tbuckley/cabot-search huggingface dataset:
Brain and Spinal Tumors of Childhood
Authors: James T. Rutka
Journal: Neuro-Oncology (2007)

Walker and colleagues have assembled an outstanding team of authors, with significant contributions from European collaborators, to write on brain and spinal tumors of childhood. While you cannot necessarily judge a book by its cover, the cover of this multiauthor text very accurately portrays the comprehensive and holistic approach taken throughout the book to address the problem of central nervous system neoplasia in children. The cover depicts advances in science with images of neuronal cells in culture and state-of-the-art neuro-imaging with an MR image of a craniopharyngioma in a child, and it also depicts the care of the psychosocial aspects of the child with an image of children playing together in a circle. The authors kindly acknowledge the work of Dr. Joachin Kuhl, a contributor to the book, who suddenly and unexpectedly died of a brain tumor during the production of the book. His enduring contribution to the book is on the topic of embryonic tumors.
The Impact of Solitary and Multiple Positive Surgical Margins on Hard Clinical End Points in 1712 Adjuvant Treatment–Naive pT2–4 N0 Radical Prostatectomy Patients
Authors: Julian Mauermann, Vincent Fradet, Louis Lacombe, Thierry Dujardin, Rabi Tiguert, Bernard Tetu, Yves Fradet
Journal: European Urology (2012)
Identification of Transformation-Related Antigen by Monoclonal Antibody on Swiss 3T3 Cells Induced by Transfection With Murine Cultured Colon 36 Tumor DNA&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Noriyuki Sato, Takashi Sato, Shuji Takahashi, Mamoru Okubo, Atsuhiko Yagihashi, Hirofumi Koshiba, Kokichi Kikuchi
Journal: JNCI Journal of the National Cancer Institute (1987)

The cell surface antigen associated with the transformed state of cells that could grow in an anchorage-independent manner was analyzed by use of techniques of DNA transfection and hybridomas secreting the monoclonal antibody (MoAb). Spleen cells of C57BL/6 mice immunized with a highly tumorigenic, chemically induced murine cultured colon 36 tumor (C-C36) of BALB/c origin were hybridized with NS-1, a hypoxanthine phosphoribosyltransferase-deficient myeloma line of BALB/c mice. Screening of hybridomas revealed an antibody that reacted with C-C36 and transformed Swiss 3T3 cells growing in soft agar after transfection of 3T3 cells with C-C36 DNA. The hybridomas that did not react with nontransformed 3T3 and the less tumorigenic BALB/c hemangioendothelioma line D10 were then selected. An MoAb was designated “#71295.” This MoAb immunoprecipitated the antigen that consisted of 65,000- and 14,000-molecular-weight components with soluble C-C36 membrane antigens. It also reacted with 2 other chemically induced syngeneic colon tumor lines, cultured colon 26 tumor line and cultured colon 51 tumor line, and with fibrosarcoma Meth A. However, #71295 was not found in NS-1, D14, and BALB/c normal thymus, liver, colon, and kidney tissues. In addition, this MoAb could not inhibit the anchorage-independent growth of C-C36 and transformed 3T3 cells. These results suggest that although the molecule defined by #71295 might not be associated with the anchorage independence of cell growth, it could be a newly expressed determinant on the cell surface that is related to the events of cell transformation.
Human T cell activation. I. Monocyte-independent activation and proliferation induced by anti-T3 monoclonal antibodies in the presence of tumor promoter 12-o-tetradecanoyl phorbol-13 acetate.
Authors: T Hara, S M Fu
Journal: The Journal of Experimental Medicine (1985)

Three monoclonal antibodies (mAb), of IgG1, IgG2a, and IgM isotypes, raised against the T3 complex, were used to probe the activation of human T cells. The IgM antibody 235 was not mitogenic for peripheral blood mononuclear cells (PMC). It efficiently blocked the proliferation of PMC induced by T cell mitogens, alloantigens, and soluble antigens. The other two antibodies were mitogenic, and behaved similarly to Leu 4 and OKT3, respectively. In T cell preparations with less than 0.1% monocytes (as assayed by nonspecific esterase staining), all three mAb were not mitogenic. They failed to induce either interleukin 2 (IL-2) receptor expression or IL-2 secretion. Addition of IL-1 failed to collaborate with anti-T3 mAb to induce these T cells to proliferate, but IL-2 enhanced T cell proliferation slightly. Monocyte-depleted T cells, however, proliferated in response to all three anti-T3 mAb, when TPA was added, in a dose-dependent manner. TPA induced a low level of IL-2 receptor expression in monocyte-depleted T cells, without inducing IL-2 secretion. Anti-T3 plus TPA induced a marked enhancement in both quantity and intensity of IL-2 receptor expression. IL-2 secretion was also detected. These results indicate that anti-T3 IgM can deliver an inductive signal despite its blockage of T cell proliferation, and that two signals are necessary and perhaps sufficient to induce human T cell activation and proliferation.
Study of Spontaneous Congestive Heart Failure in the Dog
Authors: Charles R. Wallace, William F. Hamilton
Journal: Circulation Research (1962)

Spontaneous cardiovascular disease has been found in dogs from the Savannah River Valley area, predominantly in the male house pet and hunting dog. The causes have been Dirofilariasis, chronic mitral valvular disease, and congenital cardiovascular defects. Cardiac stress in these dogs caused marked salt and water retention, increased blood volume, increased central venous and right heart pressures, and cardiac dilation and hypertrophy. These compensatory mechanisms were similar to those in man. Cardiac dilation was more pronounced in spontaneous failure than in experimental failure. Regression of cardiac dilation was very slow even after apparent compensation and clinical improvement. Plasma protein concentrations were decreased, but total extracellular protein mass was markedly increased. Sodium and potassium plasma concentrations were within normal range. Hyponatremia was occasionally observed in dogs as in man. 20 Dirofilariasis was characterized by marked pulmonary hypertension, caused primarily by pulmonary vascular changes rather than mechanical blockage. There was massive hypertrophy of the right ventricular myocardium. Heartworm dogs in congestive failure have a similar range of right heart pressure to experimental pulmonic stenosis dogs in failure. 21 Cage rest was of little therapeutic value in these dogs in congestive failure. Clinical response and physiological changes were remarkable with the use of saltabsorbing resin or digitalis compounds causing negative sodium balance. Digitalization of the dog required vigorous individual treatment controlled by clinical symptoms and P-R interval of the electrocardiogram. Acquired tolerance to digitalis required increased dosage levels every few months. The veterinary practitioner who recognizes the necessity of individual digitalization and the importance of detection and removal of thoracic fluid will be rewarded with improved clinical therapy of congestive heart failure. Experimental dogs during periods of severe cardiac stress can benefit from adequate digitalization. The similarity of biochemical and physiological changes in spontaneous heart disease, as it occurs in man and in dogs, affords an avenue for clinical research. This applicability to man is enhanced because the dog can be more comprehensively studied.
Covalent and Noncovalent Modification of Thin Filament Action
Authors: Joseph M. Metzger, Margaret V. Westfall
Journal: Circulation Research (2004)

Troponin is essential for the regulation of cardiac contraction. Troponin is a sarcomeric molecular switch, directly regulating the contractile event in concert with intracellular calcium signals. Troponin isoform switching, missense mutations, proteolytic cleavage, and posttranslational modifications are known to directly affect sarcomeric regulation. This review focuses on physiologically relevant covalent and noncovalent modifications in troponin as part of a thematic series on cardiac thin filament function in health and disease.
P581 NON-CIRRHOTIC, NON-VIRAL RELATED HEPATOCELLULAR CARCINOMA: IS IT RELATED WITH NON-ALCOHOLIC FATTY LIVER DISEASE OR MOSTLY WITH THE ASSOCIATED METABOLIC FACTORS?
Authors: H.P. Marques, H. Cortez-Pinto, A. Carvalho, A. Milheiro, V. Ribeiro, H. Gloria, E. Barroso
Journal: Journal of Hepatology (2014)
Lymphoma models for B cell activation and tolerance. III. Cell cycle dependence for negative signalling of WEHI-231 B lymphoma cells by anti-mu.
Authors: D W Scott, D Livnat, C A Pennell, P Keng
Journal: The Journal of Experimental Medicine (1986)

WEHI-231 B lymphoma cells have proven to be a useful model for the regulation of growth of normal B cells by anti-Ig reagents. We previously reported that the growth of these lymphoma cells is inhibited by heterologous or monoclonal anti-mu or anti-kappa reagents. Such cells cease to incorporate thymidine within 24-48 h of exposure to anti-Ig reagents, but are not adversely affected by antibodies directed at either class I or class II histocompatibility antigens. In fact, cell cycle analysis revealed that anti-mu causes a block in the transition of these cells from G1 to S phase. To further study the mechanism of growth inhibition, we have purified lymphoma cells in G1 by centrifugal elutriation, or enriched WEHI-231 cells at the G1/S interface by treatment with hydroxyurea, and followed their progression through the cell cycle in the presence or absence of anti-mu. Our data show that WEHI-231 B lymphoma cells receive a negative signal early in G1, since delayed addition of anti-mu (to late G1 cells) leads to no alteration in cell cycle progression at 24 h, and exposure to anti-mu during S does not alter progress through DNA synthesis and mitosis. Moreover, exposure to anti-mu for only 2 h prevents purified G1 cells from entering their first S phase. The nature of the relevant processes in early G1 is discussed in terms of models of B cell activation and tolerance induction.
Mapping of proteins from cultured fibroblasts of synovial and subcutaneous origin by high resolution two-dimensional polyacrylamide gel electrophoresis.
Authors: A Glennas, A K Thorsrud, H E Rugstad, E Jellum
Journal: Annals of the Rheumatic Diseases (1985)

Nine different cell lines of human (A) rheumatoid and (B) normal synovial fibroblasts and of (C) normal skin fibroblasts were obtained from tissue explants and grown as monolayers. The cellular protein synthesis was studied by high resolution two-dimensional polyacrylamide gel electrophoresis. Between the fourth and 10th passage of the cells in culture apparently no consistent differences were found which could be ascribed to the origin of the cells, to the rheumatoid state of the synovial tissue, or to the increasing age of the cultured fibroblasts.
<i>N</i>-Acetylcysteine Conjugate of Phenethyl Isothiocyanate Enhances Apoptosis in Growth-Stimulated Human Lung Cells
Authors: Yang-Ming Yang, Meena Jhanwar-Uniyal, Joel Schwartz, C. Clifford Conaway, H. Dorota Halicka, Frank Traganos, Fung-Lung Chung
Journal: Cancer Research (2005)

Abstract We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice. In the present study, we show that PEITC-NAC also induces apoptosis and AP-1 activity in human lung adenocarcinoma A549 cells, and that activation of AP-1 is important in PEITC-NAC induced apoptosis in these cells. PEITC-NAC induced AP-1 binding activity in A549 cells in a dose- and time-dependent manner; peak activity appeared at 10 μmol/L after 24 hours. At that time, flow cytometric analysis showed a sub-G1 peak, indicating that ∼4.5% of the cells had undergone apoptosis. When wild-type c-jun cDNA was transfected into A549 cells, PEITC-NAC–mediated apoptosis was greatly increased in the c-jun–transfected cells compared with the control vector–transfected cells, based on cell morphology and analysis of DNA fragmentation. Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 μmol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis. Bivariate flow cytometric analysis of DNA strand breaks versus DNA content showed that apoptosis induced by PEITC-NAC occurred predominantly in the G2-M phase. These findings suggest that growth-stimulated cells with an elevated basal AP-1 activity, i.e., A549 cells transfected with wild-type c-jun or treated with a tumor promoter, were more sensitive to PEITC-NAC–mediated apoptosis. The observation that PEITC-NAC induces apoptosis predominantly in growth-promoted cells, such as neoplastic cells, suggests a selective mechanism by which PEITC-NAC inhibits lung carcinogenesis.
ON THE CAUSES OF INVERSION OF THE UTERUS
Authors: L. Atthill
Journal: BMJ (1908)

laovzvrAmi~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ glancng at the table, was normal.In both these cases chloroform had been given every chance, before pushing nitro.glycerlne.. Sinoe then nitro-glycerinebas.been used in every case, with only one deatb, No. 14, where the treatment was commenced very late, perhaps too late.The value of nitro.glycerineIn Bright's disease com- menoed to exercise the minds of professional men about 1879.MurrellI had dlecovered.thatthis drug caused greatarterial relaxation., Ringer7 wrote: " Nitro.glycerineIs employed in cases of contracted kidney, to lower arterial tension; it relieves the distressiog headache of Bright's disease, and is said to increase the quantity of urine in chronic parenchymatous nephritis."The diuretic effect had further been verified by Dr. Fancourt Barnes In a case of hipspadias.Then arose In my mind the.imi- larity of condition existing In .patientssuffering from puerperal eclampsla and those suffering from uraemic con- vulsions, and thus Iwas led to try nitro.glycerinefor the former class of patients.'As regards the use of other drugs, the usual routine treatment was tried.Veneeection was used once, in addition to which one was a placenta praevia where the bleeding was neceesarily iree.Tbis case died.The hot pack was tried with No. 7, but the result was not encouraging.Chloral and bromide of potassium were nsed internally and per rectum, but failed.Saline injec- tions, per rectum, were used once, and should, perhaps, prove valuable in later stages.especially following the complication of haemorrhage.Veratrum viride, which has been highly recommended zecently, was not used.In conclusion, whilst the results quoted above neces- saily produced a great impression on my mind, yet the suggestions are not offered In a dogmatic spirit, but rather for the purpose of encouraging further investigation in this complex subject.Finally, I would suggest that the scope of the use of nitro-glycerine bypodermically m?ght be extended Into the physician's domain.It is quite possible that this series, With its results, may be only one of thoee remarkable coincidences which occur from time to time.But should the consideration of them In any way tend to a more successful treatment of these painful eases, in which the joy that should come with morning Is often turned into the sorrow of darkest night, my object will have been fully attained.
Prediction of clinical outcome in advanced hepatitis C-associated liver disease: identification of patients at the highest need for antiviral treatment and surveillance
Authors: Christoph Neumann-Haefelin, Robert Thimme
Journal: Gut (2014)

Patients infected with HCV usually have a long period of mild disease of 15–25 years. After this period, a substantial number of patients develop liver-associated morbidity and mortality, including clinical complications of liver cirrhosis such as ascites, variceal haemorrhage, hepatic encephalopathy, hepatocellular carcinoma (HCC) or liver-related death. This natural course of disease has been best described in young and mostly healthy women who were infected by a contaminated anti-D immunoglobulin preparation in East Germany in 1978/1979. Less than 2% of women with chronic HCV infection developed liver cirrhosis or HCC in the first 25 years of infection, while this number increased substantially to approximately 15% in the 35-year follow-up.1 ,2 These data were discussed controversially, since this initially mild course was partially attributed to the cohort of young, female patients with few comorbidities. A recent evaluation of a cohort of intravenous drug users (IVDU) who were followed since the 1970s, however, found a similarly slow progression of HCV-associated liver disease in this ‘real-world’ cohort. Indeed, this study analysed autopsies from 61 chronically infected subjects who had died mostly due to drug-related reasons. None of the 18 subjects who had died <15 years after HCV exposure had F3 or F4 METAVIR fibrosis stage, while 6 of 17 …
Failure of high-flow nasal cannula therapy may delay intubation and increase mortality
Authors: Byung Ju Kang, Younsuck Koh, Chae-Man Lim, Jin Won Huh, Seunghee Baek, Myongja Han, Hyun-Suk Seo, Hee Jung Suh, Ga Jin Seo, Eun Young Kim, Sang-Bum Hong
Journal: Intensive Care Medicine (2015)

Intubation in patients with respiratory failure can be avoided by high-flow nasal cannula (HFNC) use. However, it is unclear whether waiting until HFNC fails, which would delay intubation, has adverse effects. The present retrospective observational study assessed overall ICU mortality and other hospital outcomes of patients who received HFNC therapy that failed.All consecutive patients in one tertiary hospital who received HFNC therapy that failed and who then required intubation between January 2013 and March 2014 were enrolled and classified according to whether intubation started early (within 48 h) or late (at least 48 h) after commencing HFNC.Of the 175 enrolled patients, 130 (74.3 %) and 45 (25.7 %) were intubated before and after 48 h of HFNC, respectively. The groups were similar in terms of most baseline characteristics. The early intubated patients had better overall ICU mortality (39.2 vs. 66.7 %; P = 0.001) than late intubated patients. A similar pattern was seen with extubation success (37.7 vs. 15.6 %; P = 0.006), ventilator weaning (55.4 vs. 28.9 %; P = 0.002), and ventilator-free days (8.6 ± 10.1 vs. 3.6 ± 7.5; P = 0.011). In propensity-adjusted and -matched analysis, early intubation was also associated with better overall ICU mortality [adjusted odds ratio (OR) = 0.317, P = 0.005; matched OR = 0.369, P = 0.046].Failure of HFNC might cause delayed intubation and worse clinical outcomes in patients with respiratory failure. Large prospective and randomized controlled studies on HFNC failure are needed to draw a definitive conclusion.
C-C Chemokine Receptor 5 on Stromal Cells Promotes Pulmonary Metastasis
Authors: Hendrik W. van Deventer, William O'Connor, W. June Brickey, Robert M. Aris, Jenny P.Y. Ting, Jonathan S. Serody
Journal: Cancer Research (2005)

Abstract We have shown that mice that express the C-C chemokine receptor 5 (CCR5) have enhanced local tumor growth and an impaired response to vaccine therapy compared with CCR5 knockout (CCR5−/−) mice. Here, we extend these observations to evaluate the function of CCR5 in pulmonary metastasis and the mechanism underlying the diminished tumor growth in CCR5−/− mice. Lung metastases were counted in wild-type (WT) and CCR5−/− mice following the injection of 1 × 106 B16-F10 melanoma cells. These results were compared with those from syngeneic bone marrow chimeric mice formed by the transfer of WT bone marrow into irradiated CCR5−/− and CCR5−/− marrow into irradiated WT mice. Intact CCR5−/− mice developed fewer metastases than WT mice (40.2 versus 70.6; P &amp;lt; 0.05). Bone marrow chimeras formed by the transfer of WT bone marrow into CCR5−/− hosts had fewer metastases than WT hosts injected with knockout marrow (46.6 versus 98.6; P &amp;lt; 0.01). Adoptive transfer of CCR5-expressing leukocytes also failed to promote metastasis in CCR5−/− mice. However, the i.v. transfer of WT pulmonary stromal cells into CCR5−/− mice increased the number of metastases compared with transfer of CCR5−/− stromal cells (102.8 versus 26.0; P &amp;lt; 0.05). These results show for the first time that CCR5 expression on stromal and not hematopoietic cells contributes to tumor metastasis. Therefore, recently developed CCR5 inhibitors may have a novel benefit in cancer therapy.
Annexin XI Is Associated with Cisplatin Resistance and Related to Tumor Recurrence in Ovarian Cancer Patients
Authors: Jin Song, Ie-ming Shih, Ritu Salani, Daniel W. Chan, Zhen Zhang
Journal: Clinical Cancer Research (2007)

Ovarian cancer patients treated with cisplatin-based chemotherapy often develop acquired cisplatin resistance and, consequently, cancer recurrence. The precise nature of chemoresistance remains unclear. In this study, a protein identified to be associated with cisplatin resistance in ovarian cancer cells was investigated in ovarian cancer tissues to address its clinical significance.Antibody microarrays were used to identify proteins consistently differentially expressed across three pairs of cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines. Immunoblotting was used to confirm observed alteration of protein expression. The protein expression was further evaluated by immunohistochemical staining using tissue microarrays containing various human normal and malignant tissues and 164 surgical specimens derived from primary and recurrent ovarian cancer patients who underwent primary debulking surgery followed by standard chemotherapeutic regimen.Annexin XI was down-regulated in all three cisplatin-resistant cell lines as compared with their parent cells. Annexin XI expression was observed in the majority of human normal organs and decreased in some of the most common human malignancies. The expression level of Annexin XI in first recurrent ovarian cancers was much lower than that in primary ovarian cancers (P = 0.0004). Increased Annexin XI immunoreactivity in ovarian cancers seemed to prolong the disease-free interval of patients (P = 0.03). Annexin XI immunoreactivity inversely correlated with in vitro cisplatin resistance in ovarian cancers (P = 0.01).Decreased expression of Annexin XI is characteristic for cisplatin-resistant cancer cells and may contribute to tumor recurrence. Annexin XI may be a potential marker for chemoresistance and earlier recurrence of ovarian cancer patients.