tbuckley/cabot-search huggingface dataset:
Abstract No. 3 Is there a skin cancer risk with narrowband ultraviolet B phototherapy? Preliminary data from the second phase of the Dundee follow-up study
Authors: R.M.R. Hearn, R.S. Dawe, A. Kerr, K. Rahim, S.H. Ibbotson, J. Ferguson
Journal: British Journal of Dermatology (2006)

We do not know whether narrowband ultraviolet B (NB‐UVB, TL‐01) phototherapy carries any increased risk of skin cancers. Follow‐up of 126 patients treated with NB‐UVB in Germany (Weischer M, Blum A, Eberhard F et al. No evidence for increased skin cancer risk in psoriasis patients treated with broadband or narrowband UVB phototherapy: a first retrospective study. Acta Derm Venereol (Stockh) 2004; 84: 370–4) did not detect any increased skin cancer risk. Our follow‐up study (with linkage to Scottish Cancer Registry data complete to 1998) showed greater than expected (compared with age‐ and sex‐matched Scottish population) numbers of basal cell carcinomas (BCCs) in those treated with NB‐UVB (Man I, Crombie IK, Dawe RS et al. The photocarcinogenic risk of narrowband UVB (TL‐01) phototherapy: early follow‐up data. Br J Dermatol 2005; 152: 755–7). Whether the modestly increased standardized incidence rate (SIR) of 213 (95% confidence interval, CI 102–391) was due to treatment or factors such as ascertainment bias was not clear. Analysis of data from the next phase of this follow‐up study, with linkage to the Scottish Cancer Registry complete to December 2002, is ongoing. The summary phototherapy records of 4050 patients treated with NB‐UVB between 1985 and 2002 were examined. The median duration of follow‐up was 5·8 years (up to 16·7) from end of first NB‐UVB course. We now have 26 633 person‐years of follow‐up data. The most frequent primary diagnoses were: psoriasis (55%), atopic dermatitis (15·4%), polymorphic light eruption (7·7%) and chronic urticaria (3·9%). Indirect standardization, adjusting for age and sex, was used to compare numbers of skin tumours identified with numbers expected in the general Scottish population. We did not find significantly more melanomas [SIR 164 (95% CI 60–357), P = 0·16] nor squamous cell carcinomas [SIR 173 (95% CI 79–329), P = 0·08] than expected. More BCCs than expected were registered in patients who had received NB‐UVB and psoralen plus ultraviolet A [SIR 184 (95% CI 128–255), P = 0·0007] and who had received only NB‐UVB [SIR 211 (95% CI 135–314), P = 0·0007, n = 3082]. So far, these findings are reassuring. A possible explanation for the excess BCCs is a causative association between NB‐UVB exposure and BCC development. Alternatively, more BCCs may have been registered in our treated patients because of careful surveillance leading to more BCCs being detected earlier and treated with modalities leading to a histopathological diagnosis (and, therefore, registration). However, only with more prolonged follow‐up of patients who have received high cumulative numbers of treatments might a definite skin cancer risk become detectable. Therefore, we should remain cautious as we cannot dismiss the possibility that NB‐UVB is carcinogenic in humans.
Polish academy is to establish a national commission on research ethics
Authors: N. Stafford
Journal: BMJ (2011)

The Polish Academy of Sciences has taken steps to establish a national commission for research ethics, which will make Poland among the first countries in eastern Europe to have such a commission and one of only a handful in the European Union.

The academy received the mandate to found the ethics commission from Poland’s parliament, which last autumn adopted a package of new laws aimed at improving Polish science, said Andrzej Gorski, a former president of the University of Warsaw Medical School who is now a vice president at the academy.

In addition to laws dealing with funding of research projects and of research institutes, the parliament also adopted a law updating the regulation …
Alpha-1-antitrypsin content in the serum, alveolar macrophages, and alveolar lavage fluid of smoking and nonsmoking normal subjects.
Authors: G N Olsen, J O Harris, J R Castle, R H Waldman, H J Karmgard
Journal: Journal of Clinical Investigation (1975)

The content of alpha-1-antitrypsin in the serum, alveolar lavage fluid, and alveolar macrophages of smokers and nonsmokers was studied. Bronchoalveolar lavage was used to obtain alveolar fluid and macrophages from normal volunteers, and alpha-1-antitrypsin and albumin were measured using the electroimmunodiffusion technique. The serum level of inhibitor was not different between the two groups, while the total lavage fliud content of alpha-1-antitrypsin was increased in the smokers. The level of alpha-1-antitrypsin was also significantly greater (P less than 0.001) in the alveolar macrophages of the smokers suggesting the possibility of chronically increased alveolar levels in the cigarette smoker as a possible protective mechanism against proteolysis.
Varicose veins in the tropics.
Authors: A Rougemont
Journal: BMJ (1973)

Infectious MononucleosisSIR,-The "new look" at infectious mono- nucleosis by Dr. H. Pullen (12 May, p. 350), though certainly including much sound clinical information, hardly justifies the epithet "new."The very brief, almost scathing, reference to the possible aetiological role of E.B. virus will, for example, have disappointed those seeking recent information.Even a brief consideration of the past four years' work on this virus could have provided plausible reasons for some of the observations left unexplained under the headings of "Infectivity" and "Transmission."
Abstract 3778: Induction of autophagy and elimination of cancer stem-like cell in glioblastoma multiforme cells by a Magnolia officinalis active component honokiol
Authors: Chih-Jung Yao, Chuang-Ye Hong, Ping-Hsiao Shih, Chi-Tai Yeh, Ruei-Ming Chen, Shuang-En Chuang, Pei-Chun Lin, Tsu-Yi Yi, Gi-Ming Lai
Journal: Cancer Research (2011)

Abstract The anticancer effects of honokiol, an active component isolated from Chinese traditional herb Magnolia officinalis, had been noticed in recent decade. It had been reported to induce apoptosis, anti-agiogenesis and chemo/radio-sensitization on cancer cells. However, its effects on autophagy induction and cancer stem cell elimination have not yet been investigated. To more evaluate the potential of honokiol in cancer therapy, we explored its effects on these two critical events in glioblastoma multiforme (GBM) DBTRG-05MG cells. The honokiol-induced autophagy was evidenced by the time and dose-dependent increase of LC3-II in treated cells. During this autophagy induction, the phosphorylated AMP-dependent kinase alpha was dose-dependently increased in accompany with the decrease of phosphorylated mTOR protein level. In addition, the phosphorylated p38 was also markedly increased parallel with the elevation of LC3-II. Further investigation on the role of this MAPK p38 pathway in honokiol-induced autophagy is ongoing. In accordance with the growth inhibition and massive cell death induced by high dose of honokiol (50 μM), the phsphorylated Akt and Rb were dramatically suppressed in treated cells. As it is suggested that autophagy is a protective response of cancer cell to environmental stress, an autophagy inhibitor hydroxychloroquine was therefore co-administrated to enhance the effects of honokiol against GBM cells. Significantly, hydroxychloroquine augmented the honokiol-induced cell death, indicating the crucial role of autophagy in honokiol-induced anticancer effects. Moreover, honokiol appeared to have effects on the elimination of cancer stem-like cells. By UV laser-equipped flow cytometer, a small percentage of cancer stem-like side population (SP) cells was detected and sorted from another GBM cell line (GBM 8401). The expressions of stemness genes such as CD133, nestin, Oct4, NOTCH3, IHH and SMO in SP cells were much higher than those in non-SP cells. Treatment with honokiol (5 μM) for 48h decreased the percentage of GBM 8401 SP cells from 1.5% down to 0.2%. These results suggested the potential role of honokiol in GBM treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3778. doi:10.1158/1538-7445.AM2011-3778
Medulloblastoma: From Molecular Pathology to Therapy
Authors: Alessandra Rossi, Valentina Caracciolo, Giuseppe Russo, Krzysztof Reiss, Antonio Giordano
Journal: Clinical Cancer Research (2008)

Abstract Medulloblastoma is the most common malignant tumor of central nervous system in children. Patients affected by medulloblastoma may be categorized as high-risk and standard-risk patients, based on the clinical criteria and histologic features of the disease. Currently, multimodality treatment, including surgery, radiotherapy, and chemotherapy is considered as the most effective strategy against these malignant cerebellar tumors of the childhood. Despite the potential poor outcomes of these lesions, the 5-year survival stands, at present, at 70% to 80% for standard-risk patients, whereas high-risk patients have a 5-year survival of 55% to 76%. Attempts to further reduce the morbidity and mortality associated with medulloblastoma have been restricted by the toxicity of conventional treatments and the infiltrative nature of the disease. Over the past decade, new discoveries in molecular biology have revealed new insights in signaling pathways regulating medulloblastoma tumor formation. Recent advances in the molecular biology of medulloblastoma indicate that the classification of these embryonal tumors, solely based on histology and clinical criteria, may not be adequate enough. Better understanding of the growth control mechanisms involved in the development and progression of medulloblastoma will allow a better classification, leading to the improvement of the existing therapies, as well as to the development of new therapeutic approaches.
Comparable systemic bioavailability and in vivo performance for fluticasone propionate/salmeterol metered-dose and multidose dry powder (DISKUS®) inhalers in healthy subjects
Authors: R Mehta, RL Kunka, Y Yin, SMS Andrews, A Kapoor, M York, Karen Callahan, PT Daley-Yates
Journal: Journal of Allergy and Clinical Immunology (2002)
Severe diarrehoea due to small intestinal colonisation during cimetidine treatment.
Authors: W S Ruddell, M S Losowsky
Journal: BMJ (1980)

thereby permitting the fairly confident exclusion of hypertension as such as the precipitating factor.It was considered possible that phenobarbitone present in the serum might interfere with the laboratory procedure and result in artificially low oestriol values, but this was discounted after evidence showed that the behaviour of the assay was not appreciably affected by the in-vitro addition of phenobarbitone in amounts considerably above those reached during normal treatment.
SURGICAL METHODS FOR RELIEF OF PAIN
Authors: FRANCIS C. GRANT
Journal: JAMA (1941)

Cancer is only too frequently accompanied by intractable pain. Should reliance be placed on morphine and its derivatives to allay suffering, or should an attempt be made to relieve the pain by blocking afferent pathways leading from the involved area? The pain from cancer is constant and harrowing without surcease by night or day. Relief afforded by morphine is intermittent; pain ceases when the drug takes hold, then reappears. The patient bears with it as long as he can, then begs for more morphine. But section of afferent pathways, carefully planned and properly performed, can result in complete and permanent relief of pain. Unfortunately, however, the problem is not as simple as it seems. The methods at one's disposal for the relief of pain are not completely satisfactory. Chordotomy, rhizotomy, section of the branches or sensory root of the trigeminal nerve or injection of alcohol into the spinal subarachnoid space
TCT-294 Transradial versus Transfemoral Method of Two-Stent Implantation for True Bifurcation Lesions: Comparison of Immediate and Long-Term Outcomes
Authors: Zhan Gao, Bo Xu, Yuejin Yang, Zhongwei Sun, Jinqing Yuan, Jue Chen, Shubin Qiao, Yongjian Wu, Hongbing Yan, Yelin Zhao, Run-Lin Gao
Journal: Journal of the American College of Cardiology (2013)
Roads Leading to Breast Cancer
Authors: D Haber
Journal: New England Journal of Medicine (2000)

Cancer results from the accumulation of mutations in genes that regulate cellular proliferation. These mutations can occur early in the process of malignant transformation or later, during progression to an invasive carcinoma. The earliest mutations occur in the germ line, as in the case of cancer-prone families. In these instances, the inheritance of a mutated allele is commonly followed by the loss of the second allele from a somatic cell, leading to the inactivation of a tumor-suppressor gene and triggering malignant transformation. A classic example is hereditary retinoblastoma, in which there is inheritance of a mutant germ-line RB1 allele (a . . .
P265 A randomised control trial to investigate the effectiveness of PLB in the clinical setting
Authors: S. E. Roberts, F. M. Schreuder, T. Watson, M. Stern
Journal: Thorax (2011)

<h3>Introduction</h3> Pursed lips breathing (PLB) at rest increases oxygen saturation and tidal volume and reduces respiratory rate. Used with exercise it shortens the recovery period, reduces end-exercise breathlessness and improves reported physical function measured by SF-36 (Roberts SE <i>et al</i>, 2009). This study aimed to explore, in a clinical setting, the effectiveness of PLB, in the management of dyspnoea in stable COPD. <h3>Methods</h3> COPD patients referred to pulmonary rehabilitation (PR) were randomised to a control or PLB intervention group. Patients were visited twice at home over 8 weeks prior to starting PR. Each visit comprised a respiratory examination and provision of information on the PR programme; the intervention group were also taught PLB, instructed to practise this daily and to use the technique whenever troubled by breathlessness. Use of PLB was recorded in a home diary. Primary outcome measures were the Self Report Chronic Respiratory Disease Questionnaire (CRQ-SR) dyspnoea and mastery domains and the Endurance Shuttle Walk Test (ESWT). An a priori power calculation, for 80% power, was based on local PR data. Secondary outcome measures were change in Borg breathlessness, respiratory rate, heart rate and oxygen saturation on ESWT. <h3>Results</h3> 41 patients with COPD were recruited (PLB n=22, control n=19); mean (SD) age 68 (11) years, mean (SD) FEV<sub>1</sub>% predicted 47 (15.80)%. There was no statistically significant difference between groups in the primary outcome measures and in retrospect the RCT was insufficiently powered. Post hoc analysis found effect sizes for primary outcome measures were: CRQ-SR dyspnoea 0.05, mastery 0.48 and ESWT 0.44. For secondary outcome measures unpaired t-test showed a significant (p=0.02) reduction in oxygen desaturation on ESWT in favour of PLB group. <h3>Conclusion</h3> This study showed PLB practised over 8 weeks resulted in reduced physiological stress with respect to oxygen desaturation when performing a standardised endurance walk. Additionally it raises questions regarding use of a health related quality of life dyspnoea tool when investigating PLB. To date beneficial effect of PLB on dyspnoea related to exercise has only been shown using the Borg breathlessness score (Nield <i>et al</i>, 2007).
Reflectance confocal microscopy of facial lentigo maligna and lentigo maligna melanoma: a preliminary study
Authors: V. Ahlgrimm-Siess, C. Massone, A. Scope, R. Fink-Puches, E. Richtig, I.H. Wolf, S. Koller, A. Gerger, J. Smolle, R. Hofmann-Wellenhof
Journal: British Journal of Dermatology (2009)

Facial lentigo maligna (LM) and lentigo maligna melanoma (LMM) may be difficult to diagnose clinically and dermoscopically. Reflectance confocal microscopy (RCM) enables the in vivo assessment of equivocal skin lesions at a cellular level.To assess cytomorphological and architectural RCM features of facial LM/LMM.Four women and eight men aged 58-88 years presenting with facial skin lesions suspicious of LM/LMM were included. In total, 17 lesion areas were imaged by RCM before biopsy. The histopathological diagnosis of LM was made in 15 areas; the other two were diagnosed as early LMM.A focal increase of atypical melanocytes and nests surrounding adnexal openings, sheets of mainly dendritic melanocytes, cord-like rete ridges at the dermoepidermal junction (DEJ) and an infiltration of adnexal structures by atypical melanocytes were found to be characteristic RCM features of facial LM/LMM. Areas with a focal increase of atypical melanocytes and nests surrounding adnexal openings were observed at the basal layer in three cases. The remaining cases displayed these changes at suprabasal layers above sheets of mainly dendritic melanocytes. Cord-like rete ridges at the DEJ and an infiltration of adnexal structures by atypical melanocytes were observed in all cases. Previously described criteria for RCM diagnosis of melanoma, such as epidermal disarray, pleomorphism of melanocytes and pagetoid spreading of atypical melanocytes, were additionally observed.We observed a reproducible set of RCM criteria in this case series of facial LM/LMM.
A protective antiarrhythmic role of ursodeoxycholic acid in an<i>in vitro</i>rat model of the cholestatic fetal heart
Authors: Michele Miragoli, Siti H. Sheikh Abdul Kadir, Mary N. Sheppard, Nicoló Salvarani, Matilda Virta, Sarah Wells, Max J. Lab, Viacheslav O. Nikolaev, Alexey Moshkov, William M. Hague, Stephan Rohr, Catherine Williamson, Julia Gorelik
Journal: Hepatology (2011)

Intrahepatic cholestasis of pregnancy may be complicated by fetal arrhythmia, fetal hypoxia, preterm labor, and, in severe cases, intrauterine death. The precise etiology of fetal death is not known. However, taurocholate has been demonstrated to cause arrhythmia and abnormal calcium dynamics in cardiomyocytes. To identify the underlying reason for increased susceptibility of fetal cardiomyocytes to arrhythmia, we studied myofibroblasts (MFBs), which appear during structural remodeling of the adult diseased heart. In vitro , they depolarize rat cardiomyocytes via heterocellular gap junctional coupling. Recently, it has been hypothesized that ventricular MFBs might appear in the developing human heart, triggered by physiological fetal hypoxia. However, their presence in the fetal heart (FH) and their proarrhythmogenic effects have not been systematically characterized. Immunohistochemistry demonstrated that ventricular MFBs transiently appear in the human FH during gestation. We established two in vitro models of the maternal heart (MH) and FH, both exposed to increasing doses of taurocholate. The MH model consisted of confluent strands of rat cardiomyocytes, whereas for the FH model, we added cardiac MFBs on top of cardiomyocytes. Taurocholate in the FH model, but not in the MH model, slowed conduction velocity from 19 to 9 cm/s, induced early after depolarizations, and resulted in sustained re-entrant arrhythmias. These arrhythmic events were prevented by ursodeoxycholic acid, which hyperpolarized MFB membrane potential by modulating potassium conductance. Conclusion: These results illustrate that the appearance of MFBs in the FH may contribute to arrhythmias. The above-described mechanism represents a new therapeutic approach for cardiac arrhythmias at the level of MFB. (Hepatology 2011;)
Abstract 5656: Role for Sphingosine kinase 1 in head &amp; neck cancer
Authors: Keisuke Shirai, Hideki Furuya, Masayuki Wada, Jacek Bielawski, Besim Ogretmen, Yusuf A. Hannun, Lina M. Obeid, Toshihiko Kawamori
Journal: Cancer Research (2010)

Abstract Novel and effective targets for cancer therapy and prevention are increasingly important in cancer research, especially for head and neck squamous cell carcinoma (HNSCC), which is one of the most lethal cancers. A potential target for this type of cancer might be sphingosine kinase 1 (SphK1) which phosphorylates sphingosine to form sphingosine-1-phosphate (S1P) because it is a critical regulator of sphingolipid-mediated functions and the SphK1/S1P pathway has been implicated in several important biological functions including inflammation and carcinogenesis. To investigate the potential of SphK1 as a target in head and neck cancer development, we used a 4-nitroquinoline-1-oxide (4-NQO)-induced carcinogenesis tongue model in SphK1 knockout mice. All mice were treated with 4-NQO at 40 μg/ml in drinking water for 14 weeks (untreated water was available thereafter, until the end of the experiment). All animals were sacrificed at 20 weeks and animal tongues were examined. We found that SphK1 positively stained in tongue cancer induced by 4-NQO in wild type mice, and 72% SphK1 KO mice developed tongue cancer, whereas 96% of the wild type mice did (P&amp;lt;0.05). Furthermore, tongue cancer volume was significantly decreased in SphK1 KO mice (P&amp;lt;0.05). To understand how SphK1 is responsible for decreasing tongue cancer, we used a BrdU incorporation assay to evaluate cell proliferation and used a cleaved caspase-3 immunohistochemistry assay to indicate apoptosis in tongue cancer tissues. We found that tongue cancers in SphK1 KO mice had significantly less cell proliferation and increased apoptosis compared to in wild type mice (P&amp;lt;0.01 and P&amp;lt;0.001, respectively). Assaying for sphingolipid profiles in mouse blood, we found that S1P was significantly reduced in SphK1 KO mice (P&amp;lt;0.001), and that C16-ceramide was also significantly reduced in SphK1 KO mice compared to wild type mice (P&amp;lt;0.05). These data are consistent with our previous results (Cancer Lett., 256: 101-111, 2007). We also found that 4-NQO-activated phospho-Akt was reduced in tongue cancers in SphK1 KO mice, suggesting that the SphK1/S1P pathway may be involved in PI3K-Akt-mTOR pathway in HNSCC development. Our data suggest that the SphK1/S1P pathway may mediate HNSCC development and that inhibition of this pathway may be an effective and novel target for chemoprevention against HNSCC. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5656.