tbuckley/cabot-search huggingface dataset:
Comparative Physiology of the Digestive System of Vertebrates
Authors: R. Naftalin
Journal: Gut (1996)

not imposed.3Thomas and colleagues report a significantly higher rate of screen com- pliance among participants living with other participants, while those who had a diagnostic colorectal examination with negative results had significantly lower odds of complying.4Another study showed that compliance in first degree relatives ofpatients with colorectal cancer was significantly higher than in spouses (69% versus 47%, p<0-01), as was among those whose relatives died recently from col- orectal cancer.5However they found that time since diagnosis in the index case had no effect on the compliance rate, in contrast with the findings by the authors.Finally, Neilson and coworker report that compliers are found to be of higher socioeconomic classes than per- sistent non-compliers, to have more personal and family experience of illness, and to visit their dentists more regularly.6These data, in conjunction with that presented by the authors, helps us better under- stand the factors affecting compliance, while screening for colorectal cancer.
An unusual case of extramedullary blast crisis in chronic myelocytic leukaemia
Authors: Chi‐Shun Feng
Journal: American Journal of Hematology (1988)

Abstract A 27‐year‐old man with chronic myelocytic leukaemia sustained two episodes of extramedullary blast transformation. The first episode was a lymphoblastic transformation in his cervical lymph nodes, which was treated and in remission for 15 months when a second blastic transformation occurred in the meninges. All the while, the bone marrow was free from blastic crisis.
Pulsatile flow and oscillating wall shear stress in the brachial artery of normotensive and hypertensive subjects
Authors: A. C Simon, J. Levenson, P. Flaud
Journal: Cardiovascular Research (1990)

STUDY OBJECTIVE - The aim of the study was to examine oscillating arterial wall shear stress in hypertension. DESIGN - Pulsatile flow and oscillating wall shear stress were measured in brachial artery in hypertensive v normotensive subjects using pulsed Doppler apparatus. Methods were tested in four subjects using a micrometric procedure of Doppler probe displacement providing instantaneous real time velocity profiles. SUBJECTS - 19 ambulatory male patients with mild to moderate hypertension (diastolic blood pressure 95-114 mm Hg) and 11 normotensive male controls of similar age were studied. All were non-smokers. MEASUREMENTS and RESULTS - Arterial diameter and pulsatile centreline blood velocity were determined with pulsed Doppler, and blood viscosity was measured with a coaxial cylinder viscometer. Shear rates corresponding to maximum (gamma Vmax), minimum (gamma Vmin), and pulse (gamma Vpulse) velocities were evaluated with a simplified method of computation of Womersley equations. Corresponding shear stresses (tau Vmax, tau Vmin, tau Vpulse) were calculated as the product between shear rate and viscosity. The differences in wall shear rates obtained with the Womersley method and with the micrometric procedure were less than 10%. Compared to normotensives, hypertensives had greater arterial diameter [0.508(SEM0.006) v 0.446(0.014), p less than 0.001], lower maximum velocity [36.2(1.5) v 46.3(2.4) cm.s-1, p less than 0.001], lower absolute value of minimum velocity [-8.3(1.2) v -14.3(2.3) cm.s-1, p less than 0.01], lower pulse velocity [44.5(2.2) v 61.2(3.9) cm.s-1, p less than 0.001], and higher blood viscosity [4.77(0.08) v 4.28(0.09) mPa.s, p less than 0.001]. gamma and tau Vmax, Vmin and Vpulse were all lower in absolute value in hypertensives. Overall mean blood pressure in all subjects was negatively correlated to gamma Vmax (r = -0.65), tau Vmax (r = -0.46), gamma Vmin (r = -0.45), tau Vmin (r = -0.37), gamma Vpulse (r = -0.63), and tau Vpulse (r = -0.48). In hypertensives, age was correlated negatively to gamma Vmax (r = -0.44), tau Vmax (r = -0.46), gamma Vmin (r = -0.57), tau Vmin (r = -0.57), gamma Vpulse (r = -0.58), and tau Vpulse (r = -0.58). In normotensives, age was not correlated with shear parameters, except for tau Vmax (r = -0.60) and tau Vpulse (r = -0.66). CONCLUSIONS - The hypertensive state is associated with a reduction in oscillating wall shear in large arteries despite an increase in blood viscosity. Age in combination with hypertension also decreases wall shear conditions.
STUDIES ON PATHOGENIC B. COLI FROM BOVINE SOURCES
Authors: Dorothea E. Smith
Journal: The Journal of Experimental Medicine (1927)

1. The soluble specific substance obtained from a capsulated strain of B. coli is not identical with any specific substance heretofore described. It is a carbohydrate, composed of 80 per cent of hexose, probably partly of dextro- and partly of levorotatory sugar, since the rotation of the hydrolysate is low. Glucuronic acid is probably present in the molecule. 2. Crude "residue" or specific substance obtained from the uncapsulated mutant was about 100 times less active with homologous serum than similar material from the capsulated strain. This supports the view that capsular substance and soluble specific substance are the same. In cases where there is a well marked capsule, the specific substance is probably produced in greater amount and located peripherally. 3. Capsular substance is probably significant for virulence when functioning as a morphological capsule. It is present in filtrates of young culture only in very small amounts.
Platelet Phagocytosis and Processing of β-Amyloid Precursor Protein as a Mechanism of Macrophage Activation in Atherosclerosis
Authors: Guido R.Y. De Meyer, Dieter M.M. De Cleen, Susan Cooper, Michiel W.M. Knaapen, Dominique M. Jans, Wim Martinet, Arnold G. Herman, Hidde Bult, Mark M. Kockx
Journal: Circulation Research (2002)

In human occluded saphenous vein grafts, we previously demonstrated cytotoxic foam cells, presumably derived from macrophages engulfing platelets. In the present study, we investigated whether platelet phagocytosis occurs in human atherosclerotic plaques, whether this activates macrophages, and whether the platelet constituent, amyloid precursor protein (APP), was involved. Immunohistochemistry documented the presence of APP, β-amyloid peptide (Aβ, cleaved from APP), and platelets (CD9), along with inducible NO synthase (iNOS) and cyclooxygenase-2, two markers of macrophage activation, around microvessels in advanced human carotid artery plaques (n=18). Aβ colocalized with iNOS-expressing macrophages that were often surrounded by platelets. In vitro, murine J774 and human THP-1 macrophages were incubated with or without washed human platelets. Coincubation of macrophages and platelets led to platelet phagocytosis (electron and confocal microscopy) and formation of lipid-, APP-, and Aβ-containing foam cells. These expressed iNOS mRNA (reverse transcription–polymerase chain reaction) and protein and produced nitrite and tumor necrosis factor-α (ELISA). Macrophage pretreatment with 4-(2-aminoethyl)benzenesulfonyl fluoride, a protease inhibitor, reduced APP processing and inhibited NO biosynthesis induced by platelet phagocytosis but not by lipopolysaccharides. Human atherosclerotic plaques and J774 and THP-1 macrophages contained mRNA of the APP-cleaving enzyme β-secretase. This is the first demonstration of Aβ, a peptide extensively studied in Alzheimer’s disease, in human atherosclerotic plaques. It was present in activated iNOS-expressing perivascular macrophages that had phagocytized platelets. In vitro studies indicate that platelet phagocytosis leads to macrophage activation and suggest that platelet-derived APP is proteolytically processed to Aβ, resulting in iNOS induction. This represents a novel mechanism for macrophage activation in atherosclerosis.
Endothelin stimulates platelet-activating factor synthesis by cultured rat kupffer cells*1
Authors: Shamimunisa B. Mustafa, Chandrashekhar R. Gandhi, Stephen A. K. Harvey, Merle S. Olson
Journal: Hepatology (1995)

Endothelins are potent peptide mediators that elicit glycogenolytic and vasoconstrictor actions in the liver. Endothelins were found to stimulate the synthesis and release of the lipid mediator platelet-activating factor in cultured rat Kupffer cells. Endothelin-mediated synthesis of platelet-activating factor required extracellular calcium in that the calcium chelator, EGTA and nifedipine, a calcium ion channel blocker, inhibited platelet-activating factor synthesis. The phospholipase A2 inhibitor, 4-bromophenacyl bromide, strongly inhibited endothelin-induced platelet activating factor synthesis. Endothelin-stimulated platelet activating factor synthesis was inhibited after treatment of Kupffer cells with cholera toxin, whereas pertussis toxin inhibited only this response to endothelin-1. Agents that elevate intracellular cyclic AMP levels were found to inhibit endothelin-induced platelet-activating factor synthesis in Kupffer cells. Staurosporine, a protein kinase C inhibitor minimized endothelin-induced platelet-activating factor synthesis but phorbol myristate acetate, an activator of protein kinase C, did not affect endothelin-induced platelet activating factor synthesis. Thus, the current study demonstrates that activation of an endothelin receptor in cultured rat Kupffer cells results in the synthesis and release of platelet-activating factor. The importance of endothelin-mediated platelet-activating factor synthesis relates to the mechanism of intercellular signaling occurring between endothelial cells (i.e., the site of endothelin synthesis) and Kupffer cells (i.e., the site of formation of secondary mediators such as platelet-activating factor and eicosanoids) within the rat liver exposed to various types of pathophysiological episodes.
Marine Alkaloid Monanchocidin: A Proteomic-Based Screening of Protein Targets in Cisplatin-Resistant Tumor Cells
Authors: S.A. Dyshlovoy, S. Venz, A. Guzii, T. Makarieva, K. Tabakmakher, V. Stonik, S. Balabanov, C. Bokemeyer, F. Honecker
Journal: Annals of Oncology (2013)
Bacterial Effectors Target the Common Signaling Partner BAK1 to Disrupt Multiple MAMP Receptor-Signaling Complexes and Impede Plant Immunity
Authors: Libo Shan, Ping He, Jianming Li, Antje Heese, Scott C. Peck, Thorsten Nürnberger, Gregory B. Martin, Jen Sheen
Journal: Cell Host & Microbe (2008)
Loss of Suppression of Tumorigenicity 2 (ST2) Gene Reverses Sepsis-induced Inhibition of Lung Host Defense in Mice
Authors: Jacobien J. Hoogerwerf, Masja Leendertse, Catharina W. Wieland, Alex F. de Vos, J. Daan de Boer, Sandrine Florquin, Tom van der Poll
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

After surviving the initial hyperinflammatory phase, patients with sepsis display features consistent with immunosuppression, which renders the host susceptible to nosocomial infections, in particular bacterial pneumonia. Suppression of tumorigenicity 2 (ST2) is a negative regulator of Toll-like receptor signaling implicated in endotoxin tolerance.The present study sought to determine the role of ST2 in modulating host defense in the lung during sepsis, using a murine model of cecal ligation and puncture (CLP)-induced sepsis followed by a secondary infection with Pseudomonas aeruginosa via the airways.CLP or sham surgery was performed on BALB/c wild-type (WT) and ST2 knockout (KO) mice, and 24 hours later animals were challenged with 10(8) live P. aeruginosa.CLP mice demonstrated impaired clearance of Pseudomonas from their lungs and reduced pulmonary levels of tumor necrosis factor-α and IL-6 compared with sham mice. After CLP, ST2KO mice with secondary pneumonia displayed a strongly improved survival and a better bacterial clearance compared with WT mice, which was accompanied by enhanced lung inflammation. CLP did not influence the responsiveness of alveolar macrophages toward P. aeruginosa ex vivo irrespective of the st2 genotype. In contrast, CLP resulted in a reduced capacity of WT CD4(+) and CD8(+) T cells to produce IFN-γ and tumor necrosis factor-α, an immune suppressive effect that was not seen in ST2KO mice.These findings indicate that gene products of ST2 contribute to the immune-compromised state during sepsis and the ensuing disturbed homeostasis of lung host defense.
Defining and Characterizing the Progression of Type 2 Diabetes
Authors: Vivian A. Fonseca
Journal: Diabetes Care (2009)

Type 2 diabetes is a progressive disease in which the risks of myocardial infarction, stroke, microvascular events, and mortality are all strongly associated with hyperglycemia (1). The disease course is primarily characterized by a decline in β-cell function and worsening of insulin resistance. The process is manifested clinically by deteriorations in multiple parameters, including A1C, fasting plasma glucose (FPG), and postprandial glucose levels.

In this review, we will evaluate our current understanding of the role played by deteriorating β-cell function and other abnormalities linked with the progression of type 2 diabetes. An improved understanding of these abnormalities may provide the scientific groundwork for novel therapies that may help achieve and maintain good glycemic control.

### Progression from pre-diabetes to overt diabetes

Because glucose is a continuous variable, the use of thresholds to make a diagnosis is somewhat arbitrary. The term “pre-diabetes” has become well established and implies a risk of progression to overt diabetes. However, although such progression is well studied in prevention trials, little is known about the rate of progression and the characteristics of such progression in the population at large. Table 1 summarizes some of the factors associated with such progression. Nichols et al. (2) studied the progression of pre-diabetes to overt disease and observed that 8.1% of subjects whose initial abnormal fasting glucose was 100–109 mg/dl and 24.3% of subjects whose initial abnormal fasting glucose was 110–125 mg/dl developed diabetes over an average of 29.0 months (1.34 and 5.56% per year, respectively). A steeper rate of increasing fasting glucose; higher BMI, blood pressure, and triglycerides; and lower HDL cholesterol predicted diabetes development.

View this table:

Table 1 
Factors associated with progression of pre-diabetes to diabetes



The Baltimore Longitudinal Study of Aging (3) concluded that although phenotypic differences in rates of progression are partly a function of diagnostic thresholds, fasting and postchallenge hyperglycemia may represent phenotypes with distinct natural …
All Vibrio cholerae Infections Are Not Created Equal
Authors: Rosemary Harris
Journal: JAMA (1995)

To the Editor.  —The recent article by Dr Besser and colleagues 1 recommends a travel history on all patients with diarrhea and dehydration. Physicians in the United States should also be aware that cholera may no longer be limited to the third world.  I practice in the rural part of Maryland's Eastern Shore— just 90 minutes from Washington, DC, and Baltimore—and recently treated three people with cholera acquired locally. One was an elderly, homebound man who had been no further than his ground floor for 10 years. He required 500 mL/h of IV fluids to keep abreast of his stool output. A grandson is a waterman and had brought crabmeat to his home a week before the patient became ill.  The other two patients were a mother and small child who had eaten cooked crabs bought in a local market. Both did well with outpatient rehydration. Neither patient had been
Circumferential Margin Involvement Is the Crucial Prognostic Factor after Multimodality Treatment in Patients with Locally Advanced Rectal Carcinoma
Authors: Marleen J.E.M. Gosens, René A. Klaassen, Ivonne Tan-Go, Harm J.T. Rutten, Hendrik Martijn, Adriaan J.C. van den Brule, Grard A.P. Nieuwenhuijzen, J. Han J.M. van Krieken, Iris D. Nagtegaal
Journal: Clinical Cancer Research (2007)

Abstract Purpose: After preoperative (radio)chemotherapy, histologic determinants for prognostification have changed. It is unclear which variables, including assessment of tumor regression, are the best indicators for local recurrence and survival. Experimental Design: A series of 201 patients with locally advanced rectal cancer (cT3/T4, M0) presenting with an involved or at least threatened circumferential margin (CRM) on preoperative imaging (&amp;lt;2 mm) were evaluated using standard histopathologic variables and four different histologic regression systems. All patients received neoadjuvant radiochemotherapy or radiotherapy. The prognostic value of all factors was tested with univariate survival analysis of time to local recurrence and overall survival. Results: Local recurrence occurred in only 8% of the patients with a free CRM compared with 43% in case of CRM involvement (P &amp;lt; 0.0001). None of the four regression systems were associated with prognosis, not even when corrected for CRM status. However, we did observe a higher degree of tumor regression after radiochemotherapy compared with radiotherapy (P &amp;lt; 0.001). Absence of tumor regression was associated with increasing invasion depth and a positive CRM (P = 0.02 and 0.03, respectively). Conclusions: Assessment of CRM involvement is the most important pathologic variable after radiochemotherapy. Although tumor regression increases the chance on a free CRM, in cases with positive resection margins prognosis is poor irrespective of the degree of therapy-induced regression.
Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding
Authors: Samantha Scholtz, Alexander D Miras, Navpreet Chhina, Christina G Prechtl, Michelle L Sleeth, Norlida M Daud, Nurhafzan A Ismail, Giuliana Durighel, Ahmed R Ahmed, Torsten Olbers, Royce P Vincent, Jamshid Alaghband-Zadeh, Mohammad A Ghatei, Adam D Waldman, Gary S Frost, Jimmy D Bell, Carel W le Roux, Anthony P Goldstone
Journal: Gut (2013)

Roux-en-Y gastric bypass (RYGB) has greater efficacy for weight loss in obese patients than gastric banding (BAND) surgery. We hypothesise that this may result from different effects on food hedonics via physiological changes secondary to distinct gut anatomy manipulations.We used functional MRI, eating behaviour and hormonal phenotyping to compare body mass index (BMI)-matched unoperated controls and patients after RYGB and BAND surgery for obesity.Obese patients after RYGB had lower brain-hedonic responses to food than patients after BAND surgery. RYGB patients had lower activation than BAND patients in brain reward systems, particularly to high-calorie foods, including the orbitofrontal cortex, amygdala, caudate nucleus, nucleus accumbens and hippocampus. This was associated with lower palatability and appeal of high-calorie foods and healthier eating behaviour, including less fat intake, in RYGB compared with BAND patients and/or BMI-matched unoperated controls. These differences were not explicable by differences in hunger or psychological traits between the surgical groups, but anorexigenic plasma gut hormones (GLP-1 and PYY), plasma bile acids and symptoms of dumping syndrome were increased in RYGB patients.The identification of these differences in food hedonic responses as a result of altered gut anatomy/physiology provides a novel explanation for the more favourable long-term weight loss seen after RYGB than after BAND surgery, highlighting the importance of the gut-brain axis in the control of reward-based eating behaviour.
Imipramine for the treatment of fibrositis: a therapeutic trial.
Authors: A J Wysenbeek, F Mor, Y Lurie, A Weinberger
Journal: Annals of the Rheumatic Diseases (1985)

Twenty fibrositic patients were treated with imipramine 50-75 mg/day. Only two patients responded favourably. Nineteen patients stopped therapy during the initial three-month period: 14 of them due to lack of response, while two of these concomitantly disclosed side effects. The additional five patients stopped therapy mainly due to side effects, while only one of them improved with therapy. One patient, only, improved and adhered to therapy for more than three months.
A Call for More Effectively Integrating Behavioral and Social Science Principles Into Comprehensive Diabetes Care
Authors: Lawrence Fisher, Russell E. Glasgow
Journal: Diabetes Care (2007)

Research has clearly demonstrated that reductions in hyperglycemia, blood pressure, and lipids through medication and healthy living can retard diabetes progression and reduce cardiovascular risk (1). The Diabetes Prevention Program (2) has convincingly shown that healthy living and appropriate medication can reduce or even halt the progression to full diabetes for individuals with pre-diabetes. These studies used large samples of individuals who were able to adhere to the lifestyle change and medication protocols included in these clinical trials so that the effects of the interventions could be adequately documented.

Applying the results of these landmark studies to the world of clinical practice has been somewhat more difficult than anticipated (3). Providing access to care for all patients, incorporating guideline-based care in clinical practice, motivating patients to initiate and sustain the essential healthy-living life changes that diabetes requires, helping patients cope with diabetes-related distress and depression, and addressing the competing priorities in health care have slowed the full application of knowledge gained by these and related studies. In clinical practice, at national meetings, and in the literature, the question most often voiced by practicing clinicians across the diabetes-related health professions is, “How do I help activate or empower my patients to take better care of their diabetes?” Despite the general consensus that weight control, balanced diet, regular physical activity, blood glucose self-monitoring, medication management, and good diabetes emotional coping and problem solving are some of the primary, evidence-based dimensions of good diabetes self-care, most patients with diabetes continue to have chronic or episodic problems achieving these goals. These problems lead to increased morbidity and mortality, high health care costs, and often high frustration among both patients and practitioners. Despite the enormous advances in sophisticated medications and diabetes-related devices based on recent advances in genetics, biotechnology, and bio-engineering, we are left with …
Mechanochemistry of Cardiac Muscle
Authors: BRIAN M. CHANDLER, EDMUND H. SONNENBLICK, PETER E. POOL
Journal: Circulation Research (1968)

Norepinephrine increases myocardial contractility and myocardial oxygen consumption (MV · O 2 ). It is not clear whether these phenomena are directly proportional or whether there is a disproportionate increase in MV · O 2 , signifying either uncoupling of oxidative phosphorylation or a direct increase in oxidative metabolism. Accordingly, the direct conversion of chemical energy to mechanical work was studied in control and norepinephrine-treated right ventricular papillary muscles from cats. Production of adenosine triphosphate (ATP) was inhibited by iodoacetic acid and N 2 . After resting or performing variable amounts of work, the muscles were instantly frozen, and the total amount of chemical energy (∼P = creatine phosphate + ATP) used was correlated with work performed and the number of contractions. There was no change in either the initial stores of energy or in the basal rate of energy utilization following treatment with norepinephrine. However, norepinephrine-treated muscles performing isometric work used 115% as much ∼P as control muscles in only 59% as many contractions and while performing only 87% as much work. Regression analysis of these data confirmed that norepinephrine-treated muscles used a greater amount of ∼P than do control muscles. Thus the increase in contractility induced by norepinephrine results in an increase in the amount of chemical energy released disproportionate to the amount of work performed, and the "oxygen wasting" effect of norepinephrine on heart muscle results from the increased utilization of energy associated with an increased contractile state.