tbuckley/cabot-search huggingface dataset:
The utility of the ‘temporary marginal lid suture’ in facilitating Mohs surgery for tumours involving the eyelid
Authors: N. J. Mortimer, E. Tan, W. Hussain, P. J. Salmon
Journal: British Journal of Dermatology (2012)

Funding sources: none. Conflicts of interest: none declared. Madam, The application of temporary sutures placed through the tarsus of the lower eyelid is well documented in the oculoplastic and dermatological surgery literature. They are generally used as suspension sutures (Frost sutures) to reduce the risk of ectropion due to wound contraction after reconstructive procedures involving the lower eyelid.1–5 The use of temporary sutures to facilitate Mohs surgical extirpation of eyelid tumours has not previously been described. Mohs surgical excision of skin cancers involving the eyelids presents unique challenges to the surgeon. The very thin, mobile nature of eyelid skin and the need to evert the lid to incise the conjunctiva for marginal lid tumours makes the incision of tissue difficult and the harvesting and orientation of an optimal Mohs surgery specimen technically demanding. Methods to facilitate stabilization of the tissue include the use of chalazion clamps, jaeger plates and manual stretching of the skin by the surgical assistant.6, 7 We describe the use of a marginal eyelid suture to stabilize the eyelid, stretch the tissue and evert the lid when incising the conjunctiva, which in our experience is a useful tool to ensure high‐quality Mohs surgery specimens for frozen section tissue processing.
Adipose tissue reduction in mice lacking the translational inhibitor 4E-BP1
Authors: Kyoko Tsukiyama-Kohara, Francis Poulin, Michinori Kohara, Christine T. DeMaria, Alan Cheng, Zhidan Wu, Anne-Claude Gingras, Asao Katsume, Mounib Elchebly, Bruce M. Spiegelman, Mary-Ellen Harper, Michel L. Tremblay, Nahum Sonenberg
Journal: Nature Medicine (2001)
966. Synergy between Angiostatin-Endostatin and Tie-2: A Novel Anti-Angiogenic Gene Therapy for Prostate Cancer
Authors: Sudhanshu P. Raikwar, Chinghai Kao, Thomas A. Gardner
Journal: Molecular Therapy (2004)

TARGETED CANCER THERAPIES III induced a substantial anti-cancer effect in vitro and in vivo.As a further enhancement the cancer cell killing effect was improved with a tropism modification of the virus to express the knob domain of Ad3, and this improved infectivity for cancer cells.Conversely, the hTERT promoter has low activity in normal tissues, and the CRAd caused no damage to normal lung fibroblast cells.Since the telomerase activity is common in many types of cancers, these CRAds may be applicable to a wide range of tumors.We concluded that the use of hTERT promoter-based CRAds may be a potentially effective strategy for cancer treatment.
TERMINAL HYPERTHERMIA FOLLOWING INTRATHECAL STREPTOKINASE ADMINISTRATION IN A CASE OF TUBERCULOUS MENINGITIS
Authors: W L CRADDOCK, J HADDOCK-SUAREZ
Journal: Annals of Internal Medicine (1952)

Case Reports1 January 1952TERMINAL HYPERTHERMIA FOLLOWING INTRATHECAL STREPTOKINASE ADMINISTRATION IN A CASE OF TUBERCULOUS MENINGITISWALLIS L. CRADDOCK, M.D., J. HADDOCK-SUAREZ, M.D.WALLIS L. CRADDOCK, M.D.Search for more papers by this author, J. HADDOCK-SUAREZ, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-36-1-168 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptClinicians who have treated tuberculous meningitis readily welcome any suggestion which may improve results of treatment in this grave condition. Since Cathie1reported beneficial results in tuberculous meningitis from intrathecal streptokinase (a component of streptococcal fibrinolysin), several British reports2, 3have confirmed his opinions. In many institutions in England it has become routine to use this therapy, and the major effect has been a reduction in the number of cases which develop elevated intracranial pressure and internal hydrocephalus. It has been assumed that the use of this fibrinolytic enzyme should be prophylactic, in addition to its causing the liquefaction of...Bibliography1. Cathie IA: Streptokinase in treatment of tuberculous meningitis, J. Clin. Path. 2: 73 (Aug.) 1949. CrossrefMedlineGoogle Scholar2. CathieMacFarlane IAJC: Adjuvants to streptomycin in treating tuberculous meningitis, Lancet 259: 784 (Dec.) 1950. CrossrefGoogle Scholar3. WilliamsBazeley SPL: Use of streptokinase in the treatment of tuberculous meningitis, M. J. Australia 4: 690 (Nov.) 1950. CrossrefGoogle Scholar4. Stearns WH: Meningitis, Am. J. Med. 10: 746 (June) 1951. Google Scholar5. Personal communication with Carl W. Tempel, Colonel (M.C.), U. S. A., Chief Medical Service, Fitzsimons Army Hospital, Denver, Colo. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: WALLIS L. CRADDOCK, M.D.; J. HADDOCK-SUAREZ, M.D.Affiliations: Jefferson Barracks, Missouri*Received for publication June 22, 1951.From the Medical Service, Veterans Hospital, Jefferson Barracks, Missouri.Published with the permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expressed or conclusions drawn by the authors. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBiologische ProteolyseACTH and adrenal steroids in the treatment of pneumococcal meningitis in adultsANAPHYLACTIC SHOCK FROM INTRAPLEURAL STREPTOKINASE-STREPTODORNASE 1 January 1952Volume 36, Issue 1 Page: 168-171 Keywords Enzymes Hydrocephalus Hyperthermia Medical services Meningitis Surgery ePublished: 1 December 2008 Issue Published: 1 January 1952 PDF downloadLoading ...
Abstract 19626: Muscle Weakness Induces Left Ventricular Hypertrophy via Frequent Elevation of Functional Arterial Stiffness During Exercise in Patients With Hypertension
Authors: Yumi Kamada, Takashi Masuda, Daisuke Kamekawa, Shinya Tanaka, Akihiro Aoyama, Yoko Itoh, Ibuki Moriguchi, Naoyuki Kobayashi, Michihito Okubo, Emi Maekawa, Junya Ako
Journal: Circulation (2014)

Background: Hypertension (HT) characterized by autonomic imbalance, is well known to induce an inappropriate elevation of arterial stiffness resulting in left ventricular hypertrophy (LVH). On the other hand, decreased muscle strength enhances autonomic imbalance by stimulating muscle sympathetic activity during exercise even at low- or moderate-intensity. However, it is unclear whether muscle weakness induces LVH via frequent elevation of functional arterial stiffness during exercise in patients with HT. The aim of this study was to investigate the relationships among muscle strength, autonomic activity during exercise, functional arterial stiffness and LVH in them. Methods: Fifty-five patients with HT aged 68±9 years, 32 males and 23 females, participated in this study. We measured plasma brain natriuretic peptide (BNP) and LV mass index (LVMI) on echocardiogram as parameters of LV overload and LVH, respectively, and knee extension muscle strength. Patients performed a treadmill exercise test to examine heart rate recovery (HRR). We assessed the changes from baseline values of plasma noradrenalin (NA) and brachial-ankle pulse wave velocity (PWV) to those measured just after a cycle ergometer exercise test that was performed at moderate-intensity ([[Unable to Display Character: &amp;#8895;]]NA and [[Unable to Display Character: &amp;#8895;]]PWV, respectively). The HRR, [[Unable to Display Character: &amp;#8895;]]NA and [[Unable to Display Character: &amp;#8895;]]PWV were used as parameters of parasympathetic and sympathetic activities and functional arterial stiffness, respectively. We analyzed the relationships among muscle strength, HRR, [[Unable to Display Character: &amp;#8895;]]NA, [[Unable to Display Character: &amp;#8895;]]PWV, BNP and LVMI. Results: Muscle strength was negatively correlated with [[Unable to Display Character: &amp;#8895;]]NA (r=-0.23, P&lt;0.05), [[Unable to Display Character: &amp;#8895;]]PWV (r=-0.24, P&lt;0.05), BNP (r=-0.23, P&lt;0.05) and LVMI (r=-0.23, P&lt;0.05). No significant relationship was observed between muscle strength and HRR. LVMI was positively correlated with [[Unable to Display Character: &amp;#8895;]]PWV (r=0.28, P&lt;0.05). Conclusion: Muscle weakness induced LVH via frequent elevation of functional arterial stiffness caused by autonomic imbalance during exercise in patients with HT.
An Atlas of Clinical Neurology.
Authors: Roger N. Rosenberg
Journal: Annals of Internal Medicine (1977)

Developmental Diseases of the Nervous System Genetic Diseases of the Nervous System Neuroendocrinology and Systemic Metabolic Disease Coma and Intensive Care Neurology Cerebrovascular Disease Dementias and Behavioral Neurology Neuro-Oncology Movement Disorders The Epilepsies Neuromuscular Disease Infectious Diseases of the Nervous System Neuroimmunology Neurotoxic Disorders Nutritional Diseases of the Nervous System
Abstract 3392: G Protein-Coupled Receptor Kinase 2 Ablation in Cardiac Myocytes Decreases Ischemia/Reperfusion Induced Myocardial Apoptosis and Improves Cardiac Function
Authors: Erhe Gao, Qian Fan, Xiying Shang, Zheng Huang, Philip Raake, J. Kurt Chuprun, Gerald W. Dorn, Walter J Koch
Journal: Circulation (2009)
Concomitant granulocyte colony-stimulating factor and induction chemoradiotherapy in adult acute lymphoblastic leukemia: a randomized phase III trial
Authors: OG Ottmann, D Hoelzer, E Gracien, A Ganser, K Kelly, R Reutzel, T Lipp, FW Busch, M Schwonzen, G Heil
Journal: Blood (1995)
Blood Lead Levels and Hypertension
Authors: Robert P. Heaney
Journal: JAMA (2003)

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
Moonlighting Adenosine Deaminase: A Target Protein for Drug Development
Authors: Antoni Cortés, Eduard Gracia, Estefania Moreno, Josefa Mallol, Carme Lluís, Enric I. Canela, Vicent Casadó
Journal: Medicinal Research Reviews (2014)

Abstract Interest in adenosine deaminase (ADA) in the context of medicine has mainly focused on its enzymatic activity. This is justified by the importance of the reaction catalyzed by ADA not only for the intracellular purine metabolism, but also for the extracellular purine metabolism as well, because of its capacity as a regulator of the concentration of extracellular adenosine that is able to activate adenosine receptors (ARs). In recent years, other important roles have been described for ADA. One of these, with special relevance in immunology, is the capacity of ADA to act as a costimulator, promoting T‐cell proliferation and differentiation mainly by interacting with the differentiation cluster CD26. Another role is the ability of ADA to act as an allosteric modulator of ARs. These receptors have very general physiological implications, particularly in the neurological system where they play an important role. Thus, ADA, being a single chain protein, performs more than one function, consistent with the definition of a moonlighting protein. Although ADA has never been associated with moonlighting proteins, here we consider ADA as an example of this family of multifunctional proteins. In this review, we discuss the different roles of ADA and their pathological implications. We propose a mechanism by which some of their moonlighting functions can be coordinated. We also suggest that drugs modulating ADA properties may act as modulators of the moonlighting functions of ADA, giving them additional potential medical interest.
Bacterial induction of Snail1 contributes to blood-brain barrier disruption
Authors: Brandon J. Kim, Bryan M. Hancock, Andres Bermudez, Natasha Del Cid, Efren Reyes, Nina M. van Sorge, Xavier Lauth, Cameron A. Smurthwaite, Brett J. Hilton, Aleksandr Stotland, Anirban Banerjee, John Buchanan, Roland Wolkowicz, David Traver, Kelly S. Doran
Journal: Journal of Clinical Investigation (2015)

Bacterial meningitis is a serious infection of the CNS that results when blood-borne bacteria are able to cross the blood-brain barrier (BBB). Group B Streptococcus (GBS) is the leading cause of neonatal meningitis; however, the molecular mechanisms that regulate bacterial BBB disruption and penetration are not well understood. Here, we found that infection of human brain microvascular endothelial cells (hBMECs) with GBS and other meningeal pathogens results in the induction of host transcriptional repressor Snail1, which impedes expression of tight junction genes. Moreover, GBS infection also induced Snail1 expression in murine and zebrafish models. Tight junction components ZO-1, claudin 5, and occludin were decreased at both the transcript and protein levels in hBMECs following GBS infection, and this repression was dependent on Snail1 induction. Bacteria-independent Snail1 expression was sufficient to facilitate tight junction disruption, promoting BBB permeability to allow bacterial passage. GBS induction of Snail1 expression was dependent on the ERK1/2/MAPK signaling cascade and bacterial cell wall components. Finally, overexpression of a dominant-negative Snail1 homolog in zebrafish elevated transcription of tight junction protein-encoding genes and increased zebrafish survival in response to GBS challenge. Taken together, our data support a Snail1-dependent mechanism of BBB disruption and penetration by meningeal pathogens.
Evaluation of Drug Utilization Review Programs
Authors: Dale B Christensen, William H Campbell, Thomas R Fulda, Mark C Pugh, David H Smith, Earlene E Lipowski, Elgene W Jacobs, Julie W Kuhle, Robert A Crittenden
Journal: JAMA (2004)

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
CARCINOMA OF THE LUNG; A REVIEW OF 31 PROVED CASES AT THE PHILADELPHIA NAVAL HOSPITAL
Authors: Ferdinand Fetter
Journal: Annals of Internal Medicine (1943)

Article1 June 1943CARCINOMA OF THE LUNG; A REVIEW OF 31 PROVED CASES AT THE PHILADELPHIA NAVAL HOSPITALFERDINAND FETTER, M.D., F.A.C.P.FERDINAND FETTER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-18-6-978 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINCIDENCE AND ETIOLOGYThe outstanding fact about primary carcinoma of the lung is the amazing increase in its frequency during the past 30 years. Formerly bronchogenic carcinoma was considered one of the rare forms of cancer; now it has been found to be one of the commonest. Some startling facts about the frequency of this disease that were brought out by Overholt and Rumel1in a recent review of the subject are: (1) that large autopsy series show that approximately 10 per cent of all cancers start in the lung; (2) that about 15,000 people die from bronchogenic carcinoma each...Bibliography1. OVERHOLTRUMEL RHWR: Clinical studies of primary carcinoma of the lung, Jr. Am. Med. Assoc., 1940, cxiv, 735. Google Scholar2. HALPERT B: Carcinoma of the lung, Jr. Am. Med. Assoc., 1941, cxvii, 1090. CrossrefGoogle Scholar3. OSCHNERDEBAKEY AM: Carcinoma of the lung, Arch. Surg., 1941, xlii, 209. Google Scholar4. MAHERSTADERMAN PPAH: Bronchogenic carcinoma—Review of thirty verified cases, U. S. Naval Med. Bull., 1941, xxxviii, 541. Google Scholar5. OVERHOLT RH: Carcinoma of the lung as a surgical problem, Am. Jr. Surg., 1941, liv, 161. CrossrefGoogle Scholar6. HARPER FR: Bronchiogenic carcinoma of more than five years' duration treated by radiotherapy, Jr. Thorac. Surg., 1939, viii, 683. CrossrefGoogle Scholar7. BROCK RC: Pulmonary new growths: pathology, diagnosis, and treatment, Lancet, 1938, ii, 1103. CrossrefGoogle Scholar8. GRAHAM EA, in discussion of SHENSTONE S.: Experiences with total pneumonectomy, Jr. Thorac. Surg., 1942, xi, 413. Google Scholar9. PERRONELEVINSON JAJP: Primary carcinoma of the lung, ANN. INT. MED., 1942, xvii, 12. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Medical Corps United States Naval Reserve Philadelphia, Pennsylvania*Read at the Fifth Annual Round-up of Eastern Pennsylvanians of the American College of Physicians, U. S. Naval Hospital, Philadelphia, Pa., October 23, 1942. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPrimary Bronchiogenic Carcinoma 1 June 1943Volume 18, Issue 6Page: 978-987KeywordsAutopsyLung and intrathoracic tumors ePublished: 1 December 2008 Issue Published: 1 June 1943 PDF downloadLoading ...
Abstract P2-03-19: Discovery of the genes that underpin the transition to malignant phenotype of breast tumors in highly consanguineous region
Authors: Ishita Gupta, Allal Ouhtit, Somya Shanmuganathan, Hamad Al-Riyami
Journal: Cancer Research (2015)

Abstract Breast cancer (BC), a multifactorial and heterogeneous disease is a predominant women form of cancer worldwide affecting 22.9%. The rationale of this study is based on the following observations: 1) in Oman, a significantly increasing number of younger females (25-40 years) present to the clinic with advanced stage of BC; 2) in Oman, the rate of consanguinity is significantly high (52%); and 3) the transition from normal/begnin to malignant phenotype of breast tumor requires the involvement of a subset of specific genes. The long-term objective of this study is to identify and validate the subset of genes that are responsible for this malignant transformation using functional genomic studies, focus on this young age group of patients attending BC clinic (sporadic and familial). RNA samples were isolated from 40 Breast Tumors and 40 Normal tissues and analyzed by Microarray Gene Expression Profiling. Among a number of genes that were up and down regulated, BRIP1, HOXB3 and MAGED1 were identified as potential genes that might underpin the transition to the malignant phenotype; these genes were validated by RT-PCR using the same RNA samples that were examined by microarray. Pathway analysis was carried out to identify the major functional pathways connecting these genes. Ongoing sequencing of these genes using DNA extracted from the same samples will ultimately identify any genetic alteration that can affect the normal function of these genes. Functional validation assays aim to validate further the physiological relevance of these genes in tumor malignancy, and perhaps other novel genes specific to BC in the Omani population. Identification and validation of these genes will potentially pave the way towards the design of anti-cancer therapeutic strategies. Citation Format: Ishita Gupta, Allal Ouhtit, Somya Shanmuganathan, Hamad Al-Riyami. Discovery of the genes that underpin the transition to malignant phenotype of breast tumors in highly consanguineous region [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 P2-03-19.
The Effect of a Disease Management Intervention on Quality and Outcomes of Dementia Care
Authors: Barbara G. Vickrey, Brian S. Mittman, Karen I. Connor, Marjorie L. Pearson, Richard D. Della Penna, Theodore G. Ganiats, Robert W. DeMonte, Joshua Chodosh, Xinping Cui, Stefanie Vassar, Naihua Duan, Martin Lee
Journal: Annals of Internal Medicine (2006)

The investigators randomly assigned patients with dementia and their caregivers to usual care or to a coordinated system of care. In the coordinated system, care managers regularly assessed patient...
Oral tofacitinib for psoriasis: what happens with interrupted treatment?
Authors: H. Alinia, S.R. Feldman
Journal: British Journal of Dermatology (2015)

ORIGINAL ARTICLE, p 1395 Before biologics, the Holy Grail of treatment for moderate‐to‐severe psoriasis was an oral immunosuppressive agent with the efficacy of ciclosporin without ciclosporin's renal side‐effects. Bissonnette et al.1 describe such an agent, tofacitinib, an inhibitor of Janus kinase signalling. Tofacitinib has good efficacy in psoriasis (phase III study results demonstrated tofacitinib 10 mg twice daily was not inferior to etanercept 50 mg twice weekly),2 and, so far, the safety profile appears reasonably good.1 However, biologics have spoiled us. No longer is it good enough just to be a ‘clean’ immunosuppressive. The immunosuppressive effects of biologics are generally quite minimal, with immune‐related side‐effects that are quite uncommon. The long‐term side‐effect profile of tofacitinib is not, as yet, as well characterized. One advantage of tofacitinib over biologics is that many patients would prefer taking a pill to receiving an injection. Another potential advantage is that biologics lose efficacy over time,3 4 while a small molecule like tofacitinib would be expected to have less antigenicity than biologics. This might permit intermittent dosing, an approach that, owing to antigenicity, is problematic for biologics. Bissonnette et al.1 tested discontinuation/retreatment in a phase III, randomized, double‐blind, parallel‐group study of patients with chronic, moderate‐to‐severe plaque psoriasis. Patients were first treated with either tofacitinib 5 or 10 mg twice daily for 24 weeks. If patients achieved at least a 75% improvement in Psoriasis Area Severity Index (PASI 75), they were randomized to either continued therapy until week 56 or placebo for 16 weeks followed by retreatment with the previous dose for 16 weeks.1
Catastrophe in the Making: The Engineering of Katrina and the Disasters of Tomorrow <i>William R. Freudenberg, Robert Gramling, Shirley Laska, and Kai T. Erikson</i> . Washington, DC:Island Press, 2009. 209 pp. ISBN: 978-1-59726-682-6, $26.95 
Authors: David E. Schaad
Journal: Environmental Health Perspectives (2010)