tbuckley/cabot-search huggingface dataset:
US doctors were complicit in Guantanamo Bay torture, report says
Authors: H. Mooney
Journal: BMJ (2011)

Inspection of medical records, case files, and legal affidavits shows compelling evidence that the medical personnel who treated detainees at Guantanamo Bay US Naval Base in Cuba were complicit in the torture perpetrated at the base’s prison, a report says.

The paper, published in PLoS Medicine (2011;8(4):e1001027, doi:10.1371/journal.pmed.1001027), says that medical staff at the base failed to inquire into or document causes of physical injuries and psychological symptoms that they observed in the detainees.

Doctors working for the organisation Physicians for Human Rights reviewed the base’s medical records and relevant case files of nine people detained there, looking for evidence of torture and ill treatment and …
They Sent Me Here
Authors: Danielle Ofri
Journal: New England Journal of Medicine (2005)

Interview with Dr. Danielle Ofri on writing about patients’ stories. (06:20)Download “Ramonita Ortega,” I called out to the crowded waiting room. A slim, 50-ish woman with crisply trimmed gray hair followed me into my office.“They told me to give you this,” she said, smiling and shrugging, as she pushed an envelope across the desk toward me.(Figure)I've always been intrigued by who “they” are — those mystery people referred to with such assumed authority and universality. Particularly in a large city hospital, in which the staff is mammoth and constantly changing, “they” constitute a particularly encompassing force.I glanced at her chart before opening the envelope. Ms. Ortega . . .
Birmingham museum displays `The Art of Healing'
Authors: Elizabeth Rasche González
Journal: JAMA (1981)

An unorthodox "genre"—American medical art—is currently on display at the Birmingham Museum of Art in Birmingham, Ala. The exhibit, which can be viewed until March 29th, explores the interrelationship of medicine, science, and the fine arts. Entitled<i>The Art of Healing: Medicine and Science in American Art</i>, it comprises about 100 paintings, drawings, and sculptures. Art historian Dr William H. Gerdts, who wrote the catalog, notes that these works constitute an outstanding yet miscellaneous collection; selected for artistic excellence, they defy historical, stylistic, or thematic classification. Chronologically they span 300 years, beginning with one of the oldest known American portraits, an anonymous painting of Dr John Clarke (c 1664). In style, they range from neoclassic portraiture to satirical cartoons. The subjects are as diverse as Allston's<i>Christ Healing the Sick</i>; Catlin's<i>Se-non-ti-yah, Blistered Feet, a medicine man</i>; Roger's<i>Phrenology at the Fancy Ball</i>; and Warhol's Pop Art depiction of a
John Leslie Robert Barlow
Authors: Louise Barlow
Journal: BMJ (2008)

John was born in 1926 in Yorkshire to Scottish doctors, John and Louise Barlow. The family migrated to Queen Camel, Somerset, where both parents set up practice. John was educated at Epsom College, Queens’ College, Cambridge, and the Middlesex Hospital, qualifying as a physician in January 1950. He completed postgraduate work as house surgeon at Poole General Hospital (1950) and in …
Cognitive and behavioral abnormalities in children after hematopoietic stem cell transplantation for severe congenital immunodeficiencies
Authors: Penny Titman, Elizabeth Pink, Emily Skucek, Katherine O'Hanlon, Tim J. Cole, Jane Gaspar, JinHua Xu-Bayford, Alison Jones, Adrian J. Thrasher, E. Graham Davies, Paul A. Veys, H. Bobby Gaspar
Journal: Blood (2008)
Positive association between serum levels of advanced glycation end products and the soluble form of receptor for advanced glycation end products in nondiabetic subjects
Authors: Sho-ichi Yamagishi, Hisashi Adachi, Kazuo Nakamura, Takanori Matsui, Yuko Jinnouchi, Katsuhiko Takenaka, Masayoshi Takeuchi, Mika Enomoto, Kumiko Furuki, Asuka Hino, Yoshiyuki Shigeto, Tsutomu Imaizumi
Journal: Metabolism (2006)
Arterial function in nitric oxide-deficient hypertension: influence of long-term angiotensin II receptor antagonism
Authors: Jarkko Kalliovalkama, Pasi Jolma, Jari-Petteri Tolvanen, Mika Kähönen, Nina Hutri-Kähönen, Xiumin Wu, Päivi Holm, Ilkka Pörsti
Journal: Cardiovascular Research (1999)

Objective: Since the effects of angiotensin II receptor antagonism on arterial function in nitric oxide (NO)-deficient hypertension are unknown, we investigated the influence of losartan therapy (20 mg kg−1 day−1) on the control of arterial tone in NG-nitro-l-arginine methyl ester (L-NAME; 20 mg kg−1 day−1)-induced hypertension. Methods: Forty Wistar rats were divided into four groups: control, losartan, L-NAME, and losartan+L-NAME. The responses of isolated mesenteric arterial rings were examined in standard organ chambers after 8 treatment weeks. Results: Losartan therapy prevented the development of L-NAME-induced hypertension and the associated impairments of endothelium-independent relaxations to nitroprusside, isoprenaline, and cromakalim, vasodilators acting via the formation of NO, activation of β-adrenoceptors and opening of K+ channels, respectively. In addition, endothelium-dependent relaxations of noradrenaline-precontracted rings to acetylcholine during NO synthase inhibition in vitro were decreased in L-NAME rats, and clearly improved by losartan therapy. The inhibition of cyclooxygenase by diclofenac improved the responses to acetylcholine more effectively in L-NAME than losartan+L-NAME rats, but the relaxations remained decreased in L-NAME rats when compared with losartan+L-NAME rats. When hyperpolarization of smooth muscle was prevented by precontractions induced by high concentration of KCl, the responses to acetylcholine during combined NO synthase and cyclooxygenase inhibition were similar and almost abolished in all groups. Furthermore, superoxide dismutase, a scavenger of superoxide anions, enhanced the acetylcholine-induced relaxations more effectively in L-NAME than losartan+L-NAME rats, although plasma antioxidant capacity was similar in all study groups. Conclusion: Chronic L-NAME-induced hypertension was associated with attenuated arterial relaxation via endothelium-dependent and -independent mechanisms, both of which were improved by the losartan treatment. The mechanisms whereby losartan enhanced arterial relaxation in this model of experimental hypertension may have included enhanced hyperpolarization and increased sensitivity to NO in smooth muscle, and decreased vascular production of superoxide and vasoconstrictor prostanoids.
Abstract LB-502: Development of three dimensional cancer cell-CAF co-culture system
Authors: Kazuya Arai, Ruriko Sakamoto, M Itoh, Haifeng Miura
Journal: Cancer Research (2012)

Abstract Purpose A large number of cell lines have been established and used for cancer research. Monolayer culture of cancer cells alone is a simplified and effective method, however, it does not always reflect the physiological conditions. In this study, we tried to establish a simple co-culture method of cancer cells and CAF (cancer associated fibroblast), to develop three dimensional model of stroma rich tumor with cells such as pancreatic cancer and scirrhous cancer. Method Human tumor tissue samples were obtained from patients who had undergone surgery at the National Cancer Center Hospital East, Japan. Written informed consents were obtained from all patients. BxPC-3 (pancreatic cancer cell line) and A549 (lung cancer cell line) were stained with red-fluorescent dye, PKH-26. Pancreatic cancer derived- and lung cancer derived-CAF were stained with green-fluorescent dye, PKH-67. Cancer cells and CAF are seeded into the microtiter plates for 3D cell culture (NanoCulture® Plate) at a same cell number, and spheroid formation was measured by a fluorescent time lapse microscopy for 3-days. Result BxPC-3 (red) and Pancreatic CAF (green) merged well and formed mosaic spheroids. BxPC-3 (red) and lung CAF (green) did not merge and separately formed spheroids of each cell types. A549 and lung CAF merged, but A549 and Pancreatic CAF did not merge clearly. It is suggested that a specific recognition mechanisms exist by organ types or tumor types, with the adhesion between cancer cell and CAF. A) BxPC-3 and Pancreatic CAF B) BxPC-3 and lung CAF Conclusion In this study, mosaic spheroid were formed by co-culturing of same organ derived cancer cells and CAF. This co-culture system is expected as an effective tool for cancer microenvironment study and/or drug screening targeting with stroma rich tumor. 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 LB-502. doi:1538-7445.AM2012-LB-502
A HISTOLOGICAL STUDY OF THE SKIN LESIONS OF PELLAGRA
Authors: Fraser B. Gurd
Journal: The Journal of Experimental Medicine (1911)

The cutaneous lesions in pellagra consist of an early erythema, or, in occasional cases, of vesicles or bullous formations which are followed by hyperkeratosis and pigmentation, resulting in a dry, dark brown scaliness. These various lesions are similar to those normally produced by the action of sunlight, but are much more marked. The histological phenomena of the erythematous and bullous stage are those of a mild acute inflammatory reaction, together with a degeneration in the superficial layers of the corium. Following this degeneration, which involves not only the general connective tissue but the connective tissue of the blood vessels, there is a reparative change evidenced histologically by an increased cellularity of the corium and the presence of fibroblasts. The capillaries also are increased in number and much dilated. Apparently as a result of this increased vascularity of the corium, there is an increased proliferation of the epithelium resulting in a thickening of the epidermis. This increase in thickness of the epithelial layer is especially marked in the prickle cells and the stratum granulosum. In the later stages, in an effort to secure a firm basement membrane, the epithelium is seen to dip down deeply into the rarefied connective tissue. About the blood vessels during the reactionary process are found collections of lymphoid cells, a few plasma cells, but no mast cells or eosinophiles. That the irritant producing the degeneration in the corium is sunlight in the presence of some predisposing factor, is suggested by the enormous increase in pigment formation in the epithelial cells and by the large number of chromatophores in the superficial layers of the corium. This pigmentation is autochthonous in both types of cell. There is no reason for believing that the pigment is formed in the cells of the corium and thence discharged into the epithelium, or that the reverse process takes place. The predisposing factor inducing the changes in the corium is, apparently, a lessened resistance of the epithelium to the violet and ultra-violet rays, due to some metabolic insufficiency on the part of the epithelial cells. Further observation may justify the conclusion that throughout the body, pellagra is a disease essentially of the epithelium, including the nervous system, this pathological condition manifesting itself by an insufficient or altered function.
Changes in 18F-Fluorodeoxyglucose and 18F-Fluorodeoxythymidine Positron Emission Tomography Imaging in Patients with Non–Small Cell Lung Cancer Treated with Erlotinib
Authors: Linda Mileshkin, Rodney J. Hicks, Brett G.M. Hughes, Paul L.R. Mitchell, Veena Charu, Barbara J. Gitlitz, David Macfarlane, Benjamin Solomon, Lukas C. Amler, Wei Yu, Andrea Pirzkall, Bernard M. Fine
Journal: Clinical Cancer Research (2011)

Assessing clinical activity of molecularly targeted anticancer agents, especially in the absence of tumor shrinkage, is challenging. To evaluate on-treatment 18F-fluorodeoxyglucose (FDG) and/or 18F-fluorodeoxythymidine (FLT) positron emission tomography (PET) for this purpose, we conducted a prospective multicenter trial assessing PET response rates and associations with progression-free (PFS) and overall survival (OS) in 2nd/3rd-line non-small-cell lung cancer patients treated with erlotinib.PET/computed tomography (CT) scans were conducted at baseline, day (d)14 and d56 after the first daily erlotinib dose, with diagnostic CT at baseline and d56 (all scans centrally reviewed). PET partial metabolic response (PMR) was defined as a mean decrease (in ≤ 5 lesions/patient) of 15% or more maximum standardized uptake value. PFS was investigator-determined.Of 74 erlotinib-treated patients, 51 completed all imaging assessments through d56; 13 of 51 (26%) FDG-evaluable patients had PMR at d14, as did 9 of 50 (18%) FLT-evaluable patients. Four (7.8%) showed partial responses (PR) by d56 CT; all 4 had PMR by d14 FDG-PET with 3 PMRs by d14 FLT-PET. Three of the 4 patients with CT PR had evaluable archival tumor tissue; all 3 had epidermal growth factor receptor mutations. D14 and d56 PMRs by FDG or FLT were associated with improved PFS; HRs for PET responders versus nonresponders were 0.3 to 0.4. D14 FDG-PET PMR was associated with improved OS (P = 0.03) compared with FDG-PET nonresponders.Early (d14) FDG-PET PMR is associated with improved PFS and OS, even in the absence of subsequent Response Evaluation Criteria in Solid Tumors response. These data support inclusion of FDG-PET imaging in clinical trials testing novel targeted therapies, particularly those with anticipated cytostatic effects.
Genetic analysis of a kindred with familial hypobetalipoproteinemia. Evidence for two separate gene defects: one associated with an abnormal apolipoprotein B species, apolipoprotein B-37; and a second associated with low plasma concentrations of apolipoprotein B-100.
Authors: S G Young, S J Bertics, L K Curtiss, B W Dubois, J L Witztum
Journal: Journal of Clinical Investigation (1987)

In 1979 Steinberg and colleagues recognized a unique kindred with normotriglyceridemic hypobetalipoproteinemia (1979. J. Clin. Invest. 64:292-301). We have undertaken an intensive reexamination of this kindred and have studied 41 family members in three generations. In this family we document the presence of two distinct apo B alleles associated with low plasma concentrations of apolipoprotein (apo) B and low density lipoprotein (LDL) cholesterol and we trace the inheritance of these two alleles over three generations. One of the alleles resulted in the production of an abnormal, truncated apo B species, apo B-37. The other apo B allele was associated with reduced plasma concentrations of the normal apo B species, apo B-100. H.J.B., the proband, and two of his siblings had both abnormal apo B alleles and were therefore compound heterozygotes for familial hypobetalipoproteinemia. Their average LDL-cholesterol level was 6 +/- 9 mg/dl. All of the offspring of the three compound heterozygotes had hypobetalipoproteinemia, and each had evidence of only one of the abnormal apo B alleles. In the entire kindred, we identified six heterozygotes for familial hypobetalipoproteinemia who had only the abnormal apo B-37 allele and their average LDL cholesterol was 31 +/- 12 mg/dl. We identified 10 heterozygotes who had only the allele for reduced plasma concentrations of apo B-100 and their LDL cholesterol level was 31 +/- 15 mg/dl. Unaffected family members (n = 22) had LDL cholesterol levels of 110 +/- 27 mg/dl. This report describes the first kindred in which two distinct abnormal apo B alleles have been identified, both of which are associated with familial hypobetalipoproteinemia.
The Basic Position of Samuel Hahnemann
Authors: James Stephenson
Journal: JAMA (1961)

<h3>To the Editor:—</h3> Dr. Theodore Greiner in his article "Why We Rarely Know About Drugs" (<i>JAMA</i><b>177</b>:42 [July 8] 1961) essentially restates the basic position of Samuel Hahnemann, the founder of clinical pharmacology. Dr. Greiner's statement, "A more sensible attitude would be to distinguish in what way patients and their diseases have a similar response to drugs. Once a common basis is clearly described, it serves as the starting point for developing each individual therapeutic regimen. It is the task of clinical pharmacology to furnish this common basis of drug response in a form immediately available for clinical use," might be from Hahnemann's<i>Organon of Rational Healing</i>published in Leipzig in 1810. Elsewhere, Dr. Greiner speaks of "The reaction against polypharmacy and its shotgun prescriptions... in the early 1800's.... During this cycle empirical observations were neglected..." Hahnemann is, of course, generally credited by medical historians (such as Garrison) to
Malignant Melanoma and Diabetic Cutaneous Atrophy
Authors: WALTER H. C. BURGDORF
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 October 1986Malignant Melanoma and Diabetic Cutaneous AtrophyWALTER H. C. BURGDORF, M.D.WALTER H. C. BURGDORF, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-4-630_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The report of malignant melanoma in an area of diabetic cutaneous atrophy by Dr. Feldman ( 1 ) raises more questions than it answers. Dr. Feldman would have us believe that chronic skin changes in diabetes mellitus increase a patient's risk for malignant melanoma. His patient had 25 black papules and 4 pink nodules confined to areas of diabetic atrophy. The histologic diagnosis based on a punch biopsy of an unspecified lesion was "malignant melanoma, Clark's level IV and depth greater than 3.5 mm." This pathologic diagnosis implies that the author was able to identify a primary...References1. FELDMAN L. Diabetic cutaneous atrophy and malignant melanoma [Letter]. Ann Intern Med. 1985;105:142-3. LinkGoogle Scholar2. BALCHMILTON CG. Diagnosis of metastatic melanoma at distant sites. In: BALCH CM, MILTON GW, eds. Cutaneous Melanoma. Philadelphia: J.B. Lippincott Company; 1985:241. Google Scholar3. KORNBERGHARRISACKERMAN RMA. Epidermotropically metastatic malignant melanoma. Arch Dermatol. 1978;114:67-9. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1986Volume 105, Issue 4Page: 630-630KeywordsAtrophyBiopsyCutaneous melanomaDiabetes mellitusLesionsMelanoma Issue Published: 1 October 1986 PDF downloadLoading ...
SCINTIGRAPHIC EVALUATION OF NON-HODGKINʼS B-CELL LYMPHOMA PATIENTS WITH A NEW Tc-99m LABELED MONOCLONAL ANTIBODY FAB1 FRAGMENT
Authors: V. Vijayakumar, M. J. Blend, C. Bekerman, M. Kozloff, R. H. Seevers, C. M. Pinsky
Journal: Clinical Nuclear Medicine (1992)

Vijayakumar, V.; Blend, M. J.; Bekerman, C.; Kozloff, M.; Seevers, R. H.; Pinsky, C. M.* Author Information
Disease-related phenotypes in a Drosophila model of hereditary spastic paraplegia are ameliorated by treatment with vinblastine
Authors: G. Orso
Journal: Journal of Clinical Investigation (2005)

Hereditary spastic paraplegias (HSPs) are a group of neurodegenerative diseases characterized by progressive weakness and spasticity of the lower limbs. Dominant mutations in the human SPG4 gene, encoding spastin, are responsible for the most frequent form of HSP. Spastin is an ATPase that binds microtubules and localizes to the spindle pole and distal axon in mammalian cell lines. Furthermore, its Drosophila homolog, Drosophila spastin (Dspastin), has been recently shown to regulate microtubule stability and synaptic function at the Drosophila larval neuromuscular junction. Here we report the generation of a spastin-linked HSP animal model and show that in Drosophila, neural knockdown of Dspastin and, conversely, neural overexpression of Dspastin containing a conserved pathogenic mutation both recapitulate some phenotypic aspects of the human disease, including adult onset, locomotor impairment, and neurodegeneration. At the subcellular level, neuronal expression of both Dspastin RNA interference and mutant Dspastin cause an excessive stabilization of microtubules in the neuromuscular junction synapse. In addition, we provide evidence that administration of the microtubule targeting drug vinblastine significantly attenuates these phenotypes in vivo. Our findings demonstrate that loss of spastin function elicits HSP-like phenotypes in Drosophila, provide novel insights into the molecular mechanism of spastin mutations, and raise the possibility that therapy with Vinca alkaloids may be efficacious in spastin-associated HSP and other disorders related to microtubule dysfunction.
PPARgamma induces the insulin-dependent glucose transporter GLUT4 in the absence of C/EBPalpha during the conversion of 3T3 fibroblasts into adipocytes.
Authors: Z Wu, Y Xie, R F Morrison, N L Bucher, S R Farmer
Journal: Journal of Clinical Investigation (1998)

To define the molecular mechanisms that control GLUT4 expression during adipogenesis, NIH-3T3 fibroblasts ectopically expressing different adipogenic transcription factors (C/EBPbeta, C/EBPdelta, C/EBPalpha, and PPARgamma) under the control of a tetracycline-responsive inducible (C/EBPs) or a constitutive retroviral (PPARgamma) expression system were used. Enhanced production of C/EBPbeta (beta2 cell line), C/EBPbeta together with C/EBPdelta (beta/delta39 cell line), C/EBPalpha (alpha1 cell line), or PPARgamma (Pgamma2 cell line) in cells exposed to dexamethasone and the PPARgamma ligand ciglitazone (a thiazolidinedione) resulted in expression of GLUT4 mRNA as well as other members of the adipogenic gene program, including aP2 and adipsin. Focusing our studies on the beta/delta39 cells, we have demonstrated that C/EBPbeta along with C/EBPdelta in the presence of dexamethasone induces PPARgamma, adipsin, and aP2 mRNA production; however, GLUT4 mRNA is only expressed in cells exposed to ciglitazone. In addition, enhanced expression of a ligand-activated form of PPARgamma in the beta/delta39 fibroblasts stimulates synthesis of GLUT4 protein and gives rise to a population of adipocytic cells that take up glucose in direct response to insulin. C/EBPalpha is not expressed in the beta/delta39 cells under conditions that stimulate the adipogenic program. This observation suggests that PPARgamma alone or in combination with C/EBPbeta and C/EBPdelta is capable of activating GLUT4 gene expression.
Nail-Patella Syndrome: Hereditary Onchyo-Osteodysplasia Diagnosis by Tc-99m MDP Bone Scan
Authors: JOHN L. HOWARD, WARREN H. MOORE, RAMESH D. DHEKNE
Journal: Clinical Nuclear Medicine (1990)

Onchyo-osteodysplasia has been described by previous authors. It is a congenital abnormality transmitted in an autosomal dominant pattern. The karyotype and chromosomal number are normal. It is a disease primarily of the bones, nails, and kidneys, but many other organ systems may demonstrate abnormalities. The diagnosis can be made without having all the classic findings. The osseous abnormalities frequently involve the patella, pelvis, and elbow. The patella may be hypoplastic, aplastic, or dislocated. The iliac bones have bilateral “horns,” triangular bony protuberances that project posteriorly. The radial head is hypoplastic or subluxed posteriorly, leading to an increased carrying angle and often to disturbed function and decreased range of motion. Scoliosis is common. The nails, primarily on the index fingers, thumbs, and great toes, exhibit longitudinal ridging, hypoplasia, or aplasia. There may be an associated renal dysplasia or nephropathy including proteinuria.