Serotonin-Expressing Cells in the Corpus of the Stomach Originate from Bone Marrow: A Master’s Thesis

Neurogenin 3 and its downstream target NeuroD are basic helix-loop-helix transcription factors which promote endocrine differentiation in the gastrointestinal tract. However, mice lacking Ngn3 still produce several hormones in the stomach. Lineage tracing mouse models demonstrated that a majority of hormone cells in the corpus region of the stomach did not express Ngn3 or NeuroD during differentiation. Serotonin and histamine cells were entirely NeuroD-independently derived, and serotonin cells were additionally entirely Ngn3-independently derived. In this study, we isolated serotonin and histamine cells from the gastric corpus of transgenic mice expressing the fluorescent marker CFP. Serotonin cells expressed multiple mast cell markers by RT-PCR, and were found to be nearly absent in a mast cell-deficient mouse model. Labeled bone marrow transplant mice showed all serotonin cells derived from bone marrow. Histamine-expressing ECL cells, while lacking NeuroD, did not appear to express granulocyte or mast cell markers by analytical flow cytometry and RT-PCR, and resemble other enteroendocrine cell populations. Mouse gastric corpus serotonin cells, but not antral serotonin cells, are bone marrow-derived mast cells

Do changes in illness perceptions predict changes in psychological distress among oesophageal cancer survivors?

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Does risk of progression from Barrett’s esophagus to esophageal adenocarcinoma change based on the number of non-dysplastic endoscopies?

Funding: This study was funded in full by the National Institutes of Health, grant number (NIH P30DK056338‐16). The Northern Ireland Barrett’s register was funded by the UK Medical Research Council, Cancer Focus Northern Ireland (formerly the Ulster Cancer Foundation), NI HSC R&D Office, and Cancer Research UK. The Northern Ireland Cancer Registry is funded by the Public Health Agency.Peer reviewedPostprin

Socio-economic status and lifestyle factors are associated with achalasia risk: a population-based case-control study.

AIM: To evaluate the association between various lifestyle factors and achalasia risk. METHODS: A population-based case-control study was conducted in Northern Ireland, including n = 151 achalasia cases and n = 117 age- and sex-matched controls. Lifestyle factors were assessed via a face-to-face structured interview. The association between achalasia and lifestyle factors was assessed by unconditional logistic regression, to produce odds ratios (OR) and 95% confidence interval (CI). RESULTS: Individuals who had low-class occupations were at the highest risk of achalasia (OR = 1.88, 95%CI: 1.02-3.45), inferring that high-class occupation holders have a reduced risk of achalasia. A history of foreign travel, a lifestyle factor linked to upper socio-economic class, was also associated with a reduced risk of achalasia (OR = 0.59, 95%CI: 0.35-0.99). Smoking and alcohol consumption carried significantly reduced risks of achalasia, even after adjustment for socio-economic status. The presence of pets in the house was associated with a two-fold increased risk of achalasia (OR = 2.00, 95%CI: 1.17-3.42). No childhood household factors were associated with achalasia risk. CONCLUSION: Achalasia is a disease of inequality, and individuals from low socio-economic backgrounds are at highest risk. This does not appear to be due to corresponding alcohol and smoking behaviours. An observed positive association between pet ownership and achalasia risk suggests an interaction between endotoxin and viral infection exposure in achalasia aetiology

Intracranial internal carotid aneurysm causing diplopia

Internal carotid intracranial aneurysms are a relatively rare form of intracranial aneurysm that presents with diplopia, retro-orbital pain and unilateral headaches. The symptoms are progressive and the diagnosis should be considered in a patient presenting with these complaints. Underlying hypertension and advanced age are specific risk factors

Mars Science Laboratory Heatshield Aerothermodynamics: Design and Reconstruction

The Mars Science Laboratory heatshield was designed to withstand a fully turbulent heat pulse based on test results and computational analysis on a pre-flight design trajectory. Instrumentation on the flight heatshield measured in-depth temperatures in the thermal protection system. The data indicate that boundary layer transition occurred at 5 of 7 thermocouple locations prior to peak heating. Data oscillations at 3 pressure measurement locations may also indicate transition. This paper presents the heatshield temperature and pressure data, possible explanations for the timing of boundary layer transition, and a qualitative comparison of reconstructed and computational heating on the as-flown trajectory. Boundary layer Reynolds numbers that are typically used to predict transition are compared to observed transition at various heatshield locations. A uniform smooth-wall transition Reynolds number does not explain the timing of boundary layer transition observed during flight. A roughness-based Reynolds number supports the possibility of transition due to discrete or distributed roughness elements on the heatshield. However, the distributed roughness height would have needed to be larger than the pre-flight assumption. The instrumentation confirmed the predicted location of maximum turbulent heat flux near the leeside shoulder. The reconstructed heat flux at that location is bounded by smooth-wall turbulent calculations on the reconstructed trajectory, indicating that augmentation due to surface roughness probably did not occur. Turbulent heating on the downstream side of the heatshield nose exceeded smooth-wall computations, indicating that roughness may have augmented heating. The stagnation region also experienced heating that exceeded computational levels, but shock layer radiation does not fully explain the differences