tbuckley/cabot-search huggingface dataset:
Abstract 5575: Tetrandrine blocks emergence of castrate resistant phenotype in prostate cancer by promoting apoptosis and sensitizing prostate cancer cells to androgen deprivation
Authors: Sweaty Koul, Hari K. Koul
Journal: Cancer Research (2011)

Abstract Prostate cancer (PCa) is the second leading cause of cancer deaths in men, and the majority of prostate cancer deaths are a result of emergence of castrate resistant phenotype. One of the six hallmarks of cancer is resistance to apoptosis, and we hypothesized that resistance to apoptosis is in part responsible for emergence of castrate resistant phenotype in prostate cancer. Specifically we investigated the effects of Tetrandrine (TET), a bis-benzylisoquinoline alkaloid isolated from the root of Stephania tetrandra, on apoptosis of PCa cells in vitro. TET decreased viability of PCa cells. Long-term treatment with TET resulted in a dramatic increase in sub G0/G1 cell population suggestive of apoptosis. Treatment with TET resulted in decrease in anti-apoptotic proteins (Bcl-xl and survivin) and concomitant activation of caspase 3 and PARP cleavage. Moreover, Tet treatment induced DNA fragmentation and nuclear condensation, all hallmarks of apoptosis. We also observed that pretreatment with Tet sensitized LNCaP cells to androgen depletion and prevented emergence of castrate resistant phenotype in vitro culture. Moreover, Tet induced apoptosis in LNCaP C-4 and C4-B (AR positive castrate resistant prostate cancer) cells, indicated effectiveness against established castrate resistant phenotypes in prostate cancer. These results show that Tet by promoting apoptosis of prostate cancer cells and by sensitizing prostate cancer cells to androgen depletion may serve as a chemopreventive/ therapeutic agent in prostate cancer. If these results hold true in additional in vivo studies, Tet may serve as a mechanism based agent against emergence of castrate resistant prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5575. doi:10.1158/1538-7445.AM2011-5575
Calreticulin Promotes Migration and Invasion of Esophageal Cancer Cells by Upregulating Neuropilin-1 Expression via STAT5A
Authors: Feng Shi, Li Shang, Bei-Qing Pan, Xiao-Min Wang, Yan-Yi Jiang, Jia-Jie Hao, Yu Zhang, Yan Cai, Xin Xu, Qi-Min Zhan, Ming-Rong Wang
Journal: Clinical Cancer Research (2014)

We previously revealed that the calreticulin (CRT) gene is a candidate oncogene promoting cell migration and invasion and that neuropilin-1 (NRP1) is a possible effector downstream of CRT in esophageal squamous carcinoma cells. This study aims to explore the mechanisms underlying the migration and invasion of esophageal cancer cells regulated by CRT through NRP1.Quantitative reverse-transcription polymerase chain reaction, Western blot analysis, chromatin immunoprecipitation, and reporter gene assays were used to investigate the relationship between CRT and NRP1. In vitro and in vivo assays were carried out to evaluate the effects of NRP1 on malignant phenotypes of ESCC cells and tumor metastasis in NOD/SCID mice. Immunohistochemistry was performed to analyze the expression of CRT and NRP1 in esophageal squamous cell carcinomas (ESCC).Knockdown of CRT decreased the expression of NRP1. Inhibition of NRP1 reduced ESCC cell motility in vitro and experimental metastasis in vivo. Ectopic expression of NRP1 rescued the defects of cell migration and invasion in CRT-shRNA cells. CRT depletion inhibited STAT5A phosphorylation at the Y694 site via a CaMKII-independent pathway. Moreover, STAT5A directly regulated NRP1 transcription. Knockdown of CRT or NRP1 led to a downregulation of MMP2, MMP9, and FAK. Notably, positive correlation was found between CRT and NRP1 expression in ESCC tissues (P = 5.87 × 10(-5)). CRT and NRP1 coexpression was significantly associated with lymph node metastasis (P = 0.025).Our findings suggest that NRP1 is a critical downstream effector of CRT in promoting cell migration and invasion, which might contribute to the metastasis of ESCC.
A Phase 1 Study of Heat/Phenol Killed, E. coli-Encapsulated, Recombinant Modified Peanut Proteins Ara h 1, Ara h 2, and Ara h 3 (EMP-123) for the Treatment of Peanut Allergy
Authors: R. Wood, D. Stablein, A. Henning, R. Lindblab, S. Sicherer
Journal: Journal of Allergy and Clinical Immunology (2012)
Use of State Risk-Pools in Protecting the Uninsured
Authors: Bernard R. Tresnowski
Journal: JAMA (1988)

THE COUNCIL on Medical Service report, Protecting the Uninsured: Use of State Risk-Pools, 1 is a useful contribution to an unsolved national problem. We at the Blue Cross and Blue Shield Association share the American Medical Association's commitment to finding answers that will make the best use of all that the entire health care financing system can offer.  The problem of the uninsured is a challenging one, and solutions will necessarily involve sharing responsibilities of both the public and private sectors. We share the American Medical Association's commitment to answers that use what we already have in place; for example, the risk pools in 15 states that afford coverage for people with chronic medical conditions that make it impossible for them to get insurance at any price. In those states the pools have been designed to provide coverage to these individuals in a manner that is compatible and not competitive with
NEW RULING FOR HEMACYTOMETER CHAMBERS
Authors: Lewis V. Judson
Journal: JAMA (1925)

In the United States, the use of the Neubauer ruling shown in Figure 1 has been rather general for hemacytometer chambers. Professors in medical colleges, however, have had more or less difficulty in teaching the student to make the correct count because of the extra lines, which were originally added for the purpose of making the principal subdivisions of the central square millimeter area more readily discernible. Actually, these extra lines have led to confusion, resulting in erroneous counts, and the Neubauer ruling has not, therefore, been an unqualified success. A new type of ruling, shown in Figure 2, a modification of the Neubauer, was recently submitted to the Bureau of Standards for test. This new ruling clearly defines the boundaries of the major subdivisions, and it would appear to possess an advantage to the physician using the instrument in the diagnosis of disease, because of the greater certainty with
Hyaluronan fragments activate an NF-kappa B/I-kappa B alpha autoregulatory loop in murine macrophages.
Authors: P W Noble, C M McKee, M Cowman, H S Shin
Journal: The Journal of Experimental Medicine (1996)

Macrophages play an important role in the acute tissue inflammatory response through the release of cytokines and growth factors in response to stimuli such as lipopolysaccharide (LPS). Macrophage inflammatory effector functions are also influenced by interactions with the extracellular matrix (ECM). Such macrophage-ECM interactions may be important in regulating chronic inflammatory responses. Recent evidence has suggested that hyaluronan (HA), a glycosaminoglycan (GAG) component of ECM can induce inflammatory gene expression in murine macrophages. HA exists in its native form as a large polymer, but is found as smaller fragments under inflammatory conditions. The NF-kappa B/I-kappa B transcriptional regulatory system has been shown to be a critical component of the host inflammatory response. We examined the effects of high molecular weight HA and lower molecular weight HA fragments on NF-kappa B activation in mouse macrophages. Only the smaller HA fragments were found to activate NF-kappa B DNA binding activity. After HA stimulation, I-kappa B alpha mRNA was induced and I-kappa B alpha protein levels, which initially decreased, were restored. The induction of I-kappa Balpha expression was not observed for other GAGs. The time course of I-kappa B alpha protein regeneration in response to HA fragments was consistent with an autoregulatory mechanism. In support of this mechanism, in vitro translated murine I-kappa B alpha inhibited HA fragment-induced NF-kappa B DNA binding activity. The NF-kappa B DNA binding complex in HA-stimulated extracts was found to contain p50 and p65 subunits. Activation of the NF-kappa B/I-kappa B system in macrophages by ECM fragments may be an important mechanism for propagating the tissue inflammatory response.
Is it not Simpson's Acupressure Improved?
Authors: F. S. Thomas
Journal: JAMA (1889)

<h3>To the Editor:</h3> —In The Journal of January 19, under the head of " Original Articles," appears a well written article by C. S. Muscroft, M.D., of Cincinnati, viz.: " Results in Eleven Cases of a<i>New Method</i>for Arresting Bleeding in Surgical Operations," a paper read before the Section of Surgery, A. M. A., 1888. In December, 1859, the late Sir James Y. Simpson, in a communication to the Royal Medico-Chirurgical Society, of Edinburgh, presented the same method of hæmostasis, under the name of " acupressure." Does Dr. Muscroft mean by calling his method<i>new</i>, that it is not " acupressure " applied; not after the operation, in the flap, but before the flap is made? Is it not Simpson's "acupressure," improved by Muscroft? I do not wish to criticise, but ask for information. Respectfully, Council Bluffs, Iowa.
Cooperative Study of Radiologic Aspects of Renovascular Hypertension
Authors: Joseph J. Bookstein
Journal: JAMA (1977)

Abnormal urographic features were present in 60.7% of 250 patients with bilateral diseases. The urogram was relatively insensitive in the minority of patients whose lesions were of approximately equivalent severity bilaterally. In bilateral renovascular disease, the urogram demonstrated some surgical prognostic value that was not evident in unilateral renovascular disease. Furthermore, in patients with bilateral disease, the urogram was helpful in deciding between unilateral or bilateral operation.
"Angelina effect" led to more appropriate breast cancer referrals, research shows
Authors: N. Hawkes
Journal: BMJ (2014)

When the US actress Angelina Jolie announced that she had tested positive for the breast cancer gene BRCA1 and had undergone a double mastectomy, referrals for genetic counselling and testing in the United Kingdom more than doubled, remaining higher than usual for at least six months.

And these were not simply “worried well” women, a team from various cancer centres around the UK has concluded.1 The authors found no …
982 BMI1 IS A MARKER OF ACTIVATED LIVER PROGENITOR CELLS
Authors: B.A. Schotanus, B. Spee, H.S. Kruitwagen, B.B. Brinkhof, T.S.G.A.M. van den Ingh, L.C. Penning, T. Roskams
Journal: Journal of Hepatology (2010)
Effect of acetylator phenotype on efficacy and toxicity of sulphasalazine in rheumatoid arthritis.
Authors: T Pullar, J A Hunter, H A Capell
Journal: Annals of the Rheumatic Diseases (1985)

A group of 54 patients with rheumatoid arthritis (31 fast, 23 slow acetylators) treated with sulphasalazine 3 g/day were studied retrospectively. At 24 weeks no difference in the efficacy of the drug could be shown between fast and slow acetylators. In a second prospective study 40 fast acetylators were allocated to 3 g/day and 20 slow acetylators to 1.5 g/day. At 24 weeks marked improvement was seen in the fast acetylators given high dose but not the slow acetylators given low dose. It was also noted in this study that the usual ratio of fast : slow acetylators was reversed, and there is some suggestion that fast acetylators may be predisposed to more severe rheumatoid arthritis. The toxicity pattern in a total of 149 patients (83 fast, 66 slow acetylators) was also studied. Significantly more slow acetylators stopped treatment because of nausea or vomiting, or both, but serious toxicity was not confined to either group. Acetylator phenotype therefore appears important in determining the incidence of nausea and/or vomiting associated with sulphasalazine therapy in patients with rheumatoid arthritis but has no effect on the occurrence of potentially serious toxicity or efficacy. Thus prior measurement of acetylator phenotype in patients with rheumatoid arthritis confers little practical benefit in their management.
Psychiatric morbidity and physical toxicity associated with adjuvant chemotherapy.
Authors: A F Cooper, A V Hughson, C S McArdle, A R Russell, D C Smith
Journal: BMJ (1980)

Our findings support the contention of Dr Walker and his colleagues that transplant rejection can be a cause of intrarenal aneurysms, and we believe that such aneurysms represent one extreme of the wide spectrum of arterio- pathic changes that can be demonstrated by arteriography during transplant rejection.5
Hepcidin Mitigates Renal Ischemia-Reperfusion Injury by Modulating Systemic Iron Homeostasis
Authors: Yogesh Scindia, Paromita Dey, Abhinav Thirunagari, Huang Liping, Diane L. Rosin, Matteo Floris, Mark D. Okusa, Sundararaman Swaminathan
Journal: Journal of the American Society of Nephrology (2015)

Iron-mediated oxidative stress is implicated in the pathogenesis of renal ischemia–reperfusion injury. Hepcidin is an endogenous acute phase hepatic hormone that prevents iron export from cells by inducing degradation of the only known iron export protein, ferroportin. In this study, we used a mouse model to investigate the effect of renal ischemia–reperfusion injury on systemic iron homeostasis and determine if dynamic modulation of iron homeostasis with hepcidin has therapeutic benefit in the treatment of AKI. Renal ischemia–reperfusion injury induced hepatosplenic iron export through increased ferroportin expression, which resulted in hepatosplenic iron depletion and an increase in serum and kidney nonheme iron levels. Exogenous hepcidin treatment prevented renal ischemia-reperfusion–induced changes in iron homeostasis. Hepcidin also decreased kidney ferroportin expression and increased the expression of cytoprotective H-ferritin. Hepcidin-induced restoration of iron homeostasis was accompanied by a significant reduction in ischemia-reperfusion–induced tubular injury, apoptosis, renal oxidative stress, and inflammatory cell infiltration. Hepcidin–deficient mice demonstrated increased susceptibility to ischemia-reperfusion injury compared with wild-type mice. Reconstituting hepcidin-deficient mice with exogenous hepcidin induced hepatic iron sequestration, attenuated the reduction in renal H-ferritin and reduced renal oxidative stress, apoptosis, inflammation, and tubular injury. Hepcidin-mediated protection was associated with reduced serum IL-6 levels. In summary, renal ischemia–reperfusion injury results in profound alterations in systemic iron homeostasis. Hepcidin treatment restores iron homeostasis and reduces inflammation to mediate protection in renal ischemia–reperfusion injury, suggesting that hepcidin-ferroportin pathway holds promise as a novel therapeutic target in the treatment of AKI.
[188] INFLUENCE OF ANTIRETROVIRALS IN THE PROGRESSION OF LIVER FIBROSIS IN HIV/HCV COINFECTED PATIENT S. EFFECT OF HEPATOTOXICITY AND METABOLIC ABNORMALITIES
Authors: P. Barreiro, L. Martin-Carbonero, F. Blanco, P. Labraga, J. Gonzalez-Lahoz, V. Soriano
Journal: Journal of Hepatology (2007)
Macrovascular disease in type 2 diabetes: We do need animal models for in vivo studies
Authors: A NITENBERG
Journal: Cardiovascular Research (2006)

See article by Bouvet et al.  [6]  (pages 504–511) in this issue. 

Type 2 diabetes and its complications has become a major public health problem in Western countries. The number of diabetic patients in the world is estimated to be about 200 million, and prevalence of type 2 diabetes will increase not only in the West due to overweight and obesity epidemics, but also in emergent countries because of changes in eating habits.

In diabetic patients, atherosclerosis develops earlier than in other subjects and accounts for excessive morbidity and mortality [1]. Epidemiological studies have shown that cardiovascular diseases are the first cause of morbidity and mortality in patients with type 2 diabetes: coronary artery disease is increased by 3- to 4-fold, stroke is increased by 1.4- to 2.2-fold, peripheral artery diseases is increased by more than 10-fold, and 75 to 85% of hospitalisations and deaths are due to vascular complications of diabetes. Thus, in the coming years, type 2 diabetes will become the most important cause of morbidity and mortality linked to cardiovascular diseases.

Structural and functional changes in vessels of type 2 diabetic patients have been shown to be predictive of cardiovascular events. Thus, in diabetic patients, medial calcifications of lower limbs are predictive of vascular complications and death [2], and in type 2 diabetic patients with angiographically normal coronary arteries, endothelial dysfunction evidenced by coronary artery constriction induced … 

*Service de Physiologie et d'Explorations Fonctionnelles, Hopital Jean Verdier, Avenue du 14 Juillet, 93140 Bondy, France. Tel.: +33 1 48 02 65 50; fax: +33 1 48 02 65 67. Email address: alain.nitenberg{at}jvr.aphp.fr
Sweet dreams and sour awakenings
Authors: A. D Meyer
Journal: BMJ (2003)

Almost a quarter century ago Roberts and Roberts proposed in the BMJ that liquid medicines for children should be either unsweetened or sweetened with non-acidogenic substances.1 They proved a clear association between sugar sweetened drugs and dental caries in children. Since then others have pointed out the high risk of regularly using preparations containing sugar, particularly for chronically sick children.2

At a health review of a child with severe cerebral palsy, rampant carious teeth were …
Half a million French are infected with hepatitis C virus
Authors: A. Dorozynski
Journal: BMJ (1995)

At least 500000 people in France have been infected with hepatitis C virus, according to a report released last week by the minister of health, Dr Elisabeth Hubert. This is the first time that detailed statistics have been made available to evaluate the number of infections, which were previously estimated at 500000 to two million. The report is the outcome of seven epidemiological surveys carried out over the past two years by teams of experts including virologists and specialists in public health. It was prepared by the national public health network, directed by Professor Jacques Drucker.

The survey found …
Hydrogen peroxide induced changes in membrane potentials in guinea pig ventricular muscle: permissive role of iron
Authors: L. Firek, A. Beresewicz
Journal: Cardiovascular Research (1990)

Study objective – It has been proposed that oxygen free radicals trigger reperfusion arrhythmias. The mechanism of these arrhythmias is not clear. Thus, the effect of H2O2 on cellular action potentials was examined. Design – Trabecular muscles were superfused either with H2O2 alone or with H2O2 in combination with iron ions or an iron chelating agent or various scavengers of oxygen free radicals. The effect of reduction of the superfusate calcium from 1.8 to 0.2 mmol·litre−1 on H2O2 induced changes was also studied. Experimental material – Thin trabecular muscles isolated from the hearts of guinea pigs (200-300 g) of either sex were used. Measurements and main results – H2O2 (0.6 mmol·litre−1) caused a reproducible sequence of changes consisting of an initial increase in plateau height and in action potential duration, followed after 12-14 min by rapid action potential shortening accompanied by resting membrane depolarisation, reduction in action potential amplitude and dV/dtmax, and by occasional appearance of late afterdepolarisations, leading finally to loss of excitability. This sequence of changes was: (1) accelerated by higher concentrations of H2O2, FeCl3 (0.1 mmol·litre−1), and FeCl2 (0.1 mmol·litre−1); (2) prevented by dimethylthiourea (10 mmol·litre−1) and desferrioxamine (2 mmol·litre−1); (3) not influenced by superoxide dismutase (150 units·ml−1), mannitol (5-50 mmol·litre−1) or PBN (50 μmol·litre−1); and (4) not prevented by a reduction of the superfusate calcium. Conclusions – The electrophysiological alterations induced by H2O2 are caused by a hydroxyl radical formed intracellularly in the iron catalysed Fenton reaction.
Papua New Guinea 1979
Authors: JOSEPH H. MAGEE
Journal: Annals of Internal Medicine (1979)

Abroad1 May 1979Papua New Guinea 1979JOSEPH H. MAGEE, M.D.JOSEPH H. MAGEE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-90-5-849 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAs forecast by Professor Ian Maddocks (1), Papua New Guinea achieved self-government on 1 December 1973 and, with the usual numismatic and philatelic acclaim, independence from Australia on 16 September 1975. In common with other ministates of Oceania, it elected British Commonwealth status, with Queen Elizabeth II as nominal sovereign; Milne Bay's Sir John Guise became the first governor general. The health care system remains three-tiered with separate training facilities for aid post orderlies, health extension officers, and medical or dental practitioners. The University of Papua New Guinea's Faculty of Medicine is physically located at the Port Moresby General Hospital,...References1. MADDOCKS I: Papua New Guinea 1973. Ann Intern Med 78:968-969, 1973 LinkGoogle Scholar2. DUGGANPRICE GM: Hypokalemic muscular paresis in migratory Papua New Guineans. Lancet 1:649-651, 1974 CrossrefMedlineGoogle Scholar3. MAGEENARAQI JS: Port Moresby cocktail. Int J Artif Organs 1:59, 1978 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JOSEPH H. MAGEE, M.D.Affiliations: University of Papua New Guinea PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byMichael Alpers (FRS), Kuru, and Papua New Guinea: The Combined Allure of Problem, People, and Place 1 May 1979Volume 90, Issue 5Page: 849-849KeywordsHealth careHealth care facilitiesHospital medicine ePublished: 1 December 2008 Issue Published: 1 May 1979 PDF downloadLoading ...
The Relation of Pneumothorax and Other Air Leaks to Mortality in the Acute Respiratory Distress Syndrome
Authors: John G. Weg, Antonio Anzueto, Robert A. Balk, Herbert P. Wiedemann, Edward N. Pattishall, M. Anthony Schork, Leslie A. Wagner
Journal: New England Journal of Medicine (1998)

In patients with the acute respiratory distress syndrome, pneumothorax and other air leaks — any extrusion of air outside the tracheobronchial tree — have been attributed to high ventilatory pressures or volumes and linked to increased mortality.
Blood test can predict Alzheimer's disease, say US scientists
Authors: J. Wise
Journal: BMJ (2014)

Scientists have developed a blood test that uses 10 markers that they say could be used to predict with 90% accuracy whether someone will develop Alzheimer’s disease within three years.

The research, published as a letter in Nature Medicine , shows how there are differences in 10 blood phospholipids between people with pre-clinical Alzheimer’s (before the symptoms appear) and people who will not go on to develop the condition.1 The phospholipids may represent early degenerative …
Iodine-induced Hypothyroidism Due to Benziodarone (Cardivix)
Authors: M. T. Harrison, A. J. V. Cameron
Journal: BMJ (1965)

Necropsy showed that the immediate cause of death was a large pulmonary embolus.There was moderate left ventricular hyper- trophy, and the kidneys, apart from slight surface granularity, were normal.The right adrenal gland weighed 25 g., being enlarged by the presence of a bright yellow cortical adenoma; the left adrenal was macroscopically normal.Histologically the kidneys showed the changes of benign hypertension, and the adrenal adenoma consisted of large lipid-laden cells resembling zona fascicu- lata and very similar to those illustrated in earlier reports (Milne et al., 1957).