.8; P<0.001). Pharyngeal carriage of meningococcus was significantly more frequent among men released from jail (19 percent) or entering jail (17 percent) than among workers at the jails (3 percent) or community residents seen at the clinic (1 percent). Among men entering jail, those who had previously been incarcerated were more often carriers than those who had not (21 percent vs. 7 percent, P=0.03). Of the isolates from nine community residents with serogroup C meningococcal disease, eight were the same strain as that isolated from the eight inmates with serogroup C disease.In this outbreak of meningococcal disease in Los Angeles County, nearly half of community residents with the disease had contact with persons who had been in a county jail. The high rates of carriage among recidivists and released inmates suggests that the men became meningococcal carriers while in jail.
QuantiFERON to diagnose infection by Mycobacterium tuberculosis: Performance in infants and older children
Authors: Adeline Blandinières, Agathe de Lauzanne, Valérie Guérin-El Khourouj, Nadège Gourgouillon, Hélène See, Béatrice Pédron, Albert Faye, Ghislaine Sterkers
Journal: Journal of Infection (2013)
Increase in Angiotensin II Type 1 Receptor Expression Immediately After Ischemia-Reperfusion in Isolated Rat Hearts
Authors: B. C. Yang, M. I. Phillips, P. E. J. Ambuehl, L. P. Shen, P. Mehta, J. L. Mehta
Journal: Circulation (1997)

Background Myocardial ischemia is known to upregulate the systemic renin-angiotensin system, which influences myocardial ischemic events by affecting hemodynamics and hemostatic activity. This study was designed to examine whether angiotensin II (Ang II) receptor expression in the myocardium is altered immediately after ischemia-reperfusion. Methods and Results Isolated buffer-perfused Sprague-Dawley rat hearts were subjected to continuous perfusion (control, n=5) or to 25 minutes of global ischemia followed by 30 minutes of reperfusion (n=10). Autoradiographic analysis for Ang II receptors of multiple myocardial sections was performed. Whereas continuous perfusion of hearts resulted in minor changes in coronary perfusion pressure (CPP), left ventricular end-diastolic pressure (LVEDP), and developed left ventricular pressure (dLVP=LVSP−LVEDP), ischemia-reperfusion caused a marked increase in CPP and LVEDP and a decrease in dLVP, indicating severe cardiac dysfunction. Concurrently, total myocardial Ang II receptor expression was greater ( P &lt;.05) in hearts subjected to ischemia-reperfusion than in the continuously perfused control hearts. Most of the increase in Ang II receptor expression was due to an increase in type 1 receptor (AT 1 ) expression (34.6±6.5 versus 18.2±4.4 fmol/g, P &lt;.05), because Ang II type 2 receptor expression was unaffected. To examine the importance of AT 1 receptor expression, another group of isolated rat hearts (n=5) was perfused with buffer containing losartan (10 −5 mol/L) and subjected to ischemia followed by reperfusion. Perfusion of hearts with losartan attenuated the ischemia-reperfusion–induced cardiac dysfunction. Perfusion of hearts with losartan also blocked the ischemia-reperfusion–induced increase in myocardial AT 1 binding. Conclusions These observations indicate that myocardial AT 1 expression increases immediately after ischemia-reperfusion and contributes to cardiac dysfunction.
The Fat of the Land: Do Agricultural Subsidies Foster Poor Health?
Authors: Scott Fields
Journal: Environmental Health Perspectives (2004)

Ever since the Great Depression, American farmers have been the beneficiaries of a medley of subsidies and support programs meant to stabilize crop prices, keep farmers farming, and provide U.S. families with an affordable, reliable supply of food. But these programs may have had an unintended side effect. Rather than keep Americans healthy, critics say, these policies have contributed to today's obesity pandemic and other nutrition problems as well.Writing in the 2004 Annual Review of Nutrition, James Tillotson, a professor of food policy and international business at Tufts University, argues that U.S public policy encourages obesity at the expense of sound nutritional practices. "You have a whole régime here that's worked to increase agricultural efficiency," Tillotson says. And what U.S. farmers are most efficient at producing, he says, are just a few highly subsidized crops—wheat, soybeans, and especially corn.
Changing trends in hepatitis C-related mortality in the United States, 1995-2004
Authors: Matthew Wise, Stephanie Bialek, Lyn Finelli, Beth P. Bell, Frank Sorvillo
Journal: Hepatology (2008)

The disease burden and mortality from hepatitis C are predicted to increase in the United States as the number of persons with long-standing chronic infection grows. We analyzed hepatitis C mortality rates derived from US Census and multiple-cause-of-death data for 1995-2004. Deaths were considered hepatitis C–related if: (1) hepatitis C was the underlying cause of death, (2) chronic liver disease was the underlying cause and hepatitis C was a contributing cause, or (3) human immunodeficiency virus was the underlying cause and chronic liver disease and hepatitis C were contributing causes. A total of 56,409 hepatitis C–related deaths were identified. Mortality rates increased 123% during the study period (1.09 per 100,000 persons to 2.44 per 100,000), but average annual increases were smaller during 2000-2004 than 1995-1999. After peaking in 2002 (2.57 per 100,000), overall rates declined slightly, but continued to increase among persons aged 55-64 years. Overall increases were greater among males (144%) than females (81%) and among non-Hispanic blacks (170%) and Native Americans (241%) compared to non-Hispanic whites (124%) and Hispanics (84%). The 7,427 hepatitis C deaths in 2004 (mean age: 55 years), corresponded to 148,611 years of potential life lost. The highest mortality rates in 2004 were observed among males, persons aged 45-54 and 55-64 years, Hispanics, non-Hispanic blacks, and non-Hispanic Native American/Alaska Natives. Conclusion: Overall, hepatitis C mortality has increased substantially since 1995. Despite small declines in recent years, rates have continued to increase among persons aged 55-64 years. Hepatitis C is an important cause of premature mortality. (HEPATOLOGY 2008.)
Neurofibromatosis: Lymphoscintigraphic Observations
Authors: JOHN R. STY, ROBERT J. STARSHAK, GREGORY A. WOODS
Journal: Clinical Nuclear Medicine (1981)

The authors describe the lymphoscintigraphic findings in a 4-year-old child with neurofibromatosis, the principal manifestation of which was elephantiasis neuromatosa involving the right lower extremity. The lymphoscintigram demonstrated dilated lymphatics and enlarged lymph nodes.
The integrated landscape of driver genomic alterations in glioblastoma
Authors: Veronique Frattini, Vladimir Trifonov, Joseph Minhow Chan, Angelica Castano, Marie Lia, Francesco Abate, Stephen T Keir, Alan X Ji, Pietro Zoppoli, Francesco Niola, Carla Danussi, Igor Dolgalev, Paola Porrati, Serena Pellegatta, Adriana Heguy, Gaurav Gupta, David J Pisapia, Peter Canoll, Jeffrey N Bruce, Roger E McLendon, Hai Yan, Ken Aldape, Gaetano Finocchiaro, Tom Mikkelsen, Gilbert G Privé, Darell D Bigner, Anna Lasorella, Raul Rabadan, Antonio Iavarone
Journal: Nature Genetics (2013)
Urban Coccidioidomycosis and Histoplasmosis
Authors: David J. Drutz
Journal: New England Journal of Medicine (1979)

Quite suddenly, however, it launched a new attack and established itself in the business center. Residents accused the wind of "broadcasting germs," as the hotel manager put it. Whatever the reasons might be, people living in the central districts realized that their turn had come...Camus, The Plague, 1947Coccidioidomycosis and histoplasmosis are traditionally (if not always accurately) considered to be related to rural pursuits. Histoplasmosis has been associated with the clearing of land where birds have roosted, the destruction of a chicken house, spelunking, sleeping on a pillow made of chicken feathers and, most recently, cutting down a . . .
368 TRANSMIGRATION AND REVERSE TRANSMIGRATION ACROSS HUMAN HEPATIC SINUSOIDAL ENDOTHELIUM SHAPES THE SUBSEQUENT FATE OF MONOCYTE SUBSETS
Authors: H.W. Zimmermann, T. Bruns, C.J. Weston, S.M. Curbishley, K.-K. Li, E. Liaskou, D.H. Adams
Journal: Journal of Hepatology (2013)
D-Dimer in Venous Thromboembolism
Authors: Paula Bockenstedt
Journal: New England Journal of Medicine (2003)

Venous thromboembolism is an important medical problem, with an estimated incidence in the United States of 100,000 to 300,000 cases per year. Of patients presenting with symptoms suggestive of deep venous thrombosis, only 30 percent actually have the disorder. In the emergency department, where medical decisions must be made rapidly, the ability to identify, safely and accurately, the 70 percent of patients with symptoms who do not have deep venous thrombosis and likewise to identify those who do have the disorder is critical. Recent studies of the clinical diagnosis of deep venous thrombosis have shown that when risk factors and . . .
Sickle cell disease caused by heterozygosity for Hb S and novel LCR deletion: Report of two patients
Authors: Sara C. Koenig, Esmira Becirevic, Miriam S.C. Hellberg, Michael Y. Li, Jason C.C. So, Jane S. Hankins, Russell E. Ware, Lillian McMahon, Martin H. Steinberg, Hong‐Yuan Luo, David H.K. Chui
Journal: American Journal of Hematology (2009)

The b-globin gene LCR is located approximately 6 kb upstream of the embryonic epsilon-globin gene, and is made up of five DNase I hypersensitive sites (HSs), HS 1-5. LCR plays a pivotal role in regulating the expression of downstream epsilon-, (G)gamma-, (A)gamma-, delta-, and beta-globin genes in cis [1]. Deletions removing the LCR and parts of the downstream beta-globin gene cluster in patients have been described [2]. These individuals present with a (gammadeltabeta)0-thalassemia carrier phenotype. We now report two patients with severe sickle cell disease who were compound heterozygous for Hb S mutation and novel LCR deletion. In one case, HS 1-3 were deleted; in the other, HS 1-5 were deleted. In both cases, the b-like globin genes in cis to the LCR deletions were intact. Genotypically, both patients appeared to have sickle cell trait. Coinherited with either LCR deletion, these individuals presented as sickle cell disease patients. The breakpoints of these LCR deletions were defined. These results affirm that HS 2 and 3 are primarily responsible for conferring erythroid specific high-level expression of cis-linked beta-like globin genes. Furthermore, LCR deletions might cause hemolytic disease of newborns.