tbuckley/cabot-search huggingface dataset:
Cytokine response to staphylococcal exotoxins in Staphylococcus aureus septicemia
Authors: Bo Söderquist, Krysztof Kanclerski, Karl-Gössta Sundqvist, Patricia Colque-Navarro, Hans Holmberg, Tomas Vikerfors, Roland Möllby
Journal: Clinical Microbiology and Infection (1998)
Evolution of Duplicate Control Regions in the Mitochondrial Genomes of Metazoa: A Case Study with Australasian Ixodes Ticks
Authors: Renfu Shao, Stephen C. Barker, Harumi Mitani, Yayoi Aoki, Masahito Fukunaga
Journal: Molecular Biology and Evolution (2004)

To investigate the evolution pattern and phylogenetic utility of duplicate control regions (CRs) in mitochondrial (mt) genomes, we sequenced the entire mt genomes of three Ixodes species and part of the mt genomes of another 11 species. All the species from the Australasian lineage have duplicate CRs, whereas the other species have one CR. Sequence analyses indicate that the two CRs of the Australasian Ixodes ticks have evolved in concert in each species. In addition to the Australasian Ixodes ticks, species from seven other lineages of metazoa also have mt genomes with duplicate CRs. Accumulated mtDNA sequence data from these metazoans and two recent experiments on replication of mt genomes in human cell lines with duplicate CRs allowed us to re-examine four intriguing questions about the presence of duplicate CRs in the mt genomes of metazoa: (1) Why do some mt genomes, but not others, have duplicate CRs? (2) How did mt genomes with duplicate CRs evolve? (3) How could the nucleotide sequences of duplicate CRs remain identical or very similar over evolutionary time? (4) Are duplicate CRs phylogenetic markers? It appears that mt genomes with duplicate CRs have a selective advantage in replication over mt genomes with one CR. Tandem duplication followed by deletion of genes is the most plausible mechanism for the generation of mt genomes with duplicate CRs. Once duplicate CRs occur in an mt genome, they tend to evolve in concert, probably by gene conversion. However, there are lineages where gene conversion may not always occur, and, thus, the two CRs may evolve independently in these lineages. Duplicate CRs have much potential as phylogenetic markers at low taxonomic levels, such as within genera, within families, or among families, but not at high taxonomic levels, such as among orders.
Value of Determination of Specific IgE Against Recombinant Aspergillus fumigatus Allergens rAsp f1, 2, 3, 4 e 6 in the Diagnosis of Allergic Bronchopulmonary Aspergillosis
Authors: E. Oliveira, P. Giavina-Bianchi, J. Kalilz
Journal: Journal of Allergy and Clinical Immunology (2006)

RATIONALE: Allergic bronchopulmonary aspergillosis (ABPA) is a complex disease, triggered by a hypersensitivity reaction to the allergens of Aspergillus fumigatus, a fungus that opportunistically colonizes the lungs of patients with asthma. The diagnosis of ABPA is difficult. A major problem is the lack of standardized allergens used in the determination of specific IgE, but the use of recombinant allergens has been proposed to overcome this. METHODS: The aim of the present study is to evaluate whether serological tests for IgE specific to recombinant allergens of Aspergillus fumigatus (rAsp) can aid in the detection of sensitization to this fungus and in the diagnosis of ABPA. We carried out an observational, prospective, cross-sectional study in outpatient facilities for the treatment of asthma. The diagnosis of ABPA, using classical criteria, was searched in 65 asthmatics patients with immediate cutaneous reactivity to Aspergillus fumigatus. After that, serum titers of IgE against rAsp f1, 2, 3, 4 and 6 were determined. In order to compare the differences between patients with confirmed and excluded diagnosis of ABPA, we used the two-tailed Fisher's exact test. RESULTS: Although 19 of 65 patients had IgE against at least one recombinant, the disease was diagnosed in only 6 patients. One of them had IgE against all recombinant allergens tested and another one had antibody against f 3. CONCLUSIONS: The determination of serum IgE against allergens rAsp f1, 2, 3, 4 e 6 in this group wasn't helpful to make the diagnosis of ABPA, neither to detect sensitization to fungus.
Sequences in the NS5A protein of hepatitis C virus and the serum alanine aminotransferase response to interferon therapy in Japanese patients
Authors: K Nagayama, N Enomoto, N Izumi, M Kurosaki, Y Miyasaka, H Watanabe, J Itakura, C-H Chen, J Tazawa, Y Hoshino, T Ikeda, F Marumo, C Sato
Journal: Gut (2001)

BACKGROUND AND AIMS Chronic hepatitis C is a slowly progressive disease and eventually causes hepatocellular carcinoma in many patients. Although interferon (IFN) therapy has been used for viral eradication, its success rate is only about 30%. In patients in whom it has failed (non-responders), there are several patterns of serum alanine aminotransferase (ALT) values, and detection of serum HCV-RNA during and after IFN therapy and improved long term prognosis were reported in patients whose serum ALT values were normalised by IFN therapy even if HCV viraemia persisted. The present study sought to clarify the virological characteristics contributing to these differences. METHODS Complete or partial length dominant sequences of hepatitis C virus genotype 1b (HCV-1b) were determined by direct sequencing. Firstly, the complete sequences of HCV-1b genomes were determined in six non-responders; three showed normalisation of serum ALT values during IFN-α therapy and the other three did not. Subsequently, the amino acid residues that were different in the two groups were further analysed retrospectively in another 82 patients. RESULTS Comparison of the sequences suggested an association between amino acids 2154–2172 of HCV-1b and serum ALT normalisation. A retrospective analysis of 82 patients revealed that the number of amino acid substitutions in this region was the only statistically significant variable associated with ALT normalisation (odds ratio 31.0; 95% confidence interval 5.0–286) in multivariate analyses. CONCLUSIONS A HCV genomic region that correlates with the ALT response to IFN therapy appears to be present in virologically IFN ineffective patients.
Smokers with airway obstruction are more likely to quit smoking
Authors: M Bednarek
Journal: Thorax (2006)

<b>Background:</b> Chronic obstructive pulmonary disease (COPD), usually caused by tobacco smoking, is one of the leading causes of morbidity and mortality. Smoking cessation at an early stage of the disease usually stops further progression. A study was undertaken to determine if diagnosis of airway obstruction was associated with subsequent success in smoking cessation, as advised by a physician. <b>Methods:</b> 4494 current smokers (57.4% men) with a history of at least 10 pack-years of smoking were recruited from 100 000 subjects screened by spirometric testing for signs of airway obstruction. At the time of screening all received simple smoking cessation advice. 1177 (26.2%) subjects had airway obstruction and were told that they had COPD and that smoking cessation would halt rapid progression of their lung disease. No pharmacological treatment was proposed. After 1 year all subjects were invited for a follow up visit. Smoking status was assessed by history and validated by exhaled carbon monoxide level. <b>Results:</b> Nearly 70% attended a follow up visit (n = 3077): 61% were men, mean (SD) age was 52 (10) years, mean (SD) tobacco exposure 30 (17) pack-years, and 33.3% had airway obstruction during the baseline examination. The validated smoking cessation rate in those with airway obstruction was 16.3% compared with 12.0% in those with normal spirometric parameters (p = 0.0003). After correction for age, sex, nicotine dependence, number of cigarettes smoked daily, and lung function, success in smoking cessation was predicted by lower lung function, lower nicotine dependence, and lower tobacco exposure. <b>Conclusions:</b> Simple smoking cessation advice combined with spirometric testing resulted in good 1 year cessation rates, especially in subjects with airway obstruction.
Mechanism of the rejection of major histocompatibility complex class I-disparate murine skin grafts: rejection can be mediated by CD4+ cells activated by allo-class I + II antigen in CD8+ cell-depleted hosts.
Authors: E Kobayashi, K Kawai, Y Ikarashi, M Fujiwara
Journal: The Journal of Experimental Medicine (1992)

In the preceding article, we analyzed the immunohistochemical rejection mechanism of major histocompatibility complex (MHC) class I (H-2K)-disparate murine skin grafts, and showed that only CD8+ cells infiltrated at the site of the epithelial tissue of MHC class I-disparate graft. We also showed that perfect survival of MHC class I-disparate grafts were attained in thymectomized recipients treated with anti-Lyt-2 monoclonal antibody. In this report, we showed that these long-surviving allo-class I grafts were rejected in the absence of CD8+ cells by stimulation with allo-MHC class I + II-disparate graft as the second stimulation. Furthermore, it was immunohistochemically revealed that under that condition, a large number of CD4+ cells infiltrated into the epithelial tissue of these long-surviving class I grafts, which were going to be rejected 2-5 d after the transplantation of a second graft with MHC class I + II difference. This result directly shows that CD4+ cells are able to became effectors for the rejection of allo-MHC class I (H-2K) skin graft.
Smoking-Attributable Cancer Mortality in 1991: Is Lung Cancer Now the Leading Cause of Death Among Smokers in the United States?
Authors: D. R. Shopland, H. J. Eyre, T. F. Peachacek
Journal: JNCI Journal of the National Cancer Institute (1991)

Finding from the new American Cancer Society prospective study of 1.2 million men and women indicate that mortality risks among smokers have increased substantially for most of the eight major cancer sites causally associated with cigarette smoking. Lung cancer risk for male smokers doubled, while the risk for females increased more than fourfold. On the basis of the new American Cancer Society relative risks, we project that cigarette smoking alone will contribute to slightly more than 157 000 of the 514 000 total cancer deaths expected to occur in the United States in 1991. Overall, smoking directly contributes to 21.5% of all cancer deaths in women but 45% of all cancer deaths in men. It would also appear that lung cancer has now displaced cornary heart disease as the single leading cause of excess mortality among smokers in the United States. [J Natl Cancer Inst 83:1142–1148, 1991]
Advances in Palliative Medicine and End-of-Life Care
Authors: Janet L. Abrahm
Journal: Annual Review of Medicine (2010)

Palliative care improves the quality and cost-effectiveness of adult and pediatric patient care, and it decreases unwanted hospitalizations and aggressive care at the end of life. National palliative care quality standards and preferred practices can be used for benchmarking by institutions, health care systems, and accrediting bodies. Pain and symptom management and the management of delirium for patients is now possible for the vast majority of patients, even those with advanced disease. However, because of shortages of specialists providing “tertiary” palliative care, significant improvements are needed in generalist-level palliative care among oncologists, intensivists, and specialists caring for patients with advanced cardiac, pulmonary, renal, and hepatic diseases. POLST (Physician Orders for Life-Sustaining Treatment) forms are a major advance in end-of-life care. They enable patients' advance directives to be valid wherever they are cared for (home, hospital, or nursing facility).
Sex differentials in predictors of mortality for patients with adult-onset diabetes: a population-based follow-up study in Beer-Sheva, Israel.
Authors: A Biderman, I Rosenblatt, S Rosen, L M Zangwill, R Shalev, M Friger, S Weitzman
Journal: Diabetes Care (2000)

OBJECTIVE: To test the hypothesis that factors predicting mortality differ between diabetic men and women. RESEARCH DESIGN AND METHODS: A total of 498 known patients with diabetes residing in a well-defined geographical area and receiving primary health care in 3 primary care community clinics were interviewed and examined between 1988 and 1990. RESULTS: By 31 July 1998, after a mean follow-up period of 7.8 years, 148 patients (68 men and 80 women) had died (29.7%). No statistical differences in survival rate or in the specific causes of death were found between men and women. In the univariate analysis of factors examined at baseline, GHb levels were significantly higher among women who died compared with women who survived, but this was not the case for men. Conversely, a trend of higher triglyceride and uric acid levels was found for men who died compared with men who survived, but this was not the case for women. Multivariate Poisson regression analysis showed significantly higher risk ratios for mortality in men &amp;gt; or = 63 years of age, men with microalbumin excretion &amp;gt; or = 30 mg/l, and men with higher triglyceride levels. In contrast, the analysis in women showed that higher GHb and creatinine levels and a reported history of heart disease were the only factors at the baseline examination significantly and independently associated with an increased risk ratio of mortality. CONCLUSIONS: The results suggest the existence of sex-specific interactions with various metabolic factors associated with diabetes that may have a different effect on mortality for each sex.
Alterations in molecular killing mechanisms: implications in skin disease
Authors: G. De Panfilis
Journal: British Journal of Dermatology (2001)

Cytolytic T lymphocytes exert two main specific molecular killing mechanisms against target cells, namely (i) they can synthesize and release soluble cytolytic factors, and (ii) they can express effector molecules that act as ligands of receptors expressed by target cells on the cell surface; by these two pathways cytolytic T lymphocytes kill several targets, e.g. cells infected with intracellular pathogens, cells transformed by malignancy and cells producing autoantibodies. This review investigates the contribution from alterations in these molecular killing mechanisms to the pathogenesis of cutaneous diseases. In fact, molecular components involved in such killing mechanisms are often altered or distorted in skin pathology, e.g. cutaneous viral infections, skin cancer, contact hypersensitivity and autoimmune diseases with cutaneous involvement. Treatments capable of repairing the molecular components operating in such killing mechanisms could presumably favour the resolution of these skin diseases.
Academic Global Surgery
Authors: William P. Schecter
Journal: JAMA Surgery (2015)

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CCL2: a link between hepatic inflammation, fibrosis and angiogenesis?
Authors: Silvia Affò, Pau Sancho-Bru
Journal: Gut (2014)

Liver fibrosis develops as a result of an excessive accumulation of extracellular matrix mostly in the context of chronic liver injury. The progression of liver fibrosis may lead to the development of cirrhosis and eventually hepatocellular carcinoma. Only in recent years has angiogenesis been considered as a concomitant process along the progression of liver fibrosis.1 Moreover, angiogenesis has been shown to be of key importance during the development, growth and progression of hepatocellular carcinoma, one of the most vascularised tumours. However, whether angiogenesis determines the progression of liver fibrosis or is merely a consequence of fibrosis progression is still unclear.

The progression from early stages of fibrosis to cirrhosis is by definition, accompanied by structural and anatomical changes in the liver affecting liver perfusion and compromising oxygen supply. Moreover, deposition of extracellular matrix at the space of Disse prevents oxygen diffusion and promotes sinusoidal capillarisation.

But not only structural changes are behind the increased vascularisation in chronic liver diseases. Activation of hepatic stellate cells, endothelial dysfunction and recruitment of inflammatory cells determine the production of pro-angiogenic factors and a misbalance in the synthesis of vasoactive and inflammatory substances, creating a pro-angiogenic milieu.1 

The mechanisms linking inflammation, fibrosis and angiogenesis have not yet been identified and remain an open field that will certainly provide new targets for the treatment of chronic liver diseases. Upon …
Prospective Analysis of Prostate-Specific Markers in Pelvic Lymph Nodes of Patients With High-Risk Prostate Cancer
Authors: A. C. Ferrari, J. N. Eyler, M. Gao, N. N. Stone, J. Mandeli, P. Unger, R. E. Gallagher, R. Stock
Journal: JNCI Journal of the National Cancer Institute (1997)

Background: Pathologic evidence of pelvic lymph node involvement is obtained in 12%-20% of patients with localized prostate cancer that exhibits high-risk features (defined on the basis of tumor size, serum prostate-specific antigen [PSA] level, or Gleason score). The rate of systemic failure (i.e., relapse) in patients with this type of prostate cancer and no pathologic evidence of regional lymph node involvement is 55%-92% within 5 years of definitive local therapy. Since reverse transcription-polymerase chain reaction (RT-PCR) methods are likely to be more sensitive than routine pathologic examination in detecting metastatic tumor cells, we compared the ability of the two approaches to detect prostate cells in the pelvic lymph nodes of patients with localized, high-risk disease. Methods: Fifty-eight lymph node specimens isolated from 33 patients before definitive local therapy were examined. Expression of PSA and prostatespecific membrane antigen (PSM) messenger RNAs in the specimens was assessed by means of nested RT-PCR. Results: Pathologic examination identified tumor cells in the lymph nodes of four (12%) of the 33 patients, and PSA and/ or PSM expression was positive in specimens from 27 (82%) of the patients (two-sided P <.0001). The four patients with positive pathologic findings also had positive RT-PCR results. Among the 29 patients with no pathologic evidence of lymph node involvement, 23 (79%) tested positive by means of RT-PCR. In these 23 patients, PSM expression was detected more frequently than PSA expression; however, in two patients, only PSA expression was detected. Conclusions: Expression of prostate-specific markers in the pelvic lymph nodes of patients with localized, high-risk prostate cancer may indicate the presence of metastatic tumor cells. Such cells may be responsible for the high rate of systemic failure seen in these patients. Additional studies are required to determine the prognostic relevance of our findings.
Adjuvant Chemotherapy With Sequential or Concurrent Anthracycline and Docetaxel: Breast International Group 02 98 Randomized Trial
Authors: P. Francis, J. Crown, A. Di Leo, M. Buyse, A. Balil, M. Andersson, B. Nordenskjold, I. Lang, R. Jakesz, D. Vorobiof, J. Gutierrez, G. van Hazel, S. Dolci, S. Jamin, B. Bendahmane, R. D. Gelber, A. Goldhirsch, M. Castiglione-Gertsch, M. Piccart-Gebhart
Journal: JNCI Journal of the National Cancer Institute (2008)

BackgroundDocetaxel is more effective than doxorubicin for patients with advanced breast cancer. The Breast International Group 02-98 randomized trial tested the effect of incorporating docetaxel into anthracycline-based adjuvant chemotherapy and compared sequential vs concurrent administration of doxorubicin and docetaxel.
Long-lived Memory T Lymphocyte Responses After Hantavirus Infection
Authors: Heather L. Van Epps, Masanori Terajima, Jukka Mustonen, T. Petteri Arstila, Elizabeth A. Corey, Antti Vaheri, Francis A. Ennis
Journal: The Journal of Experimental Medicine (2002)

Puumala virus (PUUV) is a hantavirus that causes hemorrhagic fever with renal syndrome (HFRS), which is an important public health problem in large parts of Europe. We examined the memory cytolytic T lymphocyte (CTL) responses in 13 Finnish individuals who had HFRS between 1984 and 1995. In seven of these donors, we detected virus-specific CTL responses against the PUUV nucleocapsid (N) protein after in vitro stimulation with PUUV. Six novel CD8+ CTL epitopes were defined on the N protein and were found to be restricted by various HLA alleles including A2, A28, B7, and B8. This is the first demonstration of PUUV-specific CTL responses in humans, and the first identification of CTL epitopes on PUUV. In addition, this study provides one of the few characterizations of a human antiviral memory T cell response, without the complicating issues of virus persistence or reinfection. Interferon (IFN)-γ ELISPOT analysis showed that memory CTL specific for these epitopes were present at high frequency in PUUV-immune individuals many years after acute infection in the absence of detectable viral RNA. The frequencies of PUUV-specific CTL were comparable to or exceeded those found in other viral systems including influenza, EBV and HIV, in which CTL responses may be boosted by periodic reinfection or virus persistence.