tbuckley/cabot-search huggingface dataset:
Role of endothelin in disseminated intravascular coagulation
Authors: H. Asakura, H. Jokaji, M. Saito C. Uotani, I. Kumabashiri, E. Morishita, M. Yamazaki, T. Matsuda
Journal: American Journal of Hematology (1992)

We examined the changes in plasma levels of endothelin-1 (ET-1), a potent vasoconstrictor peptide, in 47 cases of disseminated intravascular coagulation (DIC) to investigate the role of ET-1 in DIC and its relation to multiple organ failure (MOF). A significant elevation of plasma levels of ET-1 was observed in some cases of DIC, especially in patients with sepsis, blastic crisis of chronic myelogenous leukemia, and cancer. However, no such significant elevation was observed in patients with acute promyelocytic leukemia (APL), acute leukemias except for APL, or non-Hodgkin lymphoma. Plasma levels of ET-1 were higher in patients with DIC with MOF than in those without MOF. Although the levels of ET-1 were decreased or remained low with clinical improvement in most DIC patients, the levels were further increased or remained high in patients who showed no improvement in DIC. It is suggested that ET-1 must play an important role in further progression of MOF with the vasoconstriction and microcirculatory disorders.
Incident High-Grade Squamous Intraepithelial Lesions in Senegalese Women With and Without Human Immunodeficiency Virus Type 1 (HIV-1) and HIV-2
Authors: Stephen E. Hawes, Cathy W. Critchlow, Papa Salif Sow, Papa Touré, Ibraham N'Doye, Aissatou Diop, Jane M. Kuypers, Abdoul A. Kasse, Nancy B. Kiviat
Journal: JNCI Journal of the National Cancer Institute (2006)

Background: Women infected with human immunodeficiency virus type 1 (HIV-1) and -2 may be at higher risk of developing cervical cancer than uninfected women. We assessed the relationships among human papillomavirus (HPV) types and persistence, HIV-1 and/or HIV-2 infection, and the development of high-grade cervical squamous intraepithelial lesions (HSILs) in a prospective study. Methods: We studied 627 women with and without HIV-1 and/or HIV-2 infection and high-risk HPV infection in Senegal, West Africa, who were assessed every 4 months for HSIL and HPV DNA over a mean follow-up of 2.2 years. Cox regression modeling was used to assess risks associated with development of HSIL. Results: During follow-up, 71 (11%) of 627 women developed HSIL as detected by cytology. HIV-infected women with high-risk HPV types were at greatest risk for development of HSIL. In multivariable modeling, infection with oncogenic HPV types—both persistent (hazard ratio [HR] = 47.1, 95% confidence interval [CI] = 16.3 to 136) and transient (HR = 14.0, 95% CI = 3.7 to 54)—was strongly associated with HSIL risk. In univariate analyses, HIV-positive women infected with HIV-2 were less likely to develop HSIL (HR = 0.3, 95% CI = 0.1 to 0.9) than HIV-positive women infected with HIV-1. HIV-positive women with CD4 + cell counts between 200 and 500 cells per microliter (HR = 2.2, 95% CI = 0.8 to 6.3) or fewer than 200 cells per milliliter (HR = 5.5, 95% CI = 2.0 to 15.2) were at greater risk of HSIL than HIV-positive women with CD4 counts of more than 500 cells per milliliter. High plasma HIV RNA levels were associated with increased HSIL risk (HR for each order of magnitude increase in the level of plasma HIV RNA = 1.4, 95% CI = 1.1 to 1.7; P = .005). After adjustment for HPV types and persistence, however, HIV type, plasma HIV RNA level, and CD4 count were no longer statistically significantly associated with increased risk of HSIL. Conclusions: HIV-1 and HIV-2 are associated with increased risk for development of HSIL. This risk appears to be associated primarily with increased HPV persistence that may result from immunosuppression related to HIV-1 and/or HIV-2 infection.
Delivering precision medicine in oncology today and in future—the promise and challenges of personalised cancer medicine: a position paper by the European Society for Medical Oncology (ESMO)
Authors: F. Ciardiello, D. Arnold, P.G. Casali, A. Cervantes, J.-Y. Douillard, A. Eggermont, A. Eniu, K. McGregor, S. Peters, M. Piccart, R. Popescu, E. Van Cutsem, C. Zielinski, R. Stahel
Journal: Annals of Oncology (2014)
Interaction of matrix metalloproteinases with pulmonary pollutants: Table 1–
Authors: M. Dagouassat, S. Lanone, J. Boczkowski
Journal: European Respiratory Journal (2012)

An air pollutant consists of any atmospheric substance that may harm humans, animals, vegetation or material. Various air pollutants have been reported, differing in their physicochemical characteristics. They can be grouped into four categories: gaseous pollutants ( e.g. ozone, sulfur dioxide, oxides of nitrogen, carbon monoxide and volatile organic compounds), persistent organic pollutants, heavy metals ( e.g. cadmium, lead and mercury) and particulate matter (coarse, fine and ultrafine). These pollutants can reach the respiratory system, eliciting pulmonary and/or systemic effects. These effects include inflammation, tissue remodelling and carcinogenesis: all phenomena where matrix metalloproteases (MMPs) play critical roles, given their broad effects on matrix remodelling and modulation of inflammation and cell signalling. Moreover, since expression and activity of MMPs can be induced by such stimuli, the hypothesis has been raised that MMPs could be involved in the health effects of pollutants. Until now, the implication of MMPs in these effects has been studied only for some pollutants and for a restricted selection of MMPs (mainly MMP-1, -2, -9 and -12), while evidence for a link between MMP induction/activation and health effects remains scarce. A larger number of studies is, therefore, needed in order to better understand the implication of MMPs in health effects associated with air pollution.
Management of Hyperglycemia in Type 2 Diabetes, 2015: A Patient-Centered Approach: Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes
Authors: Silvio E. Inzucchi, Richard M. Bergenstal, John B. Buse, Michaela Diamant, Ele Ferrannini, Michael Nauck, Anne L. Peters, Apostolos Tsapas, Richard Wender, David R. Matthews
Journal: Diabetes Care (2014)

In 2012, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) published a position statement on the management of hyperglycemia in patients with type 2 diabetes (1,2). This was needed because of an increasing array of antihyperglycemic drugs and growing uncertainty regarding their proper selection and sequence. Because of a paucity of comparative effectiveness research on long-term treatment outcomes with many of these medications, the 2012 publication was less prescriptive than prior consensus reports. We previously described the need to individualize both treatment targets and treatment strategies, with an emphasis on patient-centered care and shared decision making, and this continues to be our position, although there are now more head-to-head trials that show slight variance between agents with regard to glucose-lowering effects. Nevertheless, these differences are often small and would be unlikely to reflect any definite differential effect in an individual patient.

The ADA and EASD have requested an update to the position statement incorporating new data from recent clinical trials. Between June and September of 2014, the Writing Group reconvened, including one face-to-face meeting, to discuss the changes. An entirely new statement was felt to be unnecessary. Instead, the group focused on those areas where revisions were suggested by a changing evidence base. This briefer article should therefore be read as an addendum to the previous full account (1,2).

Glucose control remains a major focus in the management of patients with type 2 diabetes. However, this should always be in the context of a comprehensive cardiovascular risk factor reduction program, to include smoking cessation and the adoption of other healthy lifestyle habits, blood pressure control, lipid management with priority to statin medications, and, in some circumstances, antiplatelet therapy. Studies have conclusively determined that reducing hyperglycemia decreases the onset and progression of …
Morbid Conditions of the Kidney giving rise to Albuminuria
Authors: C. H. Jones
Journal: BMJ (1852)

IN the following communication, which I have the honour to lay before the Fellows of this Society, I purpose to present a sketch of the mor- bid conditions of the kidney which give rise to albuminous urine; to consider the essential nature of Bright's disease, so called; and the kind of treatment which pathology and experience recommend to us.So frequent is the malady, so often does it meet us in dealing with other diseases, so greatly does it mar our efforts for the cure of those diseases, and so fatal is it when arrived at its advanced stage, that no one, I think, can feel otherwise than deeply concerned to discover as much as possible of a cause so productive of evil.My descriptions of the structural lesions will principally be taken from my own examina- tions, which have been numerous; but I shall not fail to Tefer, as occasion may be, to the works of those who have thrown so much light upon the subject.One or two brief remarks upon the physiological condition of the kidney may be premised.It has been well pointed out by Mr. Bowman, how peculiarly the vascular system of the organ is disposed; how the short and wide renal artery suddenly breaks up into small straight vessels, going direct into the Malpighian tufts; how the stream of blood thus arriving in those curious capillary loops, is thence checked and stayed, not having an ample, but, on the contrary, a rather narrow channel of egress by the efferent vessel, which passes into the tubular plexus.The effect of this arrangement is, of course, to bring a more than ordinary pressure to bear on the membrane of the capillaries: this, even in their healthiest state, must be greater than that exerted by the blood on any other capillaries; but if congestion arises, or-the VOL.IV.
The synthetic triterpenoid, RTA 405, increases the glomerular filtration rate and reduces angiotensin II–induced contraction of glomerular mesangial cells
Authors: Yanfeng Ding, Rhesa D. Stidham, Ron Bumeister, Isaac Trevino, Ali Winters, Marc Sprouse, Min Ding, Deborah A. Ferguson, Colin J. Meyer, W Christian Wigley, Rong Ma
Journal: Kidney International (2012)
Lipoprotein (a) up-regulates the expression of the plasminogen activator inhibitor 2 in human blood monocytes
Authors: Christa Buechler, Heidrun Ullrich, Mirko Ritter, Mustafa Porsch-Oezcueruemez, Karl J. Lackner, Stefan Barlage, Sven Olaf Friedrich, Gert M. Kostner, Gerd Schmitz
Journal: Blood (2001)
Subcutaneous Papillomatous Cysts Produced by Bovine Papilloma Virus&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Loren D. Koller, Carl Olson
Journal: JNCI Journal of the National Cancer Institute (1971)

Papillomatous cysts developed in calves when autologous skin which had been bathed in a suspension of bovine papilloma virus (BPV) was implanted subcutaneously, or when either an area of skin inoculated with BPV or a recently developed cutaneous papilloma was buried subcutaneously. Virus-stimulated allogeneic skin implants or papilloma transplants from other calves failed to produce cysts as did non-virus-stimulated autologous skin. The cysts first developed as small cavities lined with squamous epithelium surrounded by a fibromatous capsule. By 4 months there was extensive papillomatous proliferation of the epithelium and the cysts were quite large. Scattered areas of coagulation necrosis in the epithelium began to appear at 6 months in a few cysts. By 21 months, the lining epithelium was thin and no longer hyperplastic and in someareas there was no epithelium. The content of the cysts was initially a thick, dry, caseous material that later became fluid and contained a few large clumps of keratinized epithelium. BPV and antibody to the virus were found in the cysts. When the papillomatous lining of cysts was exposed to the exterior by surgery, a typical cutaneous fibropapilloma developed.
Induction of Cardiomyocyte-Like Cells in Infarct Hearts by Gene Transfer of Gata4, Mef2c, and Tbx5
Authors: Kohei Inagawa, Kazutaka Miyamoto, Hiroyuki Yamakawa, Naoto Muraoka, Taketaro Sadahiro, Tomohiko Umei, Rie Wada, Yoshinori Katsumata, Ruri Kaneda, Koji Nakade, Chitose Kurihara, Yuichi Obata, Koichi Miyake, Keiichi Fukuda, Masaki Ieda
Journal: Circulation Research (2012)

After myocardial infarction (MI), massive cell death in the myocardium initiates fibrosis and scar formation, leading to heart failure. We recently found that a combination of 3 cardiac transcription factors, Gata4, Mef2c, and Tbx5 (GMT), reprograms fibroblasts directly into functional cardiomyocytes in vitro.To investigate whether viral gene transfer of GMT into infarcted hearts induces cardiomyocyte generation.Coronary artery ligation was used to generate MI in the mouse. In vitro transduction of GMT retrovirus converted cardiac fibroblasts from the infarct region into cardiomyocyte-like cells with cardiac-specific gene expression and sarcomeric structures. Injection of the green fluorescent protein (GFP) retrovirus into mouse hearts, immediately after MI, infected only proliferating noncardiomyocytes, mainly fibroblasts, in the infarct region. The GFP expression diminished after 2 weeks in immunocompetent mice but remained stable for 3 months in immunosuppressed mice, in which cardiac induction did not occur. In contrast, injection of GMT retrovirus into α-myosin heavy chain (αMHC)-GFP transgenic mouse hearts induced the expression of αMHC-GFP, a marker of cardiomyocytes, in 3% of virus-infected cells after 1 week. A pooled GMT injection into the immunosuppressed mouse hearts induced cardiac marker expression in retrovirus-infected cells within 2 weeks, although few cells showed striated muscle structures. To transduce GMT efficiently in vivo, we generated a polycistronic retrovirus expressing GMT separated by 2A "self-cleaving" peptides (3F2A). The 3F2A-induced cardiomyocyte-like cells in fibrotic tissue expressed sarcomeric α-actinin and cardiac troponin T and had clear cross striations. Quantitative RT-PCR also demonstrated that FACS-sorted 3F2A-transduced cells expressed cardiac-specific genes.GMT gene transfer induced cardiomyocyte-like cells in infarcted hearts.
Spirometry in the Lung Health Study: II. Determinants of short-term intraindividual variability.
Authors: P L Enright, J E Connett, R E Kanner, L R Johnson, W W Lee
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

The Lung Health Study (LHS) is a randomized clinical trial designed to determine whether a smoking intervention program and use of an inhaled bronchodilator (BD) can reduce the rate of decline of FEV1 in cigarette smokers with airflow limitation. During recruitment, spirometry was performed at second and third screening visits, a mean of 21 d apart. A total of 5,887 smokers, 35 to 60 yr of age and of whom 63% were men, met the study eligibility requirements. Smokers taking physician-prescribed BDs or with an FEV1 < 50% or > 90% predicted were excluded, as were those whose FEV1/FVC ratio was greater than 70%. Two inhalations of isoproterenol were given to determine BD response during the second visit. A serial dilution methacholine challenge test was done during the third visit to determine nonspecific airway reactivity. Ninety-five percent of the differences between FEV1 measured at the two visits were within 240 ml for women and within 320 ml for men (coefficients of repeatability). The best independent predictors of the mean short-term (between visit) intraindividual FEV1 variability were factors indicating intrinsic airway reactivity of the participants: bronchodilator response, methacholine reactivity, and the presence of wheezing; as well as factors influenced by the quality of spirometry testing: the difference between the highest and second highest FEV1s and peak flows during baseline spirometry, and the time to reach peak flow (PEFT).
Rapid expansion and long-term persistence of elevated NK cell numbers in humans infected with hantavirus
Authors: Niklas K. Björkström, Therese Lindgren, Malin Stoltz, Cyril Fauriat, Monika Braun, Magnus Evander, Jakob Michaëlsson, Karl-Johan Malmberg, Jonas Klingström, Clas Ahlm, Hans-Gustaf Ljunggren
Journal: The Journal of Experimental Medicine (2010)

Natural killer (NK) cells are known to mount a rapid response to several virus infections. In experimental models of acute viral infection, this response has been characterized by prompt NK cell activation and expansion followed by rapid contraction. In contrast to experimental model systems, much less is known about NK cell responses to acute viral infections in humans. We demonstrate that NK cells can rapidly expand and persist at highly elevated levels for &amp;gt;60 d after human hantavirus infection. A large part of the expanding NK cells expressed the activating receptor NKG2C and were functional in terms of expressing a licensing inhibitory killer cell immunoglobulin-like receptor (KIR) and ability to respond to target cell stimulation. These results demonstrate that NK cells can expand and remain elevated in numbers for a prolonged period of time in humans after a virus infection. In time, this response extends far beyond what is considered normal for an innate immune response.
Renin-Angiotensin-Aldosterone Genotype Influences Ventricular Remodeling in Infants With Single Ventricle
Authors: Seema Mital, Wendy K. Chung, Steven D. Colan, Lynn A. Sleeper, Cedric Manlhiot, Cammon B. Arrington, James F. Cnota, Eric M. Graham, Michael E. Mitchell, Elizabeth Goldmuntz, Jennifer S. Li, Jami C. Levine, Teresa M. Lee, Renee Margossian, Daphne T. Hsu
Journal: Circulation (2011)

Background— We investigated the effect of polymorphisms in the renin-angiotensin-aldosterone system (RAAS) genes on ventricular remodeling, growth, renal function, and response to enalapril in infants with single ventricle. Methods and Results— Single ventricle infants enrolled in a randomized trial of enalapril were genotyped for polymorphisms in 5 genes: angiotensinogen, angiotensin-converting enzyme, angiotensin II type 1 receptor, aldosterone synthase, and chymase. Alleles associated with renin-angiotensin-aldosterone system upregulation were classified as risk alleles. Ventricular mass, volume, somatic growth, renal function using estimated glomerular filtration rate, and response to enalapril were compared between patients with ≥2 homozygous risk genotypes (high risk), and those with &lt;2 homozygous risk genotypes (low risk) at 2 time points: before the superior cavopulmonary connection (pre-SCPC) and at age 14 months. Of 230 trial subjects, 154 were genotyped: Thirty-eight were high risk, and 116 were low risk. Ventricular mass and volume were elevated in both groups pre-SCPC. Ventricular mass and volume decreased and estimated glomerular filtration rate increased after SCPC in the low-risk ( P &lt;0.05), but not the high-risk group. These responses were independent of enalapril treatment. Weight and height z-scores were lower at baseline, and height remained lower in the high-risk group at 14 months, especially in those receiving enalapril ( P &lt;0.05). Conclusions— Renin-angiotensin-aldosterone system–upregulation genotypes were associated with failure of reverse remodeling after SCPC surgery, less improvement in renal function, and impaired somatic growth, the latter especially in patients receiving enalapril. Renin-angiotensin-aldosterone system genotype may identify a high-risk subgroup of single ventricle patients who fail to fully benefit from volume-unloading surgery. Follow-up is warranted to assess long-term impact. Clinical Trial Registration— http://www.clinicaltrials.gov . Unique identifier: NCT00113087.
Systemic immune unresponsiveness induced in adult mice by anterior chamber presentation of minor histocompatibility antigens.
Authors: J W Streilein, J Y Niederkorn, J A Shadduck
Journal: The Journal of Experimental Medicine (1980)

The ability to introduce carefully controlled numbers of viable cells into the anterior chamber of mouse eyes made it possible to examine the interrelationship between presentation of antigens into the anteior chamber and into conventional body sites and their synergistic/antagonistic effects on the immune system. P815 mastocytoma (DBA/2; H-2d) cells are syngeneic with BALB/c hosts at the major histocompatibility locus, but differ at multiple minor histocompatibility loci. When P815 cells were injected subcutaneously, they were rejected by BALB/c recipients who became specifically immune. By contrast, when P815 cells were injected intracamerally, they grew progressively into massive intraocular tumors; moreover, these BALB/c hosts proved subsequently unable to reject subcutaneously injected P815 cells, and, more impressively, failed to reject DBA/2 skin allografts placed orthotopically. Minor histocompatibility antigens, presented first through the anterior chamber of mouse eyes, elicit a suppressive rather than an aggressive host immune response that protects cells that bear these antigens from a destructive alloimmune reaction at both intracameral and systemic sites.
Early Relapse of Follicular Lymphoma After Rituximab Plus Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone Defines Patients at High Risk for Death: An Analysis From the National LymphoCare Study
Authors: Carla Casulo, Michelle Byrtek, Keith L. Dawson, Xiaolei Zhou, Charles M. Farber, Christopher R. Flowers, John D. Hainsworth, Matthew J. Maurer, James R. Cerhan, Brian K. Link, Andrew D. Zelenetz, Jonathan W. Friedberg
Journal: Journal of Clinical Oncology (2015)

Twenty percent of patients with follicular lymphoma (FL) experience progression of disease (POD) within 2 years of initial chemoimmunotherapy. We analyzed data from the National LymphoCare Study to identify whether prognostic FL factors are associated with early POD and whether patients with early POD are at high risk for death.In total, 588 patients with stage 2 to 4 FL received first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Two groups were defined: patients with early POD 2 years or less after diagnosis and those without POD within 2 years, the reference group. An independent validation set, 147 patients with FL who received first-line R-CHOP, was analyzed for reproducibility.Of 588 patients, 19% (n = 110) had early POD, 71% (n = 420) were in the reference group, 8% (n = 46) were lost to follow-up, and 2% (n = 12) died without POD less than 2 years after diagnosis. Five-year overall survival was lower in the early-POD group than in the reference group (50% v 90%). This trend was maintained after we adjusted for FL International Prognostic Index (hazard ratio, 6.44; 95% CI, 4.33 to 9.58). Results were similar for the validation set (FL International Prognostic Index-adjusted hazard ratio, 19.8).In patients with FL who received first-line R-CHOP, POD within 2 years after diagnosis was associated with poor outcomes and should be further validated as a standard end point of chemoimmunotherapy trials of untreated FL. This high-risk FL population warrants further study in directed prospective clinical trials.