tbuckley/cabot-search huggingface dataset:
Cafestol, the cholesterol-raising factor in boiled coffee, increases serum cholesterol levels in apolipoprotein E*3-leiden transgenic mice by suppression of bile acid synthesis
Authors: B. de Roos, S.M. Post, M. Vermeulen, L. Afman, M.C. Jong, V.E.H. Dahlmans, L.M. Havekes, F. Stellaard, M.B. Katan, H.M.G. Princen
Journal: Circulation (1999)
Fatal infantile cardioencephalomyopathy with COX deficiency and mutations in SCO2, a COX assembly gene
Authors: Lefkothea C. Papadopoulou, Carolyn M. Sue, Mercy M. Davidson, Kurenai Tanji, Ichizo Nishino, James E. Sadlock, Sindu Krishna, Winsome Walker, Jeanette Selby, D. Moira Glerum, Rudy Van Coster, Gilles Lyon, Emmanuel Scalais, Roger Lebel, Paige Kaplan, Sara Shanske, Darryl C. De Vivo, Eduardo Bonilla, Michio Hirano, Salvatore DiMauro, Eric A. Schon
Journal: Nature Genetics (1999)
Some people are at very low risk from heart disease
Authors: Scott Gottlieb
Journal: BMJ (1999)

Individuals at the lowest risk from three major risk factors for cardiovascular disease are significantly less likely to die from myocardial infarction or stroke than those at average risk, according to an analysis of the results of two long term studies.

The risk factors considered were lipid concentrations, blood pressure, and cigarette use ( JAMA 1999;282:2012-8).

Lead author Jeremiah Stamler, of Northwestern University Medical School, Chicago, and colleagues, analysed data from five groups of patients who participated in two long term studies of cardiovascular and non-cardiovascular mortality and life expectancy—the multiple risk factor intervention trial and the Chicago Heart Association detection project in industry.

A total of 72 144 men aged 35 to 39 years and 270 671 men aged 40 to 57 participated in the risk factor intervention trial. Information was available from three groups in the …
Prolonged elevation of serum granulysin in drug-induced hypersensitivity syndrome
Authors: N. Saito, R. Abe, N. Yoshioka, J. Murata, Y. Fujita, H. Shimizu
Journal: British Journal of Dermatology (2012)

Journal Article Prolonged elevation of serum granulysin in drug‐induced hypersensitivity syndrome Get access N. Saito, N. Saito Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Search for other works by this author on: Oxford Academic Google Scholar R. Abe, R. Abe Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Riichiro Abe. E‐mail:aberi@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar N. Yoshioka, N. Yoshioka Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Search for other works by this author on: Oxford Academic Google Scholar J. Murata, J. Murata Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Fujita, Y. Fujita Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Search for other works by this author on: Oxford Academic Google Scholar H. Shimizu H. Shimizu Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7, Kita‐ku, Sapporo 060‐8638, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 167, Issue 2, 1 August 2012, Pages 452–453, https://doi.org/10.1111/j.1365-2133.2012.10921.x Published: 01 August 2012
Missing women--revisited
Authors: A. Sen
Journal: BMJ (2003)

<h3>Abstract</h3> Telomeres are bound by dedicated protein complexes, like shelterin in mammals, which protect telomeres from DNA damage. In the nematode <i>Caenorhabditis elegans</i>, a comprehensive understanding of the proteins interacting with the telomere sequence is lacking. Here, we harnessed a quantitative proteomics approach to screen for proteins binding to <i>C. elegans telomeres</i>, and identified TEBP-1 and TEBP-2, two paralogs that associate to telomeres in vitro and in vivo. TEBP-1 and TEBP-2 are expressed in the germline and during embryogenesis. <i>tebp-1</i> and <i>tebp-2</i> mutants display strikingly distinct phenotypes: <i>tebp-1</i> mutants have longer telomeres than wild-type animals, while <i>tebp-2</i> mutants display shorter telomeres and a mortal germline, a phenotype characterized by transgenerational germline deterioration. Notably, <i>tebp-1</i>; <i>tebp-2</i> double mutant animals have synthetic sterility, with germlines showing signs of severe mitotic and meiotic arrest. TEBP-1 and TEBP-2 form a telomeric complex with the known single-stranded telomere-binding proteins POT-1, POT-2, and MRT-1. Furthermore, we find that POT-1 bridges the double- stranded binders TEBP-1 and TEBP-2, with the single-stranded binders POT-2 and MRT-1. These results describe the first telomere-binding complex in <i>C. elegans</i>, with TEBP-1 and TEBP-2, two double-stranded telomere binders required for fertility and that mediate opposite telomere dynamics.
Abstract 2164: Impact of Sirolimus-Eluting Stent and Paclitaxel-Eluting Stent on the Outcome of Patients with Sirolimus-Eluting Stent Failure: Multicenter Registry in Asia
Authors: Sunao Nakamura, Mizuki Hirose, Jang-Ho Bae, Yeo H Cahyadi, Wasan Udayachalerm, Damras Tresukosol, Sudaratana Tansuphaswadikul
Journal: Circulation (2007)

Purpose: To evaluate the Sirolimus-eluting stent (SES) and Paclitaxel-eluting stent (PES) on the outcome of patients with SES failure (SES-F). Methods: A total of 520 patients with 609 SES-F lesion...
The gene encoding ATP-binding cassette transporter 1 is mutated in Tangier disease
Authors: Marek Bodzioch, Evelyn Orsó, Jochen Klucken, Thomas Langmann, Alfred Böttcher, Wendy Diederich, Wolfgang Drobnik, Stefan Barlage, Christa Büchler, Mustafa Porsch-Özcürümez, Wolfgang E. Kaminski, Harry W. Hahmann, Kurt Oette, Gregor Rothe, Charalampos Aslanidis, Karl J. Lackner, Gerd Schmitz
Journal: Nature Genetics (1999)
Mutational spectrum and phenotypes in Danish families with hereditary angioedema because of C1 inhibitor deficiency
Authors: A. Bygum, C. R. Fagerberg, D. Ponard, N. Monnier, J. Lunardi, C. Drouet
Journal: Allergy (2010)

To cite this article: Bygum A, Fagerberg CR, Ponard D, Monnier N, Lunardi J, Drouet C. Mutational spectrum and phenotypes in Danish families with hereditary angioedema because of C1 inhibitor deficiency. Allergy 2011; 66: 76–84. Background: Hereditary angioedema (HAE), type I and II, is an autosomal dominant disease with deficiency of functional C1 inhibitor protein causing episodic swellings of skin, mucosa and viscera. HAE is a genetically heterogeneous disease with more than 200 different mutations in the SERPING1 gene. A genotype–phenotype relationship does not seem to exist in HAE, although the polymorphism c.-21T>C of exon 2 has been reported to be associated with a more severe phenotype. We aimed to establish the mutational spectrum of C1 inhibitor deficiency in Denmark and investigate the possible disease-aggravating effect of the c.-21T>C polymorphism. Methods: Hereditary angioedema was diagnosed based on clinical features and C1 inhibitor deficiency. A general severity score ranging from 0 to 10 was developed based on age at disease onset, clinical manifestations and treatment experiences. SERPING1 gene investigation was performed by exon sequencing followed by multiplex ligation-dependent probe amplification genomic rearrangement analysis in all known Danish HAE families. Results: Fifty-nine patients with HAE from 26 families were included in this study. The mean disease severity score was 7.12 [1–10], and the mean C1 inhibitor function was 26% [20–46%]. The sensitivity of the mutational screening was 96%, and 13 new mutations were found in this Danish patient cohort. Nine patients (15%) carried the c.-21T>C polymorphism, but they didn't have a more severe phenotype. Conclusion: Thirteen new mutations were identified in the Danish HAE population. No correlation between the c.-21T>C polymorphism, the biochemical values of C1 inhibitor function and the clinical severity score was found.
Statins are HDAC inhibitors: activation of p21 through release of promoter-associated HDAC1/2
Authors: Chen Ching-Chow
Journal: Cancer Research (2008)

2616   Statins are 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors broadly used for the control of hypercholesterolemia. Recently they are reported to have beneficial  effects on certain cancers. In this study, we show that statins inhibited the HDAC activity, increased the accumulation of acetylated histone H3 and the expression of p21  WAF/CIP  in human cancer cells. Computational modeling  demonstrated the direct interaction of the carboxylic acid moiety of statins with the catalytic site of HDAC2. In the subsequent enzymatic assay it was shown that lovastatin inhibited HDAC2 activity competitively with a  K  i  value of 31.6 µM. Sp1 but not p53 sites were found to be the statins-responsive element demonstrated by p21 promoter assays. DAPA and ChIP assays showed the dissociation of HDAC1/2 and association of CBP, leading to histone acetylation on the Sp1 sites of p21 promoter.  In vitro  cell proliferation and  in vivo  tumor growth were both inhibited by statins. These results suggest a novel mechanism for statins through abrogation of the HDAC activity and promoter acetylation to regulate p21 expression. Therefore, statins might serve as novel HDAC inhibitors for cancer therapy and chemoprevention.
Terrorism Assails Nation’s Psyche
Authors: Lynne Lamberg
Journal: JAMA (2005)

While humanitarian groups are not in Darfur to enact justice or political change, they say that greater international involvement is needed to put a stop to the conflict. “Our humanitarian responses are basically putting Band-Aids on the situation,” said Gillies. There are not enough peacekeeping troops in the region to prevent violence and rape in the communities and in refugee camps, noted Akwei. In addition to the immediate need for funds and personnel, there is also the issue of bringing the abusers to justice. According to Akwei, this will require increased support for investigations by the International Criminal Court “so that we don’t let the Sudanese perpetuate this myth that rape is not happening.” In June, the International Criminal Court formally announced the start of an investigation into alleged war crimes in Darfur. It has a list of individuals identified as potentially being responsible for the crimes and is in talks about initiating trials.
Abstract P164: Lipid Management in Diabetes: the REasons for Geographic And Racial Differences in Stroke (REGARDS) Study
Authors: Christopher Gamboa, Monika M Safford
Journal: Circulation (2014)

Background: The Look Ahead trial recently showed that lifestyle intervention did not lower the risk of coronary heart disease (CHD) events in diabetes, emphasizing the importance of risk factor control. This is particularly important for blacks, who have higher risks of CHD mortality than whites. We examined race-sex differences in the prevalence, awareness, treatment and control of hyperlipidemia in a large national biracial cohort with diabetes. Methods: REGARDS recruited 30,239 black and white participants ≥ 45 years of age from the 48 continental US from 2003-2007. Telephone interviews were followed by in-home visits. This analysis included participants with physician/nurse diagnosed diabetes or treatment with diabetes medication or insulin. Hyperlipidemia was defined as low density lipoprotein cholesterol &gt;100 mg/dL or statin use. We described the prevalence, awareness, treatment, and control of hyperlipidemia and calculated prevalence ratios and 95% confidence intervals comparing white men (WM) with other race-sex groups, adjusted for factors that influence health services use (sociodemographics, access to care, severity of diabetes, functional status, obesity, depressive symptoms and elevated high density lipoprotein cholesterol). Results: The race-sex distribution of the 6,497 participants with diabetes is shown in the Table. Although the prevalence of hyperlipidemia was 80-84% across race-sex groups, more white women (WW) (78%) and fewer black men (BM) (64%) were aware of their hyperlipidemia compared with WM (72%) and black women (BW) (71%). Compared to WM (80%) all other race-sex groups were less treated (WW 70%, BM 72%, BW 69%) and among the treated, less controlled (WM 77%, WW 71%, BM 62%, BW 54%). Results were similar after adjustment (Table). Conclusion: These disparities in treatment and control of hyperlipidemia in diabetes warrant further investigation, particularly among blacks, who are especially burdened by diabetes. Table. Prevalence ratios (95% CI) for hyperlipidemia prevalence, awareness, treatment, and control among participants with diabetes in REGARDS, n = 6,497.
Consultation
Authors: M. Therese Southgate
Journal: JAMA (1998)

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
Cardiorespiratory fitness and risk of heart failure: a population‐based follow‐up study
Authors: Hassan Khan, Setor Kunutsor, Rainer Rauramaa, Kai Savonen, Andreas P. Kalogeropoulos, Vasiliki V. Georgiopoulou, Javed Butler, Jari A. Laukkanen
Journal: European Journal of Heart Failure (2013)
Randomized controlled clinical trial of beta irradiation as an adjunct to trabeculectomy in open-angle glaucoma1 1The authors have no financial or proprietary interest in any products mentioned in this article.
Authors: Shafiq U Rehman, Winfried M.K Amoaku, Robert M.L Doran, Mitchel J Menage, Andrew J Morrell
Journal: Ophthalmology (2002)
Abstract 4102: p27 as a biomarker and determinant of risk for endometrial carcinoma arising in the setting of obesity
Authors: Adrienne S. McCampbell, Megan L. Mittlestedt, Ruhee Dere, Lijun Zhou, Bojana Djordjevic, Pamela T. Soliman, Qian Zhang, Caimiao Wei, Stephen D. Hursting, Karen H. Lu, Cheryl L. Walker, Russell R. Broaddus
Journal: Cancer Research (2014)

Abstract Endometrial carcinoma exhibits the strongest association with obesity of any cancer. Tumor growth is driven by PI3K/AKT activation, and opposed by tumor suppressors, including the tuberous sclerosis complex (TSC) and p27, with inactivation of TSC2 and loss of cytoplasmic misloclization of p27 both being linked to PI3K/AKT signaling. However, little is known about the involvement of p27 in the development of endometrial carcinoma arising in the setting of obesity, expecially its role in early disease progression. We found that p27 was moderatley-to-severely reduced in both “normal” endometrial glands as well as endometrial hyperplasia of obese women. Obese Tsc-2-deficient Eker rats similarly developed endometrial hyperplasia with a high frequency and short latency, and like obese women, endometrial hyperplasia that developed in obese rats exhibited loss of p27. In Eker rats, even a short duration of caloric restriction (2-4 months of age) reduced weight, increased adiponectin and lowered leptin to produce favorable leptin:adiponectin ratio, and reduced circulating insulin levels. Caloric restriction also increased p27 levels, primarily in the nucleus, and significantly decreased endometrial hyperplasia incidence by up to 50%. These data demonstrate that in the setting of obesity, loss of p27 occurs very early in progression to carcinoma. Importantly, p27 can be modulated along with weight by diet, and perhaps other lifestyle interventions that decrease risk for development of carcinoma, suggesting it may be a useful biomarker, and possible determinant of risk for endometrial carcinoma in the setting of obesity. Citation Format: Adrienne S. McCampbell, Megan L. Mittlestedt, Ruhee Dere, Lijun Zhou, Bojana Djordjevic, Pamela T. Soliman, Qian Zhang, Caimiao Wei, Stephen D. Hursting, Karen H. Lu, Cheryl L. Walker, Russell R. Broaddus. p27 as a biomarker and determinant of risk for endometrial carcinoma arising in the setting of obesity. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4102. doi:10.1158/1538-7445.AM2014-4102
Lineage commitment and developmental plasticity in early hematopoietic cells.
Authors: Koichi Akashi
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

SY07-01 

Lineage Commitment and Developmental Plasticity in Early Hematopoietic Progenitors Understanding how multipotent cells commit to each of their terminal fate potentials is an important aspect of stem cell biology. Within the hematopoietic system, the prospective isolation of stem and progenitor cell subsets by cell surface phenotype has identified the branchpoints at which major lineage decisions occur. Hematopoietic stem cells (HSCs) with self-renewal potential for a long-term or a short-term (ST) have been purified within the Lin-Sca-1+c-Kit+ fraction, which paved the way for the phenotypic discovery of lineage-restricted progenitors downstream of HSCs. The existence of phenotypically isolatable common lymphoid progenitors (CLPs) suggests that the accessibility for myelo-erythroid differentiation program is lost during the lymphoid commitment from HSCs. Although the successful isolation of common myeloid progenitors (CMPs) suggests that the granulocyte/monocyte (GM) and the megakaryocyte/erythroid (MegE) potentials are shut down simultaneously to form bifurcation of myeloid and lymphoid pathways, recent studies suggest that the loss of GM potential could be a later event in lymphoid commitment as HSCs transit to lymphoid-restricted CLPs. We found that by using mice harboring a reporter for PU.1, a transcription factor necessary for GM and lymphoid development, ST-HSCs could be divided at least into two subpopulations. ST-HSCs activating the PU.1 transcription at a low level were multipotent, while those transcribing a high level of PU.1 differentiated only into GM and lymphoid lineages. These data suggest that during the transition into CLPs, ST-HSCs sequentially and gradually lose MegE then GM potential, generating directly not only CMPs, but also the megakaryocyte/erythrocyte progenitor (MEP) and the granulocyte/monocyte progenitor (GMP). At the earliest lymphoid-committed stage, CLPs have lost both GM and MegE potentials but still retain the accessibility for multilineage differentiation programs that could be activated by ectopic transcriptional signals. They exhibited plasticity for differentiation into all myelo-erythroid lineages by the ectopic expression of transcription factors including C/EBPα, PU.1, GATA-1 and GATA-2. The induction of each lineage from CLPs could be achieved by changing the order of the expression of these transcription factors. We successfully converted CLPs even into erythrocytes, eosinophils, mast cells and basophils. These data suggest that the timing as well as the level of the expression of multiple transcription factors play a key role in hierarchical hematopoietic development from HSCs.
Site-specific phosphorylation by intracellular kinases determines the apoptotic activity of IGFBP-3 in prostate cancer
Authors: Laura Cobb, Satomi Koyama, Pinchas Cohen
Journal: Cancer Research (2007)

AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA

4393 

The IGF axis is known to play an important role in the epidemiology of many tumors, including prostate, lung and breast cancers. IGFBP-3 promotes apoptosis in cancer cells by both IGF-dependent and -independent mechanisms. We have previously shown that IGFBP-3 is rapidly internalized and localized to the nucleus, where its interactions with the nuclear receptor RXRα are important in apoptosis induction. Proteomic and bioinformatic analysis of IGFBP-3 reveals multiple consensus phosphorylation sites for kinases including CK2, PKA, PKC and cdc2. We have previously reported that phosphorylation of IGFBP-3 (S156) by DNA-PK enhances its nuclear accumulation, and is essential for its ability to interact with RXR and induce apoptosis in cultured prostate cancer cells. Indeed, IGFBP-3-S156A is completely unable to induce apoptosis in 22RV1 prostate cancer cells. Using specific chemical inhibitors, we investigated the contribution of other protein kinases to the regulation of IGFBP-3-induced apoptosis. Preventing the activation of CK2 enhanced the apoptotic potential of IGFBP-3. Using web-based proteomics software, we mapped three potential CK2 phosphorylation sites in IGFBP-3: S167, S175 and S177. These sites were mutated to Ala, and the resulting constructs were transfected in to LAPC4 and 22RV1 prostate cancer cells. WtIGFBP-3, IGFBP-3-S175A and IGFBP-3-S177A induced apoptosis to a comparable extent; however, IGFBP-3-S167A was far more potently apoptosis-inducing. Interestingly, IGFBP-3-S167A was able to induce apoptosis even in the absence of active DNA-PK, and IGFBP-3-S156A was able to induce apoptosis when CK2 activity was inhibited chemically or by using siRNA. Together, these data reveal two key regulatory phosphorylation sites in the central region of IGFBP-3. Phosphorylation of S156 by DNA-PK promotes apoptosis, whilst phosphorylation of S167 by CK2 limits the ability of IGFBP-3 to induce apoptosis in prostate cancer. Interestingly, our data suggest that the anti-apoptotic phosphorylation event induced by CK2 is dominant. These studies reveal multi-site phosphorylation of IGFBP-3 that both positively and negatively regulate its apoptotic potential. Understanding such intrinsic regulation of IGFBP-3 action may enhance the development of potential cancer therapies.