tbuckley/cabot-search huggingface dataset:
Suppression of T-cell Response in Autologous Mixed Lymphocyte-Tumor Culture by Large Granular Lymphocytes&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: A Uchida, E Klein
Journal: JNCI Journal of the National Cancer Institute (1986)

The role of large granular lymphocytes (LGL) in the autologous mixed lymphocyte-tumor culture (MLTC) was studied in cancer patients with malignant pleural effusions. When blood lymphocytes were cocultured in vitro with autologous tumor cells freshly isolated from carcinomatous pleural effusions, [3H]thymidine incorporation was weakly stimulated on day 6 in 6 of 30 samples. Removal of LGL from the responder population by treatment with the Leu-7 or Leu-11b monoclonal antibody plus complement (C') induced or augmented the proliferative response. LGL and small T-lymphocytes were isolated by discontinuous Percoll gradient centrifugation and tested separately for the proliferative response to autologous tumor. T-cells proliferated in 24 of 30 cases, while LGL showed no proliferation. Addition of LGL to autologous mixed T-cell-tumor cultures suppressed the proliferation of T-cells. LGL, however, did not inhibit T-cell proliferation induced by alloantigens and lectins. The suppressive activity of Percoll-purified LGL was not reduced by OKT3 plus C' treatment, but it was totally abrogated by Leu-11b plus C'. Supernatants produced by 24-hour culture of LGL with autologous tumor contained soluble factors that suppressed the autologous MLTC without killing the autologous tumor or T-blasts. The LGL-mediated suppression was not abolished by anti-interferon-alpha or anti-interferon-gamma antibody. Activation of T-cells in the autologous MLTC induced lytic potential restricted to autologous tumor. In the presence of LGL, T-cells failed to develop autotumor killing activity. Once autotumor killer T-cells were generated in autologous MLTC, their cytotoxicity was no longer inhibited by LGL. These results indicate that LGL from patients with carcinomatous pleural effusions suppress the capacity of autotumor-recognizing T-lymphocytes to proliferate and develop autotumor cytotoxicity in the autologous MLTC. This could explain why fresh T-cells have no cytolytic activity to autologous tumor.
Induced Sputum Derives from the Central Airways
Authors: NEIL E. ALEXIS, SHU-CHIEH HU, KIRBY ZEMAN, TODD ALTER, WILLIAM D. BENNETT
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Indirect evidence suggests that induced sputum derives from the surfaces of the bronchial airways. To confirm this experimentally, we employed a radiolabeled aerosol bolus delivery technique that preferentially deposits aerosol in the central airways in humans. We hypothesized that there would be significantly more radioactivity recovered in an induced sputum sample, and greater airways clearance of radiolabeled particles, immediately after a central versus peripheral airways deposition. Ten healthy volunteers underwent radiolabeled aerosol deposition (99mTc sulfur colloid particles) to the central and peripheral airways on separate occasions followed immediately by induced sputum or no sputum (control), while seated in front of a gamma camera. Radioactivity was measured in the selected sputum sample, processed cell pellet, and supernatant fraction. Significantly more radioactivity was present in all portions of the sputum sample after central versus peripheral airways deposition (i.e., selected sample: 15,607 counts ± 2,985 versus 943 counts ± 298, p = 0.001). Clearance from the whole lung was significantly greater 40 min after central versus peripheral airways deposition (48 ± 3% versus 5 ± 1%, p = 0.0001). Compared with control, induced sputum greatly enhanced clearance after central deposition (48 ± 3% versus 11 ± 6%, p = 0.0001), but not after peripheral deposition (5 ± 1% versus 3 ± 0.8%). These results provide direct evidence that induced sputum derives from the central airways with little or no contribution from the peripheral airways.
For Debate: Social policy as a cause of childhood accidents: the children of lone mothers
Authors: I. Roberts, B. Pless
Journal: BMJ (1995)

Almost one in five British mothers is a lone mother. Their children have injury rates that are twice those of children in two parent families. In this article the link between lone parenthood and childhood injury is examined. The increased injury rates for the children of lone mothers can be explained by the poverty, poor housing conditions, and social isolation of lone mothers in Britain. The problem of reconciling the demands of paid work with the demands of the unpaid work of childrearing is particularly difficult for lone mothers, who find themselves in a benefit dependent poverty trap. Many such mothers would seek paid work if affordable day care were available. Day care would also provide a safe environment for their children, who are otherwise exposed to the environmental hazards of poor housing. Provision of day care is a social policy that would have important effects on the health and welfare of lone mothers and their children. These effects deserve to be properly evaluated.
Durable response to 90-yttrium-Epratuzumab (hLL2) in B-cell lymphoma failing chemotherapy by using dose-fractionation schedule
Authors: Ola Lindén, F Tennvall, Eva Cavallin-Ståhl, Lennart Darte, Tomas G Ohlsson, Cecilia Hindorf, Karin Wingårdh, Sven-Erik Strand
Journal: Blood (2001)
&lt;italic&gt;Corynebacterium parvum:&lt;/italic&gt; Effects on the Biochemistry of Mouse Serum and Liver&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: S Green, A Dobrjansky
Journal: JNCI Journal of the National Cancer Institute (1979)

The ip injection of 400 µg of ZnCI2 abrogated the lethality of 800 µg of Escherlchla coll endotoxin injected ip, but not iv, into normal noninbred CD®-1 Swiss mice (median lethal dose =450 µg endotoxin). Corynebacterium parvum-treated mice (1.0 mg/mouse) became hypersensitive to both iv and ip endotoxln, and 25 µg was lethal. ZnCI2 given ip at 400 µg to C. par-vum-treated mice did not prevent endotoxin (ip or iv) lethality nor did it inhibit the release of tumor necrosis factor into the circulation. Accordingly, a search was made for alterations in the liver metabolism of trace metals, carbohydrates, and toxins that might be related to the development of endotoxin hyperreactivity in C. parvum-treated mice. An iv injection of 25 µg endotoxin into normal mice (serum zinc = 108 µg/dl ) caused serum zinc to fall to 68 µg/dl after 2 hours and to 33 µg/dl after 6 hours. Serum zinc was 79 µg/dl 2 hours after administration of 25 µg endotoxin iv in mice treated with C. parvum 4 days earlier. Mice treated with C. parvum 8 or more days earlier did not show a serum zinc response to a challenge with endotoxin. Immunologicaily inactive C. parvum (strain CN-5888), which does not induce hyperspleno-megaly or hyperreactivity to endotoxin, did not result in the loss of the serum zinc response to endotoxin. Glycogen in the livers of untreated and C. parvum-treated mice was 37.4 and 19.9 mg/g, respectively. Endotoxin (25 µg) did not cause a significant change in the amount of liver glycogen in normal mice but did result in a decrease in the amount of liver glycogen in C. par-vum-treatrd mice from 19.9 to 9.9 mg/g. Microsomes from C. parvum-treated mouse livers had significantly decreased cyto-chrome P450, aminopyrine demethylase, and lipid peroxidase. In the pyrldine nucleotide-metabolizing system, the total pyridine nucleotlde concentration in livers from C. parvum-treated mice was 50% of the normal level. The sharply lowered concentration of NADPH accounted for essentially all of this decrease. Glucose 6-phosphate dehydrogenase (Glc-6-PD), the enzyme that regenerates NADPH from NADP, was increased by 1,500% in livers from C. parvum-treated mice. The extent of the increase in Glc-6-PD activity strictly depended on the stock of mice and on the strain of C. parvum used as the reticuloendotheiial stimulating agent. The results of these studies, itemizing some of the metabolic changes that occur following immunostimulation with C. parvum and identifying a strong dependence on mouse stock, suggest that the response to C. parvum may vary considerably in different species of animals with significant metabolic consequences.
Controlled Comparison of Electrophysiological Sleep in Families of Probands With Unipolar Depression
Authors: Donna E. Giles, David J. Kupfer, A. John Rush, Howard P. Roffwarg
Journal: American Journal of Psychiatry (1998)

This study presents polysomnographic data and psychiatric history for parents and siblings of probands with unipolar depression and short REM latency, probands with unipolar depression and normal REM latency, and normal comparison probands.Parents and adult siblings (N = 252) of probands (N = 64) were evaluated for lifetime history of psychiatric disorders and were studied in the sleep laboratory for 3 nights.REM latency predicted lifetime history of major depression. Short REM latency was also associated with slow wave sleep deficits. Rate of short REM latency in relatives of depressed probands with short REM latency quadrupled the rate in relatives of both depressed probands with normal REM latency and normal probands. Lifetime risk of depression was almost twice as high in relatives of depressed probands with short REM latency as in relatives of depressed probands with normal REM latency.Short REM latency and slow wave sleep deficits are familial. Short REM latency is associated with increased risk of major depression beyond the familial risk associated with a depressed proband. Polysomnographic abnormalities also occurred in unaffected relatives. Although the data can be considered only suggestive, these findings indicate that polysomnographic abnormalities may precede the clinical expression of depression and may be useful in identifying those at highest risk for the illness.
Adjuvant chemotherapy for patients with high-grade soft-tissue sarcomas of the extremity.
Authors: A E Chang, T Kinsella, E Glatstein, A R Baker, W F Sindelar, M T Lotze, D N Danforth, P H Sugarbaker, E E Lack, S M Steinberg
Journal: Journal of Clinical Oncology (1988)

We have previously reported the results of a randomized trial that demonstrated the survival benefit of adjuvant chemotherapy in the treatment of patients with high-grade extremity sarcomas compared with no chemotherapy. This regimen included doxorubicin, cyclophosphamide, and methotrexate. This report updates and extends our experience. The median follow-up of this trial is now 7.1 years and reveals a 5-year disease-free survival of 75% and 54% for chemotherapy and no chemotherapy groups, respectively (two-sided P [P2] = .037). The 5-year overall survival for patients in this trial was 83% and 60% for the chemotherapy and no chemotherapy groups, respectively, with a trend towards improved survival in the chemotherapy arm (P2 = .124). Because of doxorubicin-induced cardiomyopathy we performed a subsequent randomized trial comparing this high-dose regimen to reduced cumulative doses of doxorubicin and cyclophosphamide without methotrexate. Eighty-eight patients were entered into this trial which has a median follow-up of 4.4 years. The 5-year disease-free and overall survival for patients treated with the reduced doses of chemotherapy was 72% and 75%, respectively, and was not significantly different from the high-dose regimen. No patients developed congestive heart failure on this study. We conclude that adjuvant chemotherapy improves disease-free survival in patients with extremity soft-tissue sarcomas. The overall survival advantage in patients receiving adjuvant chemotherapy in our initial randomized high-dose chemotherapy trial has diminished though it continues to favor the chemotherapy group. A reduced-dose chemotherapy regimen was found to be comparable to the high-dose regimen.
Abstract 213: Dystrophic iPSC-derived Cardiomyocytes Have Mislocalization of eNOS and Increased Susceptibility to Cell Death which is Reversed by the Nitrate-like Properties of Nicorandil.
Authors: Jennifer L Strande, Melanie Reiter, Courtney Gastonguay, M. Zeeshan Afzal
Journal: Circulation Research (2014)

Background: Cardiomyopathy is a leading cause of death in Duchenne and Becker muscular dystrophy (D/BMD) patients and specific therapies are lacking. Dystrophin deficiency is associated with mislocalization of nitric oxide synthase (NOS) whose dysregulation contributes to the pathogenesis of dystrophic cardiomyopathy. We have modeled dystrophic cardiomyopathy using patient-specific induced pluripotent stem cells (iPSCs) and show that DMD- and BMD- iPSC derived cardiomyocytes have mislocalization of endothelial (eNOS) but not neuronal NOS (nNOS). In this study, we determined whether nicorandil, a drug with nitrate-like properties, protects against stress-induced dystrophic cardiomyocyte injury. Methods/Results: DMD-iPSC (exon 3-6 deletion), BMD-iPSC (exon 45-53 deletion) and non-dystrophic (N)-iPSC lines were differentiated into cardiomyocytes (iCMs) and matured for 35-38 days. Immunofluorescence revealed eNOS co-localized with dystrophin along the sarcolemma in N-iCMs but not in DMD- or BMD-iCMs. eNOS also co-localized with caveolin-1 in all groups. nNOS did not co-localize with dystrophin but with the ryanodine receptor 2 in all groups. Both DMD- and BMD-iCMs have increased cell death as determined by TUNEL + staining when subject to 2 hours of metabolic stress and 4 hours of recovery (DMD: 66±3%, BMD: 29±4% vs. 1.5±0.04%; n=3-6). This was associated with dissipation of the mitochondrial membrane potential as monitored by laser-scanning confocal microscopy (DMD: complete loss, BMD: 441±168 vs. N: 891±183 AU; n=3-5). Nicorandil pretreatment was able to restore mitochondrial membrane potential and decrease cell death. The protective effects of nicorandil were abolished by ODQ, a selective inhibitor of NO-sensitive guanylyl cyclase. Conclusion: Nicorandil protects against stress-induced cell death and preserves mitochondrial function in dystrophic cardiomyocytes through its nitrite-like properties. This suggests a potential therapeutic role of nicorandil in the treatment of dystrophic cardiomyopathy.
Photodynamic therapy for actinic keratoses: procedure matters?
Authors: A. Hauschild
Journal: British Journal of Dermatology (2011)

Journal Article Photodynamic therapy for actinic keratoses: procedure matters? Get access A. Hauschild A. Hauschild Department of Dermatology, University Hospital Schleswig‐Holstein, Schittenhelmstrasse 7, 24105 Kiel, Germany E‐mail: ahauschild@dermatology.uni‐kiel.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 1, 1 January 2012, Pages 3–5, https://doi.org/10.1111/j.1365-2133.2011.10737.x Published: 01 January 2012
Rapidly progressive glomerulonephritis after immunotherapy for cancer.
Authors: M G Parker, M B Atkins, A A Ucci, A S Levey
Journal: Journal of the American Society of Nephrology (1995)

Cytokines have been used in experimental and standard protocols for immune enhancement for cancer. The combination of interleukin-2 and interferon-alpha 2 beta has been used in experimental protocols for metastatic renal cell carcinoma. A man who developed rapidly progressive renal failure after receiving this combination therapy is reported. A renal biopsy revealed a pauci-immune crescentic glomerulonephritis. Antineutrophil cytoplasmic antibodies and antiglomerular basement membrane antibodies were absent. The spectrum of renal disease and potentially related extrarenal manifestations associated with interleukin-2 and inteferon-alpha are reviewed. A pathogenesis of altered cell-mediated immunity, consistent with abnormalities in extrarenal organs after immune enhancement, is proposed.
Low-Density Lipoprotein Particle Number Is Associated With Cardiovascular Events Among Those Not Classified Into Statin Benefit Groups
Authors: Olle Melander, Dov Shiffman, Michael P. Caulfield, Judy Z. Louie, Charles M. Rowland, James J. Devlin, Ronald M. Krauss
Journal: Journal of the American College of Cardiology (2015)
The effects of chronic periodontitis and its treatment on the subsequent risk of psoriasis
Authors: J.J. Keller, H.‐C. Lin
Journal: British Journal of Dermatology (2012)

Although psoriasis and chronic periodontitis (CP) may share an underlying immune dysregulation as part of their pathologies, to date only one small-scale cross-sectional pilot study has investigated the potential association between CP and psoriasis.This study aimed to investigate the subsequent risk for psoriasis following a diagnosis of CP by utilizing a cohort study design and population-based dataset in Taiwan.In total, 115 365 patients with CP were included in the study cohort and 115 365 patients without CP were included in the comparison cohort. We individually tracked each patient for a 5-year period to identify those who had subsequently received a diagnosis of psoriasis. A Cox proportional hazards regression was performed to compute the 5-year risk of subsequent psoriasis following a diagnosis of CP.We found that the incidence rate of psoriasis during the 5-year follow-up period was 1·88 [95% confidence interval (CI) 1·77-1·99] per 1000 person-years in patients with CP and 1·22 (95% CI 1·14-1·32) per 1000 person-years in comparison patients. After censoring those who died during the follow-up period, and adjusting for monthly income and geographical region, compared with comparison patients, the hazard ratio (HR) of psoriasis for patients with CP was 1·52 (95% CI 1·38-1·70). Furthermore, the study subjects who had undergone a gingivectomy or periodontal flap operation had only a slightly higher adjusted risk of psoriasis than comparison patients (HR 1·26).This study detected an increased risk for psoriasis among patients with CP. Treatment for CP attenuated, but did not nullify, the risk for subsequent psoriasis.
Asymptomatic oesophageal and bony involvement in an HIV-negative female with pulmonary TB
Authors: Rawya Ahmed, Simon Allen, Parthipan Kanthapillai
Journal: European Respiratory Journal (2011)

A 44 year-old lady of Afro-Caribbean origin presented with a 4-months history of productive cough, night sweats and weight loss. There were no other symptoms or significant medical history. Chest auscultation revealed right-sided apical bronchial breathing and coarse crepitations mid to lower zones. Chest radiography confirmed apical cavitation and right-sided consolidation. Sputum microscopy and molecular polymerase chain reaction test showed fully sensitive mycobacterium tuberculosis (TB).  Thoracic computed tomography revealed a pneumomediastinum, oesophageal perforation and gaseous permeative infiltration of T1-T3 vertebrae.  A human immunodeficiency virus (HIV) screen was negative.  Oesophageogastroduodenoscopy was normal apart from a 2cm punched out lesion at 23cm of the oesophagus. Quadruple anti-TB therapy and enteral feeding were established via a percutaneous gastrostomy tube to avoid mediastinitis and allow healing.  Clinically occult oesophageal perforation and bony involvement in the absence of HIV infection or miliary TB has not been previously described. The mechanism of this is unclear, but may have involved a caseating mediastinal lymph node.
Impact of -1562 C/T polymorphism of MMP9 gene on COPD susceptibility in Polish patients
Authors: Iwona Gilowska, Lukasz Kasper, Katarzyna Bogacz, Jan Szczegielniak, Tomasz Dybek, Krzysztof Sladek, Marcin Czerwinski, Edyta Majorczyk
Journal: European Respiratory Journal (2014)

Introduction   One of the hypotheses of COPD development suggests protease-antiprotease imbalance,which can cause degradation of extracellular matrix. As a consequence, the decline of lung function can be observed. Matrix metalloproteinase 9 (MMP9) is a proteolytic enzyme responsible for collagen digestion, and may contribute to COPD pathogenesis. In the  MMP9  gene, a -1562 C/T polymorphism was found, and the -1562T allele is associated with increasing level of promoter activity. It may be argued that the above-mentioned allele can influence incidence of COPD.   Aims and objective   To investigate the potential role of -1562C/T polymorphism in COPD development.  Eighty-three patients diagnosed with COPD according to the GOLD criteria, and 110 healthy control individuals were enrolled in the study. All cases have Polish Caucasians ethnicity.   Methods   DNA was extracted from peripheral blood using Invisorb Spin BloodMidi Kit following the manufacturer9s instructions (Invitek, Germany).  The MMP9 -1562C/T polymorphism was typed by PCR-RFLP method using 59-GCCTGGCACATAGTAGGCCC-39 and 59-CTTCCTAGCCAGCCGGCATC-39 primers, and cutting with restriction enzyme SphI (Zhang, B. et al.  Circulation , 1999; 99: 1788-1794).   Results   The patients with COPD differed from healthy controls in frequencies of  MMP9  -1562C/T alleles (p=0.02) and genotypes (p=0.03). An association of -1562T allele with COPD in comparison with healthy controls (frequencies: 0.20 vs 0.10, respectively;OR=2.07, 95%CI=1.15-3.72) was observed using Fisher exact test as a statistical method.   Conclusion   The  MMP9 -1562T allele seems to be associated with disease susceptibility in the Polish COPD patients.
CT scanner for the pleural staging of pleural cancer: How accurate is this?
Authors: Elisa Roca, Sophie Laroumagne, Stephanie Martinez, Hervé Dutau, Philippe Astoul
Journal: European Respiratory Journal (2014)

Introduction  CT Scanner(CT) is usefull in pleural lesions assessement,but the etiological confirmation by histology is need.Thoracoscopy is the best procedure to achieve the diagnosis.CT offers information regarding to the disease extension,but its relevance for local staging in comparison to thoracoscopy assessment is questionable.To our knowledge no study have investigated the agreement between CT and thoracoscopy for the assessment of malignant pleural lesions.   Methods  100patients underwent CT before thoracoscopy,which confirmed primitive or secondary pleural cancer.Agreement between CT and thoracoscopy evaluation for local extension was analyzed using Cohen9s kappa coefficient(k) for categorical data.   Results  The comparison between CT and thoracoscopy showed:no agreement for the assessment of visceral pleural involvement and presence of lymphangitis(k=0,000,k=0,000,and k=-0,036 respectively);a slight agreement for the assessment of diaphragmatic and mediastinal pleural involvement,presence of nodules on the parietal pleura,loculated pleural effusion and lung involvement(k=0,038,k=0,186,k=0,160,k=0,040,k=0,029 respectively);and a fair agreement for the assessment of nodules on the mediastinal pleura(k=0,314).   Conclusion  CT data may be predictive of thoracoscopic features in patients with primary pleural cancer or pleural metastasis in case of nodular invasion of mediastinal pleural but failed to detect pleural lymphangitis and visceral pleural involvement, the latest being a pejorative pronostic parameter.Therefore a substantial degree of disagreement exists during the two procedures and supports thoracoscopy as the gold standard for assessment of suspicious pleural lesions.