tbuckley/cabot-search huggingface dataset:
Complement-mediated cell death induced by rituximab in B-cell lymphoproliferative disorders is mediated in vitro by a caspase-independent mechanism involving the generation of reactive oxygen species
Authors: Beatriz Bellosillo, Neus Villamor, Armando López-Guillermo, Silvia Marcé, Jordi Esteve, Elias Campo, Dolors Colomer, Emili Montserrat
Journal: Blood (2001)
Mycophenolate mofetil but not atorvastatin attenuates atherosclerosis in lupus-prone LDLr<sup>−/−</sup> mice
Authors: Sander I van Leuven, Yanice V Mendez-Fernandez, Ashley J Wilhelm, Nekeithia S Wade, Curtis L Gabriel, John J Kastelein, Erik S Stroes, Paul P Tak, Amy S Major
Journal: Annals of the Rheumatic Diseases (2011)

Rationale Recent clinical and preclinical studies have demonstrated that systemic lupus erythematosus (SLE) is associated with an increased risk for cardiovascular disease (CVD). However, unlike in the general population, little is known regarding the efficacy of atheroprotective interventions in patients with SLE. The current study aims to determine the benefit of lymphocyte inhibition on reducing the atherosclerotic burden in SLE-susceptible LDLr-deficient mice. Methods Female LDLr −/− mice were lethally irradiated and reconstituted with bone marrow from C57Bl/6 mice (LDLr.B6) or the SLE-susceptible B6. Sle1.2.3 mice (LDLr. Sle ). At 16 weeks post transplant, mice were treated with atorvastatin (10 mg/kg), mycophenolate mofetil (MMF; 40 mg/kg), or both (MMF-A) for 8 weeks, after which the extent of atherosclerosis and the presence of SLE were assessed. Results Following 8 weeks of treatment, we observed that atorvastatin-mediated reduction in cholesterol levels attenuated atherogenesis in LDLr.B6 mice but failed to significantly reduce atherosclerotic lesion size in LDLr. Sle mice, in spite of a significant reduction in serum cholesterol levels. Treatment with MMF and MMF-A attenuated atherogenesis in LDLr.B6 and LDLr. Sle mice. In addition, MMF-containing regimens inhibited recruitment of CD4+ T cells to atherosclerotic lesions in LDLr.Sle mice. In these mice, MMF also reduced the proportion of activated splenic T cells, as well as interleukin 10 secretion by T cells. With regard to lupus activity, MMF had no overt effect on anti-double-stranded DNA (dsDNA) antibody titres or kidney function and pathology. Conclusions The current study demonstrates that reduction of cholesterol levels alone is not atheroprotective in lupus-mediated atherogenesis. This is the first study to demonstrate that MMF reduces the atherosclerotic burden in a model of lupus-accelerated atherosclerosis. Our results suggest that MMF treatment may prove beneficial in preventing CVD in patients with SLE.
Abstract 4017: Identifying Protein-Protein Interactions in Single Protein Complex level by Microchannel Device
Authors: Chao-Kai Chou, Nan Jing, Hirohito Yamaguchi, Pei-Hsiang Tsou, Jun Kameoka, Mien-Chie Hung
Journal: Cancer Research (2010)

Abstract Cancer is the most threaten disease in this country and deregulations of signal pathways are often responsible for the cancer progression. Many mysteries of cancer related signal pathways have been revealed by current molecular biology research and the detection of protein-protein interactions is one of the critical techniques. The general techniques for protein-protein interactions detection include immuno-precipitation, immuno-fluorescence staining, and fluorescence resonant energy transfer. These techniques can detect specific protein in cultured cell and in tissue and have been applied in most biomedical research. However, all of them have various limitations. For instance, only two molecules could be examined in one experiment and the detection usually require long processing time with complicated procedures and large sample amount. Moreover, the detection of signals currently is still relied on X-ray film exposure or eye-direct observation that may limit the sensitivity and accuracy. We are developing a microchannel detection system in order to avoid these defects and to provide rapid and accurate detection in breast cancer signal transduction research. The principle is that nanochannel fluidics could only allow a single protein complex to pass through the detection point of fluorescence spectroscopy during examination and the result from the single protein complex could provide us most direct information of protein-protein interaction. Since the detection level is down to the single protein complex, it could highly increase the detection sensitivity. Currently, we have successful fabricated different size of microchannels and we recognized that top-down fabrication approach on transparent silicon based wafers could provide the best quality nanochannels. The channel was than integrated to the fluorescence spectroscopy for single fluorescence detection. To test the performance of the device, fluorescence antibodies were loaded into the channel and we successfully detected a single fluorescence signal during the experiment. Subsequently, we detect demonstrated that epidermal growth factor receptor (EGFR) interact with its downstream proteins Src and STAT3 in a single complex after epidermal growth factor (EGF) stimulation. However, only 1.8% of EGFR interact with both Src and STAT3 at the same time which suggests that EGFR/Src/STAT3 is a transition product in the dynamic of EGFR signal transduction. Thus, our system provides the interaction information from a single protein complex with the ratio of interactive proteins to dissect the signal transduction in dynamic aspect and will offer an effective technology. 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 4017.
BLOOD TRANSFUSION AND HTLV-I ASSOCIATED MYELOPATHY
Authors: Mitsuhiro Osame, Shuji Izumo, Akihiro Igata, Makoto Matsumoto, Tadashi Matsumoto, Shunro Sonoda, Mitsutoshi Tara, Yoshisada Shibata
Journal: The Lancet (1986)
Cottage Industry to Postindustrial Care — The Revolution in Health Care Delivery
Authors: Stephen J. Swensen, Gregg S. Meyer, Eugene C. Nelson, Gordon C. Hunt, David B. Pryor, Jed I. Weissberg, Gary S. Kaplan, Jennifer Daley, Gary R. Yates, Mark R. Chassin, Brent C. James, Donald M. Berwick
Journal: New England Journal of Medicine (2010)

U.S. health care is broken. Although other industries have transformed themselves using tools such as standardization of value-generating processes, performance measurement, and transparent reporting of quality, the application of these tools to health care is controversial, evoking fears of "cookbook medicine," loss of professional autonomy, a misinformed focus on the wrong care, or a loss of individual attention and the personal touch in care delivery. We believe that public reporting of performance with regard to appropriately designed clinical standards can overcome these concerns. The application of improvement tools is not only essential to modernizing care delivery but also the key . . .
926 NUCLEOSIDE ANALOGUE INDUCED MITOCHONDRIAL TOXICITY WITH MYOPATHY IN CHRONIC HEPATITIS B PATIENTS WITH LONG-TERM CLEVUDINE [1-(2-DEOXY- 2-FLUORO-β-L-ARABINOFURANOSYL) THYMININE, L-FMAU] THERAPY
Authors: S.Y. Park, M.K. Jung, S.W. Jeon, C.M. Cho, W.Y. Tak, Y.O. Kweon, S.K. Kim, Y.H. Choi
Journal: Journal of Hepatology (2009)
OPERATIVE TREATMENT OF CANCER OF THE UTERUS.
Authors: WIILIAM R. PRYOR
Journal: JAMA (1900)

A paper on this subject can not contain anything startlingly new until something additional regarding the nature of cancer has been discovered. Nothwithstanding that this is so, we have gained sufficient experience in its treatment to be able to make a just analysis of the various methods employed, and in this way review as it were our work in combating a disease which in America must destroy 30,000 women annually. We may also find some light in a careful study of the natural history of the disease when left unchecked, and in an analysis of the cases in which recurrence has taken place after operation. Although this paper is not to deal with the etiology of cancer, I can not refrain from calling attention to the burden of proof pointing to the theory that cancer of the uterus is caused by a parasite. And although we can not accept without
Initial effects of the grounding of the tanker Braer on health in Shetland. The Shetland Health Study Group.
Authors: D Campbell, D Cox, J Crum, K Foster, P Christie, D Brewster
Journal: BMJ (1993)

OBJECTIVE--To determine if the oil spillage from the tanker Braer had any immediate health effects on the exposed resident population. DESIGN--Cohort study with a comparison against controls, exposure status being assigned on the basis of geographical location. SETTING--Rural Shetland. SUBJECTS--All those resident on or after 5 January 1993 (day 0) within 4.5 km of the site of tanker9s grounding. Controls matched for sex and age were drawn from a general practice list 95 km distant. OUTCOME MEASURES--Demographic details; smoking and alcohol consumption; perception of health and reported presence or absence of specific symptoms; peak expiratory flow; results of haematology, liver and renal function tests, and blood and urine toxicology. RESULTS--Of subjects contacted, 420 (66%) exposed people and 92 (68%) controls were studied; 56 non-attenders were surveyed. Principal health effects arose on days 1 and 2 and were headache, throat irritation, and itchy eyes. No significant differences between those exposed and controls were found for any of the biological markers. Toxicological studies did not show any exposures that are known to affect human health. CONCLUSIONS--The study confirmed the anecdotal reports of certain acute symptoms. No evidence of pulmonary, haematological, renal, or hepatic damage was detected at the population level. Toxicological samples from exposed people did not find levels known to affect human health. Further studies are required to ascertain whether there have been any long term effects on the population.
Senescence-associated phenotypes in Akita diabetic mice are enhanced by absence of bradykinin B2 receptors
Authors: Masao Kakoki, Catherine M. Kizer, Xianwen Yi, Nobuyuki Takahashi, Hyung Suk Kim, C. Robert Bagnell, Cora Jean S. Edgell, Nobuyo Maeda, J. Charles Jennette, Oliver Smithies
Journal: Journal of Clinical Investigation (2006)

We have previously reported that genetically increased angiotensin-converting enzyme levels, or absence of the bradykinin B2 receptor, increase kidney damage in diabetic mice. We demonstrate here that this is part of a more general phenomenon - diabetes and, to a lesser degree, absence of the B2 receptor, independently but also largely additively when combined, enhance senescence-associated phenotypes in multiple tissues. Thus, at 12 months of age, indicators of senescence (alopecia, skin atrophy, kyphosis, osteoporosis, testicular atrophy, lipofuscin accumulation in renal proximal tubule and testicular Leydig cells, and apoptosis in the testis and intestine) are virtually absent in WT mice, detectable in B2 receptor-null mice, clearly apparent in mice diabetic because of a dominant mutation (Akita) in the Ins2 gene, and most obvious in Akita diabetic plus B2 receptor-null mice. Renal expression of several genes that encode proteins associated with senescence and/or apoptosis (TGF-beta1, connective tissue growth factor, p53, alpha-synuclein, and forkhead box O1) increases in the same progression. Concomitant increases occur in 8-hydroxy-2'-deoxyguanosine, point mutations and deletions in kidney mitochondrial DNA, and thiobarbituric acid-reactive substances in plasma, together with decreases in the reduced form of glutathione in erythrocytes. Thus, absence of the bradykinin B2 receptor increases the oxidative stress, mitochondrial DNA damage, and many senescence-associated phenotypes already present in untreated Akita diabetic mice.
A piece of my mind. Morning distort
Authors: F. L. Brancati
Journal: JAMA (1991)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
A phase I study of recombinant human C1 inhibitor in asymptomatic patients with hereditary angioedema
Authors: Martijn B.A. van Doorn, Jacobus Burggraaf, Tijtje van Dam, Anke Eerenberg, Marcel Levi, Cornelis E. Hack, Rik C. Schoemaker, Adam F. Cohen, Jan Nuijens
Journal: Journal of Allergy and Clinical Immunology (2005)
ICOS Receptor Instructs T Follicular Helper Cell versus Effector Cell Differentiation via Induction of the Transcriptional Repressor Bcl6
Authors: Youn Soo Choi, Robin Kageyama, Danelle Eto, Tania C. Escobar, Robert J. Johnston, Laurel Monticelli, Christopher Lao, Shane Crotty
Journal: Immunity (2011)

The nature of follicular helper CD4+ T (Tfh) cell differentiation remains controversial, including the minimal signals required for Tfh cell differentiation and the time at which Tfh cell differentiation occurs. Here we determine that Tfh cell development initiates immediately during dendritic cell (DC) priming in vivo. We demonstrate that inducible costimulator (ICOS) provides a critical early signal to induce the transcription factor Bcl6, and Bcl6 then induces CXCR5, the canonical feature of Tfh cells. Strikingly, a bifurcation between Tfh and effector Th cells was measurable by the second cell division of CD4+ T cells, at day 2 after an acute viral infection: IL2Rαint cells expressed Bcl6 and CXCR5 (Tfh cell program), whereas IL2Rαhi cells exhibited strong Blimp1 expression that repressed Bcl6 (effector Th cell program). Virtually complete polarization between Bcl6+ Tfh cells and Blimp1+ effector Th cell populations developed by 72 hr, even without B cells. Tfh cells were subsequently lost in the absence of B cells, demonstrating a B cell requirement for maintenance of Bcl6 and Tfh cell commitment via sequential ICOS signals.
DIABETIC COMA COMPLICATED BY ACUTE RETENTION OF URINE
Authors: HENRY J. JOHN
Journal: JAMA (1925)

Since insulin has been available, the hopeless aspect of coma in diabetic patients has been greatly diminished. We can now safely say that if insulin is administered soon after coma has developed, the patient will probably recover; whereas, after ten or more hours of deep coma, insulin is of little avail. In the latter case, even though the blood sugar is reduced and the chemical acidosis of the blood is partly cleared up, the patient dies. The toxic products of the acetone bodies affect especially the cardiac muscle, and cardiac failure is quite a common immediate cause of death in these cases. Thus, early and controlled treatment with insulin, together with digitalization of the heart muscle, emptying the intestinal tract, keeping the body warm, and the intravenous injection of glucose to supply both food and liquids to the body still remain our best therapeutic aids. In one of my cases
Spectral analysis of canine epicardial electrogram. Short-term variations in the frequency content induced by myocardial ischemia.
Authors: V Mor-Avi, S Akselrod
Journal: Circulation Research (1990)

Power spectra of epicardial electrograms were studied in 13 anesthetized dogs subjected to occlusion of the left anterior descending coronary artery. Electrograms were obtained from a bipolar electrode placed on the epicardial surface of the left ventricle and recorded before and after coronary occlusion. After digitization, power spectra of the first and every 50th subsequent waveform were evaluated and compared with the power spectrum of the average waveform obtained from the baseline recording. In particular, we examined variations in relative power content in three frequency ranges: 150-250 Hz, previously shown to be directly affected by myocardial ischemia; 40-150 Hz, presumably corresponding to the fine notches and slurs on the body surface QRS; and 2-40 Hz, the low-frequency range. Apart from a mild initial rise during the first 50 heart beats, the power in the high-frequency range gradually decreased, reaching 5% of the control value at wave 500. The power in the mid-frequency range showed a monotonous decrease after the occlusion and reached 16% of the control. The power in the low-frequency range showed a gradual buildup to 140% of the control after 500 heart beats. Therefore, ischemia causes a shift of the high-frequency spectral components of the local electrographic waveform to lower frequencies. Our findings and the fact that body surface ECG is produced by spatial summation of local electric potentials over the different regions of the myocardial tissue may explain two previously described effects of acute myocardial ischemia on the body surface ECG complex. First, local loss of spectral components in the range 150-250 Hz may produce a zone of reduced amplitude within a QRS complex band-pass filtered in this range. Second, displacement of power in the frequency domain may suggest an explanation to the increased incidence of visible notches and slurs on the surface QRS complex, characteristic to various myocardial pathologies.
Abstract 1702: S-adenosyl-L-methionine induces P-glycoprotein overexpression and drug resistance in human cancer cells
Authors: Tsun Yee Tsang, Chi Lam Au Yeung, Pak Lun Yau, Tim Tak Kwok
Journal: Cancer Research (2011)

Abstract P-glycoprotein (Pgp) overexpression is frequently associated with multidrug resistance in cancer cells. Pgp is an efflux pump and is encoded by human mdr1 gene. The expression of mdr1 may be regulated by promoter methylation catalyzed by DNA methyltransferases (DNMTs). S-adenosyl-L-methionine (SAMe) is an important cofactor of DNMTs. Although SAMe has been shown to regulate promoter methylation of various genes, the effect of SAMe on Pgp expression and chemosensitivity of cancer cells are however not known. The aim of the present study is to examine the role of SAMe in the regulation of Pgp expression and drug sensitivity of human cancer cells. By qRT-PCR and Western blot analyses, incubation with 1mg/ml SAMe for 24h was found to increase mdr1 mRNA and Pgp protein levels in human hepatocellular carcinoma HepG2 cells, human colorectal adenocarcinoma CaCO-2 cells and human leukemia Jurkat-T cells. Methylation specific PCR and bisulfite DNA sequencing analyses revealed that the SAMe treatment induces hypomethylation of mdr1 promoter. Moreover, SAMe decreased intracellular doxorubicin accumulation and increased doxorubicin resistance in human cancer cells as assessed by doxorubicin accumulation assay and MTT assay. Furthermore, in human colorectal carcinoma HCT-116 parent cells and DNMTs knock-out sublines, SAMe induced Pgp expression in HCT-116 parent and DNMT3b knock-out subline but not in DNMT1 and DNMT1/DNMT3b double knockout sublines. The results from the present study therefore suggest that SAMe induces hypomethylation of mdr1 promoter, Pgp expression, and thus drug resistance in human cancer cells. Furthermore, DNMT1 appeared to be important in the effect of SAMe on mdr1. 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 1702. doi:10.1158/1538-7445.AM2011-1702
Helicobacter pylori infection in childhood: risk factors and effect on growth
Authors: P Patel, M A Mendall, S Khulusi, T C Northfield, D P Strachan
Journal: BMJ (1994)

<h3>Abstract</h3> <b>Objective</b>: To investigate the current prevalence of Helicobacter pylori infection in childhood, the risk factors for infection, and the effect of infection on growth in preadolescent schoolchildren. <b>Design</b>: Population based sample of 7 year old schoolchildren followed up at age 11; data on risk20factors for infection collected at age 7; presence of infection at age 11 determined by measurement of salivary IgG against H pylori by a newly developed enzyme linked immunosorbent assay (ELISA). Height was measured at 7 and 11 years of age. <b>Subjects</b>: 554 schoolchildren from Edinburgh. <b>Results</b>: 62 (11%) children had H pylori infection.20Independent risk factors for infection were single parent families (adjusted odds ratio=2.5; 95% confidence interval 1.1 to 5.7), the 10% most crowded homes (3.1; 1.3 to 7.2), and schools serving predominantly rented housing estates (2.5; 1.0 to 6.5). School catchment area was more important than parental social class or housing tenure. Growth in height between 7 and 11 was diminished in infected children by a mean of 1.1 cm (0.3 to 2.0 cm) over four years. This growth reduction was largely confined to girls (1.6 cm over four years), among whom it correlated with salivary IgG (P=0.015). <b>Conclusion</b>: Data from salivary assay to investigate the epidemiology of H pylori suggest that factors relating to the type of community in which the child lives may now be as important for acquisition of this infection as features of the family home. The greater reduction of growth among infected girls raises the possibility that H pylori infection may delay or diminish the pubertal growth spurt.
Inducible inactivation ofNotch1 causes nodular regenerative hyperplasia in mice
Authors: Adrien Croquelois, Alex Blindenbacher, Luigi Terracciano, Xueya Wang, Igor Langer, Freddy Radtke, Markus H. Heim
Journal: Hepatology (2005)

The discovery that the human Jagged1 gene (JAG1) is the Alagille syndrome disease gene indicated that Notch signaling has an important role in bile duct homeostasis. The functional study of this signaling pathway has been difficult because mice with targeted mutations in Jagged1, Notch1, or Notch2 have an embryonic lethal phenotype. We have previously generated mice with inducible Notch1 disruption using an interferon-inducible Cre-recombinase transgene in combination with the loxP flanked Notch1 gene. We used this conditional Notch1 knockout mouse model to investigate the role of Notch1 signaling in liver cell proliferation and differentiation. Deletion of Notch1 did not result in bile duct paucity, but, surprisingly, resulted in a continuous proliferation of hepatocytes. In conclusion, within weeks after Notch1 inactivation, the mice developed nodular regenerative hyperplasia without vascular changes in the liver. (HEPATOLOGY 2005;41:487–496.)