tbuckley/cabot-search huggingface dataset:
On crying infants and clamping of cords
Authors: F. Godlee
Journal: BMJ (2011)

All babies cry, and in the first months of life they cry a lot—one to two hours a day on average, according to research quoted by Pamela Douglas and Peter Hill in their clinical review (doi:10.1136/bmj.d7772). But some cry excessively and continue with persistent crying beyond three months, and Douglas and Hill say it’s these babies and their parents who must be taken seriously. Although most will have no long term adverse effects, the strain on the family is associated with higher rates of physical abuse and postnatal depression, as well as behavioural problems in childhood (though cause and effect are hard to establish).

What can …
“Breakthrough” drugs and growth in expenditure on prescription drugs in Canada
Authors: Steven G Morgan, Kenneth L Bassett, James M Wright, Robert G Evans, Morris L Barer, Patricia A Caetano, Charlyn D Black
Journal: BMJ (2005)

Driven by increased use of prescription drugs and by shifts from old to new products, spending on drugs in Canada doubled between 1996 and 2003. 1 Which drugs drove this expenditure growth?The Canadian Patented Medicine Prices Review Board appraises the therapeutic novelty of every patented medicine in Canada to distinguish "breakthrough" drugs from other medicines.Since 1990, the board has published these appraisals in annual reports. 2 We applied the board's classifications for breakthrough drugs to total expenditures on and use of prescription drugs in the province of British Columbia (population 4.2 million).
A Panel to Predict Long-term Outcome of Infliximab Therapy for Patients With Ulcerative Colitis
Authors: Maria Theresa Arias, Niels Vande Casteele, Séverine Vermeire, Anthony de Buck van Overstraeten, Thomas Billiet, Filip Baert, Albert Wolthuis, Gert Van Assche, Maja Noman, Ilse Hoffman, Andre D’Hoore, Ann Gils, Paul Rutgeerts, Marc Ferrante
Journal: Clinical Gastroenterology and Hepatology (2014)
Elicitation of Broadly Neutralizing Influenza Antibodies in Animals with Previous Influenza Exposure
Authors: Chih-Jen Wei, Hadi M. Yassine, Patrick M. McTamney, Jason G. D. Gall, James R. R. Whittle, Jeffrey C. Boyington, Gary J. Nabel
Journal: Science Translational Medicine (2012)

The immune system responds to influenza infection by producing neutralizing antibodies to the viral surface protein, hemagglutinin (HA), which regularly changes its antigenic structure. Antibodies that target the highly conserved stem region of HA neutralize diverse influenza viruses and can be elicited through vaccination in animals and humans. Efforts to develop universal influenza vaccines have focused on strategies to elicit such antibodies; however, the concern has been raised that previous influenza immunity may abrogate the induction of such broadly protective antibodies. We show here that prime-boost immunization can induce broadly neutralizing antibody responses in influenza-immune mice and ferrets that were previously infected or vaccinated. HA stem-directed antibodies were elicited in mice primed with a DNA vaccine and boosted with inactivated vaccine from H1N1 A/New Caledonia/20/1999 (1999 NC) HA regardless of preexposure. Similarly, gene-based vaccination with replication-defective adenovirus 28 (rAd28) and 5 (rAd5) vectors encoding 1999 NC HA elicited stem-directed neutralizing antibodies and conferred protection against unmatched 1934 and 2007 H1N1 virus challenge in influenza-immune ferrets. Indeed, previous exposure to certain strains could enhance immunogenicity: The strongest HA stem-directed immune response was observed in ferrets previously infected with a divergent 1934 H1N1 virus. These findings suggest that broadly neutralizing antibodies against the conserved stem region of HA can be elicited through vaccination despite previous influenza exposure, which supports the feasibility of developing stem-directed universal influenza vaccines for humans.
Apoptosis and the subsequent generation of autoantigens as initial triggers in the pathogenesis of experimental autoimmune arthritis
Authors: S Herman, M Hoffmann, A Kny, J Smolen, G Steiner
Journal: Annals of the Rheumatic Diseases (2010)

Background Rheumatoid arthritis (RA) has a defi nite autoimmune pathogenesis.Rising evidence suggests that deregulated and/or defi cient clearance of apoptotic materials may lead to the release of potential autoantigens provoking a break in the self-tolerance mechanism.Major autoantigens in RA include immunoglobulin G, the target of rheumatoid factor (RF), citrullinated proteins and the heterogeneous nuclear ribonucleoprotein (hnRNP) A2.To gain more insight into the role of apoptotic processes in lymphoid tissues in the generation of arthritogenic autoantigens, we studied the autoimmune responses in the pristane-induced arthritis (PIA) model which shows some striking similarities with human RA, including symmetrical polyarthritis, massive bone erosion and the presence of RF and autoantibodies to hnRNP-A2.Methods Pristane (2,6,10,14-tetramethylpentadecane) was injected intradermally at the base of the tail into DA.1Frats.Lymph nodes were analysed by immunohistochemistry and immunoblotting at various time points after pristane application.The fate of potential neoantigens, particularly hnRNP-A2, during apoptosis of lymphoid cells was studied in cultured cells by inducing apoptosis with agents such as etoposide or anti-Fas antibody, or by cultivating cells in the presence of pristane/cyclodextrine complexes.To investigate apoptotic cleavage of hnRNP-A2 in vitro, caspase digestion assays were performed.Results Three days after pristane application the amount of apoptotic cells was strongly increased in draining inguinal lymph nodes of DA.1F rats compared with naïve animals.Immunoblotting analysis of inguinal lymph nodes revealed cleavage of hnRNP-A2.Furthermore, a cleaved product of hnRNP-A2 was also detected in cellular apoptosis assays performed with human peripheral blood cells and rat splenocytes.Cleavage was most pronounced after apoptosis induction via the Fas receptor.Interestingly, the cleaved product was preferentially detected in cell supernatants compared with cell lysates, whereas the intact protein was found in similar amounts in lysates and supernatants.Furthermore, both caspase 3 and caspase 6 were able to effi ciently cleave recombinant hnRNP-A2 in vitro.The in vivo relevance of these fi ndings was further strengthened by results obtained with pristane-cyclodextrine complexes which were able to induce apoptosis in both human and rat cells.Conclusion Pristane induces apoptosis in draining lymph nodes leading to cleavage of hnRNP-A2 by proteolytic enzymes such as caspase 3 or caspase 6.This suggests a mechanism for the generation of neoepitopes which are subsequently targeted by arthritogenic T cells.These data further strengthen the view of hnRNP-A2 as a key player in the pathogenesis of PIA and possibly also human RA.
Angiographic embolization for major trauma in a low-middle income healthcare setting – A retrospective review
Authors: Adil Aijaz Shah, Abdul Rehman, Adil Hussain Haider, Raza Sayani, Raza Hasnain Sayyed, Kamran Ali, Syed Nabeel Zafar, Zia-ur Rehman, Hasnain Zafar
Journal: International Journal of Surgery (2015)
Diurnal fluctuations of portal and systemic hemodynamic parameters in patients with cirrhosis
Authors: Daniel Alvarez, Diego Golombek, Patricia Lopez, Marcelo De Las Heras, Luis Viola, Susana Sanchez, Miguel Kolker, Ricardo Mastai
Journal: Hepatology (1994)

A close temporal relationship between higher levels of portal pressure during the night and the peak incidence of acute variceal bleeding has recently been demonstrated in patients with cirrhosis. Because hemodynamic changes may have a role in triggering this hemorrhagic episode, we measured systemic and portal hemodynamic parameters at 4-hr intervals for 24 hr in 12 cirrhotic patients. These results were compared with those obtained in eight healthy subjects. Cardiac output, femoral and portal blood flows were measured by Doppler technique. In cirrhotic patients, heart rate and mean arterial pressure remained constant throughout the whole study period. A marked and significant increase in portal blood flow (917 +/- 248 ml/min) (mean +/- S.D.) as compared with mesor values (649 +/- 114 ml/min, p < 0.001) was observed at midnight. This effect was accompanied by a mild but significant rise of cardiac output (from 6.5 +/- 0.7 to 6.8 +/- 0.7 l/min, p < 0.01) at 2400 hr. A significant correlation between both hemodynamic parameters was found (r = 0.78, p < 0.01). Cosinor analysis showed a significant (p < 0.05) circadian rhythm for both portal blood flow and cardiac output with an acrophase at 0050 hr. In the healthy subjects group, a significant decrease of mean arterial pressure and heart rate was observed at 2400 hr. Cosinor analysis confirmed the presence of significant rhythm for both hemodynamic parameters. In contrast with cirrhotic patients, no significant changes were observed in portal blood flow and cardiac output in healthy subjects. Our results show that in patients with cirrhosis, maximal increases in portal blood flow occur at night.(ABSTRACT TRUNCATED AT 250 WORDS)
Increased 36-Week Survival with High Oxygen Saturation Target in Extremely Preterm Infants
Authors: Ben Stenson, Peter Brocklehurst, William Tarnow-Mordi
Journal: New England Journal of Medicine (2011)

there was no effect on TmP per GFR because at 10 hours the calculation was made on the basis of nonfasting values.At 21 hours, although the TmP per GFR was appropriately calculated, on the basis of fasting values, the serum phosphorous level had returned to baseline.The rise in serum levels of 1,25-dihydroxyvitamin D is probably due to the direct stimulatory effect of calcitonin on renal 1α-hydrox y lase. 3 Recently, Gooi et al. reported that osteocytes express the calcitonin receptor and respond to calcitonin with an increase in sclerostin production. 4 Since the primary source of FGF-23 is osteocytes, these findings imply that the decline in FGF-23 levels that we observed in patients with X-linked hypophosphatemia was due to the direct effect of calcitonin on osteocytes in this disease.Our study raises the possibility that calcitonin is a therapeutic option for patients with X-linked hypophosphatemia.
Antitumor Activity of Liposome-Encapsulated Doxorubicin in Advanced Breast Cancer: Phase II Study
Authors: J. Treat, A. Greenspan, D. Forst, J. A. Sanchez, V. J. Ferrans, L. A. Potkul, P. V. Woolley, A. Rahman
Journal: JNCI Journal of the National Cancer Institute (1990)

Previous studies in animals have demonstrated liposome-encapsulated doxorubicin (LED) has substantially less cardiac toxicity than free doxorubicin but retains antitumor activity. In a phase I clinical study of LED, the maximum tolerated dose was 90 mg/m 2 and dose-limiting toxicity was considered to have been reached when granulocytopenia was produced. We used LED to treat 20 patients with advanced, measurable breast cancer. LED was given at doses of 60–75 mg/m 2 every 3 weeks as an intravenous infusion. Regression of disease was objectively measured in nine patients; in five of these patients, complete regression of the index lesion occurred. The mean duration of the responses was 7 months. Hematologic toxicity consisted of grade 1–2 leukopenia in some patients. Gastrointestinal toxicity and mucositis were generally mild and tolerable. Alopecia occurred in all patients and usually was complete. Twelve patients received cumulative doses of LED of greater than 400 mg/m 2 and were evaluated with radionuclide ventriculograms. In eight patients, the cumulative dose was greater than 500 mg/m 2 , and five had endomyocardial biopsies. Four of these biopsy results were Billingham grade 0, while one (cumulative LED dose, 750 mg/m 2 ) showed grade 1 changes with mild myofibrillar loss and dilatation of the sarcoplasmic reticulum involving less than 5% of cardiac myocytes. Two patients had decreases in left ventricular ejection fraction. One of these patients had received a total dose of LED of 630 mg/m 2 and had a decline of 13% in left ventricular ejection fraction, but had no clinical evidence of congestive heart failure and had a Billingham grade 0 endomyocardial biopsy. A second patient, who received a total dose of LED of 660 mg/m 2 plus a 300-mg/m 2 dose of free doxorubicin as adjuvant therapy more than a year prior to beginning LED treatment, had a decline of 17% in ejection fraction and developed congestive heart failure. An endomyocardial biopsy performed after failure developed showed Billingham grade 0 changes. These data show that LED has anti-tumor activity in patients with breast cancer and suggest that it is less cardio-toxic than free doxorubicin at cumulative doses of 500–880 mg/m 2 . [J Natl Cancer Inst 82: 1706–1710, 1990]
Abstract 1609: IRF1 regulates bevacizumab induced autophagy .
Authors: Ji Liang, Yuji Piao, John F. de Groot
Journal: Cancer Research (2013)

Abstract Antiangiogenic therapy is commonly being used for the treatment of recurrent glioblastoma. However, the benefits of angiogenesis inhibitors are typically transient and resistance often develops. Determining the mechanism of treatment failure of the VEGF monoclonal antibody bevacizumab for malignant glioma would provide insight into approaches to overcome therapeutic resistance. In this study, we observed up-regulation of autophagy marker expression and increased autophagosome formation after bevacizumab treatment. In order to determine genes regulating bevacizumab resistance, microarray gene expression analysis was performed on murine xenograft models of glioblastoma. Compared to control tumor tissues, we found increased transcriptional levels of STAT1/IRF1 signaling in bevacizumab resistant tumors, which were further confirmed by immunohistochemistry of bevacizumab treated tissue at the protein level. To determine whether IRF1 contributes to bevacizumab resistance, glioma stem cell lines with stable IRF1 down regulation were injected into the brains of nude mice. H&amp;E staining of 6 week treated tumor tissues showed that bevacizumab markedly reduce tumor size in the shIRF1 group compared to the control shRNA group treated with bevacizumab. We also found a decrease in autophagy marker expression and increased TUNEL staining in shIRF1 cells. These data suggest that IRF1 may regulate bevacizumab-induced autophagy, and may be one important mediator of bevacizumab resistance. Citation Format: Ji Liang, Yuji Piao, John F. de Groot. IRF1 regulates bevacizumab induced autophagy . [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 1609. doi:10.1158/1538-7445.AM2013-1609
Development of a bioartificial new intestinal segment using an acellular matrix scaffold
Authors: M. P Pahari, M. L Brown, G. Elias, H. Nseir, B. Banner, C. Rastellini, L. Cicalese
Journal: Gut (2007)

We thank Lim et al for their keen interest in our article (Gut 2006; 55: 1233-9) on the long-term results of ablation in patients with Barrett's oesophagus (BO).In this prospective, randomised controlled trial, we compared the longterm efficacy of achieving complete reversal (endoscopic and histological) between multipolar electrocoagulation (MPEC) and argon plasma coagulation (APC) in patients with BO.Patients underwent stratified randomisation by BO length, using sealed opaque envelopes.Results of this study showed that complete reversal can be maintained in ,70% of patients, irrespective of the technique, with no predictors identified associated with achieving complete reversal.In this study, we used stratified randomisation instead of simple randomisation, which allowed us to use the paired Fisher's test for determination and analyses of power and sample size.The paired Fisher's test finds whether there is a difference between two groups when the outcome is a response proportion and the difference is assessed by testing if the odds ratio (OR) is 1 or not.This works only when the subjects are stratified into groups before randomisation, as it is believed that the response proportions will vary across the strata, but that the OR is constant across the strata.In the case of our study, the strata are the BO lengths. 1 We believe that Lim et al have assumed a simple randomisation and hence used a non-paired Fisher's exact test for their sample size calculation.Crucial demographic and endoscopic features of patients and the number of ablation sessions required in the two groups were reported in this study.We agree with Lim et al that information such as the duration of each procedure for the two techniques, information on patients with BO who refused participation, and so on was not provided in the manuscript.However, as we have highlighted in our article, we reiterate that techniques such as MPEC and APC are not ready for clinical application in ablation of nondysplastic BO and should not be offered outside the research arena.The degree of long-term control of neoplasia is not as yet known.Persistence of underlying intestinal metaplasia after ablation (buried glands) carries the potential to progress to dysplasia and adenocarcinoma, a problem that cannot be ignored. 2It has also been shown that recurrent and/or persistent BO after ablative therapy still contains genetic alterations associated with malignant progression to cancer. 3At the present time, the available data do not support the application of ablative therapies for patients with non-dysplastic BO.
Access to Health Care Records After Death
Authors: David J. Robinson, Desmond O’Neill
Journal: JAMA (2007)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Acquired immune deficiency syndrome-related hyperkeratotic Kaposi’s sarcoma with severe lymphoedema: report of five cases
Authors: U.R. Hengge, K. Stocks, M. Goos
Journal: British Journal of Dermatology (2000)

Abstract Kaposi’s sarcoma (KS) is the most frequent neoplasm in acquired immune deficiency syndrome (AIDS) patients. Whereas typical cases present as erythematous, plaque or nodular lesions, hyperkeratotic variants of AIDS-associated KS are rare. We describe five patients with AIDS-associated KS with hyperkeratosis and lymphoedema as prominent features. We also speculate on its pathogenesis.
Variability of the Viscoelastic Constants Along the Aortic Axis of the Dog
Authors: RICHARD W. LAWTON
Journal: Circulation Research (1960)

The application of elastomeric theory to the study of the viscoelastic properties of the dog's aorta shows that the same value of the elastomeric parameter β may be used to describe the elastic behavior of aorta strips under both static and dynamic conditions. The variations in the parameter β and the damping fraction γ with the strip's location may be distinguished only for the extremes of the central arterial axis because of the wide variability of mechanical properties among dogs. The viscoelastic properties apparently do not correlate with the measured geometric properties of the unstressed aortic strip.
George Mason Preston
Authors: R H S Mindham
Journal: BMJ (2003)

Former general practitioner London (b Seaham Harbour, County Durham, 1935; q Guy's Hospital, London, 1960; MRCGP), died from biliary sepsis secondary to carcinoma of the pancreas on 16 August 2003.​2003.




Figure 1




At Guy's George was the outstanding student of his year, gaining an intercalated BSc in physiology with first class honours and placed top in the University of London. He was appointed lecturer in physiology at Guy's before turning to general practice in Kennington in 1968, working part time as clinical assistant in dermatology at Great Ormond Street Hospital. Later he became a police surgeon and published papers on changes in police medical work in south London. He had a lifelong interest in food and wine, rugby, music, opera, and foreign travel. He leaves his second wife, Muriel, and their two children.
In vitro neutrophil‐erythrocyte rosette formation mediated by a serum factor (IgG)
Authors: Ila Mirchandani, Margarita Palutke, Karel Kithier, Pamela Tabaczka, Jacqueline Suffian
Journal: American Journal of Hematology (1984)

Abstract In vitro neutrophil‐erythrocyte rosette (NER) formation occurred in the peripheral blood of an elderly man. This caused problems in cross‐matching for blood transfusion initially but was resolved by performing crossmatches at 37°C because this phenomenon was temperature‐dependent. NER formation was independent of complement and of the type of anticoagulant used. NERs were induced using normal control cells with the patient's plasma, serum, and the IgG fraction of serum. The resetting factor was adsorbed by heterologous group‐specific erythrocytes, but not by leukocytes. No neutrophil antibodies were identified.
Exposure to Parental Smoking in Childhood Is Associated With Increased Risk of Carotid Atherosclerotic Plaque in Adulthood
Authors: Henry W. West, Markus Juonala, Seana L. Gall, Mika Kähönen, Tomi Laitinen, Leena Taittonen, Jorma S.A. Viikari, Olli T. Raitakari, Costan G. Magnussen
Journal: Circulation (2015)

The association between passive smoking exposure in childhood and adverse cardiovascular health in adulthood is not well understood. Using a 26-year follow-up study, we examined whether childhood exposure to passive smoking was associated with carotid atherosclerotic plaque in young adults.Participants were from the Cardiovascular Risk in Young Finns Study (n=2448). Information on childhood exposure to parental smoking was collected in 1980 and 1983. Carotid ultrasound data were collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (n=1578). The proportion of children with nondetectable cotinine levels was highest among households in which neither parent smoked (84%), was decreased in households in which 1 parent smoked (62%), and was lowest among households in which both parents smoked (43%). Regardless of adjustment for potential confounding and mediating variables, the relative risk of developing carotid plaque in adulthood increased among those children with 1 or both parents who smoked (relative risk, 1.7; 95% confidence interval, 1.0-2.8; P=0.04). Although children whose parents exercised good "smoking hygiene" (smoking parents whose children had nondetectable cotinine levels) had increased risk of carotid plaque compared with children with nonsmoking parents (relative risk, 1.6; 95% confidence interval, 0.6-4.0; P=0.34), children of smoking parents with poor smoking hygiene (smoking parents whose children had detectable serum cotinine levels) had substantially increased risk of plaque as adults (relative risk, 4.0; 95% confidence interval, 1.7-9.8; P=0.002).Children of parents who smoke have increased risk of developing carotid atherosclerotic plaque in adulthood. However, parents who exercise good smoking hygiene can lessen their child's risk of developing plaque.