tbuckley/cabot-search huggingface dataset:
Effect of secretin on portal venous flow.
Authors: L Bolondi, S Gaiani, S Li Bassi, G Zironi, P Casanova, L Barbara
Journal: Gut (1990)

In this study we evaluated the effect of two different doses of secretin on portal haemodynamics (by pulsed Doppler associated with real time ultrasound) in 24 healthy humans. In 12 subjects (group A) we administered an intravenous dose of 75 clinical units of secretin and in the remaining 12 (group B) a dose of 20 CU. In all subjects the following parameters were studied before, during, and for 10 minutes after secretin administration: (a) calibre of the portal vein, (b) mean velocity of portal venous flow, and (c) volume of portal venous flow. In three subjects in each group we also evaluated the changes in flow in the superior mesenteric artery. Secretin injection induced a slight increase in both groups in comparison to basal values of portal vein calibre (mean of maximal per cent increase +25% in group A, not significant, and +16.7% in group B, not significant) and a noticeable increase of mean velocity (mean of maximal per cent increases +61.4% in group A, p less than 0.005, and +65.4% in group B, p less than 0.01) and flow volume (mean of maximal per cent increase +127% group A, p less than 0.005, and +114% group B, p less than 0.005). The magnitude of the haemodynamic changes did not differ significantly between the two groups. Doppler investigation of the superior mesenteric artery showed a marked increase of flow velocity (mean of maximal per cent increase +218% in group A and +246% in group B) and flow volume (mean of maximal per cent increase +276% in group A and +311% in group B). These data suggest that secretin has an appreciable vasoactive effect and induces a significant increase in portal venous flow even at doses much lower than those necessary for a maximal stimulation of exocrine pancreatic secretion.
Partner notification for the control of sexually transmitted infections
Authors: Catherine Mathews, David Coetzee
Journal: BMJ (2007)

<h3>Abstract</h3> <h3>Background</h3> Cold exposure may cause health problems and impaired productivity in outdoor or cold-temperature workers. The cold pressor test (CPT) is a laboratory procedure that measures cardiovascular and thermoregulatory responses to acute cold exposure such as metabolic activity in brown adipose tissue. How the body responds to acute cold exposure of a hand is not completely understood. We tested the hypothesis that the upper thorax produces heat during a single hand-CPT, which restores warmth to the cold-expose appendage. <h3>Objectives</h3> The objective was to measure skin temperature changes in the upper thoracic regions and the cold-exposed appendage during a CPT. The secondary objective was to determine if cardiovascular or psychological responses during CPT accounted for skin temperature changes. <h3>Methods</h3> 50 healthy participants immersed their right hand up to wrist level in 4 °C water for three minutes. Surface skin temperatures were imaged by infrared thermography at baseline, during CPT, and in the recovery phase. Sublingual oral temperature and water bath temperature were recorded throughout the test. Cardiovascular responses were monitored by continuous finger pulse-wave plethysmography. Peak pain and peak stress were reported by the participants on a Likert scale. <h3>Results</h3> CPT increased the systolic blood pressure (+22 mmHg, p &lt; 0.001), diastolic blood pressure (+15 mmHg, p &lt; 0.001) and heart rate (+7 beats per minute, p = 0.024). During CPT, skin temperature increased on thoracic regions including mediastinal (+0.5°C, p &lt; 0.021), sternal (+0.5°C, p &lt; 0.002), right supraclavicular (+0.3°C, p &lt; 0.042) and left supraclavicular (+0.3°C, p &lt; 0.016) regions. During CPT, the hand was cooler on ventral (−14.6°C p &lt; 0.001) and dorsal (−15.2°C p &lt; 0.001) sides, and warmed up during recovery. The ventral forearm, dorsal forearm, antecubital fossa, and adjacent medial epicondyle region were significantly cooler throughout the recovery time. The oral temperature did not change during CPT. There were no correlations between the change in mediastinal skin temperature and the sex of the participant, or changes in cardiovascular parameters, peak pain, or peak stress values. <h3>Conclusions</h3> Localized hand cooling caused a rapid warming of the thorax, dissipation of cold in the forearm, and rewarming of the hand during recovery. Thermoregulation was not dependant on pain, stress, sex, or cardiovascular changes between participants. By understanding thermoregulation, better approaches can be developed to mitigate the negative impacts of cold exposure.
Successful Use of Omalizumab in an Inadequately Controlled Type 2 Diabetic Patient With Severe Insulin Allergy
Authors: Claudia Cavelti-Weder, Bettina Muggli, Cornelia Keller, Andrea Babians-Brunner, Anna Biason-Lauber, Marc Y. Donath, Peter Schmid-Grendelmeier
Journal: Diabetes Care (2012)

A 62-year-old male patient with type 2 diabetes for 16 years developed a severe anaphylactic shock upon administration of intravenous, short-acting regular insulin. The patient’s medical history comprised allergic reactions to an unknown agent as a child as well as injection site reactions, urticaria, and dyspnea to subcutaneous NPH-insulin injections. The diagnostic work-up revealed a type 1 IgE-mediated insulin allergy by positive skin prick tests and elevated specific IgE levels against insulins of human, porcine, and bovine origin by ImmunoCAP-Assay. The insulins used were free of proinsulin. Skin prick tests with all solvents and additives of the insulin solutions were negative. Genetic sequencing of the patient’s insulin molecule revealed a normal insulin gene. Because of unsatisfactory glycemic control, specific desensitization (1) and maintenance therapy with insulin detemir was performed, but improvement of urticaria and …
Early impairment of coronary flow reserve in young men with borderline hypertension
Authors: Hanna Laine, Olli T Raitakari, Harri Niinikoski, Olli-Pekka Pitkänen, Hidehiro Iida, Jorma Viikari, Pirjo Nuutila, Juhani Knuuti
Journal: Journal of the American College of Cardiology (1998)
Extracorporeal membrane oxygenation as a bridge to allogeneic T-cell depleted hematopoietic stem cell transplantation in infants with severe combined immune deficiency: is it feasible?
Authors: Matteo Di Nardo, Franco Locatelli, Francesca Di Florio, Corrado Cecchetti, Antonio Amodeo, Sergio Rutella, Alice Bertaina
Journal: Intensive Care Medicine (2014)
CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima
Authors: Young Mi Park, Maria Febbraio, Roy L. Silverstein
Journal: Journal of Clinical Investigation (2008)

The trapping of lipid-laden macrophages in the arterial intima is a critical but reversible step in atherogenesis. However, the mechanism by which this occurs is not clearly defined. Here, we tested in mice the hypothesis that CD36, a class B scavenger receptor expressed on macrophages, has a role in this process. Using both in vivo and in vitro migration assays, we found that oxidized LDL (oxLDL), but not native LDL, inhibited migration of WT mouse macrophages but not CD36-deficient cells. We further observed a crucial role for CD36 in modulating the in vitro migratory response of human peripheral blood monocyte–derived macrophages to oxLDL. oxLDL also induced rapid spreading and actin polymerization in CD36-sufficient but not CD36-deficient mouse macrophages in vitro. The underlying mechanism was dependent on oxLDL-mediated CD36 signaling, which resulted in sustained activation of focal adhesion kinase (FAK) and inactivation of Src homology 2–containing phosphotyrosine phosphatase (SHP-2). The latter was due to NADPH oxidase–mediated ROS generation, resulting in oxidative inactivation of critical cysteine residues in the SHP-2–active site. Macrophage migration in the presence of oxLDL was restored by both antioxidants and NADPH oxidase inhibitors, which restored the dynamic activation of FAK. We conclude therefore that CD36 signaling in response to oxLDL alters cytoskeletal dynamics to enhance macrophage spreading, inhibiting migration. This may induce trapping of macrophages in the arterial intima and promote atherosclerosis.
605. Efficient AAV 1 and AAV2 Hybrid Vector for Gene Therapy of Hemophilia
Authors: Bernd Hauck, Ruian Xu, Jing Xie, Qiulan Ding, Wenman Wu, Matthew Sipler, Hongli Wang, Katherine High, Weidong Xiao
Journal: Molecular Therapy (2005)

Top of pageAbstract
Adeno-associated virus (AAV) serotype 1 (AAV1) has been shown to be more effective than the well studied AAV serotype 2 (AAV2) in muscle. In our previous study to identify muscle specific determinants on the AAV1 capsid, a series of AAV capsid mutants were generated to identify the major regions affecting AAV transduction efficiency in muscle (J Virol. 77:2768-74, 2003). Replacement of amino acids 350 to 430 of AAV2 VP1 with the corresponding amino acids from VP1 of AAV1 resulted in a hybrid vector that behaved similarly to AAV1 in vitro and in vivo in muscle. Intramuscular injection of 1|[times]|10e11 vector particles/mouse of hybrid vector carrying a human FIX transgene in CD4 KO mice resulted in levels of human FIX in the plasma of around 450 ng/ml, which were more than 4-10 fold higher than mice injected with an AAV2 vector carrying the same transgene, and reached about 75% transgene levels of AAV1 injected animals. DNA analysis of injected muscle showed 10 fold higher copy number after gene delivery with the hybrid vector compared to AAV2. A comparison of total DNA versus DNA from intact virus particles suggests a higher stability of hybrid virus particles. These results suggest that changes in the AAV capsid not only have an effect on virus-cell receptor interaction, but also influence trafficking and processing of the virus particle in the cell.

This |[ldquo]|Hybrid Vector|[rdquo]| retains the Heparin binding sites of AAV2 and therefore can be purified by a heparin-sepharose column with the same efficiency as AAV2. When tested in vivo, either in CD4 KO mice or in a hemophilic mouse model, the heparin purified hybrid vector showed a more than 10 fold higher activity than heparin-sepharose purified AAV2. This demonstrates the utility of this hybrid vector in large scale heparin-column purification generating a vector with a high expression profile for muscle directed gene delivery. Since it is only 1% different from the vector already evaluated in clinical trials of AAV2 vectors, it may be readily introduced into clinical studies.
Radionuclide Imaging of Soft Tissue Masses with Tc-99m DTPA
Authors: E. GOSHEN, I. MELLER, S. LANTSBERG, A. SAGI, M. MOSES, R. FUCHSBRAUNER, M. R. QUASTEL
Journal: Clinical Nuclear Medicine (1991)

A scintigraphic study was carried out on 48 patients presenting with palpable soft tissue masses. Imaging was carried out using Tc-99m DTPA in three phases (dynamic, blood pool after 5 minutes, followed by late scans after 2 hours). The resultant uptake of the agent was categorized as consistently positive (14 cases), initially positive but progressively negative (7 cases), initially negative but progressively positive (7 cases), and consistently negative (20 cases). Histopathologic examinations were carried out for ail cases following biopsy. A variety of malignant and benign masses were found to localize DTPA, whereas all masses that did not concentrate the agent were proven to be lipomas. In order to determine whether the uptake of DTPA bore any relationship to blood flow, additional studies using Tc-99m labeled red cells were carried out on 15 patients with soft tissue tumors. There was no correlation between blood flow or pooling and the degree of Tc-99m DTPA uptake by the palpable masses. The sensitivity of DTPA uptake as indicative of nonlipomatous tissue was 100%, and its specificity was 91%. The predictive probability that a lesion was a liopoma if there was no DTPA uptake at any phase was 100%.
Group 3 Innate Lymphoid Cells Inhibit T-Cell-Mediated Intestinal Inflammation through Aryl Hydrocarbon Receptor Signaling and Regulation of Microflora
Authors: Ju Qiu, Xiaohuan Guo, Zong-ming E. Chen, Lei He, Gregory F. Sonnenberg, David Artis, Yang-Xin Fu, Liang Zhou
Journal: Immunity (2013)
Review of Christopher Meyers.<i>A Practical Guide to Clinical Ethics Consulting: Expertise, Ethos and Power</i>.<sup>1</sup>
Authors: Armand H. Matheny Antommaria
Journal: The American Journal of Bioethics (2008)

"Review of Christopher Meyers. A Practical Guide to Clinical Ethics Consulting: Expertise, Ethos and Power. 1 ." , 8(4), pp. 72–73
The significance of gastric and duodenal histological ischemia reported on endoscopic biopsy
Authors: J. Herman, D. Chavalitdhamrong, D. Jensen, G. Cortina, A. Manuyakorn, R. Jutabha
Journal: Endoscopy (2011)

Although frequently reported, it is unknown whether pathological reports of ischemia obtained from gastroduodenal biopsies suggest a diagnosis, prognosis or a requirement for additional evaluation. The aim of this study was to review the natural history, clinical presentation, endoscopic appearance, treatments, and major clinical outcomes of patients with gastroduodenal ischemia. A case series of 14 patients with variable etiologies (seven gastric and seven duodenal) was obtained from a search of our endoscopic pathological database for reports of histological ischemia. The results were as follows. The most common presentation was upper gastrointestinal bleeding (71 %). Half of the endoscopic lesions appeared very severe (large or circumferential lesions, exudative, pseudomembranous, black or pale mucosa). There were six cases of rebleeding (43 %) and four deaths (29 %). Computed tomography scanning was frequently used (12 cases, 86 %), but led to an underlying diagnosis in only three cases. In our series, patients with underlying vascular pathology have substantial 6-month mortality (29 %).
The Role of Hospital Consultants in Clinical Directorates: The Syncromesh Report
Authors: R B Hopkinson
Journal: BMJ (1994)

The meeting from which the text of this book is drawn was organised by the Royal College of Physicians, but the account is of value to all disciplines, as the topics are important to all. The book comprehensively reviews the concept of clinical directorates and the problems associated with their application. It is very topical, reflecting the problems inherent in managing a service that is changing very - perhaps …
Coexistence of Hereditary Homocystinuria and Factor V Leiden — Effect on Thrombosis
Authors: Hanna Mandel, Benjamin Brenner, Moshe Berant, Nurith Rosenberg, Naomi Lanir, Cornelis Jakobs, Brian Fowler, Uri Seligsohn
Journal: New England Journal of Medicine (1996)

Venous and arterial thromboembolism occurs in only about one third of patients homozygous for homocystinuria, which suggests that other, contributory factors are necessary for the development of thrombosis in these patients. Factor V Leiden, an R506Q mutation in the gene coding for factor V, is the most common cause of familial thrombosis and could be a potentiating factor.We determined activated partial-thromboplastin times in the presence and absence of activated protein C and tested for the factor V Leiden mutation in 45 members of seven unrelated consanguineous kindreds in which at least 1 member was homozygous for homocystinuria.Thrombosis (venous, arterial, or both) occurred in 6 of 11 patients with homocystinuria (age, 0.2 to 8 years). All six also had the factor V Leiden mutation. One patient with prenatally diagnosed homocystinuria who was also heterozygous for factor V Leiden has received warfarin therapy since birth and has not had thrombosis (age, 18 months). Of four patients with homocystinuria who did not have factor V Leiden, none had thrombosis (ages at this writing, 1 to 17 years). Three women who were heterozygous for both homocystinuria and factor V Leiden had recurrent fetal loss and placental infarctions.Patients with concurrent homocystinuria and factor V Leiden can have an increased risk of thrombosis. Screening for factor V Leiden may be indicated in patient with homocystinuria and their family members.
Phenylalanine, other large neutral amino acids and RNA catabolites as markers for protein biosynthesis in phenylketonuria
Authors: Peter C. Clemens, Jens Gunter Burmester, Gert Wiegand, Bernhard H. Prankel, Editha Halfmann, Norbert Erb, Jürgen Müller-Wickop
Journal: Metabolism (1993)
Deletion of 7p or monosomy 7 in pediatric acute lymphoblastic leukemia is an adverse prognostic factor: a report from the Children's Cancer Group
Authors: N A Heerema, J B Nachman, H N Sather, M K La, R Hutchinson, B J Lange, B Bostrom, P G Steinherz, P S Gaynon, F M Uckun
Journal: Leukemia (2004)
A Classical Brown Adipose Tissue mRNA Signature Partly Overlaps with Brite in the Supraclavicular Region of Adult Humans
Authors: Naja Zenius Jespersen, Therese Juhlin Larsen, Lone Peijs, Søren Daugaard, Preben Homøe, Annika Loft, Jasper de Jong, Neha Mathur, Barbara Cannon, Jan Nedergaard, Bente Klarlund Pedersen, Kirsten Møller, Camilla Scheele
Journal: Cell Metabolism (2013)
Reversible male infertility due to sulphasalazine: studies in man and rat.
Authors: C O'Morain, P Smethurst, C J Dore, A J Levi
Journal: Gut (1984)

Sulphasalazine treatment for inflammatory bowel disease in man causes oligospermia, reduced sperm motility and an increased proportion of abnormal forms. On withdrawal of sulphasalazine these effects are found to be reversible and 15 pregnancies occurred at a median of 2.5 months after stopping sulphasalazine therapy. Seminal plasma concentrations of acid phosphatase fructose and PGE2 as well as the hormone profiles of patients on sulphasalazine for three months were found to be within normal limits. Sulphasalazine fed to male Sprague Dawley rats caused a dose dependent and reversible infertility with a significant reduction in litter size. Rats fed the metabolite sulphapyridine also had a reduced litter size when mated, while those fed the metabolite 59aminosalicylic acid and a polymer of 59aminosalicylic acid did not. It seems likely that the sulphapyridine moiety of sulphasalazine is responsible for the infertility seen, the effect being mediated at a late stage in sperm maturation.
Abstract 270: Cell assay on a chip to study tumor initiating cells’ heterogeneity and treatment resistance.
Authors: Weijia Zhang, Lidong Qin
Journal: Cancer Research (2013)

Abstract Recent investigations from both animal models and clinical samples have continuously supported that Tumor Initiating Cell (TIC) does exist and plays an important role in tumor metastasis and recurrence. However, TICs have a few intrinsic properties leading to their complexity in molecular targeting and inhibition. TICs are 1) heterogeneous, 2) dynamically changing states, 3) often rare and 4) lack robust biomarker combinations, thereby challenging conventional bulk in vitro experimental tools and complicating the prediction and explanation of animal study results. High throughput, in situ, and cell-by-cell measurement on TICs is a way to fully decipher TIC's molecular signature and signaling pathways. We believe such measurement can lead to 1) revolutionary implementation of TIC models; 2) identification of new therapeutic targets; and 3) reduction of breast cancer recurrence and metastasis. Microfluidics technology (1) is a candidate to serve as such type of high throughput single-cell characterization. We started pursuing such measurements a few years ago and demonstrated high throughput single-cell protein profiling on both cell lines and clinical samples. The technology, called single-cell barcode chip (SCBC), is facilitated by state-of-the-art Polydimethylsiloxane (PDMS) microfluidics protocols. The SCBC consists of down to nanoliter chambers that concentrate proteins from individual cells to a level even higher than cell culture media in conventional dish technology and contains extremely miniaturized antibody arrays to capture proteins produced by cells in these chambers. Further utilization of our SCBC platform to TICs is expected to characterize protein expression from individual breast TIC and lead to new discoveries in TIC filed. Citation Format: Weijia Zhang, Lidong Qin. Cell assay on a chip to study tumor initiating cells’ heterogeneity and treatment resistance. [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 270. doi:10.1158/1538-7445.AM2013-270
Primary Cutaneous Diphtheria
Authors: Tobias R. Funt
Journal: JAMA (1961)

Within the United States, where ulceration of the skin is but rarely caused by the Klebs-Loffler bacillus, the diagnosis of primary cutaneous diphtheria may be missed, and serious, even fatal, complications may ensue. The primary lesion, in this case of a 30-year-old man, was a pustule located on the shoulder. It developed into an indolent, intractable ulcer, shielded by an eschar clinically indistinguishable from anthrax. The skin test to diphtheria antitoxin was negative. A negative Schick test has been found not to be a criterion of immunity to cutaneous diphtheria. Intravenous administration of massive doses of penicillin was followed by dramatic recovery from the constitutional symptoms and healing of the lesion.
Problems of Duodenogastric Reflux in Tc-99m Hexa MIBI Planar, Tomographic and Bull??s Eye Display
Authors: I M HASSAN, M M J MOHAMMAD, C CONSTANTINIDES, M NAIR, N BELANI, H M ABDEL-DAYEM
Journal: Clinical Nuclear Medicine (1989)

Tc-99m Hexa MIBI (RP-30) is excreted through hepatobiliary pathways. Myocardial imaging with RP-30 is recommended 45-60 minutes after injection. During this waiting period duodenogastric reflux (DGR) is occasionally seen. Fundal activity due to duodenogastrix reflux presents problems in planar, tomographic, and Bull's eye display. The authors recommend in those cases to give the patient a light meal and wait 15-30 minutes more for the gastric activity to empty in the small intestine before starting myocardial imaging.
Partial Relief of Anginal Chest Pain by Belching
Authors: Dennis Bauman
Journal: JAMA (1977)

<h3>To the Editor.—</h3> As a staff member on an academic cardiology service, I see several patients each year with documented coronary artery disease (at least 70% obstruction of at least one major vessel by coronary arteriography) and typical angina pectoris; they obtain<i>partial</i>relief of their anginal discomfort by belching. The mechanism of this is unclear but could, at least in part, reflect the following sequence of events: angina → anxiety → air swallowing → gastric distension → sensation of lower thoracic discomfort → partial relief after belching. The purpose of this communication is to emphasize that partial relief by belching should not be interpreted as strong evidence against an ischemic origin for chest discomfort that is otherwise suggestive of angina pectoris.