tbuckley/cabot-search huggingface dataset:
INTERNAL HYDROCEPHALUS FOLLOWING REPEATED INTRAVENTRICULAR HEMORRHAGES
Authors: Francis J. Scully
Journal: Annals of Internal Medicine (1937)

Case Reports1 October 1937INTERNAL HYDROCEPHALUS FOLLOWING REPEATED INTRAVENTRICULAR HEMORRHAGESFRANCIS J. SCULLY, M.D., F.A.C.P.FRANCIS J. SCULLY, M.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-11-4-684 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSpontaneous intraventricular hemorrhage is quite rare and when it occurs is usually promptly fatal. A recurrence of such a hemorrhage is therefore quite unusual. The following case is especially interesting because of the development of an extensive internal hydrocephalus following repeated intraventricular hemorrhages.CASE REPORTMrs. J. S., aged 60, was seen in consultation with Dr. H. A. Ross of Arkadelphia on November 1, on account of a persistent headache and dizziness. On October 16 the patient had suddenly dropped over unconscious while sewing. She had previously felt well, and that morning had eaten breakfast as usual. She remained comatose...References1. HEMSATH FA: Ventricular cerebral hemorrhage in the newborn infant, pathological and etiologic study of 20 cases, Am. Jr. Obst. and Gynec., 1934, xxviii, 343. CrossrefGoogle Scholar2. COPELAND CL: Intraventricular hemorrhage, Lancet, 1934, ii, 757-758. CrossrefGoogle Scholar3. SANDSLEDERER JJM: Intraventricular hemorrhage, clinical and pathological study of three cases, Jr. Nerv. and Ment. Dis., 1927, lxv, 360-371. CrossrefGoogle Scholar4. DANDY WE: Benign encapsulated tumors in the lateral ventricles of the brain: diagnosis and treatment, Ann. Surg., 1933, xcviii, 841-845. CrossrefGoogle Scholar5. FINCHER EF: Intraventricular tumors of the cerebrum, South. Med. Jr., 1934, xxvii, 667-676. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Hot Springs, Arkansas*Received for publication August 24, 1936. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAngioma of the choroid plexus: Personal experience of 42 cases and a review of the literaturePrimary Intraventricular HemorrhageCryptic vascular malformation of the choroid plexusMicrosurgical anatomy of the choroidal arteries: Lateral and third ventriclesThird ventricular choroid plexus arteriovenous malformation simulating a colloid cystHemorrhage in bilateral choroid plexus hemangiomas demonstrated by computed tomographyArteriovenous malformation of choroid plexusDevelopmental DisordersCircumscribed Hematoma of the Lateral Ventricle Following Rupture of an Intraventricular Saccular Arterial AneurysmThalamic Angioma and Aneurysm of the Anterior Choroidal Artery with Intraventricular Hematoma 1 October 1937Volume 11, Issue 4Page: 684-686KeywordsComaHeadachesHemorrhageHydrocephalus ePublished: 1 December 2008 Issue Published: 1 October 1937 PDF downloadLoading ...
THE PLACE OF DRUG THERAPY IN THE MANAGEMENT OF UNHOSPITALIZED TUBERCULOSIS PATIENTS
Authors: A B ROBINS, A D CHAVES
Journal: Annals of Internal Medicine (1957)

Article1 October 1957THE PLACE OF DRUG THERAPY IN THE MANAGEMENT OF UNHOSPITALIZED TUBERCULOSIS PATIENTSARTHUR B. ROBINS, M.D., F.A.C.P., AARON D. CHAVES, M.D.ARTHUR B. ROBINS, M.D., F.A.C.P.Search for more papers by this author, AARON D. CHAVES, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-47-4-774 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe importance of the unhospitalized patient in the over-all tuberculosis picture has been clearly established by the findings of a recent study conducted by the U. S. Public Health Service.1 This study showed that throughout the country almost half of the significant cases of tuberculosis were at home, the majority with the disease in an advanced, presumably communicable state. This has been the situation in New York City for many years and was the reason for the adoption of a program of drug treatment for unhospitalized patients with tuberculosis by the New York City Health Department in 1953.This program...Bibliography1. Blomquist ET: The non-hospitalized tuberculosis patient, Am. J. Pub. Health 46: 149, 1956. CrossrefGoogle Scholar2. ChavesRobinsAbelesPeizerDanglerWidelock ADABHLRGD: The prevalence of streptomycin- and isoniazid-resistant strains of Mycobacterium tuberculosis in patients with newly discovered and untreated active pulmonary tuberculosis, Am. Rev. Tuberc. 72: 143, 1955. MedlineGoogle Scholar3. ChavesRobinsAbelesPeizerDanglerWidelock ADABHLRGD: Further observations on the prevalence of streptomycin- and isoniazid-resistant strains of Mycobacterium tuberculosis in patients with newly discovered and untreated active pulmonary tuberculosis, Am. Rev. Tuberc. 74: 293, 1956. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*From the Symposium on the Treatment of Tuberculosis, presented at the Thirty-eighth Annual Session of The American College of Physicians, Boston, Massachusetts, April 10, 1957.From the Bureau of Tuberculosis, Department of Health, New York, N. Y.Requests for reprints should be addressed to Arthur B. Robins, M.D., Department of Health, 125 Worth Street, New York 13, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTuberculosis 1 October 1957Volume 47, Issue 4Page: 774-781KeywordsDrug therapyDrugsPatientsPeriodic acid SchiffPrevention, policy, and public healthTuberculosis ePublished: 1 December 2008 Issue Published: 1 October 1957 PDF downloadLoading ...
B-cell–autonomous somatic mutation deficit following bone marrow transplant
Authors: Annuska M. Glas, Erwin H. N. van Montfort, Jan Storek, Emily-Gene N. Green, Roy P. M. Drissen, Viviane J. Bechtold, J. Zachary Reilly, Monja A. Dawson, Eric C. B. Milner
Journal: Blood (2000)
Abstract 13750: A Promising Highly Sensitive and Quantitative Assays of Tumorigenicity Essential for Facilitating Safety Studies of Human Induced Pluripotent Stem Cells -derived Cardiomyocytes for Future Therapeutic Application
Authors: Emiko Ito, Shigeru Miyagawa, Atsuhiro Saito, Satsuki Fukushima, Shigeo Masuda, Takuji Kawamura, Yukiko Imanishi, Nagako Sougawa, Motoko Shiozaki, Hiroko Iseoka, Akima Harada, Maki Takeda, Yoji Sato, Yoshiki Sawa
Journal: Circulation (2014)

Background: Although transplantation of cardiomyocytes derived from induced pluripotent stem cells (iPSCs) into the heart is a promising approach for heart disease, the presence of residual undifferentiated iPSCs may limit safety of this treatment. Transplantation of human iPSCs (hiPSCs) into immune-deficient mice leads to the formation of differentiated tumors comprising all three germ layers, resembling spontaneous human teratomas. Teratoma assays are considered to be a standard for demonstrating the differentiation potential of hiPSCs and hold promise as a standard for assessing the safety of hiPSC-derived cardiomyocytes intended for therapeutic applications. Methods and Results: We examined three in vitro tumorigenicity assays (soft agar colony formation assay, flow cytometry assay and quantitative real-time polymerase chain reaction [qRT-PCR] assay) and in vivo assay to detect residual undifferentiated cells. Soft agar colony formation assay was unable to detect hiPSCs. Next, we tied to detect residual undifferentiated cells by flow cytometry using six antibodies which recognize stem cell marker antigens, (Oct3/4, Nanog, SSEA-3, SSEA-4, TRA1-60, and TRA1-81). The anti-TRA1-60 antibody clearly distinguished hiPSCs from cardiomyocytes; it deteced 0.1% residual undifferentiated hiPSCs that were spiked in primary cardiomyocytes. Furthermore, to identify highly selective markers for undifferentiated hiPSCs, we compared mRNA levels of Oct3/4, Nanog, Sox2, Lin28 and Rex1 in hiPSCs and primary cardiomyocytes by qRT-PCR. Lin28 mRNA was not detected in primary cardiomyocytes, whereas the qRT-PCR assay detected 0.01% residual undifferentiated hiPSCs that were spiked in primary cardiomyocytes. In vivo study, the potency of teratoma formation was tested in immune-deficient mice. Among iPSC-derived cardiomyocytes, cells that contain more than 2% Lin28 positive fraction formed tumors. However, cell population that contained a Lin28 fraction less than 2% did not form tumors. Conclusion: We established core parameters for detecting residual tumor-forming cells. Our results provide highly sensitive and quantitative assays essential for facilitating safety studies of hiPSC-derived cardiomyocytes for future therapeutic application.
Evidence base of clinical diagnosis: The architecture of diagnostic research
Authors: D L Sackett
Journal: BMJ (2002)

Thank you for your interest in spreading the word about The BMJ.NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Username * Your Email * Send To * You are going to email the following The architecture of diagnostic research Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Issues with implementing a high‐quality lung cancer screening program
Authors: James L. Mulshine, Thomas A. D'Amico
Journal: CA A Cancer Journal for Clinicians (2014)

Answer questions and earn CME/CNE After a comprehensive review of the evidence, the United States Preventive Services Task Force recently endorsed screening with low‐dose computed tomography as an early detection approach that has the potential to significantly reduce deaths due to lung cancer. Prudent implementation of lung cancer screening as a high‐quality preventive health service is a complex challenge. The clinical evaluation and management of high‐risk cohorts in the absence of symptoms mandates an approach that differs significantly from that of symptom‐detected lung cancer. As with other cancer screenings, it is essential to provide to informed at‐risk individuals a safe, high‐quality, cost‐effective, and accessible service. In this review, the components of a successful screening program are discussed as we begin to disseminate lung cancer screening as a national resource to improve outcomes with this lethal cancer. This information about lung cancer screening will assist clinicians with communications about the potential benefits and harms of this service for high‐risk individuals considering participation in the screening process. CA Cancer J Clin 2014;64:351–363. © 2014 American Cancer Society.
Seeds of Knowledge Grow in Urban Garden
Authors: Rebecca Voelker
Journal: JAMA (2002)

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
Abstract 15674: Notch3/rbpjk Signaling Pathway in the Coronary Arteries is Involved in the Development of Heart Failure in Response to Hypertension
Authors: Astrid Monfort, Hélène Ragot, Evelyne Polidano, Regine Merval, Claude Delcayre, Christos Chatziantoniou, Jane-Lise Samuel, Alain Cohen-Solal
Journal: Circulation (2014)

Background: Notch3, a receptor expressed in vascular smooth muscle cells (VSMC), plays a key role in the integrity of resistance arteries by controlling the maturation of VSMC through RBPJk, a canonical Notch transcriptional factor. We hypothesized that Notch3 signaling pathway in the VSMCs of the coronary arteries might play a key role in the cardiac adaptation to pressure-overload. Methods: To eliminate congenital defect biases, we used mice in which conditional tamoxifen- selective deletion of RBPJk in VSMC was induced at the age of 4 weeks (SMMHC-CRE ER T2, RBP-JK loxp/loxp). Seven weeks later, hypertension was induced in control (C) mice (n= 10) and those with RBPJk deletion (SM-RBPJ-KO, n = 13) by infusion of Angiotensin 2 (Ang2) (1μg/kg/min) using Alzet minipumps after surgery. Results: In response to Ang2, SM-RBPJ-KO and control mice showed similar hypertension (159 ±7 mmHg vs 150±10 mmHg). By day 8 after surgery, SM-RBPJ-KO mice only developed a severe heart failure with anarsaca. These mice showed a decrease in shortening fraction (-42%, p&lt;0.01), a left ventricular dilatation (+15%, p&lt;0.01), and a ventricular hypertrophy (+12%, p&lt;0.05) when compared to C + Ang2. As expected, C + Ang 2 hearts showed an increase in ANP, B-MHC and Gal-3 (+76%, +55%, +46%, p&lt;0.05 respectively vs C) mRNA expressions, whereas SM-RBPJ-KO hearts exhibited even higher induction of ANP (+48%, p&lt;0.01), Gal-3 (+74%, p&lt;0.01), CD68 (+55%, p&lt;0.05) and collagen-3 (+78%, p&lt;0.01) when compared to C + Ang2. This cardiac phenotype confirmed the severe heart failure. Interestingly, immuno-morphometric analysis showed an arteriolar rarefaction in SM-RBPJ-KO + Ang2 mice associated with a lack of angiogenic signaling pathway revealed by a decrease in VEGFa and angiopoietin 2 mRNAs (-50%, and -52%, p&lt;0.05, respectively vs. C + Ang2). Conclusion: We provide evidence that in adulthood, dysfunction of the Notch3/RBPJk signaling pathway in the coronary arteries contributes in the aggravation of heart failure in response to rapid increase in blood pressure.
Abstract MP02: Dose Response Relationship Between Physical Activity and Risk of Heart Failure: A Meta-Analysis
Authors: Ambarish Pandey, Sushil Garg, Monica Khunger, Colby Ayers, Dharam Kumbhani, Benjamin Levine, James Delemos, Jarett Berry
Journal: Circulation (2015)

Background:  Prior studies have shown qualitative inverse associations between physical activity (PA)/fitness and risk for heart failure (HF). However, a comprehensive assessment of the quantitative dose response association between PA and HF risk has not been reported.   Methods:  Epidemiological studies that evaluated associations between PA/fitness and HF incidence were included. The categorical dose response association was evaluated by comparing the pooled HR for HF associated with different levels of PA (vs. lowest PA level) across studies. The continuous dose response was assessed among studies that allowed quantitative estimation of PA levels using generalized least square regression models.   Results:  After reviewing 2,314 abstracts, 14 prospective cohort studies were included (PA = 12; Fitness = 2); eight allowed quantitative estimation of PA levels. On pooled analysis, we observed 21,114 HF events among 393,486 participants (52% women) during a median follow up period of 15.5 years. The highest levels of PA were associated with significantly reduced risk of HF [Pooled HR  vs. lowest PA:  0.68 (0.62-0.73)]. Furthermore, higher levels of PA were associated with lower risk of HF in categorical as well as continuous dose response analyses ( Figure ). Compared to participants reporting no leisure time PA, those who engaged in guideline recommended minimum levels of PA (500 MET*min/week, 2008 US Federal Guidelines) had only modest reductions in HF risk [HR: 0.90(0.87 - 0.92)]. In contrast, a substantial risk reduction was observed among individuals engaging in advanced guidelines recommended PA levels [1000 MET-min/week, HR: 0.81(0.76 - 0.85)]. The magnitude of HF risk reduction associated with highest levels of PA was similar in men and women with no significant interaction by sex. [P interaction : 0.64].   Conclusion:  There is an inverse dose response relationship between PA and HF risk. Higher doses of PA in excess of the current guideline recommended minimum PA levels might be required to significantly reduce the risk of HF.
Transcriptional signature associated with response to Aplidin® (Plitidepsin) in human T-cell lymphoma cell lines
Authors: Nerea Martínez, Margarita Sánchez-Beato, Paloma de la Cueva, M. Victoria Moneo, Miguel Aracil, Juan Carlos Tercero, José Jimeno, MiguelAngel Piris
Journal: Clinical Cancer Research (2006)

B13   Aplidin ® (Plitidepsin) is a marine compound with antitumoral activity that produces cell cycle G1 arrest, G2 blockage, and apoptosis in different tumor cell types. It was previously described that high concentrations of Plitidepsin (400-500 nM) produced activation of the mitogen activated protein kinases JNK, p38 and ERK; additional studies done at concentrations closer to average IC50 values (i.e. 50 nM) also support the findings of JNK activation. Inhibition of VEGF autocrine loop, reducing VEGF secretion and down-regulation of the VEGFr-1 has also been described. Phase II clinical studies are currently underway in a variety of solid tumors and hematological malignancies.The aim of this study was to investigate the functional changes and molecular signature induced by Plitidepsin in human T cell lymphoma. Therefore, a panel of 5 human T cell lymphoma cell lines was treated with clinically relevant concentrations of Plitidepsin (20 nM). The IC50 of these cell lines are between 10 and 40 nM.Cells were collected at different points of treatment, 0, 6, 24, 48 and 72 hours, for flow cytometry analysis (FACS) and RNA extraction. Cells treated with DMSO were used as controls. Plitidepsin treatment produced apoptosis, measured by Annexin V.To obtain the gene expression signature in response to Plitidepsin in the cell lines studied, a cDNA microarray containing 9300 genes relevant in cancer and drug resistance was used.Genes deregulated at each time-point of treatment in at least 3 of the 5 cell lines were selected. Only those genes whose deregulation was maintained at least in 2 time-points of the treatment were considered. This analysis revealed upregulation of 86 genes and downregulation of 66 genes in response to Plitidepsin. Among the upregulated genes, a group of genes related with apoptosis, such as CASP7, RHOB (Ras homolog gene), BNIP1 (bcl2 interacting protein), CYCS (cytochrome C), the Serine/threonine-protein kinase SGK, and the Mitochondrial ribosomal protein MRPS30, and with signal transduction such as JUN, were found, whereas some genes related with cell cycle check points, such as CDKN2C, CDC45L, CENPF (centromer protein), the cyclins CCNG1, CCNG2 and CCNB2, were downregulated. The heat shock protein HSP70 was also downregulated in response to Plitidepsin treatment. This gene expression signature is comparable to the one previously obtained in B cells (AML and ALL cell lines), although some differences, which can be explained by the different sensibility to Plitidepsin of B or T cells, have been found.
Chronology of Cholelithiasis
Authors: Henry Y.I. Mok, Ellen R.M. Druffel, William M. Rampone
Journal: New England Journal of Medicine (1986)

We investigated the natural history of cholelithiasis in 59 samples of stones from the gallbladder or common bile duct in 15 patients, using as a tracer for the timing of stone formation the 14C released into the environment during nuclear weapons testing. The ages of the stones were correlated with the dates of onset of symptoms and with other clinical data. None of 11 symptomatic patients had symptoms or complications until at least two years (mean +/- SD, 8.0 +/- 5.1 years) after stone formation began. There was a lag time of 11.7 +/- 4.6 years between initial stone formation and cholecystectomy. The growth rates of stones from 11 symptomatic patients and 4 asymptomatic patients were similar (2.6 +/- 1.4 and 2.6 +/- 1.1 mm per year). Studies of two stones retrieved from the common bile duct showed that one had the same age as a cholecystic stone; the other, removed two years after cholecystectomy, apparently grew in the common bile duct. The long latency period between the formation of gallstones and the onset of symptoms indicates that interruption of the natural progression of gallstone disease is potentially possible with medical therapy.
Abstract 9012: Ablation of Neutral Cholesterol Ester Hydrolase 1 Accelerates Oxysterol-induced Macrophage Apoptosis by Aggravating Endoplasmic Reticulum Stress.
Authors: Motohiro Sekiya, Jun-ichi Osuga, Masaki Igarashi, Hiroaki Okazaki, Shun Ishibashi
Journal: Circulation (2010)

An excess of cholesterol and/or oxysterols induces apoptosis in macrophages, contributing to the development of advanced atherosclerotic lesions. In foam cells, these sterols are stored in esterified forms, which are mainly hydrolyzed by two enzymes: neutral cholesterol ester hydrolase 1 (Nceh1) and hormone-sensitive lipase (Lipe). A deficiency in either enzyme leads to accelerated growth of atherosclerotic lesions in mice. However, it is poorly understood how the esterification and hydrolysis of sterols are linked to apoptosis. While attempting to examine the intracellular structures of the Nceh1-deficient macrophages using transmission electron microscopy, we found the characteristic features of apoptosis such as condensed nuclei predominantly in Nceh1-deficient macrophages under normal culture conditions. We examined several apoptotic stimuli, and 25-hydroxycholesterol (25-HC) strikingly induced apoptosis in Nceh1-deficient macrophages (10.5% in wild-type vs 86.1% in Nceh1-deficient macrophages upon in...