tbuckley/cabot-search huggingface dataset:
Change in Defense Mechanisms During Long-Term Dynamic Psychotherapy and Five-Year Outcome
Authors: J. Christopher Perry, Michael Bond
Journal: American Journal of Psychiatry (2012)

Research suggests that defense mechanisms may underlie other aspects of functioning and psychiatric symptoms. The authors examined whether defenses change in accordance with the hierarchy of defense adaptation during long-term dynamic psychotherapy and whether such change is associated with long-term outcomes on other measures.Twenty-one adults with depressive, anxiety, and/or personality disorders entered long-term dynamic psychotherapy (mean=248 weeks) and subsequent follow-along (mean duration, 5.1 years). Measures of functioning and symptoms were gathered in periodic follow-along interviews, external to the therapy. A median of eight psychotherapy sessions over 2.5 years for each participant were rated using the Defense Mechanism Rating Scales quantitative method.Overall, the lowest (action) and highest (high adaptive) defense levels in the hierarchy of defenses improved significantly, as did overall defensive functioning (median effect size=0.71, 95% CI=0.01-1.83). Overall defensive functioning still remained below the healthy-neurotic range. A higher number of axis I disorders and childhood histories of sexual abuse and witnessing violence were associated with a slower rate of improvement in defenses. Change in defenses within therapy by 2.5 years was highly associated with significant levels of change at 5 years in external measures of both functioning (rs=0.60) and symptoms (rs=0.58), controlling for initial levels.Change in defensive functioning in long-term psychotherapy largely follows the hierarchy of defense adaptation. The relationship to long-term improvement in outcomes suggests that defenses be considered candidates for mediating improvement in functioning and symptoms.
Similarity of the Impact of Type 1 and Type 2 Diabetes on Cardiovascular Mortality in Middle-Aged Subjects
Authors: Auni Juutilainen, Seppo Lehto, Tapani Rönnemaa, Kalevi Pyörälä, Markku Laakso
Journal: Diabetes Care (2008)

To compare the risk of cardiovascular disease (CVD) death and the impact of hyperglycemia on the risk of CVD mortality associated with type 1 diabetes to that associated with type 2 diabetes.The study comprised 173 participants with type 1 diabetes, 834 participants with type 2 diabetes, and 1,294 nondiabetic participants, aged 45-64 years at baseline and free of CVD. The age of onset of diabetes was >30 years in both diabetic groups.During an 18-year follow-up, 86 participants with type 1 diabetes, 567 participants with type 2 diabetes, and 252 nondiabetic participants died. CVD mortality rates per 1,000 person-years were 23.1 (95% CI 16.9-31.9) in type 1 diabetic, 35.3 (30.8-40.4) in type 2 diabetic, and 4.6 (3.8-5.7) in nondiabetic participants. Adjusted hazard ratios for CVD mortality in participants with type 1 diabetes versus no diabetes was 3.6 (95% CI 2.2-5.7) in men and 13.3 (6.9-22.5) in women and in participants with type 2 diabetes versus no diabetes 3.3 (2.5-4.5) in men and 10.1 (6.7-17.4) in women. An increment of 1 unit (%) of GHb increased CVD mortality by 52.5% (95% CI 28.4-81.3) in type 1 diabetic subjects and by 7.5% (4.3-10.8) in type 2 diabetic participants.The impact of type 1 and type 2 diabetes on CVD mortality was similar. The effect of increasing hyperglycemia on the risk of CVD mortality was more profound in type 1 than in type 2 diabetic subjects.
Oral Immunotherapy for Fish Allergy Using a Hypoallergenic Decomposed Fish Meat
Authors: Y. Nakajima, Y. Kondo, Y. Mori, S. Otaka, Y. Okubo, K. Tanaka, K. Yamawaki, C. Inuo, N. Hirata, S. Suzuki, I. Tsuge, T. Kondo, K. Osajima, Y. Itagaki, A. Urisu
Journal: Journal of Allergy and Clinical Immunology (2015)
A novel p63 sterile alpha motif (SAM) domain mutation in a Japanese patient with ankyloblepharon, ectodermal defects and cleft lip and palate (AEC) syndrome without ankyloblepharon
Authors: K. Tsutsui, Y. Asai, A. Fujimoto, M. Yamamoto, M. Kubo, N. Hatta
Journal: British Journal of Dermatology (2003)

We present a sporadic case of a Japanese female infant with ectodermal dysplasia, complete cleft lip and palate, severe skin erosions at birth and recurrent scalp infection. She had typical clinical features of ankyloblepharon, ectodermal defects and cleft lip and palate (AEC) syndrome without ankyloblepharon. Histological and immunohistochemical analyses showed reduced granular cell layers and aberrant expression of the p63 protein in the suprabasal keratinocytes. Mutation analysis of the exon 13 of p63 gene revealed a heterozygous in-frame 3-bp insert (c. 538-539 ins TTC) encoding additional amino acid residues (F). This is the first report of sterile alpha motif domain mutation except for single nucleotide transitions.
Smoke-free legislation reduces exposure in children
Authors: Vandana Gupta
Journal: Thorax (2008)

Smoke-free legislation was introduced in Scotland in March 2006. The CHETS study investigated changes in children’s exposure to second-hand smoke due to a change in legislation resulting in changes to parental smoking patterns.

In this cross-sectional study, surveys were performed by primary school children (mean age 11.4 years) in the same schools …
Critical Role of the Axonal Guidance Cue EphrinB2 in Lung Growth, Angiogenesis, and Repair
Authors: Arul Vadivel, Tim van Haaften, Rajesh S. Alphonse, Gloria-Juliana Rey-Parra, Lavinia Ionescu, Al Haromy, Farah Eaton, Evangelos Michelakis, Bernard Thébaud
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Rationale: Lung diseases characterized by alveolar damage currently lack efficient treatments. The mechanisms contributing to normal and impaired alveolar growth and repair are incompletely understood. Axonal guidance cues (AGC) are molecules that guide the outgrowth of axons to their targets. Among these AGCs, members of the Ephrin family also promote angiogenesis, cell migration, and organogenesis outside the nervous system. The role of Ephrins during alveolar growth and repair is unknown.Objectives: We hypothesized that EphrinB2 promotes alveolar development and repair.Methods: We used in vitro and in vivo manipulation of EphrinB2 signaling to assess the role of this AGC during normal and impaired lung development.Measurements and Main Results: In vivo EphrinB2 knockdown using intranasal siRNA during the postnatal stage of alveolar development in rats arrested alveolar and vascular growth. In a model of O2-induced arrested alveolar growth in newborn rats, air space enlargement, loss of lung capillaries, and pulmonary hypertension were associated with decreased lung EphrinB2 and receptor EphB4 expression. In vitro, EphrinB2 preserved alveolar epithelial cell viability in O2, decreased O2-induced alveolar epithelial cell apoptosis, and accelerated alveolar epithelial cell wound healing, maintained lung microvascular endothelial cell viability, and proliferation and vascular network formation. In vivo, treatment with intranasal EphrinB2 decreased alveolar epithelial and endothelial cell apoptosis, preserved alveolar and vascular growth in hyperoxic rats, and attenuated pulmonary hypertension.Conclusion: The AGC EphrinB2 may be a new therapeutic target for lung repair and pulmonary hypertension.
Chronic nonocclusive coronary artery constriction impairs ventricular function, myocardial structure, and cardiac contractile protein enzyme activity in rats.
Authors: J M Capasso, A Malhotra, P Li, X Zhang, J Scheuer, P Anversa
Journal: Circulation Research (1992)

To determine the effects of chronic nonocclusive coronary constriction on cardiac hemodynamics, structural integrity, and contractile protein enzyme activity, the left coronary artery was narrowed in rats, and measurements of ventricular performance, magnitude, and distribution of tissue damage and myofibrillar Mg2+ and Ca2+ myosin ATPase activities were evaluated 1 month later. In the presence of coronary artery stenosis averaging 58%, three levels of involvement of global cardiac performance were identified, and the rats were divided accordingly. In the first group, only left ventricular end-diastolic pressure (LVEDP) was increased; in the second group, LVEDP and left ventricular +dP/dt and/or -dP/dt were affected; and in the third group, LVEDP, left ventricular +dP/dt and -dP/dt, and right ventricular end-diastolic pressure were impaired. Thus, left ventricular moderate dysfunction, severe dysfunction, and failure occurred with coronary narrowing. On a structural basis, coronary constriction resulted in an ongoing process characterized by acute myocytolytic necrosis and foci of replacement fibrosis in different stages of healing. The number of these lesion profiles in the left ventricular myocardium increased 4.7-, 4.4-, and 8.3-fold in rats with moderate dysfunction, severe dysfunction, and failure, respectively. Biochemically, Mg(2+)-ATPase activity of myofibrils increased biventricularly when moderate dysfunction was present. However, this parameter decreased with the appearance of severe dysfunction, reaching control values in ventricular failure. Ca2+ myosin ATPase activity was reduced in the left ventricle of rats with severe dysfunction and failure, whereas it was elevated in the right ventricle of rats with severe dysfunction. In conclusion, a fixed lesion of the left main coronary artery with a modest reduction in vessel luminal diameter generates a conditioned state of the heart characterized by a continuous loss of myocytes and replacement scarring, which, in combination with alterations in contractile protein enzyme activity, may be responsible for a number of abnormalities in cardiac dynamics ranging from moderate dysfunction to pump failure.
Referral Patterns, Treatment Choices, and Outcomes in Locoregional Esophageal Cancer: A Population-Based Analysis of Elderly Patients
Authors: Ewout W. Steyerberg, Bridget Neville, Jane C. Weeks, Craig C. Earle
Journal: Journal of Clinical Oncology (2007)

PURPOSE To determine the impact of demographics and comorbidity on access to specialists' services, treatment, and outcome for patients with locoregional esophageal cancer. PATIENTS AND METHODS We performed a retrospective cohort study of 3,538 patients older than age 65 years who were diagnosed with locoregional esophageal cancer between 1991 and 1999 in one of 11 regions monitored by the Surveillance, Epidemiology, and End Results tumor program. We examined linked Medicare claims for assessment by a surgeon, radiation oncologist, or medical oncologist and subsequent treatment with surgery, radiation, or chemotherapy. Logistic regression analyses were performed for seeing a specialist and for undergoing treatment according to age, sex, race, socioeconomic status, geographic region, and presence of comorbidities. Cox proportional hazards analyses were performed to estimate hazard ratios (HRs) for survival with and without adjustment for treatment received. Results Seeing a cancer specialist depended especially on age and region of diagnosis. These same factors were also related to subsequent treatment decisions, but associations were reversed in some regions, such that treatment depended less on region. Older patients had poorer survival (HR = 2.0 for 85+ v 65 to 69 years), which was partly explained by treatment received (HR decreased to 1.5 when adjusted for treatment). CONCLUSION Older patients have less intensive treatment of esophageal cancer, which is explained by both a lower rate of seeing a cancer specialist and by less intensive treatment once seen. Referring physicians and treating specialists must ensure that elderly patients are not deprived of the opportunity to consider all of their treatment options.
Is there a difference in the incidence of metastasis at diagnosis of lung cancer between smokers and non smokers
Authors: Anoma Siribaddana, Srimati Waidyasekara, Kapila Senevirathna, Kanchana Dissanayake, Manil Pieris
Journal: European Respiratory Journal (2013)

Background

Since the degree of suspicion of lung cancer in nonsmokers is less would it lead to a delay in diagnosis? Or would etiologies other than smoking cause more aggressive, disseminated cancers? T he objective was to find out differences of incidence in metastasis at presentation in smokers and nonsmokers

Methodology

This prospective study was carried out in Teaching hospital kandy Sri Lanka for one year from January to December 2013.All patients who had histologicaly proven lung cancer were recruited. Their smoking history was obtained using an interviewer administered questionnaire. Staging was done by CT thorax, neck and upper abdomen, and in some cases with imaging of spine and brain. Patients with pleural effusions had pleural aspiration for cytology and pleural biopsy. Staging was done using TNM 7th revision .Smokers and nonsmokers were compared using chi square test.

Results

Total 71

Gender N %

males 61 85.92

females 10 14.10

Mean age 62.8, Standard deviation +/- 11.26

View this table:

Age distribution





View this table:

Incidence of metastasis at diagnosis by group





Conclusion

Nonsmokers have a statistically significant higher chance of having metastasis at the time of diagnosis than smokers.
NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway
Authors: Tomohiro Watanabe, Naoki Asano, Stefan Fichtner-Feigl, Peter L. Gorelick, Yoshihisa Tsuji, Yuko Matsumoto, Tsutomu Chiba, Ivan J. Fuss, Atsushi Kitani, Warren Strober
Journal: Journal of Clinical Investigation (2010)

Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular epithelial cell protein known to play a role in host defense at mucosal surfaces. Here we show that a ligand specific for NOD1, a peptide derived from peptidoglycan, initiates an unexpected signaling pathway in human epithelial cell lines that results in the production of type I IFN. Detailed analysis revealed the components of the signaling pathway. NOD1 binding to its ligand triggered activation of the serine-threonine kinase RICK, which was then able to bind TNF receptor-associated factor 3 (TRAF3). This in turn led to activation of TANK-binding kinase 1 (TBK1) and IkappaB kinase epsilon (IKKepsilon) and the subsequent activation of IFN regulatory factor 7 (IRF7). IRF7 induced IFN-beta production, which led to activation of a heterotrimeric transcription factor complex known as IFN-stimulated gene factor 3 (ISGF3) and the subsequent production of CXCL10 and additional type I IFN. In vivo studies showed that mice lacking the receptor for IFN-beta or subjected to gene silencing of the ISGF3 component Stat1 exhibited decreased CXCL10 responses and increased susceptibility to Helicobacter pylori infection, phenotypes observed in NOD1-deficient mice. These studies thus establish that NOD1 can activate the ISGF3 signaling pathway that is usually associated with protection against viral infection to provide mice with robust type I IFN-mediated protection from H. pylori and possibly other mucosal infections.
CD50 (intercellular adhesion molecule 3) stimulation induces calcium mobilization and tyrosine phosphorylation through p59fyn and p56lck in Jurkat T cell line.
Authors: M Juan, O Viñas, M R Pino-Otín, L Places, E Martínez-Cáceres, J J Barceló, A Miralles, R Vilella, M A de la Fuente, J Vives
Journal: The Journal of Experimental Medicine (1994)

The leukocyte differentiation antigen, CD50, has been recently identified as the intercellular adhesion molecule 3 (ICAM-3), the third counter-receptor of leukocyte function-associated antigen 1 (LFA-1). This molecule seems to be specially involved in the adhesion events of the initial phases of the immune response. To characterize the role of CD50 in leukocyte interactions, the different molecular events induced after cross-linking of CD50 on T cell-derived Jurkat cell line have been analyzed. When cells were incubated with anti-CD50 mAbs and cross-linked with polyclonal goat anti-mouse immunoglobulins, a rise in intracellular calcium concentration ([Ca2+]i) was observed. This increase in [Ca2+]i was mainly due to the uptake of extracellular Ca2+. This Ca2+ flux involved tyrosine phosphorylations and was further increased by CD3 costimulation. These data, together with those obtained by phosphotyrosine (P-Tyr) immunoprecipitation and in vitro kinase assays, suggested the involvement of protein-tyrosine kinases (PTK) in CD50 transduction pathways. By using specific antisera, the presence of p56lck and p59fyn protein tyrosine kinases (PTK) was clearly demonstrated in the CD50 immunoprecipitates. These findings suggest that the interaction of CD50 with its natural ligand (LFA-1) may result in T lymphocyte activation events, in which CD50 could play a very active role after antigen triggering.
Phase II study of Cloretazine for the treatment of adults with recurrent glioblastoma multiforme1
Authors: Michael A. Badruddoja, Kara Penne, Annick Desjardins, David A. Reardon, Jeremy N. Rich, Jennifer A. Quinn, Sith Sathornsumetee, Allan H. Friedman, Darell D. Bigner, James E. Herndon, Ann Cahill, Henry S. Friedman, James J. Vredenburgh
Journal: Neuro-Oncology (2006)

Cloretazine (VNP40101M) is a newly synthesized alkylating agent belonging to a novel class of alkylating agents called 1,2-bis(sulfonyl)hydrazines. Agents that belong to this class do not produce vinylating and chloroethylating species, and hence this class of alkylating agents is thought to have minimal systemic toxicity. Cloretazine produces two short-lived active species: 1,2-bis(methylsulfonyl)-1-(2-chloroethyl) hydrazine (a chloroethylating species) and a thiophilic carbamoylating methylisocyanate species. The chloroethylating species preferentially produces lesions at the O(6) position of guanine. The methylisocyanate species may inhibit O(6)-alkylguanine-DNA alkyltransferase, an important mechanism of resistance against alkylating agents. The purpose of this study was to determine the efficacy and tolerability of Cloretazine in patients with recurrent glioblastoma multiforme. The basis for the determination of efficacy was the proportion of patients alive without evidence of disease progression six months after initiation of treatment. Patients with recurrent glioblastoma multiforme received Cloretazine (300 mg/m(2)) intravenously every six weeks. Radiographic response, survival data, and toxicity were assessed. Thirty-two patients were enrolled. Median age was 56 years; 24 patients (75%) were men. At six months, two patients were alive and progression free, so the six-month progression-free survival (PFS) was 6%. The median PFS was 6.3 weeks. There were no objective radiographic responses. Twelve patients had stable disease for at least one cycle, but only two patients received more than three cycles. Nine patients experienced grade 4 thrombocytopenia and three patients experienced grade 4 neutropenia. Cloretazine administered every six weeks was relatively well tolerated, although this schedule has insignificant activity for patients with recurrent glioblastoma multiforme.
The abnormal lower oesophageal sphincter in pernicious anaemia
Authors: R. L. Farrell, O. T. Nebel, A. T. McGuire, D. O. Castell
Journal: Gut (1973)

Lower oesophageal sphincter pressure has been studied in pernicious anaemia patients and controls using an infused open-tipped system. Resting sphincter pressure was significantly (p < 0.01) lower in the pernicious anaemia patients. After gastric acidification with 0.1 N HCl pressure fell significantly (p < 0.01) in both groups. Following subsequent alkalinization, lower oesophageal sphincter pressure for controls rose significantly (p < 0.001). For pernicious anaemia patients the pressure after alkali was not greater than resting levels. Graded intravenous doses of pentagastrin in controls resulted in a peak pressure change of 38.5 +/- 4.9 mm Hg after the 0.8 mug/kg dose. For patients the peak pressure change was only 13.0 +/- 5.2 mm Hg and occurred after 0.4 mug/kg. Cholinergic stimulation with edrophonium (10 mg) produced a peak pressure change of 20.6 +/- 2.6 mm Hg in controls but only 3.5 +/- 1.0 mm Hg in pernicious anaemia patients (p < 0.001). In addition, no change in lower oesophageal sphincter pressure occurred in patients after stimulation with subcutaneous betazole (1.5 mg/kg). In conclusion, the lower oesophageal sphincter in pernicious anaemia is characterized both by a low resting pressure and a decreased response to endogenous and exogenous stimuli. These results suggest a primary end organ defect and most likely indicate abnormal smooth muscle function in pernicious anaemia. Resting sphincter pressure levels and edrophonium response in age-matched subjects indicate that these changes are not due to aging alone.
A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance
Authors: Christopher B. Newgard, Jie An, James R. Bain, Michael J. Muehlbauer, Robert D. Stevens, Lillian F. Lien, Andrea M. Haqq, Svati H. Shah, Michelle Arlotto, Cris A. Slentz, James Rochon, Dianne Gallup, Olga Ilkayeva, Brett R. Wenner, William S. Yancy, Howard Eisenson, Gerald Musante, Richard S. Surwit, David S. Millington, Mark D. Butler, Laura P. Svetkey
Journal: Cell Metabolism (2009)
Baseline features and clinical results in patients excluded from randomization from a large international trial of reperfusion strategies in acute myocardial infarction: The CADILLAC Registry
Authors: Mark A. Turco, David A. Cox, Eulogio Garcia, James E. Tcheng, John J. Griffin, Giulio Guagliumi, Thomas D. Stuckey, John D. Carroll, Cindy L. Grines, Barry D. Rutherford, Steve Slack, Martin Fahy, Roxana Mehran, Alexandra J. Lansky, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2003)