tbuckley/cabot-search huggingface dataset:
Limits to liver transplantation in the UK
Authors: S P PEREIRA, R WILLIAMS
Journal: Gut (1998)

In recent years, the number of liver transplants performed in the UK and the Republic of Ireland has been increasing by approximately 10% per year, rising from 509 in 1992 to 687 in 1995. Over the same period, the number of solid organ donors notified to the UK Transplant Support Service Authority (UKTSSA) has remained relatively static (951 in 1992, and 966 in 1995).1 In 1996, however, there was a fall in the number of liver donors for the first time, with only 691 donors accepted compared with 724 in 1995.2 3 In parallel with this decrease in organ availability, there was a 5% decline in the number of liver transplants (from 687 in 1995 down to 652 in 1996) and a corresponding 9% fall in the number of cadaveric kidneys transplanted.3 Although transplant activity has since increased (692 liver transplants in 19972), such statistics show the fragility of the current balance between solid organ availability and transplantation in the UK. Given that up to 30% of livers from potential donors are unsuitable for organ donation for medical reasons,4 the number of patients transplanted each year is unlikely to be maintained, let alone increased, unless organ availability can be improved.

Although the waiting list for liver transplantation in the UK is still relatively short, it has increased by 30% over the past two years, from 138 patients on the active waiting list at the end of 1995, to 180 patients in December 1997.2 3 Median times from listing to transplantation for chronic liver disease have also risen, from 30 to 38 days in 1995/96.2 These waiting times are still much lower than those of the USA and countries in continental Europe which have a much higher prevalence of liver disease than the UK, …
Recruiting African American Women to Participate in Hereditary Breast Cancer Research
Authors: Chanita Hughes Halbert, Kiyona Brewster, Aliya Collier, ChaChira Smith, Lisa Kessler, Benita Weathers, Jill E. Stopfer, Susan Domchek, E. Paul Wileyto
Journal: Journal of Clinical Oncology (2005)

This study evaluated the process of recruiting African American women to participate in genetic counseling research for BRCA1 and BRCA2 (BRCA1/2) mutations with respect to referral, study enrollment, and participation in genetic counseling.
Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.
Authors: R J Sung, W A Shapiro, E N Shen, F Morady, J Davis
Journal: Journal of Clinical Investigation (1983)

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.
Clearance of chronic plaque psoriasis by anthralin—subjective and objective assessment and comparison with photochemotherapy
Authors: JANET MARKS, SARAH ROGERS, BILL CHADKIRK, SAM SHUSTER
Journal: British Journal of Dermatology (1981)

Journal Article Clearance of chronic plaque psoriasis by anthralin—subjective and objective assessment and comparison with photochemotherapy Get access JANET MARKS, JANET MARKS Department of Dermatology, University of Newcastle upon Tyne, NE1 4LP Search for other works by this author on: Oxford Academic Google Scholar SARAH ROGERS, SARAH ROGERS Department of Dermatology, University of Newcastle upon Tyne, NE1 4LP Search for other works by this author on: Oxford Academic Google Scholar BILL CHADKIRK, BILL CHADKIRK Department of Dermatology, University of Newcastle upon Tyne, NE1 4LP Search for other works by this author on: Oxford Academic Google Scholar SAM SHUSTER SAM SHUSTER Department of Dermatology, University of Newcastle upon Tyne, NE1 4LP Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 105, Issue s20, 1 August 1981, Pages 96–99, https://doi.org/10.1111/j.1365-2133.1981.tb01020.x Published: 01 August 1981
TWEAK induces liver progenitor cell proliferation
Authors: Aniela Jakubowski, Christine Ambrose, Michael Parr, John M. Lincecum, Monica Z. Wang, Timothy S. Zheng, Beth Browning, Jennifer S. Michaelson, Manfred Baestcher, Bruce Wang, D. Montgomery Bissell, Linda C. Burkly
Journal: Journal of Clinical Investigation (2005)

Progenitor ("oval") cell expansion accompanies many forms of liver injury, including alcohol toxicity and submassive parenchymal necrosis as well as experimental injury models featuring blocked hepatocyte replication. Oval cells can potentially become either hepatocytes or biliary epithelial cells and may be critical to liver regeneration, particularly when hepatocyte replication is impaired. The regulation of oval cell proliferation is incompletely understood. Herein we present evidence that a TNF family member called TWEAK (TNF-like weak inducer of apoptosis) stimulates oval cell proliferation in mouse liver through its receptor Fn14. TWEAK has no effect on mature hepatocytes and thus appears to be selective for oval cells. Transgenic mice overexpressing TWEAK in hepatocytes exhibit periportal oval cell hyperplasia. A similar phenotype was obtained in adult wild-type mice, but not Fn14-null mice, by administering TWEAK-expressing adenovirus. Oval cell expansion induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) was significantly reduced in Fn14-null mice as well as in adult wild-type mice with a blocking anti-TWEAK mAb. Importantly, TWEAK stimulated the proliferation of an oval cell culture model. Finally, we show increased Fn14 expression in chronic hepatitis C and other human liver diseases relative to its expression in normal liver, which suggests a role for the TWEAK/Fn14 pathway in human liver injury. We conclude that TWEAK has a selective mitogenic effect for liver oval cells that distinguishes it from other previously described growth factors.
Life after shock
Authors: Amy Maxmen
Journal: The Journal of Experimental Medicine (2009)

Lethal shock is subverted by crippling a family of G proteins in endothelial cells, according to Korhonen and colleagues on page [411][1].

![Figure][2] 

Mice without endothelial Gq/G11 survived allergen-induced shock.



Bee stings or other allergens can cause anaphylactic shock in severely
Respiratory syncytial virus: a sleeping giant?
Authors: D. M. Fleming, A. J. Elliot
Journal: European Respiratory Journal (2007)

The study by Jansen et al. 1 in the present issue of the European Respiratory Journal focuses on the impact of influenza and respiratory syncytial virus (RSV) on mortality and hospital admissions. As in many other similar publications, it emphasises the significance of RSV (and influenza) in all age groups and not just children, in whom the impact is already well recognised 1. In common with other similar studies, the evidence presented is derived by linking independent data on virus circulation (mainly from specimens sampled in children) with data on healthcare utilisation. As such, it falls short of direct linkage between cause and effect, although this has been demonstrated in experimental studies, which have included wild-type virus in addition to low temperature attenuated strains. In one of these studies, McKay et al. 2 administered wild-type virus to 20 human volunteers, and nine of them developed upper respiratory tract symptoms.

In community-based observational cohort studies between 1977 and 1981, Monto and Sullivan 3 demonstrated average RSV isolation rates of 56 per 100 person-yrs in children aged 0–4 yrs, seven in those aged 5–19 yrs and somewhat less in older people. RSV demonstrated a clearer seasonality than other viruses studied. Zambon et al . 4 identified RSV in nose/throat virology specimens from community-based persons of all ages with influenza-like illness. Several studies have shown high rates of laboratory-confirmed infection in older people and especially in persons with chronic respiratory disease 5, 6. Basing their findings on serological studies, Dowell et al. 5 considered RSV to be one of the four most common pathogens identified in cases of lower respiratory tract infection in hospitalised adults, but went on to comment that none of the 57 cases of RSV infection included in the study were diagnosed during their period of hospitalisation. In an excellent …
Smallpox: A Case with Minimal Lesions
Authors: T. P. Evans
Journal: BMJ (1947)

many of whom have never known consistency or stability, always keeping in view our goal, which is that, if at all possible, the child shall eventually return home.We have aimed at a combination of routine with latitude, and of kindness and understanding with the gradual development of a really con- structivq attitude towards the child. (3)Play therapy has been widely utilized both as individual and as group treatment, and for the older children talks and discussions.(4) We have invited the parents to attend regularly for interviews, and in
Bacteria as the cause of ulcerative colitis
Authors: M. CAMPIERI
Journal: Gut (2001)

Ulcerative colitis (UC) is a chronic inflammatory condition of the large bowel of unknown aetiology, characterised by the presence of bloody diarrhoea and mucus associated with a negative stool culture for bacteria, ova, or parasites.

This definition finds its historical rationale in the first supposed description of the disease by Wilks and Moxon more than one century ago (1875)1; they reported a case of bloody colitis that was apparently not caused by dysenteric pathogens. Later, Sir William Hale-White reported upon occasional patients with severe ulceration of the colon not due to tuberculosis, typhoid fever, or malignant disease. The origin remained obscure, however, and he felt this condition should not be confused with bacillary dysentery.2 

Since these first descriptions, are there now data supporting a non-bacterial origin of the disease as suggested, or have we found evidence to support a bacterial role in the onset of symptoms?

In the last decade, the dogma that no bacteria could grow in the acid milieu of the stomach has been systematically destroyed by the evidence that an infective agent, Helicobacter pylori , is responsible for gastric/duodenal disease.3 If only a few thousand bacteria can cause gastritis, can we be so sure that among the billions of bacteria living within the colon some strains are not responsible for the onset of intestinal inflammation or for its perpetuation?

During the period 1938–1954, the only drug available for treatment of UC was sulphasalazine (SASP). Nanna Svartz used SASP, which is composed of a sulphonamide-sulphapyridine and a salicylate-5-aminosalicylic acid (5-ASA). Because of its anti-bacterial activity, it was postulated that the onset of UC might have some linkage with bacteria.4Though we know today that 5-ASA is the active part of SASP,5 a recent meta-analysis showed a trend towards a superior efficacy of …
Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats.
Authors: N Bank, H S Aynedjian
Journal: Journal of Clinical Investigation (1990)

The effect of progressive increases in intraluminal glucose concentration on proximal tubule sodium absorption was studied in normal and streptozotocin diabetic rats by microperfusion. Each tubule was perfused twice, with and without glucose added to the perfusion fluid. Net sodium and water absorption were markedly enhanced by 300-500 mg% intraluminal glucose in both normal and diabetic rats. Substituting the transported but nonmetabolized glucose analogue, alpha-methyl D-glucoside for glucose also resulted in marked stimulation of sodium absorption, whereas substituting bicarbonate and acetate for chloride in the perfusion solution inhibited the effect of glucose. These observations suggest that the stimulation of sodium absorption by glucose was mediated by the brush border Na/glucose cotransporter. Sodium concentration and osmolality were found to fall markedly to hypotonic levels when high glucose concentrations were in the perfusion fluid. This luminal hypotonicity may be an important driving force for proximal fluid absorption. In poorly controlled diabetes, high filtered glucose concentrations may lead to enhanced proximal sodium and water absorption, which could in turn contribute to volume expansion, hypertension, and renal hypertrophy.
A neurocognitive mechanism for folk biology?
Authors: Remo Job, Luca Surian
Journal: Behavioral and Brain Sciences (1998)

Atran's putative module for folk biology is evaluated with respect to evidence from patients showing category-specific impairments for living kinds. Existing neuropsychological evidence provides no support for the primacy of categorization at the generic species level. We outline reasons for this and emphasize that such claims should be tested using inductive reasoning tasks.
Ultralow-Power Electronics for Biomedical Applications
Authors: Anantha P. Chandrakasan, Naveen Verma, Denis C. Daly
Journal: Annual Review of Biomedical Engineering (2008)

The electronics of a general biomedical device consist of energy delivery, analog-to-digital conversion, signal processing, and communication subsystems. Each of these blocks must be designed for minimum energy consumption. Specific design techniques, such as aggressive voltage scaling, dynamic power-performance management, and energy-efficient signaling, must be employed to adhere to the stringent energy constraint. The constraint itself is set by the energy source, so energy harvesting holds tremendous promise toward enabling sophisticated systems without straining user lifestyle. Further, once harvested, efficient delivery of the low-energy levels, as well as robust operation in the aggressive low-power modes, requires careful understanding and treatment of the specific design limitations that dominate this realm. We outline the performance and power constraints of biomedical devices, and present circuit techniques to achieve complete systems operating down to power levels of microwatts. In all cases, approaches that leverage advanced technology trends are emphasized.
Association Between Plasma Levels of Monocyte Chemoattractant Protein-1 and Long-Term Clinical Outcomes in Patients With Acute Coronary Syndromes
Authors: James A. de Lemos, David A. Morrow, Marc S. Sabatine, Sabina A. Murphy, C. Michael Gibson, Elliott M. Antman, Carolyn H. McCabe, Christopher P. Cannon, Eugene Braunwald
Journal: Circulation (2003)

Background— Monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 appears to play a critical role at multiple stages in atherosclerosis, including the initiation of the fatty streak, promotion of plaque instability, and remodeling after myocardial infarction. Methods and Results— MCP-1 was measured from frozen plasma specimens in 279 healthy volunteers and 2270 patients with acute coronary syndromes enrolled in the Oral Glycoprotein IIb/IIIa Inhibition with Orbofiban in Patients with Unstable Coronary Syndromes (OPUS-TIMI) 16 trial. Median [25th, 75th percentiles] MCP-1 levels were 157 [124, 196] pg/mL in healthy volunteers and 178 [128, 238] pg/mL in the OPUS-TIMI 16 population ( P &lt;0.001). In OPUS-TIMI 16, baseline MCP-1 levels were associated with older age, female sex, hypertension, diabetes, prior coronary disease, and renal insufficiency ( P &lt;0.01 for each) but not with smoking status, body mass index, ejection fraction, troponin I or C-reactive protein. After adjustment for differences in baseline characteristics, ECG changes, troponin I, and C-reactive protein, an MCP-1 level &gt;75th percentile (corresponding to the 90th percentile in the healthy volunteers) was associated with an increased risk of death or myocardial infarction through 10 months of follow-up (adjusted hazard ratio, 1.53; 95% CI, 1.09 to 2.14; P =0.01). Conclusions— In a large cohort of patients with acute coronary syndromes, an elevated baseline level of MCP-1 was associated both with traditional risk factors for atherosclerosis as well as an increased risk for death or myocardial infarction, independent of baseline variables. Because it appears to play a crucial role at multiple stages of atherosclerosis, MCP-1 is attractive as a surrogate biomarker and merits further study as a potential therapeutic target.
Blockade of the Stromal Cell–Derived Factor-1/CXCR4 Axis Attenuates <i>In vivo</i> Tumor Growth by Inhibiting Angiogenesis in a Vascular Endothelial Growth Factor–Independent Manner
Authors: Bayasi Guleng, Keisuke Tateishi, Miki Ohta, Fumihiko Kanai, Amarsanaa Jazag, Hideaki Ijichi, Yasuo Tanaka, Miwa Washida, Keita Morikane, Yasushi Fukushima, Takao Yamori, Takashi Tsuruo, Takao Kawabe, Makoto Miyagishi, Kazunari Taira, Masataka Sata, Masao Omata
Journal: Cancer Research (2005)

The interaction between the chemokine receptor CXCR4 and its specific ligand, stromal cell-derived factor-1 (SDF-1/CXCL12), mediates several cellular functions. In cancer, SDF-1-positive or CXCR4-positive cells of various lineages are detected within tumor tissues. Recent intensive research has indicated the possibility that blocking CXCR4 could reduce the metastatic potential of cancer cells. Here, we show that the inhibition of the SDF-1/CXCR4 axis decreases the growth of s.c. gastrointestinal tumors through the suppression of tumor neoangiogenesis. The neutralization of CXCR4 suppressed the growth in vivo of tumors derived from mouse Colon38 and PancO2 cells, whereas it did not affect the growth of Colon38 and PancO2 cells in vitro. This attenuation of tumor growth was found to be independent of the expression of CXCR4 by the cancer cells themselves, because CXCR4 knocked-down Colon38 cells grew similarly to control cells. Furthermore, CD31-positive tumor capillaries were reduced to 45% (P < 0.001) and intratumor blood flows were decreased to 65% (P < 0.01) by blockade of CXCR4. The vascular endothelial growth factor (VEGF) concentration in the tumors was not affected by the neutralization of CXCR4. Taken together with the detection of CXCR4-positive endothelial cells in the tumor tissues, the findings suggest that the antiangiogenic effects of the blockade of CXCR4 are related to a reduction of the establishment of tumor endothelium independently of VEGF inhibition. Our data indicate that the SDF-1/CXCR4 pathway might be a general target for anticancer strategies and that blocking this system could be cooperatively effective in combination with other antiangiogenic therapies, such as blockade of VEGF.
Criteria for the Recognition of Pulmonary Emboli
Authors: J. O'Neal Humphries
Journal: JAMA (1976)

EFFECTIVE therapy can reduce to a fraction the risk of recurrent pulmonary emboli. However, failure to recognize the disorder continues to be one of the major causes of disability and death. An organized approach to the assessment of the patient with suspected recent pulmonary embolus is as important as any individual test. One of the first decisions is when to initiate therapy. This decision will have to be made on the clinical estimation of how likely the possibility is that the patient has had an embolus. If the clinical picture is typical or even highly suspicious, intravenous heparin therapy should be initiated immediately. On the other hand, if pulmonary embolization seems unlikely and is being considered only as an outside possibility, it is prudent to withhold treatment and gather further evidence as expediently as possible. <h3>Clinical Presentation</h3> A careful search of the history for suggestive symptoms, often nonspecific and subtle,
Management dilemmas in acute pulmonary embolism
Authors: Robin Condliffe, Charlie A Elliot, Rodney J Hughes, Judith Hurdman, Rhona M Maclean, Ian Sabroe, Joost J van Veen, David G Kiely
Journal: Thorax (2013)

<h3>Background</h3> Physicians treating acute pulmonary embolism (PE) are faced with difficult management decisions while specific guidance from recent guidelines may be absent. <h3>Methods</h3> Fourteen clinical dilemmas were identified by physicians and haematologists with specific interests in acute and chronic PE. Current evidence was reviewed and a practical approach suggested. <h3>Results</h3> Management dilemmas discussed include: sub-massive PE, PE following recent stroke or surgery, thrombolysis dosing and use in cardiac arrest, surgical or catheter-based therapy, failure to respond to initial thrombolysis, PE in pregnancy, right atrial thrombus, role of caval filter insertion, incidental and sub-segmental PE, differentiating acute from chronic PE, early discharge and novel oral anticoagulants. <h3>Conclusion</h3> The suggested approaches are based on a review of the available evidence and guidelines and on our clinical experience. Management in an individual patient requires clinical assessment of risks and benefits and also depends on local availability of therapeutic interventions.