tbuckley/cabot-search huggingface dataset:
Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.
Authors: P A Mackowiak, M Marling-Cason, J W Smith, J P Luby
Journal: Journal of Clinical Investigation (1984)

Cytomegalovirus (CMV) and other viruses within the herpes group have recently been shown to induce Fc receptors in infected monolayers. We have examined the possibility that such receptors might facilitate the adherence of antibody-coated bacteria to CMV-infected cells. To do this, we infected confluent human embryonic lung (HEL) cell monolayers with CMV (strain AD 169) and then used a double radiolabel assay to measure adherence of Escherichia coli 06 to both infected and control monolayers. We examined infected monolayers 48 h after viral seeding, at which time 30-60% of the cells exhibited characteristic cytopathic changes. We compared the adherence of untreated E. coli 06 with the adherence of E. coli 06 that had been preincubated for 1 h at 37 degrees C with either nonimmune or anti-E. coli 06 antiserum. Pretreatment of the E. coli 06 with specific antiserum significantly enhanced its adherence to CMV-infected, but not to control, monolayers (P less than 0.01 by the Mann-Whitney U test). We did not see such enhancement when we used anti-E. coli 06 antiserum to treat a nontypable E. coli. The augmented adherence of antibody-coated E. coli 06 to CMV-infected monolayers was abrogated by pretreating the monolayers with nonimmune serum or purified Fc fragments, but not by pretreating with IgA, IgM, or 1 mM trypan blue. Preincubating HEL cell monolayers with 100 U/ml human leukocyte interferon for 72 h at 37 degrees C did not affect the adherence of antibody-coated E. coli 06 to the monolayers. To determine if antibody-coated bacteria that adhered to the surface of CMV-infected monolayers might themselves act as receptors for microorganisms with Fc binding potential, we compared the adherence of Cowan strain Staphylococcus aureus to CMV-infected and control monolayers that had been preincubated with antibody-coated E. coli 06. The S. aureus adhered significantly better to the former monolayers (P less than 0.001). These results illustrate a previously unrecognized mechanism by which certain herpesviruses might enhance the adherence of secondary pathogens to nonphagocytic cell populations. Such a mechanism, if active in vivo, might facilitate the colonization of mucosal surfaces by these pathogenic microorganisms, and in this way might contribute to both the reported predisposition of CMV-infected patients to secondary infections and to the high prevalence of S. aureus in the vaginal flora of women with histories of genital herpes.
Vitamin E as an Antioxidant of the Lung
Authors: Ingrid Kolleck, Pranav Sinha, Bernd Rüstow
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Section:ChooseTop of pageAbstract <<VITAMIN E IS AN INTEGRAL ...HIGH-DENSITY LIPOPROTEIN ...HDL-SPECIFIC RECEPTORS EX...EFFECT OF VITAMIN E DEPLE...VITAMIN E CONCENTRATION A...OPEN QUESTIONS OF VITAMIN...ReferencesCITING ARTICLES
<i>MicroRNA-146a</i>and<i>Ets-1</i>gene polymorphisms in ocular Behçet's disease and Vogt–Koyanagi–Harada syndrome
Authors: Qingyun Zhou, Shengping Hou, Liang Liang, Xinyu Li, Xiaoyu Tan, Lin Wei, Bo Lei, Aize Kijlstra, Peizeng Yang
Journal: Annals of the Rheumatic Diseases (2012)

MicroRNA-146a (miR-146a) is involved in certain immune-mediated diseases. Transcription factor Ets-1 strongly affects miR-146a promoter activity and directly regulates miR-146a expression. This study was performed to investigate the association of miR-146a and Ets-1 gene polymorphisms with Behçet's disease (BD) and Vogt-Koyanagi-Harada (VKH) disease in a Chinese Han population.A total of 809 patients with BD, 613 patients with VKH and 1132 normal controls were genotyped for miR-146a/rs2910164, rs57095329 and rs6864584, Ets-1/rs1128334 and rs10893872 using a PCR restriction fragment length polymorphism assay. miR-146a expression was examined in peripheral blood mononuclear cells (PBMCs) by real-time PCR. Cytokine production by PBMCs was measured by ELISA.A significantly decreased frequency of the homozygous rs2910164 CC genotype and C allele was observed in patients with BD compared with controls (pc(a)=1.24×10(-5), OR 0.61; pc(a)=1.33×10(-4), OR 0.75, respectively). MiR-146a expression in GG cases was 2.45-fold and 1.99-fold higher, respectively, than that in CC cases and GC cases. There was no association of the other four single nucleotide polymorphisms (SNPs) with BD. There was also no association of these five SNPs with its main clinical features. No associations were found with the five SNPs tested or with its clinical manifestations in VKH disease. Interleukin (IL)-17, tumour necrosis factor (TNF)α and IL-1β production from rs2910164 CC cases was markedly lower than that in GG cases. No effect of genotype was observed on IL-6 and monocyte chemoattractant protein (MCP)-1 production and IL-8 expression was slightly higher in CC cases.Our study identified a strong association of rs2910164 of miR-146a with BD in a Chinese population and decreased expression of miR-146a and certain proinflammatory cytokines in individuals carrying the CC genotype.
Modulation of Hypertonicity-Induced Aquaporin-1 by Sodium Chloride, Urea, Betaine, and Heat Shock in Murine Renal Medullary Cells
Authors: Fuminori Umenishi, Shigemi Yoshihara, Takefumi Narikiyo, Robert W. Schrier
Journal: Journal of the American Society of Nephrology (2005)

Aquaporin-1 (AQP1) expression is induced by hypertonicity in renal medullary cells. The purpose of the present study was to elucidate the role of sodium chloride (NaCl), urea, betaine, and heat shock on hypertonicity-induced AQP1 expression in cultured murine renal medullary-K2 (mIMCD-K2) cells. AQP1 expression was maximally induced under mild hypertonic medium supplemented with 100 mM NaCl (N100), whereas severe hypertonic medium supplemented with 150 mM NaCl (N150) caused little AQP1 induction. The reduction of AQP1 expression in N150 was associated with reduced cell viability. When cells were exposed continuously to N100, hypertonicity-induced AQP1 expression was elevated, whereas the return to isotonic medium reduced AQP1 expression in a time-dependent manner. The half-life of AQP1 protein in isotonic conditions was approximately 4 h, whereas hypertonicity markedly increased its half-life. These results indicate that hypertonicity plays an important role in AQP1 induction, stability, and degradation. On the contrary, urea inhibited hypertonicity-induced AQP1 expression in a dose-dependent manner. The addition of organic osmolyte betaine in N150 enhanced hypertonicity-induced AQP1 expression, whereas it decreased AQP1 expression in N100. This suggests that the excessive accumulation of betaine may counteract hypertonic stress and thus attenuate hypertonicity-induced AQP1 expression. Heat shock treatment promoted hypertonicity-induced AQP1 and heat shock protein 70 (HSP70) expression in both N100 and N150, suggesting an effect on the stability of hypertonicity-induced AQP1 expression. Taken together, NaCl, urea, betaine, and heat shock that regulate hypertonicity-induced AQP1 expression are potentially important factors in urinary concentration and contribute to the steady-state level of AQP1 expression.
Cancer Incidence Trends Among Asian American Populations in the United States, 1990-2008
Authors: S. L. Gomez, A.-M. Noone, D. Y. Lichtensztajn, S. Scoppa, J. T. Gibson, L. Liu, C. Morris, S. Kwong, K. Fish, L. R. Wilkens, M. T. Goodman, D. Deapen, B. A. Miller
Journal: JNCI Journal of the National Cancer Institute (2013)

BackgroundNational cancer incidence trends are presented for eight Asian American groups: Asian Indians/Pakistanis, Chinese, Filipinos, Japanese, Kampucheans, Koreans, Laotians, and Vietnamese.
Identification of a novel surface protein on activated CD4+ T cells that induces contact-dependent B cell differentiation (help).
Authors: S Lederman, M J Yellin, A Krichevsky, J Belko, J J Lee, L Chess
Journal: The Journal of Experimental Medicine (1992)

CD4+ T lymphocytes provide contact-dependent stimuli to B cells that are critical for the generation of specific antibody responses in a process termed T helper function. The surface structures on activated CD4+ T cells that mediate this function are not fully known. We previously reported the isolation of a functionally unique subclone of the Jurkat leukemic T cell line (D1.1) that constitutively expressed contact-dependent helper effector function. To identify T cell surface molecules that mediate contact-dependent T helper function, a monoclonal antibody (mAb), designated 5c8, was generated that inhibits D1.1-mediated B cell activation and immunoprecipitates a novel 30-kD protein structure from surface-iodinated D1.1 cells. Normal CD4+ T cells express 5c8 antigen (Ag) transiently 5-6 h after activation by phorbol myristate acetate and phytohemagglutinin with maximal expression 5-6 h after activation and absence of expression by 24 h. In contrast, neither resting nor activated CD8+ T cells express 5c8 Ag. In functional studies, mAb 5c8 inhibits the ability of fixed, activated CD4+ T cells to induce B cell surface CD23 expression. In addition, mAb 5c8 inhibits the ability of CD4+ T cells to direct terminal B cell differentiation driven by pokeweed mitogen. Taken together, these data suggest that 5c8 Ag is a novel, activation-induced surface T cell protein that is involved in mediating a contact-dependent element of the helper effector function of CD4+ T lymphocytes.
The variability of female reproductive ageing
Authors: E. R. te Velde
Journal: Human Reproduction Update (2002)

The delay in childbearing is an important societal change contributing to an increasing incidence of subfertility. The prevailing concept of female reproductive ageing assumes that the decline of both quantity and quality of the oocyte/follicle pool determines an age-dependent loss of female fertility. There is an apparent discrepancy between the ability to maintain a regular ovulatory cycle pattern and the several years earlier cessation of female fertility. This latter is largely explained by an age-related increase of meiotic non-disjunction leading to chromosomal aneuploidy and early pregnancy loss, such that most embryos from women ⩾40 years old are chromosomally abnormal and rarely develop further. The final stage of reproductive ageing–-the occurrence of menopause–-shows a huge variation between women. Age at last birth in natural fertility populations, which marks the end of female fertility, shows an identically wide variation as age at menopause, but occurs on average 10 years earlier. Given the high heritability for age at menopause, the variation in both age of menopause and last birth are probably under genetic control by the same set of genes. Some of those genes must carry heritable variants which modulate the rate of ovarian ageing and give rise to the wide age variations for the various phases of reproductive ageing.
Interleukin-10 Ablation Promotes Tumor Development, Growth, and Metastasis
Authors: Takashi Tanikawa, Cailin Moira Wilke, Ilona Kryczek, Grace Y. Chen, John Kao, Gabriel Núñez, Weiping Zou
Journal: Cancer Research (2011)

Abstract Interleukin-10 (IL-10) is a broadly acting immune inhibitory cytokine that is generally thought to support tumor growth. Here we challenge this view with evidence that genetic ablation of IL-10 in the mouse significantly heightens sensitivity to chemical carcinogenesis, growth of transplanted tumors, and formation of metastases. Tumor growth in IL-10–deficient (IL-10−/−) mice was associated with an increased level of myeloid-derived suppressor cells (MDSC) and CD4+Foxp3+ regulatory T (Treg) cells in both the tumor microenvironment and the tumor-draining lymph nodes. IL-10−/− MDSCs express high levels of MHC and IL-1, and they efficiently induced formation of Treg cells. IL-1 signaling blockade reduced tumor growth mediated by IL-10 deficiency, associated with a partial rescue of tumor infiltration and function of effector T cells and a decrease in tumor angiogenesis and tumor infiltration by Treg cells. Taken together, our findings establish that endogenous IL-10 inhibits inflammatory cytokine production and hampers the development of Treg cells and MDSCs, two key components of the immunosuppressive tumor microenvironment, thereby inhibiting tumor development, growth, and metastasis. Cancer Res; 72(2); 420–9. ©2011 AACR.
Mechanisms of Anemia in CKD
Authors: Jodie L. Babitt, Herbert Y. Lin
Journal: Journal of the American Society of Nephrology (2012)

Anemia is a common feature of CKD associated with poor outcomes. The current management of patients with anemia in CKD is controversial, with recent clinical trials demonstrating increased morbidity and mortality related to erythropoiesis stimulating agents. Here, we examine recent insights into the molecular mechanisms underlying anemia of CKD. These insights hold promise for the development of new diagnostic tests and therapies that directly target the pathophysiologic processes underlying this form of anemia.
Angiotensin II Stimulates Calcineurin Activity in Proximal Tubule Epithelia through AT-1 Receptor-Mediated Tyrosine Phosphorylation of the PLC-γ1 Isoform
Authors: Janice P. Lea, Shao G. Jin, Brian R. Roberts, Michael S. Shuler, Mario B. Marrero, James A. Tumlin
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. Angiotensin II (AngII) contributes to the maintenance of extracellular fluid volume by regulating sodium transport in the nephron. In nonepithelial cells, activation of phospholipase C (PLC) by AT-1 receptors stimulates the generation of 1,4,5-trisphosphate (IP3) and the release of intracellular calcium. Calcineurin, a serine-threonine phosphatase, is activated by calcium and calmodulin, and both PLC and calcineurin have been linked to sodium transport in the proximal tubule. An examination of whether AngII activates calcineurin in a model of proximal tubule epithelia (LLC-PK1 cells) was performed; AngII increased calcineurin activity within 30 s. An examination of whether AngII activates PLC in proximal tubule epithelia was also performed after first showing that all three families of PLC isoforms are present in LLC-PK1 cells. Application of AngII increased IP3 generation by 60% within 15 s, which coincided with AngII-induced tyrosine phosphorylation of the PLC-γ1 isoform also observed at 15 s. AngII-induced tyrosine phosphorylation was blocked by the AT-1 receptor antagonist, Losartan. Subsequently, an inhibitor of tyrosine phosphorylation blocked the AngII-induced activation of calcineurin, as did coincubation with an inhibitor of PLC activity and with an antagonist of the AT-1 receptor. It is therefore concluded that AngII stimulates calcineurin phosphatase activity in proximal tubule epithelial cells through a mechanism involving AT-1 receptor–mediated tyrosine phosphorylation of the PLC isoform.
Alternative Health Service
Authors: P. J. Bishop
Journal: BMJ (1974)

quantities by the Radiochemical Centre for use by investigators, who are continually evaluating its properties.'We have had the opportunity of testing this2 and comparing it with the silicate and with yttrium-90 citrate from France.The silicate consistently gave good retention in the knee, equivalent to that previously found with the resin col- loid, while the ferric hydroxide-based col- loid and the citrate were less well retained in the knee.In addition the citrate was associated with early lymph node uptake of considerable amounts of radioisotope.We have also analysed the chromosomal damage noted after treatment with these four radiocolloids and have found a low rate of chromosomal damage-equivalent to that after iodine-131 treatment for hyperthy- roidism-with the ferric hydroxide and sili- cate forms of yttrium-90.With the citrate there was considerably more chromosomal damage, roughly equivalent to that found with gold-198.4You mention that there is a reduction of lymph node uptake with hydrocortisone.This is noted only when using gold-198, with which there is a very considerable lymph node uptake of radioactivity.We have attempted the same work with yttrium-90 silicate, but because there is very little lymph node uptake with this latter preparation we have been unable to demonstrate material differences between hydrocortisone-treated patients and control patients in terms of lymph node uptake.-Iam, etc.,
Anal canal pressure profile: a reappraisal as determined by rapid pullthrough technique.
Authors: S M McHugh, N E Diamant
Journal: Gut (1987)

Previous station pull through techniques of anal canal pressure measurement have not truly represented the differences among individuals and between sexes in the length and pressure profile of the anal canal. Furthermore, the techniques commonly used in anal canal pressure determination have not been adequately compared or standardised. Therefore, a mechanised rapid pull through technique using an 8-lumen, 4-quadrant, continuously perfused catheter was evaluated and used to define the anal canal pressure profile. For measurement of the resting anal canal pressures, this technique was compared with the more usual station pull through technique in 12 subjects. There were no differences in resting pressure recorded by either technique with infusion rates ranging from 0.5 to 1.2 cc/min/orifice and over a range of catheter withdrawal rates of 0.19 to 0.48 cm/sec. Twenty two subjects (12 men/10 women) had their anal canal pressure profiles assessed using the rapid pull through technique. Anal canal length representing the mean of four axes differed between the sexes (p less than 0.005) and the difference was largely accounted for by a decrease in length of the anterior axis in women. A standardisation technique was used to account for between subject variation and for a more accurate between sex comparison of the pressure profiles. Significant differences in radial symmetry were found between the sexes. In the anterior axis the pressure was higher distally in women, while in the anterior and lateral axes the pressure was higher proximally in men. Anteriorly in women the highest pressures were exerted over a much shorter canal length than in men. We conclude that the usual station pull through technique can give reliable resting pressure measurements in the anal canal. The rapid pull through technique described herein, however, used a flexible catheter system which follows the normal anal canal and rectal contours, allows a more appropriate assessment of the anal sphincter profile, and provides findings that are consistent with the known local anatomy.
A potential new target for asthma therapy: A Disintegrin and Metalloprotease 10 (ADAM10) involvement in murine experimental asthma
Authors: J. A. Mathews, J. Ford, S. Norton, D. Kang, A. Dellinger, D. R. Gibb, A. Q. Ford, H. Massay, C. L. Kepley, P. Scherle, A. D. Keegan, D. H. Conrad
Journal: Allergy (2011)

To cite this article: Mathews JA, Ford J, Norton S, Kang D, Dellinger A, Gibb DR, Ford AQ, Massay H, Kepley CL, Scherle P, Keegan AD, Conrad DH. A potential new target for asthma therapy: A Disintegrin and Metalloprotease 10 (ADAM10) involvement in murine experimental asthma. Allergy 2011; 66: 1193–1200. Background: Elevated levels of CD23, a natural regulator of IgE production, have been shown to decrease the signs of lung inflammation in mice. The aim of this study was to study the involvement of ADAM10, the primary CD23 sheddase, in experimental asthma. Methods: ADAM10 was blocked either by using mice with a B-cell-specific deletion of the protease or pharmacologically by intranasal administration of selective ADAM10 inhibitors. Airway hypersensitivity (AHR) and bronchoaveolar lavage fluid (BALF) eosinophilia and select BALF cytokine/chemokine levels were then determined. Results: Using an IgE and mast cell–dependent mouse model, B-cell-specific ADAM10−/− mice (C57B/6 background) exhibited decreased eosinophilia and AHR when compared with littermate (LM) controls. Treatment of C57B/6 mice with selective inhibitors of ADAM10 resulted in an even further decrease in BALF eosinophilia, as compared with the ADAM10−/− animals. Even in the Th2 selective strain, Balb/c, BALF eosinophilia was reduced from 60% to 23% respectively. In contrast, when an IgE/mast cell–independent model of lung inflammation was used, the B-cell ADAM10−/− animals and ADAM10 inhibitor treated animals had lung inflammation levels that were similar to the controls. Conclusions: These results thus show that ADAM10 is important in the progression of IgE-dependent lung inflammation. The use of the inhibitor further suggested that ADAM10 was important for maintaining Th2 levels in the lung. These results thus suggest that decreasing ADAM10 activity could be beneficial in controlling asthma and possibly other IgE-dependent diseases.
Mucus clearance with three chest physiotherapy regimes in cystic fibrosis: a comparison between postural drainage, PEP and physical exercise
Authors: L Lannefors, P Wollmer
Journal: European Respiratory Journal (1992)

The effects of three different regimes of chest physiotherapy were compared in this cross-over study. Mucus clearance was monitored in nine clinically stable cystic fibrosis (CF) patients. The patients performed: 1) postural drainage with thoracic expansion exercises + forced expiration technique (FET) in the left decubitus position; 2) positive expiratory pressure (PEP)-mask breathing + FET; and 3) physical exercise on a bicycle ergometer + FET. All treatments had the same duration and FET was standardized. Mucus clearance was assessed using a technique based on measurement of the elimination of inhaled radiolabelled particles. Mean clearance of tracer from the right lung by postural drainage, PEP and physical exercise was 18% (range 10-29%), 20% (12-43%), 16% (8-25%), respectively, and from the left lung 20% (8-42%), 15% (5-23%) and 13% (5-17%), respectively. The differences were not statistically significant. Surprisingly, postural drainage (PD) was the most effective technique in the left, dependent lung in 7 of the 9 patients.
Moyamoya Disease and Moyamoya Syndrome
Authors: R. Michael Scott, Edward R. Smith
Journal: New England Journal of Medicine (2009)

Moyamoya disease is a cerebrovascular condition predisposing affected patients to stroke in association with progressive stenosis of the intracranial internal carotid arteries and their proximal branches. Patients with characteristic moyamoya vasculopathy plus associated conditions are categorized as having moyamoya syndrome. This review describes the demographic characteristics, pathogenesis, evaluation, and treatment of moyamoya disease and syndrome.
A randomized phase II trial comparing every 3-weeks carboplatin/paclitaxel with every 3-weeks carboplatin and weekly paclitaxel in advanced non-small cell lung cancer
Authors: M.A. Socinski, A. Ivanova, K. Bakri, J. Wall, M.Q. Baggstrom, T.A. Hensing, A. Mears, M. Tynan, J. Beaumont, A.H. Peterman, H.B. Niell
Journal: Annals of Oncology (2005)