tbuckley/cabot-search huggingface dataset:
Resection and Primary Anastomosis in Necrotizing Enterocolitis
Authors: Niyi Ade-Ajayi, Edward Kiely, David Drake, Rob Wheeler, Lewis Spitz
Journal: Journal of the Royal Society of Medicine (1996)

Necrotizing enterocolitis (NEC) is the most common surgical emergency in the newborn. Up to half of babies with NEC develop advanced disease requiring surgical intervention. Options include peritoneal drainage under local anaesthetic, enterostomy only, resection and enterostomies, and resection with primary anastomosis. Resection with enterostomies is favoured by many paediatric surgeons but management of neonatal enterostomies can be difficult. The outcome of 26 infants undergoing surgery for advanced NEC over a 2-year period is reviewed. Resection and primary anastomosis was possible in 18 infants of whom two (11%) died. Recurrent NEC developed in four (22%) and strictures in three (17%) of these infants. An initial enterostomy was fashioned in eight infants, three following resection of necrotic intestine and five as a proximal diverting stoma in infants with pan-intestinal involvement. Five of these eight infants died (63%), giving an overall mortality of 27%. Primary anastomosis is an effective procedure following resection of grossly involved intestine in infants with NEC. The mortality and morbidity in this series compared well with those reported for staged procedures.
A Perspective on Confidentiality
Authors: ERIC A. PLAUT
Journal: American Journal of Psychiatry (1974)

The confidentiality of communications from psychiatric patients is threatened from many directions. The traditional stance of psychiatrists has been to proclaim total confidentiality as the principle and then to make exceptions. As third-party payers, peer review structures, and governmental agencies erode the exclusively dyadic doctor-patient relationship, the traditional stance no longer suffices. What is needed is a thorough understanding of the forces involved and a set of principles to help assess the real needs for confidentiality in a variety of psychiatrist-patient interactions.
Abstract 2196: Are METs Achieved at the Heart Rate of 100 Beats Per Minute Superior to Maximal METs as a Predictor of Cardiovascular Mortality?
Authors: Vy-Van Le, Sandra Mandic, Teferi Mitidu, Ricardo Oliveira, Jonathan Myers, Victor Froelicher
Journal: Circulation (2008)

Submaximal exercise testing can be useful for testing individuals with limitations to performing maximal exercise. Recent studies suggested that workload at a fixed submaximal heart rate (HR) of 10...
Differential cooperation of oncogenes with p53 and Bax to induce apoptosis in rhabdomyosarcoma
Authors: Alan C Taylor, Katja Schuster, Pamela P McKenzie, Linda C Harris
Journal: Molecular Cancer (2006)

Abstract Background Deregulated expression of oncogenes such as MYC and PAX3-FKHR often occurs in rhabdomyosarcomas. MYC can enhance cell proliferation and apoptosis under specific conditions, whereas PAX3-FKHR has only been described as anti-apoptotic. Results In order to evaluate how MYC and PAX3-FKHR oncogenes influenced p53-mediated apoptosis, rhabdomyosarcoma cells were developed to independently express MYC and PAX3-FKHR cDNAs. Exogenous wild-type p53 expression in MYC transfected cells resulted in apoptosis, whereas there was only a slight effect in those transfected with PAX3-FKHR. Both oncoproteins induced BAX, but BAX induction alone without expression of wild-type p53 was insufficient to induce apoptosis. Data generated from genetically modified MEFs suggested that expression of all three proteins; MYC, BAX and p53, was required for maximal cell death to occur. Conclusion We conclude that cooperation between p53 and oncoproteins to induce apoptosis is dependent upon the specific oncoprotein expressed and that oncogene-mediated induction of BAX is necessary but insufficient to enhance p53-mediated apoptosis. These data demonstrate a novel relationship between MYC and p53-dependent apoptosis, independent of the ability of MYC to induce p53 that may be important in transformed cells other than rhabdomyosarcoma.
Increased endothelial-derived microparticles in ventilator-induced lung injury
Authors: Eleftheria Letsiou, Saad Sammani, Joe G. Garcia, Steven M. Dudek
Journal: European Respiratory Journal (2014)

Ventilator-induced lung injury (VILI) is a consequence of mechanical ventilation and contributes to the pathophysiology of lung injury syndromes. The role of the vascular endothelium in VILI remains largely unknown. Endothelial microparticles (EMPs) are membrane vesicles shed by activated or apoptotic cells. We have previously demonstrated that human lung endothelial cells (EC) exposed to pathologic cyclic stretch (in vitro model of VILI) shed increased numbers of EMPs that mediate lung injury. In this study, we characterize EMPs in a murine model of VILI. C57BL/6J mice were subjected to high tidal volume (40mL/kg) mechanical ventilation (VILI). Spontaneously breathing (SB) mice served as control. After 4h, blood/BAL were collected and microparticles (MPs) were isolated by differential centrifugation. MPs were quantified after staining with a marker of endothelial activation, CD62E (Flow cytometry). Plasma MPs were also analyzed by immunoblotting for VE-cadherin. The purity and characteristics (size 0.1 to 1μm) of the isolated MP populations were confirmed by electron microscopy and flow cytometry. VILI-mice exhibited significant lung injury and increased circulating CD62E positive MPs (1.38-fold) compared to SB mice. In addition, MP lysates contained increased VE-cadherin levels in VILI-challenged mice compared to SB. We next determined the levels of EMPs in the alveolar space. CD62E(+) BAL MPs were increased by 1.87-fold in VILI-challenged mice compared to SB mice. Our results suggest that high levels of EMPs in blood and BAL during mechanical ventilation may represent VILI-induced endothelial dysfunction. EMPs are promising novel biomarkers and mediators of lung injury. Funding: AHA.
Lymphoreticular Tumors in Sao Paulo, Brazil&lt;xref ref-type="fn" rid="FN1"&gt;1&lt;/xref&gt;
Authors: Correa, P., O'Conor, G. T., Machado, Jesus Carlos, Jamra, Michel, Okuyama, Mario H., Marigo, Carlos
Journal: JNCI Journal of the National Cancer Institute (1973)

Journal Article Lymphoreticular Tumors in Sao Paulo, Brazil Get access P. Correa, P. Correa Co-Editor Search for other works by this author on: Oxford Academic PubMed Google Scholar G. T. O'Conor, G. T. O'Conor Co-Editor Search for other works by this author on: Oxford Academic PubMed Google Scholar Jesus Carlos Machado, M.D., Jesus Carlos Machado, M.D. Hospital do Cancer, Instituto Butantan; Hospital das Clinicas; Hospital do Servidor Publico do Estado de São Paulo; and Hospital da Santa Casa de Misericordia, Sao Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Michel Jamra, Michel Jamra Hospital do Cancer, Instituto Butantan; Hospital das Clinicas; Hospital do Servidor Publico do Estado de São Paulo; and Hospital da Santa Casa de Misericordia, Sao Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Mario H. Okuyama, Mario H. Okuyama Hospital do Cancer, Instituto Butantan; Hospital das Clinicas; Hospital do Servidor Publico do Estado de São Paulo; and Hospital da Santa Casa de Misericordia, Sao Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Carlos Marigo Carlos Marigo Hospital do Cancer, Instituto Butantan; Hospital das Clinicas; Hospital do Servidor Publico do Estado de São Paulo; and Hospital da Santa Casa de Misericordia, Sao Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 50, Issue 6, June 1973, Pages 1651–1655, https://doi.org/10.1093/jnci/50.6.1651 Published: 01 June 1973
The Mozart Effect
Authors: John R Hughes, William H James
Journal: Journal of the Royal Society of Medicine (2001)

It is a matter of concern that most contemporary academic psychology focuses on cognition rather than on the emotions. Professor Jenkins reviews the putatively beneficial effect of Mozart's music on spatial ability. However no-one doubts that civilized music beneficially affects the emotions too. So an important unanswered question arises: does uncivilized music adversely affect our emotions? I write as a cyclist who for 50 years has narrowly escaped death at the hands of London's motorists. My experience is that (those few) motorists listening to Mozart are a more docile safe lot than those listening to loud pop music. The causal nexus could lie in either direction, but might some ‘road rage’ be due to an overdose of pop music? It would be interesting to play loud music to motorists in a driving simulator. Would the music induce them to be even more willing to mow down the odd cyclist?
Abstract 1337: Attenuation of the Leptin-Induced Hypertrophy by NF-kB Inhibition Requires Activation of AMPK in Neonatal Cardiomyocytes
Authors: Venkatesh Rajapurohitam, Sabzali Javadov, Daniel M Purdham, Morris Karmazyn
Journal: Circulation (2007)

Introduction: Leptin, a 16 kDa product of the obesity gene, has been shown to be elevated in patients with heart failure. Recently we demonstrated that leptin induces hypertrophy in cultured cardiomyocytes, however the molecular mechanisms underlying the hypertrophic effect of leptin remain to be elucidated. In the present study we investigated whether nuclear factor-kB (NF-kB) and adenosine monophosphate-activated kinase (AMPK) are key mediators in leptin-induced cardiac hypertrophy. Methods and Results: Leptin (3.1 nM) treatment for 24 hrs increased cell surface area by 40% (P&lt;0.002) as measured by Sigma scan software. The increase in cell surface area was completely blocked by NF-kB activation inhibitor (1μM) and AICAR (1 mM), the AMPK activator (P&lt;0.001). Incubation with leptin for 24 hrs had no effect on PRKA-α (α-subunit of AMPK) but upregulated the PRKAβ2 (β-subunit of AMPK) gene by 85% (P&lt;0.04) as determined by real-time PCR. In contrast, AICAR treatment increased the PRKA-α by 256% (P&lt;0.02) but not the PRKA-β gene. The leptin-dependent 90% increase in α-skeletal actin, a hypertrophic marker gene was inhibited by AICAR (P&lt;0.01). Western blot analysis revealed that leptin treatment for 5 min increased the phosphorylation of IkBs, a group of cytoplasmic NF-kB inhibitors by 51% (P&lt;0.03). Phosphorylation triggers their degradation and allows NF-kB to translocate into the nucleus. Leptin-induced IkB-α phosphorylation was associated with significant activation of NF-kB p65 by phosphorylation at Ser536 which is important for translocation into the nucleus. Inhibition of NF-kB induced upregulation of P-Thr172-AMPK but not P-Ser485 AMPK levels. Cglitazone (5 μM), a potent and selective PPAR-γ ligand, or AICAR treatment for 30 min significantly upregulated the expression of P-Thr172-AMPK while leptin had no effect. In addition, AICAR treatment for 24 hrs increased the expression of PPAR-γ by 450% (P&lt;0.006), FATCD36 by 35% (P&lt;0.03) and GLUT1 by 220% (P&lt;0.03). Conclusion : Attenuation of leptin-induced hypertrophy by NF-kB inhibition is mediated by AMPK activation. The anti-hypertrophic effect of AMPK activation is mediated through upregulation of PPAR-γ, FATCD36 and GLUT1 genes expression responsible for maintaining energy homeostasis.
T cells subpopulations and cytokine responses to tuberculosis antigens in blood of smoking and nonsmoking tuberculosis patients
Authors: Natalia Makarova, Tatyana Vaneeva, Nailya Kulikovskaya, Vitaliy Litvinov
Journal: European Respiratory Journal (2013)

Background: Smoking can influence immune responses in TB patients.  Objective: We investigated whether some blood T cell subpopulations and cytokine responses to TB, PHA antigens differ in TB smoking and TB nonsmoking patients. Methods: Of 35 new diagnosed TB patients enrolled (mean 32,3 years old), 13 (37 %) were smoking. The circulating quantity and percentages of CD3+, CD4+, CD8+, CD4+CD25+, CD4+HLa-DR+ in peripheral blood were estimated by multi-color flow cytometry analysis. Also we evaluated levels of IFN-g, TNF-a, IL-2 in ELISA after the induction in blood with CFP10-ESAT6-TB7.7 and PHA antigens.  Results: No statistically proven differences in T cell subpopulations were observed in smoking and nonsmoking TB patients. Smoking TB patients had lower levels of IFN-g induced by CFP10-ESAT6-TB7.7 (M±m 60,5±23,7, 95% CI for Mean 8,7-112,2, vs 113±33,4, 95% CI for Mean 43,4-182,6 in nonsmoking) and IL-2 induced by CFP10-ESAT6-TB7.7 (69,8±26,7, 95% CI for Mean 11,7-127,9; vs 172,6±50,5, 95% CI for Mean 67,6-277,5). But in smoking TB patients PHAinduced IFN-g was statistically higher than in nonsmoking (M±m 348,6±63,8 vs 170,4±38,4; Mann-Whitney Test p=0,031). TNF-a response to both antigens had no statistically proven differences in smoking and nonsmoking groups.   Conclusion:  In smoking TB patients nonspecific INF-g production prevail, but TB-specific INF-g production is lower than in nonsmoking TB patients. So the processes of TB granuloma forming and recovery can be modified in smoking TB patients.
Intraarterial cisplatin and concurrent radiation for locally advanced bladder cancer.
Authors: L Eapen, D Stewart, C Danjoux, P Genest, N Futter, D Moors, A Irvine, J Crook, S Aitken, L Gerig
Journal: Journal of Clinical Oncology (1989)

Between 1983 and 1987 25 patients with invasive bladder cancer (16 stage tumor 3 (T3) and nine stage T4) were treated with intraarterial cisplatin and concurrent radical radiation (20/25) or intraarterial cisplatin, concurrent preoperative radiation, and cystectomy (5/25). One patient died from treatment-related toxicity. Other toxicities have been what one would expect from the individual treatment modalities except for a sensory sacral root neuropathy in 11 of 24 (46%) patients. Twenty-three of 24 (96%) patients achieved a complete response (CR) and the projected actuarial 2-year survival is 90%. Only one of the 23 complete responders has had an invasive local recurrence. The excellent complete local response and survival rates achieved warrant further study of the combination of intraarterial cisplatin and radiation as a bladder-preserving strategy.
Does venous blood gas analysis provide accurate estimates of hemoglobin oxygen affinity
Authors: Fabienne Huber, Tsogyal D. Latshang, Jeroen Goede, Konrad E. Bloch
Journal: European Respiratory Journal (2011)

Background: Polycythemia occurs in conditions with chronic hypoxemia including lung and heart disease, polycythemia vera, hemoglobinopathies and in certain neoplasms. Arterial blood gas analysis and assessment of hemoglobin oxygen affinity by the PO2 with oxygen saturation of 50% (P50) are used to evaluate potential causes of secondary polycythemia. We investigated accuracy of a simplified estimation of P50 from venous blood in comparison to tonometry, the gold standard for measurement of P50.

Methods: In 50 patients referred for evaluation of polycythemia pH, PO2 and SO2 were measured in venous blood (ABL 700 series, Radiometer, Copenhagen) and P50v was derived by standard equations (Severinghaus, J Appl Physiol 1979;46:599). Tonometry was performed to obtain P50t (Hemoxanalyzer, TCS, New Hope, PA). Agreement of P50v and P50t was analyzed.

Results: The mean P50t was 25.8 (range 17.4-34.1) mmHg. The mean difference (bias) of P50v and P50t was 0.5 mmHg, the limits of agreement (95% CI) were -5.15 to +6.09 mmHg. The sensitivity and specificity of P50v to identify patients with P50t outside the normal range (23-27 mmHg) were 5 and 77%, respectively.

Conclusions: Estimates of P50 based on venous blood gas analysis and standard equations have a low bias compared to tonometry. However, the precision of P50v is not sufficiently high to replace P50t in the evaluation of individual patients with suspected disturbances of hemoglobin oxygen affinity.
Acyclovir prophylaxis and fever during remission-induction therapy of patients with acute myeloid leukemia: a randomized, double-blind, placebo-controlled trial.
Authors: O J Bergmann, S C Mogensen, S Ellermann-Eriksen, J Ellegaard
Journal: Journal of Clinical Oncology (1997)

PURPOSE A randomized, double-blind, placebo-controlled trial was performed to estimate the preventive effect of the antiherpetic drug acyclovir on fever, incidence of bacteremia, use of antibiotics, and presentation of infections in patients with acute myeloid leukemia (AML). PATIENTS AND METHODS Ninety herpes simplex virus (HSV)-seropositive patients aged 18 to 84 years were included. Forty-five patients received acyclovir (800 mg by mouth daily) and 45 placebo. The patients were examined daily for 28 days from the initiation of remission-induction chemotherapy. RESULTS Fever developed in all patients in both groups. Acyclovir prophylaxis postponed the development of an oral temperature &gt; or = 38.0 degrees C by 3 days (95% confidence interval [CI], 1 to 4 days; P = .03) and the initiation of antibacterial treatment by 3 days (95% CI, 1 to 5 days; P = .008). The duration of fever, use of antibacterial treatment, incidence of bacteremia, and need for systemic antifungal therapy were not affected by acyclovir prophylaxis. At fever development, acyclovir prophylaxis affected the incidence and localization pattern of oral ulcers. Thus, in the acyclovir group, the number of nonfungal oral infections was reduced (relative risk, 0.45 [95% CI, 0.24 to 0.85]) and mainly located on the soft palate (relative risk, 2.49 [95% CI, 1.19 to 5.22]). CONCLUSION Acyclovir prophylaxis has an impact on fever development, but not on the duration of fever or the need for antibiotics. It does not reduce the incidence of bacteremia, but the presentation of acute oral infections is changed.
Murine lung airway fibroblasts drive fibrosis through STAT4 signaling after cigarette smoke exposure
Authors: Tillie Hackettt, Steven Zhou, Joanne Wright, Andrew Churg
Journal: European Respiratory Journal (2012)

Cigarette smoke-induced emphysema and small airway remodeling (SAR) are the anatomic bases of chronic obstructive lung disease (COPD), but the pathogenesis of these changes is unclear and current treatments for COPD are minimally effective. We exposed wild type (WT) and STAT4-/- mice to cigarette smoke for 6 months and found that STAT4-/- mice are protected against smoke-induced small airway remodeling but not emphysema. Unexpectedly, we observed that STAT4 is expressed in cultured murine wild type (WT) lung parenchyma-derived and airway-derived fibroblasts, but to a much greater extent in the latter. The same phenomenon was seen in cultured human parenchymal and airway fibroblasts. WT airway fibroblasts proliferated faster than STAT4-/- airway fibroblasts, whereas there was no difference between strains for parenchymal fibroblasts. IL-12 is up-regulated in human and mouse lungs after smoke exposure, and treatment with IL-12 caused phosphorylation of STAT4 in WT airway fibroblasts. Exposure of WT airway, but not parenchymal, fibroblasts to IL-12 caused increased expression of collagen 1α1 and TGFβ, factors involved in SAR, whereas STAT4-/- fibroblasts were unresponsive to IL-12. STAT4 thus controls proliferation and matrix production in airway but not parenchymal fibroblasts, and smoke-induced IL-12 can drive small airway remodeling via STAT4 signaling. These findings suggest that treatment with clinically available anti IL-12p40 drugs might provide a new completely approach to preventing SAR in cigarette smokers.
LSC 2013 abstract - miRNA-based identification of SEC14L3 deregulation in murine experimental asthma
Authors: Sabine Bartel, Nikola Schulz, Fabian Theis, Francesca Alessandrini, Shinji Takenaka, Oliver Eickelberg, Susanne Krauss-Etschmann
Journal: European Respiratory Journal (2013)

Background: MicroRNAs are small non-coding RNAs essential for immune function and lung development. Previously, we had found increased pulmonary expression of miR-17, -144 & miR-21, correlating with decreased mRNA & protein levels of the putative targets CREB1 and its co-activators CRTC 1&3 in mice with ova-induced asthma. Expressions were modulated by in vitro overexpression/silencing of the miRNAs. We now hypothesized that miR-17, -144 &-21 regulate CREB1/CRTC-mediated gene transcription in experimental asthma and sought to identify new targets of relevance for asthma.  Methods: Murine lung epithelial cells (MLE-12) or human bronchial epithelial cells (16-HBE) were transfected with precursor miRNAs/antimiRs. Expression of miRNAs/targets was evaluated by RT-qPCR and Western blotting. For selection of CREB1 targets down-regulated genes in lungs of mice with ova-induced asthma were screened for CRE elements in their promoter region. Lung sections were histologically assessed by periodic acid schiff (PAS) stain and SEC14L3 immunostaining.  Results: Among the 35 candidate CREB1 targets we chose SEC14L3 & LTBP4 as both were already brought into context with asthma. Their mRNA expressions were influenced by in vitro overexpression/ silencing of the candidate miRNAs in a CREB1-dependent manner. For SEC14L3 we confirmed this in vivo deregulation on protein level by western blot and immunostainings of lung sections, where it coincided with goblet cell metaplasia.  Conclusion: Using miRNA profiles as preselection tools, we identified SEC14L3 as new target that might be useful for monitoring the integrity of the respiratory epithelium in experimental asthma.
10-yr follow-up results of NSABP B-32, a randomized phase III clinical trial to compare sentinel node resection (SNR) to conventional axillary dissection (AD) in clinically node-negative breast cancer patients.
Authors: Thomas B. Julian, Stewart J. Anderson, David N. Krag, Seth P. Harlow, Joseph P. Costantino, Takamaru Ashikaga, Donald L. Weaver, Eleftherios P. Mamounas, Norman Wolmark
Journal: Journal of Clinical Oncology (2013)

1000 Background: NSABP B-32, the largest surgical prospective randomized phase III trial was designed to compare overall survival (OS), disease-free survival (DFS), and morbidity between SNR alone vs SNR + AD in SN negative (-) pts. We present 10 yr outcome data for primary endpoints as well as updated data on the effect of occult metastases, found later in the SN by central, detailed pathologic analysis. Methods: 5,611 women with operable, clinically N0, invasive breast cancer were randomized to SNR + AD (Group [Grp] 1) or to SNR alone with AD only if SNs were positive (Grp2). 3,989 (71.1%) of 5,611 pts were SN-. 3,986 (99.9%) of these SN- pts had follow-up information: Grp 1: 1,975, Grp 2:2,011. Median time on study was 9.4 yrs. Cox proportional hazard models adjusting for study stratification variables were used to compare OS and DFS between the two groups. Two-sided p values were used. HR values &gt; 1 indicate a more favorable outcome in Grp 1 Results: At 10 yrs, there continues to be no significant difference in OS between the two groups (HR: 1.11, p = 0.27). 10 yr Kaplan-Meier (K-M) estimates for OS are 87.8% for SNR alone and 88.9% for SNR + AD. There continues to be no significant difference in DFS between the two groups (HR: 1.01, p=0.92). 10-yr K-M estimates for DFS were 76.9% for both groups. Occult nodal disease was originally detected in 3,884 pts (15.8%) with SN- on initial H and E analysis. Comparisons between the groups with and without occult disease yielded an adjusted HR for OS: 1.25 (p = 0.08) with an absolute difference at 10 yrs of 2.8% and a HR for DFS: 1.24 (p = 0.018) with an absolute difference of 4.1%. The cumulative incidences of local-regional events were low (10-yr values: SNR 4.0%, SNR+AD, 4.3%) and not significant (HR: 0.95, p = 0.77). Conclusions: At 10 yrs there continues to be no significant differences in OS and DFS between SNR and SNR + AD in pts with negative SN. The relative increase in risk of DFS and OS for pts with occult SN metastases remains stable. Support: PHS grants: NSABP: U10CA-12027, U10CA-37377, U10CA-69651, U10CA-69974; VT Ca Cntr: P30 CA22435; DNK: 5RO1CA074137 NCI Dpt HHS. Clinical trial information: NCT00003830.