tbuckley/cabot-search huggingface dataset:
Patient Survival after Human Albumin Administration
Authors: Mahlon M. Wilkes, Roberta J. Navickis
Journal: Annals of Internal Medicine (2001)

To test the hypothesis that albumin administration is not associated with excess mortality.Computer searches of the MEDLINE and EMBASE databases, the Cochrane Library, and Internet documents; hand searching of medical journals; inquiries to investigators and medical directors; and review of reference lists.Randomized, controlled trials comparing albumin therapy with crystalloid therapy, no albumin, or lower doses of albumin.Two investigators independently extracted data. The primary end point was relative risk for death. Criteria used to assess methodologic quality were blinding, method of allocation concealment, presence of mortality as a study end point, and crossover. Small-trial bias was also investigated.Fifty-five trials involving surgery or trauma, burns, hypoalbuminemia, high-risk neonates, ascites, and other indications were included. Albumin administration did not significantly affect mortality in any category of indications. For all trials, the relative risk for death was 1.11 (95% CI, 0.95 to 1.28). Relative risk was lower among trials with blinding (0.73 [CI, 0.48 to 1.12]; n = 7), mortality as an end point (1.00 [CI, 0.84 to 1.18]; n = 17), no crossover (1.04 [CI, 0.89 to 1.22]; n = 35), and 100 or more patients (0.94 [CI, 0.77 to 1.14]; n = 10). In trials with two or more such attributes, relative risk was further reduced.Overall, no effect of albumin on mortality was detected; any such effect may therefore be small. This finding supports the safety of albumin. The influence of methodologic quality on relative risk for death suggests the need for further well-designed clinical trials.
Long-term Efficacy of Maintenance Bacillus Calmette-Guérin versus Maintenance Mitomycin C Instillation Therapy in Frequently Recurrent TaT1 Tumours without Carcinoma In Situ: A Subgroup Analysis of the Prospective, Randomised FinnBladder I Study with a 20-Year Follow-up
Authors: Riikka Järvinen, Eero Kaasinen, Anna Sankila, Erkki Rintala
Journal: European Urology (2009)
MicroRNA145 Targets BNIP3 and Suppresses Prostate Cancer Progression
Authors: Xueqin Chen, Jing Gong, Hao Zeng, Ni Chen, Rui Huang, Ying Huang, Ling Nie, Miao Xu, Juan Xia, Fang Zhao, Wentong Meng, Qiao Zhou
Journal: Cancer Research (2010)

The putative tumor suppressor miR145 is transcriptionally regulated by TP53 and is downregulated in many tumors; however, its role in prostate cancer is unknown. On the other hand, BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3) is overexpressed in various tumors, including prostate cancer, and may transcriptionally repress the apoptosis-inducing factor (AIF) gene. Although BNIP3 transcription is controlled by hypoxia-inducible factor 1alpha (also elevated in prostate cancer), we postulated the posttranscriptional regulation of BNIP3 by miR145 through bioinformatics analysis, and herein we experimentally showed that miR145 negatively regulated BNIP3 by targeting its 3'-untranslated region. Artificial overexpression of miR145 by using adenoviral vectors in prostate cancer PC-3 and DU145 cells significantly downregulated BNIP3, together with the upregulation of AIF, reduced cell growth, and increased cell death. Artificial overexpression of wild-type TP53 in PC-3 cells (which lack TP53 protein) and DU145 cells (in which mutated nonfunctioning TP53 is expressed) significantly upregulated miR145 expression with consequent effects on BNIP3 and cell behavior as with miR145 overexpression. Analysis of prostate cancer (n = 134) and benign prostate (n = 83) tissue sample showed significantly decreased miR145 and increased BNIP3 expression in prostate cancer (P < 0.001), particularly in those with tumor progression, and both molecular changes were associated with unfavorable outcome. Abnormalities of the miR145-BNIP3 pair as part of TP53-miR145-BNIP3-AIF network may play a major role in prostate cancer pathogenesis and progression.
Acute gastric dilatation--a delayed complication of percutaneous endoscopic gastrostomy.
Authors: S Ghosh, M A Eastwood, K R Palmer
Journal: Gut (1993)

Acute gastric dilatation presenting 15 months after a percutaneous endoscopic gastrostomy is reported. The gastric dilatation was associated with local sepsis around the gastrostomy and resolved after removal of the gastrostomy tube.
Energy and Human Health
Authors: Kirk R. Smith, Howard Frumkin, Kalpana Balakrishnan, Colin D. Butler, Zoë A. Chafe, Ian Fairlie, Patrick Kinney, Tord Kjellstrom, Denise L. Mauzerall, Thomas E. McKone, Anthony J. McMichael, Mycle Schneider
Journal: Annual Review of Public Health (2013)

Energy use is central to human society and provides many health benefits. But each source of energy entails some health risks. This article reviews the health impacts of each major source of energy, focusing on those with major implications for the burden of disease globally. The biggest health impacts accrue to the harvesting and burning of solid fuels, coal and biomass, mainly in the form of occupational health risks and household and general ambient air pollution. Lack of access to clean fuels and electricity in the world's poor households is a particularly serious risk for health. Although energy efficiency brings many benefits, it also entails some health risks, as do renewable energy systems, if not managed carefully. We do not review health impacts of climate change itself, which are due mostly to climate-altering pollutants from energy systems, but do discuss the potential for achieving near-term health cobenefits by reducing certain climate-related emissions.
Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase
Authors: Carl Nathan, Noel Calingasan, Jon Nezezon, Aihao Ding, M. Scott Lucia, Krista La Perle, Michele Fuortes, Michael Lin, Sabine Ehrt, Nyoun Soo Kwon, Junyu Chen, Yoram Vodovotz, Khatuna Kipiani, M. Flint Beal
Journal: The Journal of Experimental Medicine (2005)

Brains from subjects who have Alzheimer's disease (AD) express inducible nitric oxide synthase (iNOS). We tested the hypothesis that iNOS contributes to AD pathogenesis. Immunoreactive iNOS was detected in brains of mice with AD-like disease resulting from transgenic expression of mutant human beta-amyloid precursor protein (hAPP) and presenilin-1 (hPS1). We bred hAPP-, hPS1-double transgenic mice to be iNOS(+/+) or iNOS(-/-), and compared them with a congenic WT strain. Deficiency of iNOS substantially protected the AD-like mice from premature mortality, cerebral plaque formation, increased beta-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of beta-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD.
Responses of Tracheobronchial Receptors to Inhaled Furosemide in Anesthetized Rats
Authors: TOMOKO SUDO, FUMIAKI HAYASHI, TAKASHI NISHINO
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Inhalation of furosemide, a loop diuretic, has shown favorable effects on experimentally induced cough, bronchoconstriction, and dyspnea. The effect of inhaled furosemide on tracheobronchial receptors was studied in anesthetized, spontaneously breathing rats. Single unit or pauci unit activity was recorded from the right vagus nerve. Tracheobronchial receptors were classified into slowly and rapidly adapting receptors (SARs and RARs, respectively), based on their adaptation index (AI), which was derived from the decrease in spike frequency (sf) over 2 s, expressed as a percentage of the peak firing rate. There were 43 SARs (AI ⩽ 25%) and eight RARs (AI ⩾ 50%). Inhalation of furosemide (n = 29) increased the slope of airway pressure (Paw) versus sf of SARs from 8.6 to 14.8 Hz/cm H2O with an increase in sf at Paw = 0 cm H2O from 18.0 to 49.5 Hz, resulting in an upward shift of the line. Neither inhalation of vehicle (n = 9) nor intravenous injection of furosemide (n = 5) changed this relationship. In addition, inhalation of furosemide attenuated the activity of RARs. These findings indicate that SARs are sensitized and RARs desensitized by inhalation of furosemide. We discuss possible mechanisms for this, and its relevance to clinical problems of dyspnea, bronchoconstriction, and cough.
Cutaneous Melanoma Subtypes Show Different BRAF and NRAS Mutation Frequencies
Authors: Gerald Saldanha, Linda Potter, Philip DaForno, J. Howard Pringle
Journal: Clinical Cancer Research (2006)

BRAF mutations are present in two thirds of cutaneous melanomas and many of the rest have NRAS mutations. However, cutaneous melanoma is a heterogeneous disease with many clinicopathologic subtypes. Of these, the majority fits into four categories: superficial spreading, nodular, lentigo maligna, and acral lentiginous melanoma (ALM). Thus far, there is very limited data combining BRAF and NRAS mutation analysis to explore differences between cutaneous melanoma subtypes. The aim of this study was to address this issue.The frequency of BRAF and NRAS hotspot mutations, in exons 15 and 2, respectively, was assessed in 59 cutaneous melanomas comprising superficial spreading, nodular, lentigo maligna, and ALM using single-strand conformational polymorphism and RFLP-PCR analysis.Only 2 of 21 (9.5%) ALM showed BRAF exon 15 mutation compared with 9 of 14 (64.3%) superficial spreading malignant melanomas, 4 of 11 (36.4%) nodular melanomas, and 7 of 13 (53.4%) lentigo maligna melanomas (P < 0.01). However, our key finding is that the combined analysis of BRAF exon 15 and NRAS exon 2 showed that there were no significant differences in the overall mutation frequency between subtypes. In particular, 9 of 19 (47.4%) ALM without BRAF exon 15 mutation had an NRAS exon 2 mutation.We show that the overall BRAF/NRAS frequency in mutation hotspots is not significantly different among cutaneous melanoma subtypes. These data show that mitogen-activated protein kinase pathway activation may be important in all major subtypes of cutaneous melanoma, although the mechanism by which this is achieved varies.
Rates and Outcomes of Follicular Lymphoma Transformation in the Immunochemotherapy Era: A Report From the University of Iowa/Mayo Clinic Specialized Program of Research Excellence Molecular Epidemiology Resource
Authors: Brian K. Link, Matthew J. Maurer, Grzegorz S. Nowakowski, Stephen M. Ansell, William R. Macon, Sergei I. Syrbu, Susan L. Slager, Carrie A. Thompson, David J. Inwards, Patrick B. Johnston, Joseph P. Colgan, Thomas E. Witzig, Thomas M. Habermann, James R. Cerhan
Journal: Journal of Clinical Oncology (2013)

This study sought to characterize transformation incidence and outcome for patients with follicular lymphoma (FL) in a prospective observational series begun after diffusion of rituximab use.
K <sup>+</sup> Currents in Human Coronary Artery Vascular Smooth Muscle Cells
Authors: Maik Gollasch, Christian Ried, Rostislav Bychkov, Friedrich C. Luft, Hermann Haller
Journal: Circulation Research (1996)

K+ channels and their currents are important in vascular tone regulation and are potential therapeutic targets; however, K+ channels in human coronary artery vascular smooth muscle cells (VSMCs) have received little attention. We examined K+ currents in freshly isolated VSMCs from human coronary arteries (n=368 from 32 human hearts) with conventional patch-clamp or perforated-patch techniques with nystatin. We detected four different K+ currents: (1) the delayed rectifier K+ current, IK(dr); (2) the Ca2+-activated K+ current, IK(Ca); (3) the nonrectifying noninactivating outward ATP-dependent K+ current, IK(ATP); and (4) the spontaneous transient outward K+ current, IK(STOC). K+ channels underlying spontaneous transient outward currents probably represent a single clustered population of Ca2+-activated K+ channels functionally associated with Ca2+ release channels in the sarcoplasmic reticulum. Inwardly rectifying K+ currents were not observed. K+ currents were unevenly distributed in that they were not uniformly exhibited by all cells. The most prominent K+ currents were IK(Ca) (100%) and IK(dr) (46%). IK(STOC)s, which have not been previously described in humans, were present in 67% of VSMCs. IK(ATP) was small under physiological conditions; however, IK(ATP) increased markedly after cell stimulation with exogenous or endogenous coronary vasodilators. Thus, IK(ATP) may be particularly relevant in ischemia and could be of special importance as a therapeutic target. We conclude that human coronary VSMCs have unique K+ currents that differ sufficiently from those of other species, thus making the investigation of human material clinically relevant. The findings suggest potential avenues for further therapeutic research.
NF-κB Gene Signatures and p53 Mutations in Head and Neck Squamous Cell Carcinoma
Authors: Robert L. Ferris, Jennifer R. Grandis
Journal: Clinical Cancer Research (2007)

Head and neck squamous cell carcinoma (HNSCC) has traditionally been attributed to carcinogen exposure, through heavy tobacco and ethanol consumption. Disruption of tumor suppressor pathways, notably regulated through p53 and Rb, has served as a paradigm for studying HNSCC carcinogenesis and the
Randomized Trial of an Intervention to Improve Mammography Utilization Among a Triracial Rural Population of Women
Authors: Electra Paskett, Cathy Tatum, Julia Rushing, Robert Michielutte, Ronny Bell, Kristie Long Foley, Marisa Bittoni, Stephanie L. Dickinson, Ann Scheck McAlearney, Katherine Reeves
Journal: JNCI Journal of the National Cancer Institute (2006)

Mammography is underused by certain groups of women, in particular poor and minority women. We developed a lay health advisor (LHA) intervention based on behavioral theories and tested whether it improved mammography attendance in Robeson County, NC, a rural, low-income, triracial (white, Native American, African American) population.
Thermosensitive N-isopropylacrylamide–N–propylacrylamide-vinyl pyrrolidone terpolymers: Synthesis, characterization and preliminary application as embolic agents
Authors: Xiaowei Li, Wenguang Liu, Guixiang Ye, Bingqi Zhang, Dunwan Zhu, Kangde Yao, Zuoqin Liu, Xizhong Sheng
Journal: Biomaterials (2005)
Epidemiology and transmission of HIV-2. Why there is no HIV-2 pandemic
Authors: K. M. De Cock
Journal: JAMA (1993)

Although human immunodeficiency virus type 1 (HIV-1) and HIV-2 share modes of transmission, their epidemiologic characteristics differ and international spread of HIV-2 has been very limited. Recently, the prevalence of infection with HIV-1 but not HIV-2 has increased rapidly in different West African countries, where HIV-2 was probably present earlier. Among 19,701 women of reproductive age tested in Abidjan, Ivory Coast, between 1988 and 1992, the prevalence of HIV-1 infection increased from 5.0% to 9.2%, while that of HIV-2 declined from 2.6% to 1.5%. Differences in viral load may be responsible: reported results of virus culture and polymerase chain reaction assays suggest that at high CD4+ T-lymphocyte counts viral load is lower in HIV-2-infected than in HIV-1-infected persons; the efficacy of heterosexual and perinatal transmission of HIV-2 is less efficient than that of HIV-1 at this stage. At low (< 0.20 x 10(9)/L [< 200/microL]) CD4+ T-lymphocyte counts, virus isolation is equally successful for both viruses, and the efficacy of heterosexual transmission is similar. Differences in HIV-1 and HIV-2 natural history are reflected in differences in viral load, that for HIV-2 being lower until immunodeficiency is severe. Differences in viral load throughout most of the natural history of infection appear to correlate with lower transmissibility of HIV-2 than HIV-1, and are the likeliest explanation for their markedly different global epidemiology.
THE IMMUNOLOGICAL BASIS OF ACQUIRED CELLULAR RESISTANCE
Authors: G. B. Mackaness
Journal: The Journal of Experimental Medicine (1964)

The resistance developed by mice during infection with Listeria monocytogenes, Brucella abortus, or Mycobacterium tuberculosis is not specifically directed against the infecting organism. The processes involved in the induction of acquired resistance, however, are highly specific and seem to depend upon two factors: a state of immunological reactivity of the host and the presence of the specific microbial antigens to which the host has become reactive. When these two coexist in the tissues the host is found to be non-specifically resistant. It is suggested that resistance, which was shown to depend upon an altered state of host macrophages, may be due to the interaction of antigen and a specific antibody adsorbed to the surface of host macrophages; and that the antibody involved in the reaction is perhaps identical with the antibody which confers the state of delayed-type hypersensitivity. The results are discussed in relation to the question of latent infection and infection immunity.
Antidepressants are a rational complementary therapy for the treatment of Alzheimer's disease
Authors: Marwa Aboukhatwa, Laura Dosanjh, Yuan Luo
Journal: Molecular Neurodegeneration (2010)

Abstract There is a high prevalence rate (30-50%) of Alzheimer's disease (AD) and depression comorbidity. Depression can be a risk factor for the development of AD or it can be developed secondary to the neurodegenerative process. There are numerous documented diagnosis and treatment challenges for the patients who suffer comorbidity between these two diseases. Meta analysis studies have provided evidence for the safety and efficacy of antidepressants in treatment of depression in AD patients. Preclinical and clinical studies show the positive role of chronic administration of selective serotonin reuptake inhibitor (SSRI) antidepressants in hindering the progression of the AD and improving patient performance. A number of clinical studies suggest a beneficial role of combinatorial therapies that pair antidepressants with FDA approved AD drugs. Preclinical studies also demonstrate a favorable effect of natural antidepressants for AD patients. Based on the preclinical studies there are a number of plausible antidepressants effects that may modulate the progression of AD. These effects include an increase in neurogenesis, improvement in learning and memory, elevation in the levels of neurotrophic factors and pCREB and a reduction of amyloid peptide burden. Based on this preclinical and clinical evidence, antidepressants represent a rational complimentary strategy for the treatment of AD patients with depression comorbidity.
White Adipose Tissue Cells Are Recruited by Experimental Tumors and Promote Cancer Progression in Mouse Models
Authors: Yan Zhang, Alexes Daquinag, Dmitry O. Traktuev, Felipe Amaya-Manzanares, Paul J. Simmons, Keith L. March, Renata Pasqualini, Wadih Arap, Mikhail G. Kolonin
Journal: Cancer Research (2009)

Abstract The connection between obesity and accelerated cancer progression has been established, but the mediating mechanisms are not well understood. We have shown that stromal cells from white adipose tissue (WAT) cooperate with the endothelium to promote blood vessel formation through the secretion of soluble trophic factors. Here, we hypothesize that WAT directly mediates cancer progression by serving as a source of cells that migrate to tumors and promote neovascularization. To test this hypothesis, we have evaluated the recruitment of WAT-derived cells by tumors and the effect of their engraftment on tumor growth by integrating a transgenic mouse strain engineered for expansion of traceable cells with established allograft and xenograft cancer models. Our studies show that entry of adipose stromal and endothelial cells into systemic circulation leads to their homing to and engraftment into tumor stroma and vasculature, respectively. We show that recruitment of adipose stromal cells by tumors is sufficient to promote tumor growth. Finally, we show that migration of stromal and vascular progenitor cells from WAT grafts to tumors is also associated with acceleration of cancer progression. These results provide a biological insight for the clinical association between obesity and cancer, thus outlining potential avenues for preventive and therapeutic strategies. [Cancer Res 2009;69(12):5259–66]
Effect of Altitude on the Heart and the Lungs
Authors: Peter Bärtsch, J. Simon R. Gibbs
Journal: Circulation (2007)

T his review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level.We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals.These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively.One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail.Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the highaltitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension.
Overexpression of Phosphorylated Mammalian Target of Rapamycin Predicts Lymph Node Metastasis and Prognosis of Chinese Patients with Gastric Cancer
Authors: Guanzhen Yu, Jiejun Wang, Ying Chen, Xi Wang, Jun Pan, Gang Li, Zhiliang Jia, Qiang Li, James C. Yao, Keping Xie
Journal: Clinical Cancer Research (2009)

Abstract Purpose: We determined the expression of mammalian target of rapamycin (mTOR) and its activated form, p-mTOR, in Chinese patients with gastric cancer and its clinical effects and underlying mechanisms. Experimental Design: Tissue microarray blocks containing gastric cancer tissue and matched noncancer gastric tissue specimens obtained from 1,072 patients were constructed. Expression of total mTOR and p-mTOR in these specimens was analyzed using immunohistochemical studies and confirmed by Western blotting. Results: The overall rates of total mTOR and p-mTOR overexpression were 50.8% (545 of 1,072) and 46.5% (499 of 1,072), respectively. The p-mTOR overexpression was significantly correlated with total mTOR overexpression. Overexpression of total mTOR protein was significantly correlated with tumor differentiation, T1/T2 tumors, and stage I/II/III disease, whereas p-mTOR overexpression was significantly correlated with lymph node metastasis and all stage disease. The Cox proportional hazards model revealed that the overexpression of p-mTOR, but not total mTOR, was an independent prognostic factor for gastric cancer. The overexpression of p-mTOR also predicted the angiogenic phenotype of human gastric cancer and regulated angiogenesis of gastric cancer cells. Conclusions: Increased activation of mTOR is frequent in human gastric cancer and overexpression of p-mTOR is an independent prognostic factor, suggesting that mTOR pathway could be a potential target for therapy of this malignancy.