tbuckley/cabot-search huggingface dataset:
Erratum: Triad3A, an E3 ubiquitin-protein ligase regulating Toll-like receptors
Authors: Tsung-Hsien Chuang, Richard J Ulevitch
Journal: Nature Immunology (2004)

Nature Immunology 5, 495–502 (2004). In Figure 3b, the conditions above the blot were mislabeled and in Figure 6e, HKSA and OspA were mislabeled. They are labeled correctly here. Nature Immunology regrets these errors.
Abstract 5022: Early progenitor cells but not late luminal progenitor cells preserve in invasive breast carcinoma.
Authors: Kevin J. Zhang, Suling Liu, Nava Siegelmann-Danieli, Ping L. Zhang
Journal: Cancer Research (2013)

Abstract Background CD133 and CD117 represent markers of human breast tissue differentiation. CD133 is an early progenitor marker while CD117 represents late luminal progenitor marker (Lim, et al, Nature Medicine 2009). Morphologic expression of the two markers has not been well established in paraffin embedded tissue of human breast lesions. Design In this study, we evaluated CD133 and C117 expression in different human breast lesions. Group 1 consisted of 15 benign breast cases (5 reduction mammoplasty cases with no significant pathology and 10 fibroadenoma or fibrocystic changes). Group 2 (malignant group 2) included 13 breast cases with invasive ductal carcinoma (IDC). Group 3 (malignant group 3) was composed of 12 BRCA-mutant breast cases but only six cases had IDC. All sections from paraffin embedded tissue were immunohistochemically stained for CD133 (AC133 clone) and CD117 (monoclonal antibody). Expression of the two markers in normal breast glands adjacent to lesions (normal controls), benign lesions (benign controls) and IDC were evaluated and positive rate was calculated. Results Both CD133 and CD117 were expressed in normal breast glands (normal controls) of all three groups and benign breast lesions (Table 1). However, the expression of CD133 was detected in the majority of IDC lesions as compared to low positive percent of CD117 expression in both groups 2 and 3 (Table 1). Recombined tumor cases, based on the molecular luminal status, also showed 56 - 70% CD133 positivity but 0 - 20% CD117 positivity in IDC cells. Table 1. CD133 and CD117 in benign and malignant breast lesions Group 1, total Group 2, total Group 3, total CD133+ in normal 15/15 (100%) 13/13 (100%) 12/12 (100%) CD117+ in normal 15/15 (100%) 13/13 (100%) 11/12 (91%) Group 1, Benign Lesions Group 2, Invasive cancer Group 3 Invasive cancer CD133+ in lesions 10/10 (100%) 8/13 (61%) 4/6 (67%) CD117+ in lesions 9/10 (90%) 1/13 (8%) 1/6 (17%) Conclusions We show that normal breast glands expressed both CD133 and CD117, compatible with the presence of stem cell niche in normal breast ducts and acini. However our data suggest that in IDC, there is presence of early progenitor cells but not late luminal progenitor cells, regardless of the molecular luminal status, supporting the view that cancer stem cells exist in the invasive breast carcinoma. Citation Format: Kevin J. Zhang, Suling Liu, Nava Siegelmann-Danieli, Ping L. Zhang. Early progenitor cells but not late luminal progenitor cells preserve in invasive breast carcinoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5022. doi:10.1158/1538-7445.AM2013-5022
S154 Is there a role for IL-33 in the pathogenesis of pulmonary arterial hypertension?
Authors: D. Shao, F. Perros, M. Humbert, G. Caramori, L. Price, I. Addcock, S. Wort
Journal: Thorax (2010)

<h3>Introduction and objectives</h3> IL-33 is a 31KDa cytokine which is a member of the IL-1 family. It resides in the nucleus of endothelial and epithelial cells as a chromatin-associated factor in vivo. IL-33 is thought to be released from stressed or necrotic, but not apoptotic, endothelial or epithelial cells in response to cell injury or infection, acting as an endogenous 'alarmin', to alert the immune system of cell and tissue damage. IL-33 is then able to bind to its receptor (ST2) on immune cells, thereby stimulating immunoregulatory activity through induction of NF-κB and mitogen-activated protein kinases, as well as enhancing the production of the Th2 cytokines IL-5 and IL-13. There is increasing evidence that IL-33 may have a protective role in terms of endothelial integrity and function. As the pathogenesis of pulmonary arterial hypertension (PAH) is thought to involve endothelial cell dysfunction, we were interested to see whether there may be a role for IL-33 in this condition. <h3>Methods</h3> RT-PCR for IL-33 was performed on human pulmonary arterial cells (HPAECs) derived from normal healthy controls and patients with idiopathic PAH. siRNA IL-33 knockdown was performed using smartpool duplexes on normal HPAECs. RT-PCR was then performed using QuantiTec primer assays. <h3>Results</h3> IL-33 mRNA expression was decreased 2.1-fold in PAH patient samples (0.369±0.02, n=10) compared to controls (0.761±0.06, n=14) p&lt;0.005. In normal human lung tissue, intense IL-33 staining was shown in the ECs nuclear in blood vessels. It is also worth to note that there was little or no IL-33 staining in non-ECs. siRNA knockdown IL-33 in HPAECs resulted in a 1.8±0.22, 1.3±0.13 and 1.4±0.20 (n=3) fold increase of mRNA IL-6, BMP-9 and ST2 mRNA, respectively; whereas RANTES, fractalkine and cathepsin-L mRNA was decreased by 1.5±0.03, 1.7±0.01 and 2.1±0.17 fold respectively (n=3) (Abstract S154 Figure 1). <h3>Conclusion</h3> IL-33mayplay an important role in the pathogenesis of PAH through regulating the expression ofcytokines and chemokines known to be involved in vascular remodelling. In particular, it is of interest that Il-33 may regulate IL-6 production and ST2 which acts as an endogenous IL-33 inhibitor.
Autologous Transplantation of Granulocyte Colony–Stimulating Factor–Mobilized Peripheral Blood Mononuclear Cells Improves Critical Limb Ischemia in Diabetes
Authors: Pingping Huang, Shangzhu Li, Mingzhe Han, Zhijian Xiao, Renchi Yang, Zhong Chao Han
Journal: Diabetes Care (2005)

OBJECTIVE— To assess the application of autologous transplantation of granulocyte colony–stimulating factor (G-CSF)–mobilized peripheral blood mononuclear cells (PBMNCs) in the treatment of critical limb ischemia (CLI) of diabetic patients and to evaluate the safety, efficacy, and feasibility of this novel therapeutic approach. RESEARCH DESIGN AND METHODS—Twenty-eight diabetic patients with CLI were enrolled and randomized to either the transplant group or the control group. In the transplant group, the patients received subcutaneous injections of recombinant human G-CSF (600 μg/day) for 5 days to mobilize stem/progenitor cells, and their PBMNCs were collected and transplanted by multiple intramuscular injections into ischemic limbs. All of the patients were followed up after at least 3 months. RESULTS—At the end of the 3-month follow-up, the main manifestations, including lower limb pain and ulcers, were significantly improved in the patients of the transplant group. Their laser Doppler blood perfusion of lower limbs increased from 0.44 ± 0.11 to 0.57 ± 0.14 perfusion units (P &amp;lt; 0.001). Mean ankle-brachial pressure index increased from 0.50 ± 0.21 to 0.63 ± 0.25 (P &amp;lt; 0.001). A total of 14 of 18 limb ulcers (77.8%) of transplanted patients were completely healed after cell transplantation, whereas only 38.9% of limb ulcers (7 of 18) were healed in the control patients (P = 0.016 vs. the transplant group). No adverse effects specifically due to cell transplantation were observed, and no lower limb amputation occurred in the transplanted patients. In contrast, five control patients had to receive a lower limb amputation (P = 0.007, transplant vs. control group). Angiographic scores were significantly improved in the transplant group when compared with the control group (P = 0.003). CONCLUSIONS—These results provide pilot evidence indicating that the autologous transplantation of G-CSF–mobilized PBMNCs represents a simple, safe, effective, and novel therapeutic approach for diabetic CLI.
Why doctors don't read research papers
Authors: Christopher W Ide
Journal: BMJ (2005)

Editor—Having written or co-written several original research papers and review articles during my professional life, I believe that one of the reasons that we don't read research papers is because, despite protestations to the contrary, editors regularly seem to indulge in behaviour that goes against all the principles of good writing, including insisting on the use of po-faced titles which do not even attract the reader's attention in the first place.1
Overloading human aortic smooth muscle cells with low density lipoprotein-cholesteryl esters reproduces features of atherosclerosis in vitro.
Authors: J L Goldstein, R G Anderson, L M Buja, S K Basu, M S Brown
Journal: Journal of Clinical Investigation (1977)

Human aortic smooth muscle cells accumulate only small amounts of cholesteryl esters in tissue culture, even when incubated for prolonged periods with high levels of plasma low density lipoprotein (LDL). This failure to overaccumulate LDL-cholesteryl esters is due to an LDL-mediated feedback suppression of the activity of the cell surface LDL receptor, a regulatory action that limits the rate at which the cells take up LDL. This regulatory system can be bypassed by incubating smooth muscle cells with LDL that has been given a strong positive charge by covalent linkage with N,N-dimethyl-1,3-propanediamine (DMPA-LDL). The unregulated uptake of DMPA-LDL produces a massive deposition of cholesteryl esters in the form of inclusions within the cell. These inclusions take up lipid stains and exhibit positive birefringence with formée crosses that are typical of liquid crystals of cholesteryl esters. By electron microscopy, the cholesteryl ester inclusions appear as homogeneous gray cytoplasmic lipid droplets. The current studies demonstrate that the unregulated uptake of LDL-cholesteryl esters by human aortic smooth muscle cells can reproduce in vitro the major biochemical and morphological alterations that occur within smooth muscle cells in vivo during the process of atherosclerosis.
Searching the Medical Literature
Authors: ERIC T. RUMSEY
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 June 1986Searching the Medical LiteratureERIC T. RUMSEY, M.L.S.ERIC T. RUMSEY, M.L.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-6-889_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The article by Haynes and colleagues (1) is very useful. We use the National Library of Medicine (NLM) and the Bibliographic Retrieval Service (BRS) systems to search MEDLINE, and our experience generally confirms what Haynes and colleagues report. However, the sample searches used by Haynes and colleagues to test the different systems were relatively simple and straightforward (an obvious advantage in doing an objective study of many systems). For searches such as these, NLM is indeed a perfectly adequate system, and it probably is the least expensive, as the study shows. As searches become more complicated, however,...Reference1. HAYNES R, MCKIBBON K, and WALKER C. Computer searching of the medical literature: an evaluation of MEDLINE searching systems. Ann Intern Med. 1985;103:812-6. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ERIC T. RUMSEY, M.L.S.Affiliations: University of Iowa Health Sciences Library Iowa City, IA 52242 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1986Volume 104, Issue 6Page: 889-889KeywordsLibraries ePublished: 1 December 2008 Issue Published: 1 June 1986 PDF downloadLoading ...
Macrophage-Specific Expression of Mannose-Binding Lectin Controls Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice
Authors: Robert A. Matthijsen, Menno P.J. de Winther, Dian Kuipers, Ingeborg van der Made, Christian Weber, M. Veronica Herias, Marion J.J. Gijbels, Wim A. Buurman
Journal: Circulation (2009)

With consideration of the central role of the innate immune system in atherogenesis and mannose-binding lectin (MBL) as an innate regulator of immunity, the role of MBL in experimental and human atherosclerosis was assessed.With the use of immunohistochemistry and polymerase chain reaction, deposition and gene expression of MBL-A and -C were assessed in murine atherosclerosis from mice deficient for the low-density lipoprotein receptor (LDLR(-/-)) after 10 or 18 weeks of high-fat feeding. MBL was present and was produced in 10-week-old lesions, whereas deposition and gene expression were minimal after 18 weeks of high-fat feeding and absent in healthy vasculature. Interestingly, deposition of MBL-A and -C differed: MBL-A predominantly localized in upper medial layers, whereas MBL-C was found in and around intimal macrophages. To further study the role of local MBL production by monocytic cells in atherosclerosis, LDLR(-/-) mice with MBL-A and -C(-/-) monocytic cells were construed by bone marrow transplantation. Mice carrying MBL-A and -C double deficient macrophages had increased (30%) atherosclerotic lesions compared with wild-type controls (P=0.015) after 10 weeks of high-fat diet. Subsequently, analysis of MBL deposition and gene expression in advanced human atherosclerotic lesions revealed the presence of MBL protein in ruptured but not stable atherosclerotic lesions. Putatively in agreement with murine data, no MBL gene expression could be detected in advanced human atherosclerotic lesions.These results are the first to show that MBL is abundantly present and locally produced during early atherogenesis. Local MBL expression, by myeloid cells, is shown to critically control development of atherosclerotic lesions.
Primary Extra-Adrenal Pheochromocytoma Positive I-123 MIBG Imaging with Negative I-131 MIBG Imaging
Authors: BARRY L. SHULKIN, BRAHM SHAPIRO, ISAAC R. FRANCIS, RICHARD DORR, SHAIO-WEL SHEN, JAMES C. SISSON
Journal: Clinical Nuclear Medicine (1986)

I-131 metaiodobenzylguanidine (I-131 MIBG) is a well established imaging agent that reliably detects pheochromocytoma. In some patients, however, I-131 MIBG may fail to localize pheochromocytoma. I-123 MIBG has several potential advantages over I-131 MIBG, and these advantages may enable locating pheochromocytomas which have eluded other techniques, including I-131 MIBG imaging. A patient with primary extraadrenal pheochromocytoma is described who illustrates the superiority of I-123 MIBG for the imaging of pheochromocytoma.
GRAFTING WITH FROG SKIN
Authors: H. W. M. Kendall
Journal: BMJ (1916)

MDICAL JOUR1IAIIntestinies.-Theappendices epiploicae of the transverse colon were swollen and haemorrhagic.The mesentery contained suany calcareous masses as large as small haricot beans.The lymphatic glands were not enlarged.The presacral haemolymph glands were enlarged.Kidneus.-Weighed 7 oz.each.On section they were pale in colour and in the pyramidal portion of each kidney were two pale-green areas about the size of a large pea.The other .abdominalorgans were apparentlv normal.*Marrow.-The shaft of the tibia contained marrow of a pale yellow colour with complete absence of any red coloration; that in the head of the tibia was pale yellow.The marrow of the ribs and sternum was greyish-brown in colour. MIicroscopic Examiiinationt.IHeart.-The spaces between the muscular bundles were in- filtrated with leucocytes of the myeloblastic type.Liver.-The periphery of the lobules was packed with cells ,with the appearance of myeloblasts.Much free browni-coloured pigment was presenit towards the periphery of the lobules.
Effect of rate-dependent left bundle branch block on global and regional left ventricular function.
Authors: D A Bramlet, K G Morris, R E Coleman, D Albert, F R Cobb
Journal: Circulation (1983)

Seven subjects with rate-dependent left bundle branch block (RDLBBB) and 13 subjects with normal conduction (control group) underwent upright bicycle exercise radionuclide angiography to determine the effects of the development of RDLBBB on global and regional left ventricular function. Six of the seven subjects with RDLBBB had atypical chest pain syndromes; none had evidence of cardiac disease based on clinical examination and either normal cardiac catheterization or exercise thallium-201 scintigraphy. Radionuclide angiograms were recorded at rest and immediately before and after RDLBBB in the test group, and at rest and during intermediate and maximal exercise in the control group. The development of RDLBBB was associated with an abrupt decrease in left ventricular ejection fraction (LVEF) in six of seven patients (mean decrease 6 +/- 5%) and no overall increase in LVEF between rest and maximal exercise (65 +/- 9% and 65 +/- 12%, respectively). In contrast, LVEF in the control group was 62 +/- 8% at rest and increased to 72 +/- 8% at intermediate and 78 +/- 7% at maximal exercise. The onset of RDLBBB was associated with the development of asynchronous left ventricular contraction in each patient and hypokinesis in four of seven patients. All patients in the control group had normal wall motion at rest and exercise. These data indicate that the development of RDLBBB is associated with changes in global and regional ventricular function that may be confused with development of left ventricular ischemia during exercise.
EMASCULATION AND OVARIOTOMY AS A PENALTY FOR CRIME AND THE REFORMATION OF CRIMINALS.Read before the Illinois State Medical Society, May 15, 1894.
Authors: ROBERT BOAL
Journal: JAMA (1894)

Political and social economists and humanitarians within the past third of a century have spent much time, thought and effort upon the best and most effective means of punishing crime and reforming the vicious and criminal classes of societv. The tendency of the present age is to abandon in a great measure the cruel, retaliatory and vindictive punishments for criminal offenses. As we have advanced in morals and a higher civilization the disposition to punish criminals by demanding a penalty in kind, an eye for an eye and a tooth for a tooth, has undergone a marked change, not that crime is more tolerated, or criminals more readily forgiven, but because we have more enlightened and intelligent views of the causes of crime and the antecedents, surroundings and conditions which affect the lives and form the characters of the guilty. We have now a clearer perception of the responsibility of the
Abstract 2325: Increase in neuroblastoma metastasis after dual inhibition of VEGF and Notch
Authors: Alejandro Garcia, Debarshi Banerjee, Jan K. Kitajewski, Jessica J. Kandel, Darrell J. Yamashiro
Journal: Cancer Research (2012)

Abstract Purpose: Vascular endothelial growth factor (VEGF) inhibition is a validated cancer treatment. However, even in responsive tumors, acquired resistance is common. Notch proteins also function as key angiogenic effectors, and cross-regulate VEGF expression, raising the question of whether combined treatment would enhance tumor suppression. We hypothesized that dual VEGF/Notch blockade would inhibit tumor growth in experimental SY5Y neuroblastoma. Methods: SY5Y neuroblastoma cells were lentivirally transfected to express Notch1-decoy (N1D) or GFP (control). Proliferation was assessed in vitro under both hypoxia and normoxia using BrdU assays. To examine the effect of N1D on tumor growth, 10[6] cells were xenografted intrarenally in nude mice and treated with placebo or bevacizumab (BV) twice a week. Tumor progression was monitored by bioluminescence. Metastatic burden in target organs was quantified by bioluminescence and histology. Vascular disruption due to N1D and BV treatment was evaluated by immunostaining. IACUC approval was obtained for all experiments. Results: Expression of soluble N1D was confirmed by immunoblotting conditioned media. SY5Y+N1D cells proliferated more rapidly in hypoxia than control SY5Y+GFP cells (p&amp;lt;0.01). In vivo, BV treatment alone significantly reduced tumor growth as compared to placebo (p=0.026). However, combined treatment (N1D + BV) did not further reduce SY5Y tumor growth as compared to BV treatment alone (p=0.684). Interestingly, dual-treated mice developed higher metastatic burdens in liver than mice treated with either agent alone or controls by bioluminescence (p=0.006). By histology, dual-treated mice displayed a higher incidence of liver metastasis (7/9 mice) vs. mice treated with BV only (3/10 mice). Immunostaining demonstrated disruption of tumor vessel architecture in BV- and N1D + BV-treated mice. Conclusion: Dual VEGF/Notch targeting of SY5Y tumors resulted in increased metastatic burden, without affecting primary tumor growth, as compared to either treatment alone. Recent data indicates that tumoral hypoperfusion can promote progression, potentially by selecting for biologically aggressive behaviors. Our results suggest that dual Notch/VEGF blockade causes an enhanced propensity to metastasize. These data warrant further preclinical investigation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2325. doi:1538-7445.AM2012-2325
Right sinus of Valsalva-right atrial fistula secondary to nonpenetrating chest trauma: a case report with description of noninvasive diagnostic features.
Authors: A DeSa'Neto, M B Padnick, K B Desser, N G Steinhoff
Journal: Circulation (1979)

A sinus of Valsalva-right atrial fistula secondary to nonpenetrating chest trauma is described. Echocardiogrpahy demonstrated diastolic fluttering of the anterior tricuspid valve, suggesting a left-to-right shunt at the level of the right atrium. External jugular venous pulse tracings revealed large alpha waves and attenuation of the y descent. Cardiac catheterization disclosed a fistulous communication between the right sinus of Valsalva and right atrium. After surgical repair of the fistula, the ultrasonic recording and external pulse tracing reverted to normal. We believe this is the first description of such a shunt after blunt thoracic trauma.
Medial Ptosis of the Kidney
Authors: George C. Prather
Journal: New England Journal of Medicine (1948)

PROBABLY on more than one occasion urologists have examined patients for pain or discomfort that, because of its character and location, was thought to be of renal origin, only to find the pyelographic studies normal. In at least a few of these cases the symptoms may be due to medial ptosis of the kidney.Caudal mobility of the kidney with the body in the vertical or upright position (ptosis of the kidney) has been known for many years as a clinical entity, with alternate periods of popularity and disrepute. This paper is not directly concerned with that subject.Little or . . .