tbuckley/cabot-search huggingface dataset:
Easy ways to resist change in medicine
Authors: Allen F Shaughnessy, David C Slawson
Journal: BMJ (2004)

fall into three main categories: traction techniques (Hippocrates, 3 Stimson 4 ) leverage techniques (Kocher, 5 Milch 6 ), and scapular manipulation. 7ocher's manoeuvre was originally described in 1870. 5The affected arm is flexed at the elbow and adducted against the side of the body.The forearm is rotated externally and the upper arm lifted in a sagittal plane as far as possible and finally internally rotated.There have been many adjustments to this widely used technique, especially as the additional torque resulting from adduction and internal rotation have been associated with humeral shaft fractures in elderly people. 8 9 To perform Kocher's manoeuvre the surgeon must abduct and externally rotate his own arm, this means the fibres of the sternocostal head of his pectoralis major are maximally stretched.If a patient is not well sedated or has not received adequate analgesia he or she is more likely forcefully to resist the reduction.This results in a sudden uncoordinated eccentric contraction of the surgeon's pectoralis major muscle, which in our case resulted in a pectoralis major rupture.If adequate sedation and pain relief are not possible, reduction under general anaesthetic may be necessary to minimise the risk of complications for both the patient and the doctor.
α-Chemokine CXCL10 and β-chemokine CCL2 serum levels in patients with hepatitis C–associated cryoglobulinemia in the presence or absence of autoimmune thyroiditis
Authors: Alessandro Antonelli, Clodoveo Ferri, Poupak Fallahi, Silvia Martina Ferrari, Silvia Frascerra, Angelo Carpi, Andrea Nicolini, Ele Ferrannini
Journal: Metabolism (2008)
2014 MERS-CoV Outbreak in Jeddah — A Link to Health Care Facilities
Authors: Ikwo K Oboho, Sara M Tomczyk, Ahmad M Al-Asmari, Ayman A Banjar, Hani Al-Mugti, Muhannad S Aloraini, Khulud Z Alkhaldi, Emad L Almohammadi, Basem M Alraddadi, Susan I Gerber, David L Swerdlow, John T Watson, Tariq A Madani
Journal: New England Journal of Medicine (2015)

A marked increase in the number of cases of Middle East respiratory syndrome coronavirus (MERS-CoV) infection occurred in Jeddah, Saudi Arabia, in early 2014. We evaluated patients with MERS-CoV infection in Jeddah to explore reasons for this increase and to assess the epidemiologic and clinical features of this disease.We identified all cases of laboratory-confirmed MERS-CoV infection in Jeddah that were reported to the Saudi Arabian Ministry of Health from January 1 through May 16, 2014. We conducted telephone interviews with symptomatic patients who were not health care personnel, and we reviewed hospital records. We identified patients who were reported as being asymptomatic and interviewed them regarding a history of symptoms in the month before testing. Descriptive analyses were performed.Of 255 patients with laboratory-confirmed MERS-CoV infection, 93 died (case fatality rate, 36.5%). The median age of all patients was 45 years (interquartile range, 30 to 59), and 174 patients (68.2%) were male. A total of 64 patients (25.1%) were reported to be asymptomatic. Of the 191 symptomatic patients, 40 (20.9%) were health care personnel. Among the 151 symptomatic patients who were not health care personnel, 112 (74.2%) had data that could be assessed, and 109 (97.3%) of these patients had had contact with a health care facility, a person with a confirmed case of MERS-CoV infection, or someone with severe respiratory illness in the 14 days before the onset of illness. The remaining 3 patients (2.7%) reported no such contacts. Of the 64 patients who had been reported as asymptomatic, 33 (52%) were interviewed, and 26 of these 33 (79%) reported at least one symptom that was consistent with a viral respiratory illness.The majority of patients in the Jeddah MERS-CoV outbreak had contact with a health care facility, other patients, or both. This highlights the role of health care-associated transmission. (Supported by the Ministry of Health, Saudi Arabia, and by the U.S. Centers for Disease Control and Prevention.).
Muscular FDG Uptake After Chewing Chewing Gum in a Patient With Hodgkin Disease
Authors: Jacqueline Vock, Freimut D. Juengling, Thomas Krause, Michael Wissmeyer
Journal: Clinical Nuclear Medicine (2007)

A 42-year-old man with Hodgkin disease of the mediastinum (initial stage IIIB) was referred for restaging after completion of chemotherapy. The CT scan showed complete remission, the FDG PET revealed intense and symmetric uptake in the buccal and parapharyngeal region, whereas the sites of the initial manifestations did not show any pathologic uptake. The only clinical finding was a symmetric hypertrophy of the masseteric muscles. Precise anamnesis revealed that the patient regularly chews chewing gum and that he had done so in the uptake period before FDG PET imaging.
Plasma Proteins and the Gastrointestinal Tract
Authors: Graham H. Jeffries, Halsted R. Holman, Marvin H. Sleisenger
Journal: New England Journal of Medicine (1962)

LEAKAGE of plasma proteins into the gastrointestinal tract is a major cause of hypoproteinemia in many diseases1 2 3 4 5 6 and, indeed, may play an important part in the normal degradation of plasma proteins.7 8 9 10 Early clinical studies described a syndrome of hypoproteinemia inexplicable by decreased synthesis or external loss of plasma protein.11 12 13 14 Studies of I131 turnover in patients with this syndrome showed an increase in albumin catabolism, but did not indicate the mechanism and site of this protein degradation.11 , 12 , 14 , 15 Hydrolysis of plasma proteins entering the gastrointestinal lumen, with reabsorption of their amino acids, delayed the recognition of this site of plasma protein loss, . . .
THE DIABETIC ACUTE ABDOMEN: A TYPICAL CASE
Authors: R. D. Lawrence, C. G. Millman, F. E. Pilkington
Journal: BMJ (1931)

The treatment of neuritis by electricity was advocated by the late Dr. Naunton Davies some thirty years ago.He published his results in the Bristol Medico-Chirlrgical Journal in June, 1915, stating that the method was applicable only to interstitial neuritis in which there is hyperaemia and exudation in the nerve sheath.The diseased areas are limnited in extent, the spots are often the size of a split pea, or smaller, the nierve between them being free from trouble.If a spot is overlooked, pain may remain in that spot, and radiate over a wide field.
THE PROPERDIN SYSTEM AND IMMUNITY
Authors: Ralph J. Wedgwood, Harold S. Ginsberg, Louis Pillemer
Journal: The Journal of Experimental Medicine (1956)

Detailed experiments are presented which indicate that the properdin system is an inhibitor of Newcastle disease virus. Viral inhibition required all known components of the properdin system: properdin, all four components of complement and magnesium; the removal of any one constituent resulted in a loss of inhibition; the replacement of the constituent restored antiviral effect. The inhibition of virus was temperature-dependent. The process of inhibition by serum resulted in a decrease in the amount of properdin available in the serum without any measurable effect on the components of complement. The prolonged incubation of inactive serum-virus mixtures with cation-exchange resin resulted in the restoration of some, but not all, of the hemagglutinating activity of the virus. The requirements of the properdin system and the implication of these findings were discussed.
INFLUENCE OF LIGHT ENVIRONMENT ON THE ORGANIC CONSTITUTION OF NORMAL RABBITS WITH ESPECIAL REFERENCE TO THE ACTION OF NEON LIGHT
Authors: Wade H. Brown
Journal: The Journal of Experimental Medicine (1928)

The influence of light environment on the organic constitution of normal rabbits was studied by comparing the weights of organs of animals that had been living under cerrtain conditions for long periods of time. It was found that the light environment produced an effect on the physical constitution of the rabbits which was comparable to the effects produced on the functional activity of the same animals.
An Outbreak of Organic Dust Toxic Syndrome in a College Fraternity
Authors: William T. Brinton
Journal: JAMA (1987)

An explosive outbreak of a febrile respiratory illness occurred among members of a college fraternity. The preponderant signs and symptoms were muscle aches, cough, and low-grade fever. All illnesses occurred within 1.3 to 13 hours of attendance at a party where there was a dense airborne dust from straw that had been laid on the floor. Of the 67 fraternity members who attended the party and answered a questionnaire, 55 became ill (attack rate, 82%). Risk of illness was higher for those who spent more time at the party. Duration of illness ranged from 4.5 hours to seven days. Results of serological studies did not demonstrate an allergic or viral cause for these illnesses. The clinical and epidemiologic features of this outbreak were characteristic of organic dust toxic syndrome, an acute respiratory illness caused by inhalation of molds growing on hay, silage, or other agricultural products.
Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil
Authors: Rathnagiri Polavarapu, Douglas R. Spitz, Julia E. Sim, Mark H. Follansbee, Larry W. Oberley, Amir Rahemtulla, Amin A. Nanji
Journal: Hepatology (1998)

Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation ( r = −.92, P &lt; .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE- and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury.
449. Sca-1+ Cell-Based Gene Therapy with a Modified Fibroblast Growth Factor 2 (FGF2) Increased Endosteal/Trabecular Bone Formation in Mice
Authors: Susan L. Hall, K.-H. William Lau, Shin-Tai Chen, Matilda H.-C. Sheng, Apurva K. Srivastava, Henry J. Klamut, Jon E. Wergedal, Daila S. Gridley, Subburaman Mohan, David J. Baylink
Journal: Molecular Therapy (2006)

A major problem in bone-wasting diseases such as osteoporosis is the loss of endosteal bone that results in reduced bone strength and increased fracture risk. Recent advances in gene therapy raise the possibility that ex vivo gene therapy with a bone-forming gene may be used to enhance endosteal bone formation. However, a successful strategy requires that the transduced cells remain at the endosteal bone sites. Sca-1+ cells are a desirable cell vehicle because of their ability to home and engraft into the bone marrow cavity. This study assessed the feasibility of an ex vivo Sca-1+ cell-based systemic FGF2 gene therapy to promote endosteal bone formation. To maximize our chances of demonstrating a biological effect, the human FGF2 transgene was modified to increase protein secretion and stability by adding the BMP2/4 hybrid signal sequence and mutating two key cysteines in the FGF2 molecule. Retro-orbital injection of Sca-1+ cells transduced with the MLV-FGF2 vector into sub-lethally irradiated stem cell deficient (W41/W41) mice resulted in long-term engraftment, marked elevation in serum FGF2, and dose-related endosteal bone formation. Ten weeks post transplantation, serum FGF2 levels in mice transplanted with MLV-GFP-transduced Sca-1+ cells (controls) averaged 36|[plusmn]|6 pg/mL, whereas the serum FGF2 level in mice transplanted with FGF2-expressing cells was significantly increased but highly variable (2502|[plusmn]|2459 pg/mL, p 4,000 pg/mL), endosteal bone formation was so robust that the marrow space was completely filled with bony tissues. There was insufficient calcium available for mineralization of the newly formed bone, leading to hypocalcemia, secondary hyperparathyroidism, and osteomalacia. However, these undesirable side effects appeared to be dose-related. Thus, it may be possible to minimize adverse effects while maximizing efficacy by optimizing transgene expression. In conclusion, these data demonstrate the massive power of our approach to target and deliver a systemic gene therapy to the endosteal bone surface, and provide compelling test-of-principle evidence for the feasibility of a Sca-1+ cell-based ex vivo systemic FGF2 gene therapy to promote endosteal bone formation.
Heterogeneity of Pathogenetic Mechanisms in Aplastic Anemia
Authors: NABIH I. ABDOU
Journal: Annals of Internal Medicine (1981)

The mechanisms responsible for the bone marrow failure in 21 aplastic anemia patients were studied by the colony-forming units in culture assay (CFU-C). Twelve patients had no detectable in-vitro defect that could be responsible for the low CFU-C numbers. Three patients had suppressor T cells that inhibited CFU-C (p less than 0.001); one of two patients responded to antithymocyte globulin therapy and the third recovered spontaneously. Three patients had serum inhibitory immunoglobulins directed against their marrow CFU-C; plasmapheresis resulted in recovery of bone marrow function. Three patients had abnormalities at the colony-stimulating factor level: Two had inhibitors of colony-stimulating factor, corrected in vitro and in vivo by indomethacin and cholinergic agonists (p less than 0.01); and the third had colony-stimulating factor generation defect, corrected in vitro and in vivo by lithium. Testing for cellular or humoral suppressor factors directed against precursor cells or for abnormalities at the colony-stimulating factor level gives helpful guidelines to therapy in aplastic anemia.
β-tubulin Induced Murine Model of Autoimmune Hearing Loss and Regulation of T Cell Cytokines of the Mice
Authors: S.H. Cho, B. Zhou, J. Glickstein, M.H. Kermany, C. Cai, Q. Cai, W. Liu, T.J. Yoo
Journal: Journal of Allergy and Clinical Immunology (2007)
Effect of Long-Term Exposure to Insulin Lispro on the Induction of Antibody Response in Patients With Type 1 or Type 2 Diabetes
Authors: S. Edwin Fineberg, Jie Huang, Rocco Brunelle, K. S. Gulliya, James H. Anderson
Journal: Diabetes Care (2003)

To determine the long-term effects of insulin lispro on inducing lispro-specific, insulin-specific, and cross-reactive (reactive with both insulin lispro and human insulin) antibodies.A multinational, multicenter combination of controlled and noncontrolled, open-label studies of 4.5 years' duration was designed to evaluate the long-term immunologic profile of subcutaneously administered insulin lispro. A total of 1,221 patients (men and women; 12-81 years of age) with type 1 or type 2 diabetes were enrolled. Circulating anti-insulin antibodies were measured using radioimmunoassays.Insulin-specific and lispro-specific antibody responses were within the background noise levels of the assays. Significant elevations of antibody were confined to a cross-reactive antibody response. Antibody levels resulting from prior exposure to long- and short-acting insulins changed little after transfer to insulin lispro and remained within or near the baseline levels. De novo exposure to insulin lispro resulted in increases in cross-reactive but not insulin- or lispro-specific antibody levels. Cross-reactive insulin antibodies developed more readily in patients with type 1 diabetes than in those with type 2 diabetes. Long-term antibody responses tended to decrease over time and returned to baseline or near-baseline levels by the end of the long-term studies. No evidence of an anamnestic antibody response could be found in individuals treated intermittently with insulin lispro.The immunogenic profile of patients treated with insulin lispro was comparable to that of patients treated with recombinant human insulin. Inductions of significant levels of specific or cross-reactive antibodies were not observed in patients who had received insulin previously. No significant antibody-dependent increases in insulin dosage requirements were noted in these patients. The incidence of insulin allergy was not different from that in patients treated with recombinant regular human insulin.
Anti-tumor necrosis factor α treatment promotes apoptosis and prevents liver regeneration in a transgenic mouse model of chronic hepatitis C
Authors: Erwin Daniel Brenndörfer, Malin Weiland, Lars Frelin, Emma Derk, Gustaf Ahlén, Jian Jiao, Johannes Georg Bode, Matti Sällberg
Journal: Hepatology (2010)

Tumor necrosis factor α (TNFα) has been implicated in a variety of inflammatory diseases, and anti-TNFα has been shown to improve therapy when added to standard of care in chronic hepatitis C virus (HCV) infection. In addition, patients with chronic HCV have increased serum levels of TNFα and the macrophage-attracting chemokine (C-C motif) ligand 2 (CCL2). A mouse model of chronic HCV with hepatic nonstructural (NS) 3/4A protein expression mimics the human infection through a reduced response to double-stranded RNA and cleavage of the T cell protein tyrosine phosphatase. The mice also display a resistance to TNFα in vivo. We therefore analyzed the relationship between NS3/4A and TNFα. Wild-type and NS3/4A-transgenic (Tg) mice were treated with TNFα/D-galactosamine (D-galN), acting through the TNF receptor 1 on hepatocytes and macrophages, or lipopolysaccharide (LPS)/D-galN, acting through Toll-like receptor 4 on sinusoidal endothelial cells, macrophages, and dendritic cells. Mice were analyzed for hepatic signaling, liver damage, TNFα, and CCL2. Similar to HCV-infected humans, NS3/4A-Tg mice displayed elevated basal levels of TNFα and CCL2. Treatment of NS3/4A-Tg mice with TNFα/D-galN or LPS/D-galN led to increased hepatic nuclear factor kappa B (NFκB) activation, increased TNFα and CCL2 levels, decreased apoptosis, and increased hepatocyte regeneration. Importantly, blocking NFκB activation (bortezomib) or administering anti-TNFα (infliximab) 4 hours after LPS/D-galN injection reversed the resistance of NS3/4A-Tg mice to TNFα-induced liver injury. Conclusion: Resistance to TNFα seen in NS3/4A-Tg mice is explained by a hepatoprotective effect of NFκB and TNFα. Hence, anti-TNFα agents block these effects and are antiviral by promoting hepatocyte apoptosis and preventing hepatocyte regeneration. (Hepatology 2010;.)
A Case of Varicose Aneurysm of the Femoral Artery and Vein
Authors: C. H. Y. Godwin
Journal: BMJ (1887)

1i'RB MB1?iT4sft IWw ,' 1271, cataract in both eyes, and is wittia a few months of completing her century.She took a fortnight to consider my proposal, and then, exercising the undoubted prerogative of her sex, and perhaps, also, at such an exceptionally advanced age, a wise discretion declined it.In three of the four cases I have mentioned I had performed a preliminary iridectomy some months before the removal of the cataracts, and I shall in future, if opportunity favour me, adopt a similar pre- caution in operating upon patients of advanced age, as I am convinced that by so doing a higher average of success is achieved.Mr. Higgens, not long ago, published a series of cataract-operations on old people in which he had obtained very excellent results, and I hope that his experience and my own may encourage others to attempt the storming of these ancient citadels, for the gift of sight is none the less prized and gratefully welcomed by the aged, because it comes to them in the sunset of their life.
Role of primacy of birth in HLA-identical sibling transplantation
Authors: Christoph Bucher, Martin Stern, Andreas Buser, Dominik Heim, Michael Paulussen, Jörg Halter, Dimitrios Tsakiris, Armin Droll, Sandrine Meyer-Monard, Andre Tichelli, Jakob Passweg, Alois Gratwohl
Journal: Blood (2007)
Delayed ischemic preconditioning contributes to renal protection by upregulation of miR-21
Authors: Xialian Xu, Alison J. Kriegel, Yong Liu, Kristie Usa, Domagoj Mladinov, Hong Liu, Yi Fang, Xiaoqiang Ding, Mingyu Liang
Journal: Kidney International (2012)

Delayed ischemic preconditioning effectively protects kidneys from ischemia-reperfusion injury but the mechanism underlying renal protection remains poorly understood. Here we examined the in vivo role of microRNA miR-21 in the renal protection conferred by delayed ischemic preconditioning in mice. A 15-min renal ischemic preconditioning significantly increased the expression of miR-21 by 4 h and substantially attenuated ischemia-reperfusion injury induced 4 days later. A locked nucleic acid-modified anti-miR-21 given at the time of ischemic preconditioning knocked down miR-21 and significantly exacerbated subsequent ischemia-reperfusion injury in the mouse kidney. Knockdown of miR-21 resulted in significant upregulation of programmed cell death protein 4, a proapoptotic target gene of miR-21, and substantially increased tubular cell apoptosis. Hypoxia-inducible factor-1α in the kidney was activated after ischemic preconditioning and blockade of its activity with a decoy abolished the upregulation of miR-21 in cultured human renal epithelial cells treated with the inducer cobalt chloride. In the absence of ischemic preconditioning, knockdown of miR-21 alone did not significantly affect ischemia-reperfusion injury in the mouse kidney. Thus, upregulation of miR-21 contributes to the protective effect of delayed ischemic preconditioning against subsequent renal ischemia-reperfusion injury.