The trefoil factor family (TFF) peptides are important in gastro-intestinal mucosal protection and repair. Their mechanism of action remains unclear and receptors are sought. We aimed to identify and characterise proteins binding to TFF2. A fusion protein of mouse TFF2 with alkaline phosphatase was generated and used to probe 2-D protein blots of mouse stomach. The resulting spots were analysed by MS. The protein identified was characterised by bioinformatics, rapid amplification of cDNA ends, in situ hybridisation (ISH) and immunohistochemistry (IHC). Functional assays were performed in gastrointestinal cell lines. A single major murine protein was identified and named blottin. It was previously unknown as a translated product. Blottin is also present in rat and human; the latter gene is also known as GDDR. The predicted full-length proteins are 184 amino acids long (20 kDa), reducing to 164 amino acids (18 kDa) after signal peptide cleavage. ISH of gastrointestinal tissues shows abundant blottin mRNA in gastric surface and foveolar epithelium. IHC shows cytoplasmic staining for blottin protein, and by immunoelectron microscopy in mucus granules and Golgi stacks. Previous work showed that blottin is down-regulated in gastric cancers. Blottin contains a BRICHOS domain, and has 56% similarity with gastrokine-1. Cultured HT-29 cells express blottin and show increased DNA synthesis with antiblottin antibody; however, this effect is reversed by the immunising peptide. We have identified and characterised a TFF2-binding protein produced by gastric epithelium. Blottin may play a role in gastrointestinal mucosal protection and modulate gut epithelial cell proliferation.

BackgroundThis study assessed the symptom severity of patients with advanced cancer in a palliative care unit and explored the factors associated with symptom improvement.MethodsThis study was conducted in a palliative care unit in Taiwan between October 2004 and December 2009. Symptom intensity was measured by the “Symptom Reporting Form”, and graded on a scale of 0 to 4 (0 = none, and 4 = extreme). These measures were assessed on the 1st, 3rd, 5th, and 7th Day in the palliative care unit. The study data comprised routine clinical records and patients’ demographic data. Generalized estimating equation (GEE) was used to assess the symptom improvement, and investigate the factors associated with the symptom reporting form scores.ResultsAmong the 824 recruited patients with advanced cancer, pain (78.4 %), anorexia (64.4 %) and constipation (63.5 %)were the most common and severe symptom. After controlling for other factors in the multivariate GEE model, the day of palliative care administration was a significant factor associated with all of the scales, except Days 7 on the dyspnoea and oedema scales and Day 5 on the anxiety scale. In addition, patients aged ≥ 65 years exhibited significantly lower scores on the pain, sleep disturbance, depression, and anxiety scales than did those aged < 65 years. Moreover, female patients exhibited higher scores on the vomiting, anorexia, oedema, depression, and anxiety scales than did male patients. Furthermore, patients with gastrointestinal tract cancer exhibited higher scores on the constipation, vomiting, anorexia, oedema, depression, and anxiety scales and lower scores on the dyspnoea scale than did those with lung cancer. Patients with breast cancer exhibited higher scores on the oedema scale and lower scores on the anxiety scale. Patients with genitourinary cancer exhibited higher scores on the vomiting and oedema scales and lower scores on the dyspnoea scale. Patients with head, neck, and oral cancer exhibited lower scores on the oedema scale alone.ConclusionThe symptom severity declined during the first week in the palliative care unit. In addition, differences in sex and primary cancer sites may contribute to varying degrees of symptom improvement.Electronic supplementary materialThe online version of this article (doi:10.1186/s12904-016-0105-8) contains supplementary material, which is available to authorized users.

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This study aims to assess the interactive effect of marital status and shift work on family function. A population-based sample of 1,438 nurses between the ages of 20–45 yr was recruited from Taiwan during the period from July 2005 to April 2006 using a mailed questionnaire. The self-administered questionnaire contained information about demographic data, work status, shift work schedule, and the Family APGAR (Adaptation, Partnership, Growth, Affection, and Resolve) Scale, to evaluate family function. Compared to day shift nurses, non-night and rotation shift nurses had 1.53- and 1.38-fold (95% CI=1.09–2.14 and 1.01–1.88) risk to have poor family function after adjusting for other covariates. Married nurses, by contrast, had a 0.44-fold (95% CI=0.29–0.66) risk to have poor family function compared to single nurses. In addition, married nurses who worked non-night or rotation shifts had a significantly higher percent of poor family function than those married nurses working day shifts; however, similar results were not replicated in single nurses. We concluded that shift work and marital status could influence family function.

IntroductionAlthough statin therapy is beneficial to patients with ischemic stroke, statin use, and intracerebral hemorrhage (ICH) remain a concern. ICH survivors commonly have comorbid cardiovascular risk factors that would otherwise warrant cholesterol‐lowering medication, thus emphasizing the importance of assessing the characteristics of statin therapy in this population.MethodsWe performed a cohort study by using 10 years of data collected from the National Health Insurance Research Database in Taiwan. We enrolled 726 patients admitted for newly diagnosed ICH from January 1, 2001 to December 31, 2010. The patients were categorized into high‐ (92), moderate‐ (545), and low‐intensity (89) statin groups, and into hydrophilic (295) and lipophilic (431) statin groups. The composite outcomes included all‐cause mortality, recurrent ICH, ischemic stroke, transient ischemic attack, and acute coronary events.ResultsThe patients in the low‐intensity group did not differ significantly from the patients in the high‐intensity group in risk of all‐cause mortality (adjusted hazard ratio [aHR] = 0.65, 95% confidence interval [CI] = 0.28–1.55) and recurrent ICH (aHR = 0.66, 95% CI = 0.30–1.44). In contrast, the patients in the hydrophilic group had a significantly lower risk of recurrent ICH than did those in the lipophilic group (aHR = 0.69, 95% CI = 0.48–0.99). We determined no significant differences in other composite endpoints between hydrophilic and lipophilic statin use.ConclusionHydrophilic statin therapy is associated with a reduced risk of recurrent ICH in post‐ICH patients. The intensity of statin use had no significant effect on recurrent ICH or other components of the composite outcome. Additional studies are required to clarify the biological mechanisms underlying these observations.

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BackgroundThe contribution of bone marrow-derived cells to epithelial tissues in the inflamed gut remains controversial. Recent reports have suggested that cell fusion between bone marrow-derived cells and the intestinal epithelium takes place in inflammatory conditions.MethodsIn attempts to confirm this, we have undertaken gender mis-matched bone marrow (BM) transplants from male Swiss Webster (SWR) mice to B and T cell-deficient female Rag2 KO mice which, 4 weeks later, were given 5% dextran sodium sulphate in drinking water to induce acute colitis. A further BM-treated group of animals with a graft versus host-like condition was also studied. We developed a new method to combine up to three brightfield or fluorescent lectin- or immuno-histochemical signals with fluorescent in situ hybridisation for the Y and X chromosomes to enable us unequivocally to identify BM-derived male cells which presented as different cell types in the gastrointestinal tract.Principal FindingsIn rolled preparations of whole intestines we scanned around 1.5 million crypts at many tissue levels. In no instance did we see a Y chromosome-positive cell in the epithelial compartment, which was not also CD45-positive. We saw no evidence of cell fusion, based on combined X and Y chromosome analysis. Levels of CD45-positive stromal and lymphoid cells and pericryptal myfibroblasts (positive for α-smooth muscle actin) increased with time up to a plateau, which resembled the level seen in untreated control grafted animals. We saw very few Y chromosome-positive endothelial cells in intestinal stromal vessels.ConclusionsWe conclude that whole BM transplantation does not result in intestinal epithelial engraftment in this model. Our new methods can usefully assist in multi-signal analyses of cell phenotypes following BM transplant and in models of chimaerism and regenerative medicine.

This paper establishes a method of clonality analysis using the reverse transcription-polymerase chain reaction (RT-PCR) to amplify X-linked G6PD transcripts on defined cell populations microdissected from archival, paraffin-embedded tissue sections. Four known monoclonal low-grade B-cell lymphomas from females who were heterozygous (informative) at the 1131 exonic polymorphic locus of the G6PD gene were used to validate the method. Lymphoma and reactive lesions in each case were separated by microdissection. In order to preserve the intact RNA species in the lesion, sections were digested on the slides before microdissection. A one-step RT-PCR was performed with a single pair of primers, one of which contained a mismatched base adjacent to the polymorphic site, to generate a PvuI cutting site. Successful amplification and allele identification by PvuI digestion were achieved from all RNA samples studied. Three of four samples from non-neoplastic reactive lesions showed two bands with equal intensity, representing transcription of the two alleles of the G6PD gene, while the corresponding tumour samples demonstrated a biased intensity in one allele, indicating monoclonality. To assess the method further, the clonal nature of in situ and invasive breast cancers was examined, along with adjacent normal breast tissue and hyperplastic lesions from three informative females from our archives. Apart from the clusters of normal terminal duct-lobular units, all lesions were monoclonal. This result is in agreement with data derived from other X-linked gene studies and loss of heterozygosity (LOH) analyses of pre-invasive breast disease. The results suggest that the clonality analysis method presented here is simple and reliable, and is therefore potentially applicable in a wide range of pathological conditions.