Between feminism and anorexia: An autoethnography

Critical feminist work on eating disorders has grown substantially since its establishment in the 1980s, and has increasingly incorporated the use of anorexic stories, voices and experiences. Yet rarely do such accounts offer the anorexic a space to respond to the now established feminist conceptions of the problem which structure the books or articles in which they appear. Anorexic, or recovered anorexic, voices are used by the researcher to interpret the role played by gender, even whilst the subjects are invited to respond to and critique, medical and popular discourses on the disorder. This lack of dialogue is all the more striking in the context of the feminist aim to fight ‘back against the tendency to silence anorexic women’s’ own interpretations of their starving, treatment and construction (Saukko, 2008: 34). As someone who suffered from anorexia for 20 years, this article offers an autoethnographic account of my experience of encountering the feminist literature on anorexia in a bid to speak back, or enter into a dialogue between feminist politics and eating disorder experience

A retrospective review and multi-specialty, evidence-based guideline for the management of necrotising otitis externa

BACKGROUND: Necrotising otitis externa is a progressive infection of the external auditory canal which extends to affect the temporal bone and adjacent structures. Progression of the disease process can result in serious sequelae, including cranial nerve palsies and death. There is currently no formal published treatment guideline.OBJECTIVE: This study aimed to integrate current evidence and data from our own retrospective case series in order to develop a guideline to optimise necrotising otitis externa patient management.METHODS: A retrospective review of necrotising otitis externa cases within NHS Lothian, Scotland, between 2013 and 2018, was performed, along with a PubMed review.RESULTS: Prevalent presenting signs, symptoms and patient demographic data were established. Furthermore, features of cases associated with adverse outcomes were defined. A key feature of the guideline is defining at-risk patients with initial intensive treatment. Investigations and outcomes are assessed and treatment adjusted appropriately.CONCLUSION: This multi-departmental approach has facilitated the development of a succinct, systematic guideline for the management of necrotising otitis externa. Initial patient outcomes appear promising.</p

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie

Staphylococcus aureus endocarditis associated with injecting new psychoactive substances

Background Staphylococcus aureus infective endocarditis (IE) associated with injection of new psychoactive substances (NPS) in Edinburgh from 2014 to 2016 was observed. We compared these infections with a series of S. aureus IE cases in a non-injecting population within Edinburgh. Methods NPS-associated S. aureus IE diagnosed between 1 January 2014 and 31 May 2016 in persons who inject drugs (PWID) were compared with a series of S. aureus IE cases from non-PWID. Results There was a fourfold increase in the annual incidence of S. aureus IE, mainly due to NPS use in PWID. A larger vegetation diameter was seen on echocardiogram in PWID vs non-PWID (median 1.7 cm vs 0.65 cm; p = 0.009) with more embolic complications in PWID (15 PWID vs 1 non-PWID; p = 2.1 x 10-7) but no difference in 90-day mortality (2 PWID vs 4 non-PWID; p = 0.39). Conclusions NPS-associated S. aureus IE correlated with complications, such as deep organ embolic abscesses, that were different from non-PWID S. aureus IE. The alarming increase in incidence resolved with targeted public health and legislative measures

Epstein–Barr virus antibody level and gastric cancer risk in Korea: a nested case–control study

BACKGROUND: Few cohort studies have investigated Epstein-Barr virus (EBV) infection before the occurrence of gastric cancer. METHODS: Among 14 440 cohort participants, 100 incident gastric cancer cases were individually matched to two controls. Epstein-Barr virus antibodies IgG and IgA against viral capsid antigen (VCA), EBV nuclear antigen (EBNA) antibody IgG, and early antigen (EA) antibody IgG were measured using enzyme immunoassays (EIAs). RESULTS: The highest titres of VCA IgG (odds ratio (OR): 1.37, 95% confidence interval (CI): 0.62-3.06) or EBNA IgG (OR: 0.87, 95% CI: 0.51-1.46) were not associated with gastric cancer risk. CONCLUSION: Higher levels of VCA IgG or EBNA IgG were not associated with increased risk of gastric adenocarcinoma in Koreans.Akiba S, 2008, CANCER SCI, V99, P195, DOI 10.1111/j.1349-7006.2007.00674.xKoshiol J, 2007, BRIT J CANCER, V97, P1567, DOI 10.1038/sj.bjc.6604063Tedeschi R, 2007, AM J EPIDEMIOL, V165, P134, DOI 10.1093/aje/kwj332Gwack J, 2006, BRIT J CANCER, V95, P639, DOI 10.1038/sj.bjc.6603309Ouburg S, 2005, EUR J GASTROEN HEPAT, V17, P1213Chan D, 2005, J RES PRACT INF TECH, V37, P267HERRERAGOEPFERT R, 2005, WORLD J GASTROENTERO, V11, P6096CORREA P, 2004, GASTRIC CANCER, V7, P9Macsween KF, 2003, LANCET INFECT DIS, V3, P131Gartner BC, 2003, CLIN DIAGN LAB IMMUN, V10, P78, DOI 10.1128/CDLI.10.1.78-82.2003Burgess DE, 2002, BRIT J CANCER, V86, P702, DOI 10.1038/sj/bjc/6600107YOO KY, 2002, ASIAN PAC J CANCER P, V3, P85Chien YC, 2001, NEW ENGL J MED, V345, P1877Bruu AL, 2000, CLIN DIAGN LAB IMMUN, V7, P451Shinkura R, 2000, J MED VIROL, V60, P411Akre O, 1999, INT J CANCER, V82, P1Tokunaga M, 1998, CANCER EPIDEM BIOMAR, V7, P449*IARC, 1997, EPSTEINBARR VIR KAP, V8LEVINE PH, 1995, INT J CANCER, V60, P642LEHTINEN T, 1993, CANCER CAUSE CONTROL, V4, P187GESER A, 1982, INT J CANCER, V29, P397

Promoter methylation of CDKN2A and lack of p16 expression characterize patients with hepatocellular carcinoma

<p>Abstract</p> <p>Background</p> <p>The product of CDKN2A, p16 is an essential regulator of the cell cycle controlling the entry into the S-phase. Herein, we evaluated CDKN2A promoter methylation and p16 protein expression for the differentiation of hepatocellular carcinoma (HCC) from other liver tumors.</p> <p>Methods</p> <p>Tumor and corresponding non-tumor liver tissue samples were obtained from 85 patients with liver tumors. CDKN2A promoter methylation was studied using MethyLight technique and methylation-specific PCR (MSP). In the MethyLight analysis, samples with ≥ 4% of PMR (percentage of methylated reference) were regarded as hypermethylated. p16 expression was evaluated by immunohistochemistry in tissue sections (n = 148) obtained from 81 patients using an immunoreactivity score (IRS) ranging from 0 (no expression) to 6 (strong expression).</p> <p>Results</p> <p>Hypermethylation of the CDKN2A promoter was found in 23 HCCs (69.7%; mean PMR = 42.34 ± 27.8%), six (20.7%; mean PMR = 31.85 ± 18%) liver metastases and in the extralesional tissue of only one patient. Using MSP, 32% of the non-tumor (n = 85), 70% of the HCCs, 40% of the CCCs and 24% of the liver metastases were hypermethylated. Correspondingly, nuclear p16 expression was found immunohistochemically in five (10.9%, mean IRS = 0.5) HCCs, 23 (92%; mean IRS = 4.9) metastases and only occasionally in hepatocytes of non-lesional liver tissues (mean IRS = 1.2). The difference of CDKN2A-methylation and p16 protein expression between HCCs and liver metastases was statistically significant (p < 0.01, respectively).</p> <p>Conclusion</p> <p>Promoter methylation of CDKN2A gene and lack of p16 expression characterize patients with HCC.</p

Simulating Microdosimetry in a Virtual Hepatic Lobule

The liver plays a key role in removing harmful chemicals from the body and is therefore often the first tissue to suffer potentially adverse consequences. To protect public health it is necessary to quantitatively estimate the risk of long-term low dose exposure to environmental pollutants. Animal testing is the primary tool for extrapolating human risk but it is fraught with uncertainty, necessitating novel alternative approaches. Our goal is to integrate in vitro liver experiments with agent-based cellular models to simulate a spatially extended hepatic lobule. Here we describe a graphical model of the sinusoidal network that efficiently simulates portal to centrilobular mass transfer in the hepatic lobule. We analyzed the effects of vascular topology and metabolism on the cell-level distribution following oral exposure to chemicals. The spatial distribution of metabolically inactive chemicals was similar across different vascular networks and a baseline well-mixed compartment. When chemicals were rapidly metabolized, concentration heterogeneity of the parent compound increased across the vascular network. As a result, our spatially extended lobule generated greater variability in dose-dependent cellular responses, in this case apoptosis, than were observed in the classical well-mixed liver or in a parallel tubes model. The mass-balanced graphical approach to modeling the hepatic lobule is computationally efficient for simulating long-term exposure, modular for incorporating complex cellular interactions, and flexible for dealing with evolving tissues

Detection of oncogenic virus genomes and gene products in lung carcinoma

We investigated a series of 122 cases of small cell lung carcinomas and non-small cell lung carcinomas for the presence of several viruses that are known to be oncogenic in humans. Thus, viral genomes (DNA) and/or RNA transcripts and/or proteins of human papillomaviruses (HPV) 16, 18, 31, 33, 51, Epstein–Barr virus (EBV), human herpesvirus 8 (HHV-8), human cytomegalovirus (HCMV) and simian virus 40 (SV40) were investigated on tissue sections (prepared in tissue microarrays) with different techniques of immunohistochemistry and in situ hybridisation. None of the cases displayed a single positive tumour cell for all the viruses tested whatever the technique applied. Of note, in five cases of tumours with lymphoid infiltrates, we detected scattered EBV (EBER)-positive bystander lymphocytes. In three cases, a faint nuclear staining was found with the anti-latent nuclear antigen/LANA1 (HHV-8) antibody. These cases were checked by PCR with two sets of primers (orf 26 and orf 75) and remained negative for this latter virus. Taken together, our data strongly suggest that the conventional human oncogenic viruses (HPV, EBV, HCMV, HHV-8 and SV40) are unlikely to play some role in the development of lung carcinomas

Variability in depression prevalence in early rheumatoid arthritis: a comparison of the CES-D and HAD-D Scales

<p>Abstract</p> <p>Background</p> <p>Depression is common in rheumatoid arthritis (RA), however reported prevalence varies considerably. Two frequently used instruments to identify depression are the Center for Epidemiological Studies Depression (CES-D) scale, and the Hospital Anxiety and Depression Scale (HADS). The objectives of this study were to test if the CES-D and HADS-D (a) satisfy current modern psychometric standards for unidimensional measurement in an early RA sample; (b) measure the same construct (i.e. depression); and (c) identify similar levels of depression.</p> <p>Methods</p> <p>Data from the two scales completed by patients with early RA were fitted to the Rasch measurement model to show that (a) each scale satisfies the criteria of fit to the model, including strict unidimensionality; (b) that the scales can be co-calibrated onto a single underlying continuum of depression and to (c) examine the location of the cut points on the underlying continuum as indication of the prevalence of depression.</p> <p>Results</p> <p>Ninety-two patients with early RA (62% female; mean age = 56.3, SD = 13.7) gave 141 sets of paired CES-D and HAD-D data. Fit of the data from the CES-D was found to be poor, and the scale had to be reduced to 13 items to satisfy Rasch measurement criteria whereas the HADS-D met model expectations from the outset. The 20 items combined (CES-D13 and HADS-D) satisfied Rasch model expectations. The CES-D gave a much higher prevalence of depression than the HADS-D.</p> <p>Conclusion</p> <p>The CES-D in its present form is unsuitable for use in patients with early RA, and needs to be reduced to a 13-item scale. The HADS-D is valid for early RA and the two scales measure the same underlying construct but their cut points lead to different estimates of the level of depression. Revised cut points on the CES-D13 provide comparative prevalence rates.</p