tbuckley/cabot-search huggingface dataset:
Recurrent virus meningitis.
Authors: J P Anderson
Journal: BMJ (1969)

NMICA JOUMUNL uria (Meyer-Betz, 1911) and an association with alcohol overlooked or regarded as incidental.For example, Elek and Anderson (1953) described "paroxysmal paralytic myoglobinuria" in a woman after the ingestion of a "few gins," and more recently Schutta et al. (1969) reported the cases of three patients with "paroxysmal idiopathic myoglobinuria," all of whom were heavy drinkers.So far as we are aware the above is the first example of the condition described in this country, but it seems possible that myopathy due to alcohol may be commoner than is generally realized, and a history of alcoholism in patients with a neuro- muscular disorder should be considered as of possible aetio- logical significance.We wish to thank Dr.
Risks of all-cause and suicide mortality in mental disorders: a meta-review
Authors: Edward Chesney, Guy M. Goodwin, Seena Fazel
Journal: World Psychiatry (2014)

A meta-review, or review of systematic reviews, was conducted to explore the risks of all-cause and suicide mortality in major mental disorders. A systematic search generated 407 relevant reviews, of which 20 reported mortality risks in 20 different mental disorders and included over 1.7 million patients and over a quarter of a million deaths. All disorders had an increased risk of all-cause mortality compared with the general population, and many had mortality risks larger than or comparable to heavy smoking. Those with the highest all-cause mortality ratios were substance use disorders and anorexia nervosa. These higher mortality risks translate into substantial (10-20 years) reductions in life expectancy. Borderline personality disorder, anorexia nervosa, depression and bipolar disorder had the highest suicide risks. Notable gaps were identified in the review literature, and the quality of the included reviews was typically low. The excess risks of mortality and suicide in all mental disorders justify a higher priority for the research, prevention, and treatment of the determinants of premature death in psychiatric patients.
The Mesangial Cell Revisited
Authors: Detlef Schlo[Combining Diaeresis]ndorff, Bernhard Banas
Journal: Journal of the American Society of Nephrology (2009)

Mesangial cells and their matrix form the central stalk of the glomerulus and are part of a functional unit interacting closely with endothelial cells and podocytes. Alterations in one cell type can produce changes in the others. The cytokines generated by mesangial cells, endothelial cells, and podocytes that tridirectionally and interactively influence cognate receptors on receiver cells are not fully defined. The existence of cytokine cross-talk seems very likely, given the observations that podocyte injury frequently results in mesangial cell proliferation, whereas mesangial cell injury leads to foot process fusion and proteinuria. Another potentially fruitful area of future research is the role of mesangial cells as local modulators of innate and adaptive immune responses. Thus, mesangial cell research still holds much promise.
Synchronous Presentation of B-Cell Chronic Lymphocytic Leukemia/Small-Cell Lymphoma and Colon Adenocarcinoma Within the Same Mesenteric Lymph Nodes and a Single Liver Metastasis
Authors: Nicola Silvestris, Francesco Alfredo Zito, Maria Grazia Fiore, Gianni Simone, Stefania Tommasi, Giovanni Izzi, Attilio Guarini, Giuseppe Colucci
Journal: Journal of Clinical Oncology (2010)
3p Microsatellite Alterations in Exhaled Breath Condensate from Patients with Non–Small Cell Lung Cancer
Authors: Giovanna E. Carpagnano, Maria Pia Foschino-Barbaro, Giuseppina Mulé, Onofrio Resta, Stefania Tommasi, Anita Mangia, Francesco Carpagnano, Gaetano Stea, Antonia Susca, Giuseppe Di Gioia, Mario De Lena, Angelo Paradiso
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

The still-high mortality for lung cancer urgently requires the availability of new, noninvasive diagnostic tools for use in early diagnosis and screening programs. Recently, exhaled breath condensate (EBC) has been proposed as a useful tool to obtain biological information on lung cancer disease. This study provides, for the first time, evidence that DNA alterations already described in lung cancer are detectable in EBC from patients with non-small cell lung cancer (NSCLC) and in healthy subjects. Thirty patients with histologic evidence of NSCLC and 20 healthy subjects were enrolled in the present study. All subjects had allelotyping analysis of DNA from EBC (EBC-DNA) and from whole blood (WB-DNA) of a selected panel of five microsatellites (D3S2338, D3S1266, D3S1300, D3S1304, D3S1289) located in chromosomal region 3p. Results from healthy subjects and subjects with cancer, and from EBC and WB, were compared. In addition, the relationships with smoking habit and clinicopathologic tumor features were considered. Microsatellite alterations (MAs) were found in 53% of EBC-DNA and in 10% of WB-DNA loci investigated in patients with NSCLC (p < 10(-6)); conversely, MAs were present only in 13% of EBC-DNA and in 2% of WB-DNA informative loci in healthy subjects. In patients with NSCLC, a direct association between number of MAs detected in EBC-DNA and tobacco consumption was observed. We conclude that EBC-DNA is highly sensitive in detecting MA information unique to patients with lung cancer. Furthermore, MA information seems to be directly related with tobacco consumption, and is potentially applicable to screening and early diagnostic programs for patients with NSCLC.
Interleukin‐32: A new proinflammatory cytokine involved in hepatitis C virus‐related liver inflammation and fibrosis
Authors: Alexander R. Moschen, Teresa Fritz, Andrew D. Clouston, Ilka Rebhan, Oliver Bauhofer, Helen D. Barrie, Elizabeth E. Powell, Soo-Hyun Kim, Charles A. Dinarello, Ralf Bartenschlager, Julie R. Jonsson, Herbert Tilg
Journal: Hepatology (2011)

Interleukin 32 (IL-32) is a recently described proinflammatory cytokine that activates p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB), thereby inducing proinflammatory cytokines such as IL-1β and tumor necrosis factor alpha (TNF-α). We investigated the role of IL-32 in patients with chronic hepatitis C virus (HCV) infection. Steady-state hepatic messenger RNA (mRNA) levels of IL-32 were determined in a cohort of 90 subjects; anti-IL-32 staining was used in a second cohort of 132 consecutive untreated chronic HCV patients. Correlations with histological features of steatosis, inflammation, and fibrosis were made. In vitro, endogenous IL-32 in monocytes and in the human hepatoma cell line Huh-7.5 were examined. The effects of IL-32-overexpression and IL-32-silencing on HCV replication were studied using HCV luciferase reporter viruses. There were highly significant positive associations between hepatic IL-32 mRNA expression and liver steatosis, inflammation, fibrosis, smooth muscle actin (SMA) area, and serum alanine aminotransferase (ALT) levels. IL-32 protein expression was positively associated with portal inflammation, SMA area, and ALT. In vitro, IL-1β and TNF-α significantly induced IL-32 expression in human Huh-7.5 cells. Alone, stimulation with interferon alpha (IFN-α) did not induce IL-32 expression in Huh-7.5. However, IFN-α exerted a significant additive effect on TNF-α-induced but not IL-1β-induced IL-32 expression, particularly in CD14+ monocytes. This effect was dependent both on NF-κB and Jak/STAT signaling. Viral infection of Huh-7.5 cells resulted in a significant (11-fold) induction of IL-32 mRNA expression. However, modulation of IL-32 in Huh-7.5 cells by overexpression or silencing did not influence HCV virus replication as determined by luciferase assays.IL-32 is a novel proinflammatory cytokine involved in HCV-associated liver inflammation/fibrosis. IL-32 is expressed by human hepatocytes and hepatoma cells and its expression is regulated by proinflammatory stimuli.
Continued Exposure to Maternal Distress in Early Life Is Associated with an Increased Risk of Childhood Asthma
Authors: Anita L. Kozyrskyj, Xiao-Mei Mai, Patrick McGrath, Kent T. HayGlass, Allan B. Becker, Brian MacNeil
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Evidence is emerging that exposure to maternal distress in early life plays a causal role in the development of childhood asthma.Because much of the data are from high-risk cohorts, we undertook a birth cohort study in a complete population of children to test this association.Using Manitoba, Canada's, health care and prescription databases, this longitudinal study assessed the association between maternal distress during the first year of life and onward, and asthma at age 7 in a 1995 birth cohort of 13,907 children.Maternal distress was defined on the basis of health care or prescription medication use for depression or anxiety. Asthma status was derived from health care and prescription records for asthma, using a definition validated by comparison to pediatric allergist diagnosis. Multiple logistic regression was used to determine the likelihood of asthma (odds ratio [OR], 95% confidence interval [95% CI]). Independent of well-known asthma risk factors, our population-based study of a non-high-risk cohort demonstrated an increased risk of childhood asthma (OR, 1.25; 95% CI, 1.01-1.55) among children exposed to continued maternal distress from birth until age 7. Exposure to maternal depression and anxiety limited to the first year of life did not have a demonstrable association with subsequent asthma. Of interest, we observed that the risk of asthma associated with continued maternal distress was increased in children living in high- versus low-income households (OR, 1.44; 95% CI, 1.12-1.85).Maternal distress in early life plays a role in the development of childhood asthma, especially if it continues beyond the postpartum period.
The concept of quarantine in history: from plague to SARS
Authors: G GENSINI
Journal: Journal of Infection (2004)

The concept of 'quarantine' is embedded in health practices, attracting heightened interest during episodes of epidemics. The term is strictly related to plague and dates back to 1377, when the Rector of the seaport of Ragusa (then belonging to the Venetian Republic) officially issued a 30-day isolation period for ships, that became 40 days for land travellers. During the next 100 years similar laws were introduced in Italian and in French ports, and they gradually acquired other connotations with respect to their original implementation. Measures analogous to those employed against the plague have been adopted to fight against the disease termed the Great White Plague, i.e. tuberculosis, and in recent times various countries have set up official entities for the identification and control of infections. Even more recently (2003) the proposal of the constitution of a new European monitoring, regulatory and research institution has been made, since the already available system of surveillance has found an enormous challenge in the global emergency of the severe acute respiratory syndrome (SARS). In the absence of a targeted vaccine, general preventive interventions have to be relied upon, including high healthcare surveillance and public information. Quarantine has, therefore, had a rebound of celebrity and updated evidence strongly suggests that its basic concept is still fully valid.
Probenecid as a sensitizer of bisphosphonate-mediated effects in breast cancer cells
Authors: Regina Ebert, Jutta Meissner-Weigl, Sabine Zeck, Jorma Määttä, Seppo Auriola, Sofia Coimbra de Sousa, Birgit Mentrup, Stephanie Graser, Tilman D Rachner, Lorenz C Hofbauer, Franz Jakob
Journal: Molecular Cancer (2014)

Anti-resorptive bisphosphonates (BP) are used for the treatment of osteoporosis and bone metastases. Clinical studies indicated a benefit in survival and tumor relapse in subpopulations of breast cancer patients receiving zoledronic acid, thus stimulating the debate about its anti-tumor activity. Amino-bisphosphonates in nM concentrations inhibit farnesyl pyrophosphate synthase leading to accumulation of isopentenyl pyrophosphate (IPP) and the ATP/pyrophosphate adduct ApppI, which induces apoptosis in osteoclasts. For anti-tumor effects μM concentrations are needed and a sensitizer for bisphosphonate effects would be beneficial in clinical anti-tumor applications. We hypothesized that enhancing intracellular pyrophosphate accumulation via inhibition of probenecid-sensitive channels and transporters would sensitize tumor cells for bisphosphonates anti-tumor efficacy. MDA-MB-231, T47D and MCF-7 breast cancer cells were treated with BP (zoledronic acid, risedronate, ibandronate, alendronate) and the pyrophosphate channel inhibitors probenecid and novobiocin. We determined cell viability and caspase 3/7 activity (apoptosis), accumulation of IPP and ApppI, expression of ANKH, PANX1, ABCC1, SLC22A11, and the zoledronic acid target gene and tumor-suppressor KLF2. Treatment of MDA-MB-231 with BP induced caspase 3/7 activity, with zoledronic acid being the most effective. In MCF-7 and T47D either BP markedly suppressed cell viability with only minor effects on apoptosis. Co-treatment with probenecid enhanced BP effects on cell viability, IPP/ApppI accumulation as measurable in MCF-7 and T47D cells, caspase 3/7 activity and target gene expression. Novobiocin co-treatment of MDA-MB-231 yielded identical results on viability and apoptosis compared to probenecid, rendering SLC22A family members as candidate modulators of BP effects, whereas no such evidence was found for ANKH, ABCC1 and PANX1. In summary, we demonstrate effects of various bisphosphonates on caspase 3/7 activity, cell viability and expression of tumor suppressor genes in breast cancer cells. Blocking probenecid and novobiocin-sensitive channels and transporters enhances BP anti-tumor effects and renders SLC22A family members as good candidates as BP modulators. Further studies will have to unravel if treatment with such BP-sensitizers translates into preclinical and clinical efficacy.
Twist1 and Hopx determine function and persistence of pathogenic memory/effector T cells
Authors: I. Albrecht, K. Hradilkova, K. Westendorf, M. Weber, A. Radbruch, H.-D. Chang
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Introduction</h3> T helper (Th) lymphocytes support the initiation and maintenance of autoimmune inflammation through secretion of cytokines and provision of B cell help leading to the generation of longlived plasma cells secreting pathogenic autoantibodies. In particular Th type 1 (Th1) and Th17 cells, which promote inflammation through the secretion of IFN-γ, tumour necrosis factor-α and interleukin-17, have been implicated in the pathogenesis of autoimmunity. The critical role of CD4<sup>+</sup> Th cells has been demonstrated by the clinical benefit achieved through the depletion of Th cells with an anti-CD4 antibody in refractory rheumatoid arthritis patients. However, unwanted side-effects of sustained CD4 lymphopenia and the associated induced immunodeficiency call for the development of more advanced approaches allowing the selective elimination of disease-causing Th cells. This requires a better understanding of the biology of pathogenic Th cells and the identification of selective biomarkers. <h3>Material and methods</h3> The authors wanted to investigate the mechanisms involved in the transition from acute to chronic inflammation and identify selective biomarkers allowing the identification of pathogenic Th cells. Following the rationale that Th cells involved in chronic autoimmune inflammation have a history of repeated (auto-)antigen contact, the authors have compared the transcriptomes of Th1 and Th2 cells which they have stimulated only once to Th cells which they have stimulated several times. <h3>Results</h3> The authors could identify the two genes, twist1 and hopx, to be specifically upregulated in repeatedly stimulated, pro-inflammatory Th1 cells. Twist1 is a helix-loop-helix transcription factor whose expression increments with each restimulation. Twist1 is highly expressed in CD4<sup>+</sup> T cells isolated directly from the site of inflammation in patients with, for example, rheumatoid arthritis and inflammatory bowel disease, but not in T cells isolated from the peripheral blood. When twist1 is downregulated in Th1 cells by RNA interference in the murine ovalbumin-induced arthritis model, inflammation is augmented, indicating that twist1 is an intrinsic regulator of inflammation. Inhibition of hopx expression in Th1 cells leads to an impairment in their ability to persist in vivo. Accordingly, hopx-deficient mice have fewer effector/memory Th1 cells in steady-state. Th1 cells, which lack expression of hopx, are not able to induce inflammation in the murine transfer colitis model or the ovalbumin-induced arthritis model. <h3>Conclusions</h3> Twist1 and hopx qualify as selective biomarkers allowing the identification of pro-inflammatory, pathogenic Th1 cells. The importance of twist1 and hopx for the function and persistence of pathogenic Th1 cells may offer novel opportunities for the selective targeting of such cells.
Long-Term Vitamin C Treatment Increases Vascular Tetrahydrobiopterin Levels and Nitric Oxide Synthase Activity
Authors: Livius V. d’Uscio, Sheldon Milstien, Darcy Richardson, Leslie Smith, Zvonimir S. Katusic
Journal: Circulation Research (2003)

In cultured endothelial cells, the antioxidant, L-ascorbic acid (vitamin C), increases nitric oxide synthase (NOS) enzyme activity via chemical stabilization of tetrahydrobiopterin. Our objective was to determine the effect of vitamin C on NOS function and tetrahydrobiopterin metabolism in vivo. Twenty-six to twenty-eight weeks of diet supplementation with vitamin C (1%/kg chow) significantly increased circulating levels of vitamin C in wild-type (C57BL/6J) and apolipoprotein E (apoE)--deficient mice. Measurements of NOS enzymatic activity in aortas of apoE-deficient mice indicated a significant increase in total NOS activity. However, this increase was mainly due to high activity of inducible NOS, whereas eNOS activity was reduced. Significantly higher tetrahydrobiopterin levels were detected in aortas of apoE-deficient mice. Long-term treatment with vitamin C restored endothelial NOS activity in aortas of apoE-deficient mice, but did not affect activity of inducible NOS. In addition, 7,8-dihydrobiopterin levels, an oxidized form of tetrahydrobiopterin, were decreased and vascular endothelial function of aortas was significantly improved in apoE-deficient mice. Interestingly, vitamin C also increased tetrahydrobiopterin and NOS activity in aortas of C57BL/6J mice. In contrast, long-term treatment with vitamin E (2000 U/kg chow) did not affect vascular NOS activity or metabolism of tetrahydrobiopterin. In vivo, beneficial effect of vitamin C on vascular endothelial function appears to be mediated in part by protection of tetrahydrobiopterin and restoration of eNOS enzymatic activity.
CONVULSIVE STATES AND COMA IN CASES OF ISLET CELL ADENOMA OF THE PANCREAS
Authors: PAUL F. A. HOEFER, SAMUEL A. GUTTMAN, IRVING J. SANDS
Journal: American Journal of Psychiatry (1946)

This report is an analysis of neurological and psychiatric manifestations observed in 27 patients suffering from verified adenoma of the islet cell apparatus of the pancreas. In addition relevant laboratory data, mainly those related to the glucose metabolism and in the last 11 patients also the EEG findings are discussed. The clinical data were arranged in four groups: (1) autonomic-visceral, (2)somatic-neurological, (3) "psychomotor" manifestations and (4) seizures and seizure fragments. These four groups of data are then discussed in terms of anatomic-physiological levels using concepts established by Himwich. Our findings differ in several important aspects from those found in therapeutic insulin shock. An attempt is made to understand the reasons for this divergence. Glucose tolerance curves in a majority of our cases are diabetic in pattern and often also in level. "Flat" curves are the exception in our experience. The EEG findings are those to be expected in patients whose cerebral metabolism is depressed. In addition suggestive "convulsive" patterns such as spike-and-wave bursts are found in most of our patients, even those who had no clinical convulsive seizures.
Selective Profiling of Proteins in Lung Cancer Cells from Fine-Needle Aspirates by Matrix-Assisted Laser Desorption Ionization Time-of-Flight Mass Spectrometry
Authors: Joseph M. Amann, Pierre Chaurand, Adriana Gonzalez, James A. Mobley, Pierre P. Massion, David P. Carbone, Richard M. Caprioli
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) has been used to analyze tumor sections and can determine tumor type, nodal involvement, and survival, and shows promise in predicting therapeutic response. Our purpose was to develop a method compatible with MALDI-TOF MS that allows selective analysis of cancer cells in mixed clinical samples such as fine-needle aspirates. Experimental Design: Lung cancer cell lines were cytocentrifuged onto metal-coated, transparent glass slides and used for optimization of fixation, staining, and RBC lysis protocols. Fine-needle aspirates from human tumors and mouse model tumors were used to provide fresh tissue samples for determining the feasibility of this method. Results: The MALDI-TOF MS compatible fixation and staining techniques provided high-resolution cellular morphology, which allowed identification and selective spotting of tumor cells. The RBC lysis step efficiently removed contaminating RBC yielding spectra nearly free from hemoglobin peaks. Protein profiles of fine-needle aspirates were found highly reproducible and similar to the profiles of the tissue from which they were obtained. Using this method, we were able to differentiate between xenograft tumors derived from two different human cell lines, A549 and H460. Conclusion: This procedure results in the production of high-quality, cancer cell–specific protein profiles. This highly reproducible technique could be applied to many other types of mixed clinical samples and has the potential to be very useful in the clinical diagnosis, classification, and, potentially, the individualized treatment of cancer patients.
INTERACTION OF HISTOCOMPATIBILITY (HL-A) ANTIBODIES AND COMPLEMENT WITH SYNCHRONIZED HUMAN LYMPHOID CELLS IN CONTINUOUS CULTURE
Authors: S. Ferrone, N. R. Cooper, M. A. Pellegrino, R. A. Reisfeld
Journal: The Journal of Experimental Medicine (1973)

The interaction of histocompatibility (HL-A) antibodies and complement with synchronized human lymphoid cells in continuous culture has been investigated. The sensitivity of cultured lymphoid cells to HL-A antibody-mediated lysis in the cytotoxic test, the extent of activation of the complement system, the degree to which labeled complement components are bound, and the ability of these cells to absorb HL-A alloantibodies do not vary significantly during the cell growth cycle. The constancy of histocompatibility antigen expression throughout the growth cycle of cultured cells suggests that these cell surface markers are an essential part of membrane cytoarchitecture and could well play a critical role in determining the normal function of the cell membrane.