tbuckley/cabot-search huggingface dataset:
Sources of toxoplasma infection in pregnant women: European multicentre case-control study Commentary: Congenital toxoplasmosis---further thought for food
Authors: A J C Cook
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objective:</b> To determine the odds ratio and population attributable fraction associated with food and environmental risk factors for acute toxoplasmosis in pregnancy. <b>Design:</b> Case-control study. <b>Setting:</b> Six large European cities. <b>Participants:</b> Pregnant women with acute infection (cases) detected by seroconversion or positive for anti-<i>Toxoplasma gondii</i> IgM were compared with pregnant women seronegative for toxoplasma (controls). <b>Main outcome measures:</b> Odds ratios for acute infection adjusted for confounding variables; the population attributable fraction for risk factors. <b>Results:</b> Risk factors most strongly predictive of acute infection in pregnant women were eating undercooked lamb, beef, or game, contact with soil, and travel outside Europe and the United States and Canada. Contact with cats was not a risk factor. Between 30% and 63% of infections in different centres were attributed to consumption of undercooked or cured meat products and 6% to 17% to soil contact. <b>Conclusions:</b> Inadequately cooked or cured meat is the main risk factor for infection with toxoplasma in all centres. Preventive strategies should aim to reduce prevalence of infection in meat, improve labelling of meat according to farming and processing methods, and improve the quality and consistency of health information given to pregnant women.
Treatment of gallstones with piezoelectric lithotripsy and oral bile acids
Authors: Gilles Pelletier, Jean Delmont, Raymond Capdeville, Henri Mosnier, Jean-Michel Raymond, Denis Collet, François-Xavier Caroli, Jean Moreaux, Marcel Guivarc'h, Michel Amouretti, Jacques Perissat, Pascal Guivarch, Serge Erlinger, Jean-Pierre Etienne
Journal: Journal of Hepatology (1991)
Abstract 12282: A Decrease in Mitochondrial, but Not Cytosolic, Iron Protects Against Cardiac Ischemia-Reperfusion Damage Through a Reduction in ROS
Authors: Hsiang-Chun Chang, Rongxue Wu, Hossein Ardehali
Journal: Circulation (2014)

Introduction: Iron is essential for the activity of several cellular proteins, but excess free iron can cause cellular damage through production of reactive oxygen species (ROS). Iron accumulation in mitochondria, the major site of cellular iron homeostasis, leads to cardiomyopathy. However, it is not known whether a reduction in baseline mitochondrial (as opposed to cytosolic) iron can protect against ischemia-reperfusion (I/R) injury in the heart. We hypothesized that since mitochondria are the major site of iron homeostasis and that mitochondrial iron can lead to oxidative damage, a reduction in mitochondrial iron at baseline would be sufficient to protect against I/R injury. Results: Transgenic (TG) mice with cardiomyocyte-specific overexpression of the mitochondrial iron export protein ATP-binding cassette (ABC)-B8 had significantly lower mitochondrial iron in the heart than nontransgenic (NTG) littermates at baseline, but their cardiac function and the expression of key antioxidant systems were similar to NTG littermates. In response to I/R, TG mice displayed significantly less apoptosis and lipid peroxidation products and better preserved cardiac function than NTG littermates, suggesting that a reduction in mitochondrial iron protects against I/R injury. To confirm these results, we next took a pharmacological approach to assess the effects of a reduction in mitochondrial vs cytosolic iron on the response to I/R using 2,2’-bipyridyl (BPD, a mitochondria-accessible iron chelator) and deferoxamine (DFO, an iron chelator that can only reduce cytosolic iron). Treating rat cardiomyoblast H9C2 cells with BPD but not DFO significantly lowered chelatable mitochondrial iron and protected against H 2 O 2 induced cell death, and pretreatment with BPD but not DFO protected mice against I/R injury and reduced ROS production, suggesting that a reduction in baseline mitochondrial, but not cytosolic, iron is sufficient to protect against I/R injury. Conclusions: Our findings demonstrate that selective reduction in mitochondrial iron is protective in I/R injury. Thus, targeting mitochondrial iron with selective iron chelators may provide a novel approach for treatment of ischemic heart disease.
Abstract P6-05-01: Endoplasmic reticulum resident protein transmembrane protein 33 (TMEM33) induces apoptosis via UPR signaling and autophagy in breast cancer cells
Authors: Rong Hu, Xiyuan Zhang, Leena Hilakivi-Clarke, Usha Kasid, Robert Clarke
Journal: Cancer Research (2015)

Abstract Breast cancer is the most common cancer type in women, with expected incidence of around 232,670 new cases in the US alone each year. Endoplasmic reticulum stress (EnR stress) and the related unfolded protein response (UPR) are activated in breast cancer cells to promote cell survival and endocrine resistance. TMEM33 is a novel transmembrane protein that resides in the endoplasmic reticulum (EnR) and has been shown to activate two of the UPR branches (PERK; IRE1α). However, the cellular functions and underlying mechanism of this EnR resident protein remains largely unknown. In this study, we show that overexpression of TMEM33 induces robust cell death in breast cancer cells. TMEM33 overexpression strongly activates the pro-death JNK-p53 pathway, possibly through the activation of IRE1α. We also observe a significant inhibition of the downstream survivin (also called BIRC5), which is known to inhibit cell death by binding to caspases and blocking their activation. We further show that either the blockage of JNK activation with a small molecule inhibitor, or the overexpression of survivin, protects cells against TMEM33-induced apoptosis. In addition, we demonstrate that TMEM33 overexpression induces autophagy in breast cancer cells (changes in LC3 and p62 expression). Inhibition of autophagy with either the autophagy inhibitor chloroquine, or by knockdown of the autophagy gene Atg5, further sensitizes breast cancer cells to TMEM33 overexpression. Conversely, cell death induced by TMEM33 is decreased by overexpression of the autophagy gene Beclin 1. The findings in this study demonstrate that the novel EnR resident protein TMEM33 induces cell death by activating the IRE1α-JNK-p53-survivin pathway in breast cancer cells. Paradoxically, autophagy is also activated by TMEM33 but the prosurvival action is generally not sufficient to block all of the cell death signaling. Citation Format: Rong Hu, Xiyuan Zhang, Leena Hilakivi-Clarke, Usha Kasid, Robert Clarke. Endoplasmic reticulum resident protein transmembrane protein 33 (TMEM33) induces apoptosis via UPR signaling and autophagy in breast cancer cells [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P6-05-01.
Abstract 4191: Whole exome sequencing of a case of olfactory neuroblastoma
Authors: SooJin Cha, Se-Hoon Lee, Jong-Il Kim, Jong-Yeon Shin
Journal: Cancer Research (2014)

Abstract Purpose: Olfactory neuroblastoma (ONB) is an unusual malignancy occurred in sinonasal tract and molecular characteristics were poorly understood. Here we analyzed sequence of a fresh tissue from an olfactory neuroblastoma patient through whole exome sequencing to identify ONB-specific mutations. Methods: We examined fresh tumor sample with matched peripheral blood from a patient diagnosed olfactory neuroblastoma. All procedures were approved by IRB in Seoul National University Hospital. He was 30 years old and had chemotherapy, surgery and radiotherapy. He had a recurrent disease with metastasis to bones and lymph nodes, and tumor tissue was obtained from a lymph node. Genomic DNA was isolated from a dissected tissue and whole exome library was constructed using Agilent SureSelectXT Human All Exon V4+UTRs (71Mb). Sequencing was performed by Illumina HiSeq2000 platform with paired-end 101bp reads and sequenced data was aligned to human reference genome g1k v37 using Burrows-Wheeler Aligner (BWA). Then, a series of bioinformatical tools were used such as SAMtools, PICARD, the Genome Analysis Toolkit (GATK) and MuTect to list up potential candidate genes. These genes were filtered out considered as germline variants informed in database like dbSNP, 1000 genome project and exome sequencing project 6500 (esp6500). Final candidate genes were identified by manual curation based on cancer gene classification of public database and publications. Results: Our approach generated 15Gb and 17Gb of mapped sequence, with 97.91% and 98.43% of the target regions covered at least 10X depth in tumor and normal sample, respectively. After processing and filtering, we identified 8 candidate cancer genes including 5 somatic nucleotide variants (SNVs; CDKN2C, NBPF1, NBPF10, TGFBR2 and TP53) and 3 insertion/deletion mutations (ACVR1B, AR and CARD11). Among SNVs, CDKN2C showed stopgain SNV resulted in truncated mutation and the same mutation in TP53 were recurrently reported in COSMIC database. Cancer gene candidate indel mutations included 2 frameshift insertions (ACVR1B and CARD11) and 1 nonframeshift insertion (AR). Conclusions: We analyzed a patient of olfactory neuroblastoma using our WES pipeline and several genes were identified to candidate cancer gene mutations which should be validated in large number of samples. Citation Format: SooJin Cha, Se-Hoon Lee, Jong-Il Kim, Jong-Yeon Shin. Whole exome sequencing of a case of olfactory neuroblastoma. [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 4191. doi:10.1158/1538-7445.AM2014-4191
Sharing an Agenda for Children
Authors: D Satcher
Journal: JAMA (2001)

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
Ligand Activation of Peroxisome Proliferator–Activated Receptor β Inhibits Colon Carcinogenesis
Authors: Holly E. Marin, Marjorie A. Peraza, Andrew N. Billin, Timothy M. Willson, Jerrold M. Ward, Mary J. Kennett, Frank J. Gonzalez, Jeffrey M. Peters
Journal: Cancer Research (2006)

Abstract There is considerable debate whether peroxisome proliferator–activated receptor β/δ (PPARβ/δ) ligands potentiate or suppress colon carcinogenesis. Whereas administration of a PPARβ ligand causes increased small intestinal tumorigenesis in Apcmin/+ mice, PPARβ-null (Pparb−/−) mice exhibit increased colon polyp multiplicity in colon cancer bioassays, suggesting that ligand activation of this receptor will inhibit colon carcinogenesis. This hypothesis was examined by treating wild-type (Pparb+/+) and Pparb−/− with azoxymethane, coupled with a highly specific PPARβ ligand, GW0742. Ligand activation of PPARβ in Pparb+/+ mice caused an increase in the expression of mRNA encoding adipocyte differentiation–related protein, fatty acid–binding protein, and cathepsin E. These findings are indicative of colonocyte differentiation, which was confirmed by immunohistochemical analysis. No PPARβ-dependent differences in replicative DNA synthesis or expression of phosphatase and tensin homologue, phosphoinositide-dependent kinase, integrin-linked kinase, or phospho-Akt were detected in ligand-treated mouse colonic epithelial cells although increased apoptosis was found in GW0742-treated Pparb+/+ mice. Consistent with increased colonocyte differentiation and apoptosis, inhibition of colon polyp multiplicity was also found in ligand-treated Pparb+/+ mice, and all of these effects were not found in Pparb−/− mice. In contrast to previous reports suggesting that activation of PPARβ potentiates intestinal tumorigenesis, here we show that ligand activation of PPARβ attenuates chemically induced colon carcinogenesis and that PPARβ-dependent induction of cathepsin E could explain the reported disparity in the literature about the effect of ligand activation of PPARβ in the intestine. (Cancer Res 2006; 66(8): 4394-401)
Differential Effects of Anti-Fas Ligand and Anti-Tumor Necrosis Factor α Antibodies on Acute Graft-Versus-Host Disease Pathologies
Authors: Koichi Hattori, Takao Hirano, Hiroaki Miyajima, Norifumi Yamakawa, Masatoshi Tateno, Kazuo Oshimi, Nobuhiko Kayagaki, Hideo Yagita, Ko Okumura
Journal: Blood (1998)
386. Intra-Arterial Adenoviral Mediated β2Adrenergic Receptor (AR) Gene Delivery Induces Neoangiogenesis in Rat Ischemic Hindlimb
Authors: Guido Iaccarino, Vincenzo Cerullo, Michele Ciccarelli, Gennaro Galasso, Daniela Sorriento, Walter J. Koch, Federico Piscione, Lucio Pastore, Francesco Salvatore, Bruno Trimarco
Journal: Molecular Therapy (2004)

Top of pageAbstract
We have shown that β2AR gene delivery to the endothelium corrects impaired endothelial vasodilation in hypertensive rats. Endothelium mediates other vascular biology responses, including neoangiogenesis; furthermore, during chronic ischemia there is local adrenergic activation. Based on this background, we tested the hypothesis that increasing the number of endothelial β2AR in ischemic districts would result in neoangiogenesis. We used the rat ischemic hind limb (HL) model in 15 WKY rats, by legating the right common femoral artery. Through means of an incision made distal to the ligature, we injected intraarterially a solution containing 5∗109PFU of recombinant adenovirus encoding for the human β2 AR (ADβ2AR, n=8), the naturally occurring, signaling challenged ILE164 variant of the human β2AR (ADβ2-164AR, n=5) or an empty virus (ADEV, n=7) and incubate for 15 minutes while venous blood return from the HL was blocked. After 15 days, we performed selective HL digital angiographies in live anaesthetized rats, with a computer controlled injection during i.a. nitroglycerin (20 μg i.a.) to induce maximal vasodilation. We estimated blood flow (BF) measuring the number of angiography frames needed by the contrast medium to reach the origin of the dorsal paw artery from the injection (TFC). HL perfusion was also assessed by dyed beads dilution, injecting in the abdominal aorta 108 dyed beads, and measuring the release of dye in the digested gastrocnemious samples of the ischemic HL. As reference we used the contralateral non ischemic muscle. We also counted the capillary (<10μ diameter) per muscle fiber density (C/F) on tibial muscle sections stained with isolectin B4. The non ischemic HL of ADβ2AR, ADβ2-164AR and ADEV rats showed similar TFCs (4.9±0.18, 5.3±0.65 and 5.1±0.2 TFC, ns). ADβ2AR, ADβ2-164AR and ADEV ischemic HL presented greater TFCs compared to the non ischemic HL but the ADβ2AR TFCs were significantly reduced to ADEV and ADβ2-164AR (11±2.5; 23±6.8 and 30±0.1 respectively, p<0.001). BF estimated by dyed microspheres dilution was higher in the ADβ2AR vs the ADEV and ADβ2-164AR ischemic HL (fold of non ischemic control: 1.9±0.6, 0.5±0.14, and 0.45±1 respectively, p<0.05). Finally, capillary density was higher in ADβ2AR compared to ADβ2-164AR and ADEV (0.82±0.04, 0.56±0.03 and vs 0.53±0.03 C/F respectively, p<0.001). In conclusion, our data show that ADβ2AR increases blood flow in ischemic HL, suggest a role for endothelial β2AR in neoangiogenesi, which might be impaired in patients harbouring the ILE164 variant of the b2AR gene.
A small suberythemal ultraviolet B dose every second week is sufficient to maintain summer vitamin D levels: a randomized controlled trial
Authors: M.K.B. Bogh, A.V. Schmedes, P.A. Philipsen, E. Thieden, H.C. Wulf
Journal: British Journal of Dermatology (2011)

Journal Article A small suberythemal ultraviolet B dose every second week is sufficient to maintain summer vitamin D levels: a randomized controlled trial Get access M.K.B. Bogh, M.K.B. Bogh Department of Dermatology, Copenhagen University Hospital, Bispebjerg, Bispebjerg Bakke 23, 2400 Copenhagen NV, Denmark Morten K.B. Bogh. E‐mail: bogh@dadlnet.dk Search for other works by this author on: Oxford Academic Google Scholar A.V. Schmedes, A.V. Schmedes Department of Clinical Biochemistry, Lillebaelt Hospital, Vejle, Denmark Search for other works by this author on: Oxford Academic Google Scholar P.A. Philipsen, P.A. Philipsen Department of Dermatology, Copenhagen University Hospital, Bispebjerg, Bispebjerg Bakke 23, 2400 Copenhagen NV, Denmark Search for other works by this author on: Oxford Academic Google Scholar E. Thieden, E. Thieden Department of Dermatology, Copenhagen University Hospital, Bispebjerg, Bispebjerg Bakke 23, 2400 Copenhagen NV, Denmark Search for other works by this author on: Oxford Academic Google Scholar H.C. Wulf H.C. Wulf Department of Dermatology, Copenhagen University Hospital, Bispebjerg, Bispebjerg Bakke 23, 2400 Copenhagen NV, Denmark Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 2, 1 February 2012, Pages 430–433, https://doi.org/10.1111/j.1365-2133.2011.10697.x Published: 01 February 2012 Article history Accepted: 14 October 2011 Published: 01 February 2012
Abstract 5929: Osteopontin Predicts Mortality in Patients With Pulmonary Hypertension
Authors: Mark Rosenberg, Joachim F Meyer, Ekkehard Gruenig, Matthias Lutz, Dirk Lossnitzer, Rita Wipplinger, Hugo A Katus, Norbert Frey
Journal: Circulation (2009)

Background: The extracellular matrix protein Osteopontin (OPN) was found upregulated in several animal models of cardiac failure and appears to play an important role in myocardial remodeling. More...
Neutrophils interact with adenovirus vectors via the β2-Integrin CD11b
Authors: Daniel A. Muruve, Matthew J. Cotter
Journal: Molecular Therapy (2004)

Gene therapy is a therapeutic strategy that may potentially treat a multitude of clinically important conditions. To these ends, adenovirus vectors (Ad-vectors) are a promising means to deliver specific genes of interest to target cells. The efficacy of Ad-vectors is limited by the innate immune response against these infectious particles. Following transduction in vivo, Ad-vectors activate the innate immune system resulting in rapid vector clearance and acute inflammation of transduced tissues. The infiltration of effector leukocytes, such as neutrophils, is a hallmark of the innate immune response and may play a major role in Ad-vector clearance. The aims of this work were to explore neutrophil-Ad-vector interactions and to identify the essential molecules mediating this interaction. C57/B6 mice were administered a Cy2-labeled first generation Ad-vector, AdLuc, intravenously and sacrificed at 3 hours. Neutrophil populations were isolated from the liver and analyzed by flow-cytometry for fluorescence. Compared to vehicle, neutrophils from Cy2-AdLuc treated mice demonstrated significant vector uptake confirming an important role for these innate cells in the host response to Ad-vectors. To further study Ad-vector neutrophil interactions, purified populations of human peripheral blood neutrophils were incubated with Cy2-AdLuc and analyzed using fluorescence microscopy and flow cytometry. Ad-vector uptake by neutrophils increased significantly over 20-60 minutes. Neutrophil uptake of Ad-vectors did not require viral capsid RGD motifs since internalization of the RGD-deleted Ad-vector, AdL.PB over 20-60 minutes was similar to AdLuc. Neutrophil pre-incubation with a blocking anti-CD11b mAb (ICRF44), but not control IgG, inhibited Ad-vector uptake demonstrating that this β2-integrin is required for Ad-vector internalization. To determine activation, neutrophil L-selectin expression was determined by flow cytometry following incubation with AdLuc. L-selectin expression, decreased significantly over 60 minutes following incubation with AdLuc consistent with neutrophil activation. These data confirm that neutrophils interact significantly with and are activated by Ad-vectors. Furthermore, neutrophil-expressed CD11b, but not viral capsid RGD motifs, is essential for adenoviral uptake. Future studies will focus on elucidating the mechanism of Ad-vector-mediated neutrophil activation and its role in vector clearance in vivo.
Abstract 64: A p53 activating mutation drives metastatic high-grade serous ovarian cancer arising from the ovary in mice
Authors: Jaeyeon Kim, Donna M. Coffey, Lang Ma, Martin M. Matzuk
Journal: Cancer Research (2014)

Abstract The tumor suppressor p53 is the most frequently mutated gene in high-grade serous ovarian cancer, or high-grade serous carcinoma (HGSC) − the most common and deadliest ovarian cancer. Yet it remains unknown whether p53 mutation can drive HGSC. To address this, we have incorporated a p53 activating mutation, p53R172H, into conditional Dicer-Pten double-knockout (DKO) mice, generating triple-mutant (TKO) mice. Like DKO mice, these TKO mice develop fallopian-tube-originated HGSCs, aggressively metastasizing inside the abdominal cavity, inducing ascites, and killing the mice. Then, unlike DKO mice, when both fallopian tubes are surgically removed from TKO mice, TKO ovaries alone are capable of developing HGSCs, which also metastasize to the abdominal cavity, including the omentum, diaphragm, and mesentery. This finding indicates that p53 mutation can drive HGSC in the ovary. To further examine the ability of p53 mutation to drive ovarian HGSC, we have generated p53R172H-Pten double-mutant mice (DMu), a control line for TKO mice. Intriguingly, 30% of the DMu mice (12/40 mice) develop metastatic HGSCs in the ovary, which spread to the abdominal cavity before killing the mice, just like TKO mice with fallopian tubes removed. Unlike TKO and DKO mice, however, DMu mice show no sign of tumor in the fallopian tube. Our new mouse models of ovarian cancer therefore show that p53 mutation indeed can initiate and drive metastatic HGSCs arising from the ovary. Clinically, our study suggests that besides the fallopian tube, the ovary can serve as a source of high-grade serous ovarian cancer. (Grant support: Ovarian Cancer Research Fund (OCRF); Marsha Rivkin Ovarian Cancer Challenge Grant; F32 NCI National Research Service Award (NRSA); K99/R00 NCI Pathway to Independence Award) Citation Format: Jaeyeon Kim, Donna M. Coffey, Lang Ma, Martin M. Matzuk. A p53 activating mutation drives metastatic high-grade serous ovarian cancer arising from the ovary in mice. [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 64. doi:10.1158/1538-7445.AM2014-64
Abstract 13180: Poor Adherence to Medication is an Independent Risk Factor for Adverse Clinical Outcomes in Heart Failure with Reduced Ejection Fraction (HFrEF) but not Heart Failure with Preserved Ejection Fraction (HFpEF)
Authors: Naoko Kato, Koichiro Kinugawa, Etsuko Nakayama, Takako Tsuji, Yumiko Kumagai, Chikako Miura, Masayoshi Nagayama, Tetsuya Sumiyoshi, Hitonobu Tomoike, Ryozo Nagai
Journal: Circulation (2012)