tbuckley/cabot-search huggingface dataset:
Superior Demonstration of Splenosis by Heat-Denatured Tc-99m Red Blood Cell Scintigraphy Compared With Tc-99m Sulfur Colloid Scintigraphy
Authors: Ian Hagan, Richard Hopkins, Iain Lyburn
Journal: Clinical Nuclear Medicine (2006)

A 41-year-old woman who had undergone splenectomy 24 years previously after a road traffic accident was investigated for deranged liver function tests after an upper respiratory tract infection. Subsequent serology confirmed acute Epstein-Barr virus infection. Abdominal ultrasound demonstrated a solid nodule between the liver and right kidney. Computed tomography (CT) of the abdomen identified 5 further nodules around the stomach and in the lower abdomen. A Tc-99m sulfur colloid study was performed to confirm a suspected diagnosis of splenosis. Uptake could be clearly identified in only 3 of the nodules, so a Tc-99m heat-denatured red blood cell (RBC) study was undertaken. This showed clear uptake in all of the identified nodules as well as uptake in smaller nodules not perceived on CT, thus confirming the diagnosis of splenosis and demonstrating the superior sensitivity of heat-denatured RBC scintigraphy in the identification of heterotopic splenic tissue.
Age at death from cystic fibrosis.
Authors: P. A. Lewis
Journal: BMJ (1989)

babies have?Emery has suggested that these babies may have been more likely to have been admitted to a special care baby unit, where they will usually have been placed prone.6My recently born first child (boy, born in winter, of low birth weight) was placed supine bearing in mind our own work on sleeping position and the risk associated with these other characteristics.A few weeks later, however, he had an acute upper respiratory tract infection which he could sleep through only if placed prone.He has had another infection since then and is currently in the throes of his third.On each occasion he could comfortably sleep only in the prone position and he always sleeps prone now.I note that the only two control babies in the Hong Kong study who were normally placed supine were in hospital.Is the reason that some Chinese families break an almost universal cultural norm and place their babies prone to do with the fact that those babies have acute upper respiratory tract infections or other conditions which might make sleeping supine difficult-and is this the "cause" of their increased risk of cot death rather than the sleeping position itself?
1138-42 13-year follow-up of the German angioplasty surgery investigation
Authors: Jan Kaehler, Ralf Koester, Hans-Juergen Rupprecht, Thomas Ischinger, Roland Jahns, Albrecht Vogt, Martin Lampen, Rainer Hoffmann, Thomas Meinertz, Christian W Hamm
Journal: Journal of the American College of Cardiology (2004)
Expression profiling of persistent polyclonal B-cell lymphocytosis suggests constitutive expression of the AP-1 transcription complex and downregulation of Fas-apoptotic and TGFβ signalling pathways
Authors: C H Lawrie, R Shilling, X Troussard, H Cattan, H Mossafa, F Pezzella, J Boultwood, J S Wainscoat, C S R Hatton
Journal: Leukemia (2008)
NHS devolved to Scotland and Wales
Authors: J. Warden
Journal: BMJ (1997)

Differences in the way that the health service is run in England, Scotland, and Wales will increase further when its functions are devolved to separate elected bodies within the next three years. Government proposals for a Scottish parliament and a Welsh assembly, subject to referendums in September, will transfer responsibility for health from the respective secretaries of state and the British government.

The Scottish parliament especially will have direct legislative power on most health matters, including the NHS, its funding, medical …
In vivo and in vitro exposure to PCB 153 reduces long-term potentiation.
Authors: R J Hussain, J Gyori, A P DeCaprio, D O Carpenter
Journal: Environmental Health Perspectives (2000)

We examined the effects of gestational and lactational exposure to polychlorinated biphenyl (PCB) 153 (2,4,5,2',4',5'-hexaCB) on the magnitude of long-term potentiation (LTP) observed in the CA1 region of hippocampal brain slices prepared from rats at 30 days of age. We compared these actions to those observed when PCB 153 is dissolved in normal Krebs-Ringer solution and perfused on slices from control rats of the same age. In vivo exposure was at three dose levels (1. 25, 5, and 20 mg/kg/day) from gestational day 3 through weaning at postnatal day 21. Although responses to low-frequency stimulation of the Schaffer collateral pathway in exposed animals were not different from controls, significantly reduced LTP was induced after tetanic stimulation, even at the lowest dose studied. We observed a comparable depression of LTP when control slices were perfused with Krebs-Ringer that had been equilibrated with PCB 153 in a generator column. Neither in vivo nor in vitro exposure significantly altered the input-output curves obtained before tetanic stimulation, but both suppressed the increase in response observed in controls after tetanic stimulation. Because LTP is thought to be correlated with learning ability, these observations may provide at least a partial mechanism to explain the reduction of intelligence quotient observed in humans exposed to PCBs early in development.
Abstract 1054: S100B affects cell signaling in malignant melanoma
Authors: Kira Gianni, Michele I. Vitolo, Paul T. Wilder, Stuart S. Martin, David J. Weber
Journal: Cancer Research (2011)

Abstract Establishing the mechanism by which S100B effects ERK and its downstream proteins will provide valuable insight into the role of S100B in the progression of melanoma and potentially aid in developing new pharmacological drugs. S100B is a 21.5 kDa symmetric homodimer that is highly conserved and expressed in a number of tissues and cell lines, including melanocytes. Generally, low levels of S100B have trophic effects, while higher levels are problematic, as is the case in human malignant melanoma. S100B is an effective and widely used prognostic marker for malignant melanoma, with increased levels of serum S100B being predictive of disease stage, increased recurrence, and low overall survival. It has previously been found that S100B directly interacts with the tumor suppressor protein p53, down-regulating its protein levels, thereby allowing damaged cells to proliferate and mutations to propagate. S100B has also been implicated in several other signaling pathways, including the MAPK pathway (BRAF-MEK-ERK). The initial hypothesis tested was that S100B inhibits the phosphorylation of ERK targets in a calcium-dependent manner. To evaluate the significance of S100B in melanoma cell lines, stable S100B knock-down clones were created using lentiviral shRNA particles. The extent of the knock-down varies among the clones and shows a correlation between the level of remaining S100B and the level of phosphorylated ERK, where the clone with the least amount of S100B also has the lowest level of phosphorylated ERK. The clones also display a decreased rate of proliferation measured with both an MTT based assay, as well as with electrical impedance. Over-expression studies were also conducted where normal human S100B, but not a mutant S100B incapable of binding calcium, results in increased phosphorylated ERK, but decreased phosphorylated RSK at Thr573. To determine if S100B was interacting with RSK directly, pull-down assays were performed, and RSK was detected in S100B pull-downs in the presence of calcium; however, it was not detected in the presence of the calcium chelator EDTA. In conclusion, we demonstrate that the calcium-binding protein S100B affects the MAPK pathway by simultaneously increasing phosphorylated ERK and decreasing phosphorylated RSK, together which are consistent with the increased growth rates and cancer progression. 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 1054. doi:10.1158/1538-7445.AM2011-1054
Abstract 3180: Altered β-catenin phosphorylation pattern in human prostate cancer
Authors: Cheng Du, Chuanyou Zhang, Md. Helal U. Biswas, K.C. Balaji
Journal: Cancer Research (2010)

Abstract Protein kinase D1 (PKD1) phosphorylates β-catenin at Thr112 and Thr120. The phosphorylation is required for β-catenin membrane trafficking via trans Golgi network (TGN). Data presented in this study indicate that activation of PKD1 shrinks the cytoplasmic pool of β-catenin which mainly is the non-phosphorylation (S33/S37/T41/S45) isoform of β-catenin, suggesting that PKD1 interacts with Wnt/GSK3β signaling pathway. The phosphorylated Thr120 β-catenin (pT120) isoform predominately locates at membrane fraction in cultured prostate cancer cell line C4-2. A newly developed phospho-threonine antibody specifically targeting the pT120 of β-catenin shows accumulation of pT120 β-catenin in TGN in normal prostate tissues. Our study demonstrates that distribution of Thr120 phosphorylated β-catenin is distinct in normal and malignant prostate tissues. In 16/22 (72%) of normal prostate tissues, the pT120 β-catenin is enriched at TGN. In contrast, only 15/200 (7.5%; p &amp;lt; 0.001) of prostate cancer samples had accumulation of pT120 β-catenin in TGN. A vast majority of cancer samples (92.5%) lacking of TGN staining shows the pT120 β-catenin distributed diffusely in cytoplasm, nucleus and plasma membrane. can be more discriminatory compared to conventional β-catenin antibody staining. We propose that β-catenin T120 phosphospecific antibody can be used to study alteration in subcellular distribution of β-catenin and possibly as biomarker in prostate and other tissues, which may facilitate risk stratification or predict disease outcomes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3180.
1072-215 Depressive symptoms are associated with reduced heart rate variability in individuals without coronary artery disease
Authors: Viola Vaccarino, Rachel Lampert, Forrester Lee, J.Douglas Bremner, Jerome L Abramson, Nancy Murrah, Nadeem Afzal, Faiz A Cheema, Jack Goldberg
Journal: Journal of the American College of Cardiology (2004)
Glia Maturation Factor Gamma (GMFG): A Cytokine-Responsive Protein During Hematopoietic Lineage Development and Its Functional Genomics Analysis
Authors: Ying Shi, Ling Chen, Lance A. Liotta, Hong-Hui Wan, Griffin P. Rodgers
Journal: Genomics Proteomics & Bioinformatics (2006)

Abstract Human hematopoiesis was evaluated using the techniques of controlled stem cell differentiation, two-dimensional gel electrophoresis-based proteomics, and functional genomics. We provide the first report that glia maturation factor gamma (GMFG) is a cytokine-responsive protein in erythropoietin-induced and granulocyte-colony stimulating factor-induced hematopoietic lineage development. Results from global functional genomics analysis indicate that GMFG possesses several other features: hematopoietic tissue-specific gene expression, a promoter concentrated with high-score hematopoiesis-specific transcription factors, and possible molecular coevolution with a rudimentary blood/immune system. On the basis of our findings, we hypothesize that GMFG is a hematopoietic-specific protein that may mediate the pluripotentiality and lineage commitment of human hematopoietic stem cells.
SHARP Project has detected new HIV diagnoses
Authors: L. Sathia, S. Duncan
Journal: BMJ (2011)

NK cells express an activating FcR (FcγRIIIa) that mediates Ab-dependent cellular cytotoxicity and the production of immune modulatory cytokines in response to Ab-coated targets. IL-21 has antitumor activity in murine models that depends in part on its ability to promote NK cell cytotoxicity and IFN-γ secretion. We hypothesized that the NK cell response to FcR stimulation would be enhanced by the administration of IL-21. Human NK cells cultured with IL-21 and immobilized IgG or human breast cancer cells coated with a therapeutic mAb (trastuzumab) secreted large amounts of IFN-γ. Increased secretion of TNF-α and the chemokines IL-8, MIP-1α, and RANTES was also observed under these conditions. NK cell IFN-γ production was dependent on distinct signals mediated by the IL-21R and the FcR and was abrogated in STAT1-deficient NK cells. Supernatants derived from NK cells that had been stimulated with IL-21 and mAb-coated breast cancer cells were able to drive the migration of naive and activated T cells in an in vitro chemotaxis assay. IL-21 also enhanced NK cell lytic activity against Ab-coated tumor cells. Coadministration of IL-21 and Ab-coated tumor cells to immunocompetent mice led to synergistic production of IFN-γ by NK cells. Furthermore, the administration of IL-21 augmented the effects of an anti-HER2/<i>neu</i> mAb in a murine tumor model, an effect that required IFN-γ. These findings demonstrate that IL-21 significantly enhances the NK cell response to Ab-coated targets and suggest that IL-21 would be an effective adjuvant to administer in combination with therapeutic mAbs.
Teaching laparoscopic surgery: the need for guidelines
Authors: C M S Royston, M R J Lansdown, W A Brough
Journal: BMJ (1994)

There is a risk that minimally invasive surgery will fall into disrepute unless adequate steps are taken to reassure the public. Some form of accreditation after a recognised training scheme would go a long way towards allaying these fears. The cost of training surgeons must be addressed. Adequate training will probably pay dividends in reduced litigation. The royal colleges should be responsible for maintaining standards of teaching on recognised courses, setting criteria for accreditation, and supervising a national audit of all laparoscopic procedures.Laparoscopy was introduced to the UK in 1989. Today, about 33% of surgeons performing laparoscopic cholecystectomy were self-taught. No guidelines for laparoscopic procedures exist. Perforation of the bowel during laparoscopy causing peritonitis and death of a London woman resulted in private London hospitals requiring consultant surgeons to have accreditation before performing laparoscopic procedures. Some trust hospitals bar surgeons who have had problems with these procedures from performing any laparoscopy. The Royal College of Surgeons and surgical societies interested in minimally invasive surgery should be responsible for laparoscopic training and accreditation of surgeons. They would need to establish criteria for accreditation and a mechanism of appeal for surgeons who fail accreditation. Such action would allay public anxieties. 3 consultant surgeons have taught courses for laparoscopic cholecystectomy and laparoscopic hernia repair. They have done demonstrations or proctorships at 29 UK hospitals. These surgeons suggest that the ideal training for a laparoscopic procedure includes, in order, a video, a pelvitrainer, hands-on training, and training under an experienced surgeon at his/her hospital (proctorship). It is best if at least 2 surgeons from the same hospital undergo the training simultaneously. After successful completion of training as deemed by the proctor, the trainee should receive accreditation. The surgeons advise that laparoscopic training first be limited to consultant surgeons until there are enough trained surgeons who can train junior surgeons. The UK government has set up 3 minimally invasive centers in London, Leeds, and Scotland, where commercial companies instead of the Royal College of Surgeons will do the training. A comprehensive evaluation should be conducted to determine true incidence of mortality and complications.
Abstract 3091: A sumoylation-dependent transcriptional subprogram is required for Myc-driven tumorigenesis
Authors: Jessica D. Kessler, Kristopher T. Kahle, Tingting Sun, Kristen L. Meerbrey, Michael R. Schlabach, Earlene M. Schmitt, Samuel O. Skinner, Qikai Xu, Mamie Z. Li, Zachary C. Hartman, Mitchell Rao, Peng Yu, Rocio Dominguez-Vidana, Anthony C. Liang, Nicole L. Solimini, Ronald J. Bernardi, Bing Yu, Tiffany Hsu, Ido Golding, Ji Luo, C. Kent Osborne, Chad Creighton, Susan G. Hilsenbeck, Rachel Schiff, Chad A. Shaw, Stephen J. Elledge, Thomas F. Westbrook
Journal: Cancer Research (2012)

Abstract Myc is an oncogenic transcription factor frequently dysregulated in human malignancies. While the transcriptional programs and other functions of Myc have been intensively studied, there remains no effective strategy for inhibiting Myc in patients. To search for pathways that support the Myc oncogenic program, we employed a next-generation RNAi screen for Myc-synthetic lethal (MySL) genes. Using this strategy, we have identified several cellular processes required to tolerate oncogenic Myc. Key among these is the core sumoylation machinery, and we define the Sumo-activating enzyme (SAE) as a central component in this MySL network. Loss of SAE drives synthetic lethality with Myc, and the enzymatic activity of SAE is required to support the Myc oncogenic state. Inactivation of SAE leads to mitotic catastrophe and cell death selectively upon Myc hyper-activation. Mechanistically, depletion of SAE switches a subprogram of Myc transcriptional targets governing mitotic spindle function from activated to repressed, a subprogram we term Sumoylation-dependent Myc Switchers, or SMS genes. Notably, SMS genes are required to tolerate Myc hyper-activation, and SAE and the SMS program are required for Myc-dependent breast cancer cell survival in vitro and tumor growth and progression in vivo. Importantly, patient survival significantly correlates with levels of SAE and SMS gene expression in Myc-high tumors. Collectively, these studies reveal a mitotic vulnerability of Myc-driven cancers and demonstrate that inhibiting sumoylation can selectively impair mitosis and survival in an oncogenic Myc-dependent manner. We propose that drugs targeting SAE and its downstream SMS targets may have therapeutic benefits for patients with Myc-driven cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3091. doi:1538-7445.AM2012-3091
Letter: Treatment of aspergillosis.
Authors: R H George, A J Bint
Journal: BMJ (1974)

together with uterine contractions and signs of fetal irritability.Relief was achieved with a pethidine injection.The relationship of the heparin injection to the uterine contraction was noticed but we decided to continue the treatment.After the second dose of heparin six hours later the patient immediately had the same abdominal pain, which was again relieved by pethidine.At this point we became sure that the uterine contractions were due to the heparin injections.Heparin was stopped, no other anticoagulants were given, and the patient was treated conservatively.So far as we know no such reaction to heparin has been reported before.We thought of a small retroplacental haemorrhage due to heparin as a possible cause of pain, but the speed of the reaction and the relatively small dose of heparin and absence of complications afterwards made this un- likely.-Weare, etc.,
Sacral Neuromodulation for Refractory Lower Urinary Tract Dysfunction: Results of a Nationwide Registry in Switzerland
Authors: Thomas M. Kessler, Eric Buchser, Sylvain Meyer, Daniel S. Engeler, Abdul-Wahab Al-Khodairy, Ulf Bersch, Christophe E. Iselin, Bruno Roche, Daniel M. Schmid, Brigitte Schurch, Stephane Zrehen, Fiona C. Burkhard
Journal: European Urology (2006)
Islamic Bioethics at the End of Life: Why<i>Mukallaf</i>Status Cannot Be the Criterion of Defining the Life That Should Be Saved
Authors: Shahram Ahmadi Nasab Emran
Journal: The American Journal of Bioethics (2015)

In the absence of serious methodological works on Islamic bioethics, the work by Padela and Mohiuddin (2015) with their effort in constructing an Islamic approach to end-of-life issues is timely an...
Immune system versus tumor: shifting the balance in favor of DCs and effective immunity
Authors: Howard L. Kaufman, Mary L. Disis
Journal: Journal of Clinical Investigation (2004)

Despite the initial excitement over cancer vaccines, the clinical effectiveness of immunotherapy has been disappointing. The suppressive milieu present within established tumors inhibits effective immune responses, although new strategies are emerging to manipulate the local tumor microenvironment and shift the balance back to a proinflammatory environment, promote DC activation, and enhance tumor immunity .
Staging Non-Hodgkin Lymphoma
Authors: J. O. Armitage
Journal: CA A Cancer Journal for Clinicians (2005)

Non-Hodgkin Lymphomas are always treatable and frequently curable malignancies. However, choosing the most appropriate therapy requires accurate diagnosis and a careful staging evaluation. New patients with non-Hodgkin Lymphoma should have their tumors classified using the World Health Organization classification. The specific choice of therapy is dependent on a careful staging evaluation. Patients with non-Hodgkin Lymphoma are assigned an anatomic stage using the Ann Arbor system. However, patients should also be classified using the International Prognostic Index. New insights into the biology of the lymphomas in the coming years might well improve our ability to evaluate patients and choose therapy.
Marfan syndrome and mitral valve prolapse
Authors: Arthur E. Weyman, Marielle Scherrer-Crosbie
Journal: Journal of Clinical Investigation (2004)

Mitral valve prolapse (MVP), an abnormal displacement into the left atrium of a thickened and redundant mitral valve during systole, is a relatively frequent abnormality in humans and may be associated with serious complications. A recent study implicates fibrillin-1, a component of extracellular matrix microfibrils, in the pathogenesis of a murine model of MVP. This investigation represents an initial step toward understanding the mechanisms involved in human MVP disease and the development of potential treatments.
Salt-Losing Nephritis
Authors: Arthur H. Levere, Laurence G. Wesson
Journal: New England Journal of Medicine (1956)

THE phenomenon of excessive loss of salt in the urine of patients with chronic Bright's disease has been known for many years. Peters and his coworkers,1 in 1929, described patients with renal disease who had excessive excretion of chloride in the urine in spite of markedly decreased serum chloride concentrations. By giving large amounts of salt, they found it possible to maintain serum chloride at normal values. They suggested that in some cases of nephritis salt deprivation was dangerous and, indeed, recommended supplemental sodium chloride to prevent salt depletion.In 1944 Thorn, Koepf and Clinton2 first reported the clinical implications . . .
CIRCULATING MICRO-RNA 133A AS PREDICTOR OF MYOCARDIAL SALVAGE AND CLINICAL PROGNOSIS IN PATIENTS WITH ACUTE REPERFUSED ST-ELEVATION MYOCARDIAL INFARCTION
Authors: Ingo Eitel, Patrick Dieterich, Volker Adams, Georg Fuernau, Phillip Lurz, Steffen Desch, Suzanne de Waha, Gerhard Schuler, Holger Thiele
Journal: Journal of the American College of Cardiology (2012)