Irrational Beliefs and Attention Bias Towards Symptoms-Related Stimuli in Maintaining Gastrointestinal Symptoms: Results from a Pilot Study

Abstract

Recent etiopathogenic theories of gastrointestinal conditions state that information processing biases can be a possible major factor involved in the aetiology and maintenance of these conditions. This exploratory study investigated the role of attention biases (AB) towards symptoms-related cues in gastrointestinal patients with respect to symptom maintenance, simultaneously taking into consideration the role of irrational beliefs. We included 32 patients diagnosed with gastrointestinal conditions. Patients completed a battery of psychological tests and an experimental task aimed to measure the preferential attention processing of linguistic stimuli related to gastrointestinal symptoms when they compete for attention resources with neutral stimuli. AB was positively related to irrational beliefs [r(31) = .376, p = .037] and analgesics use [r(32) = .518, p = .002], but not to self-report gastrointestinal symptoms [r(30) = −.165, p = .382]. Irrational beliefs correlated with pain catastrophizing [r(31) = .373, p = .039], but not to gastrointestinal symptoms, pain intensity, visceral sensitivity or negative emotions; however, pain catastrophizing correlated with all of these. Taken together, our results suggest that core irrational beliefs action as general vulnerability factors that trigger specific implicit and explicit cognitive mechanisms (i.e., AB, pain catastrophizing) involved in the onset and maintenance of symptoms. Future experimental studies should test the robustness of these results in larger samples and aim to further advance our understanding of how cognitive factors interact and potentiate each other in generating and maintaining debilitating suffering.

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Magnetic resonance analysis of malignant transformation in recurrent glioma

Background

Patients with low-grade glioma (LGG) have a relatively long survival, and a balance is often struck between treating the tumor and impacting quality of life. While lesions may remain stable for many years, they may also undergo malignant transformation (MT) at the time of recurrence and require more aggressive intervention. Here we report on a state-of-the-art multiparametric MRI study of patients with recurrent LGG.

Methods

One hundred and eleven patients previously diagnosed with LGG were scanned at either 1.5 T or 3 T MR at the time of recurrence. Volumetric and intensity parameters were estimated from anatomic, diffusion, perfusion, and metabolic MR data. Direct comparisons of histopathological markers from image-guided tissue samples with metrics derived from the corresponding locations on the in vivo images were made. A bioinformatics approach was applied to visualize and interpret these results, which included imaging heatmaps and network analysis. Multivariate linear-regression modeling was utilized for predicting transformation.

Results

Many advanced imaging parameters were found to be significantly different for patients with tumors that had undergone MT versus those that had not. Imaging metrics calculated at the tissue sample locations highlighted the distinct biological significance of the imaging and the heterogeneity present in recurrent LGG, while multivariate modeling yielded a 76.04% accuracy in predicting MT.

Conclusions

The acquisition and quantitative analysis of such multiparametric MR data may ultimately allow for improved clinical assessment and treatment stratification for patients with recurrent LGG.

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Antimutagenic Compounds of White Shrimp (Litopenaeus vannamei): Isolation and Structural Elucidation

According to the World Health Organization, cancer is the main cause of mortality worldwide; thus, the search of chemopreventive compounds to prevent the disease has become a priority. White shrimp (Litopenaeus vannamei) has been reported as a source of compounds with chemopreventive activities. In this study, shrimp lipids were extracted and then fractionated in order to isolate those compounds responsible for the antimutagenic activity. The antimutagenic activity was assessed by the inhibition of the mutagenic effect of aflatoxin B1 on TA98 and TA100 Salmonella tester strains using the Ames test. Methanolic fraction was responsible for the highest antimutagenic activity (95.6 and 95.9% for TA98 and TA100, resp.) and was further separated into fifteen different subfractions (M1–M15). Fraction M8 exerted the highest inhibition of AFB1 mutation (96.5 and 101.6% for TA98 and TA100, resp.) and, after further fractionation, four subfractions M8a, M8b, M8c, and M8d were obtained. Data from 1H and 13C NMR, and mass spectrometry analysis of fraction M8a (the one with the highest antimutagenic activity), suggest that the compound responsible for its antimutagenicity is an apocarotenoid.

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Pathologic stage following preoperative chemoradiotherapy underestimates the risk of developing distant metastasis in rectal cancer: A comparison to staging without preoperative chemoradiotherapy

Background and Objectives

There is still little evidence of a relationship between pathologic stage with or without preoperative chemoradiotherapy (CRT) in rectal cancer. The aim of this study was to investigate the prognostic implication of the preoperative-CRT pathologic stage (ypStage) by comparing it to the pathologic stage without preoperative-CRT (pStage).

Methods

Between July 2004 and December 2012, 774 consecutive patients who received radical surgery for histologically diagnosed rectal adenocarcinoma (clinical stage I–III) were included.

Results

A total of 674 surviving patients were followed-up for a median of 43.4 months. Five-year local recurrence (LR) -free survival rates were similar for each ypStage and the corresponding pStage. In contrast, 5-year distant metastasis (DM) -free survival rates were poorer for each ypStage than for the corresponding pStage. The hazard ratio increased with a decrease in pathological stages (Stage I: 3.5, Stage II: 2.2, and Stage III: 1.4).

Conclusions

ypStage in rectal cancer is a good prognostic factor in predicting LR and DM. Although the ypStage can stratify patients according to the risk of developing DM, the risk as determined by the ypStage could be higher than that of corresponding pStage, especially in patients showing a higher degree of downstaging. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.

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Consideration in lower extremity reconstruction following oncologic surgery: Patient selection, surgical techniques, and outcomes

The goal for reconstruction following oncologic surgery involves providing adequate coverage allowing subsequent adjuvant therapy, preserving function, and to have a reasonable aesthetic outcome. Patients with soft tissue tumors of the lower extremity have en bloc tumor resections with wide margins for local control followed by reconstruction. This reconstructive algorithm demonstrates survival rates equivalent to amputation, with success approaching 95%. Attempting limb salvage has now become the mainstay standard for reconstructing defects following excision of lower extremity cancers. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.

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Quantification of adipose transfer viability using a novel, bioluminescent murine model

Publication date: Available online 23 February 2016
Source:Journal of Plastic, Reconstructive & Aesthetic Surgery
Author(s): A.A. Gassman, K.K. Kao, J.P. Bradley, J.C. Lee
Fat grafting has highly variable long-term results. Research efforts to improve the reliability of fat grafting are limited by inefficient methods to evaluate fat engraftment. In this work, we describe a novel animal model for quantitative evaluation of fat grafting using in-vivo bioluminescence of adipocytes from luciferase expressing mice. Subcutaneous adipose tissue from GFP and luciferase-expressing FVB mice were obtained. The samples were homogenized, decanted, and injected into the dorsal skin folds of wildtype FVB mice. Viability of the transferred tissue was examined over a 28-day time period with quantitative bioluminescence after luciferin injection. All animals demonstrated viable adipose transfer with bioluminescence detectable on days 0, 1, 7, 14, and 28. This animal model may be used for non-invasive, longitudinal studies, to quantify the fat engraftment process.



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Long non-coding RNA PVT1 promotes non-small cell lung cancer cell proliferation through epigenetically regulating LATS2 expression

Long non-coding RNAs (lncRNAs) are a novel class of transcripts with no protein coding capacity, but with diverse functions in cancer cell proliferation, apoptosis and metastasis. The lncRNA PVT1 is 1716 nt in length and located in the chr8q24.21 region, which also contains the myelocytomatosis (MYC) oncogene. Previous studies demonstrated that MYC promotes PVT1 expression in primary human cancers. However, the expression pattern and potential biological function of PVT1 in non-small cell lung cancer (NSCLC) is still unclear. Here we found that PVT1 was up-regulated in 105 human NSCLC tissues compared with normal samples. High expression of PVT1 was associated with a higher TNM stage and tumor size, as well as poorer overall survival. Functional analysis revealed that knockdown of PVT1 inhibited NSCLC cell proliferation and induced apoptosis both in vitro and in vivo. RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription. Furthermore, ectopic expression of LATS2 increased apoptosis and repressed LAD cell proliferation by regulating the Mdm2-p53 pathway. Taken together, our findings indicated that PVT1/EZH2/LATS2 interactions might serve as new target for LAD diagnosis and therapy.

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The Bromodomain BET inhibitor JQ1 Suppresses Tumor Angiogenesis in Models of Childhood Sarcoma

The bromodomain and extra terminal domain (BET) inhibitor, JQ1 has marked antitumor activity against several hematologic malignancies as well as solid tumor models. Here we investigated its activity in vitro and in vivo against models of childhood rhabdomyosarcoma and Ewing sarcoma. In vitro, JQ1 (but not the inactive enantiomer JQ1R) inhibited cell proliferation, and increased G1 fraction of cells, although there was no correlation between cell line sensitivity and suppression of c-MYC or MYCN. In vivo, xenografts showed significant inhibition of growth during the period of treatment, and rapid regrowth after treatment was stopped, activity typical of antiangiogenic agents. Further, xenografts derived from cell lines intrinsically resistant or sensitive to JQ1 in vitro had similar sensitivity in vivo as xenografts. Further investigation showed that JQ1 reduced tumor vascularization. This was secondary to both drug-induced down regulation of tumor-derived growth factors and direct effects of JQ1 on vascular elements. JQ1 suppressed VEGF-stimulated vascularization of Matrigel plugs in mice, and in vitro suppressed differentiation, proliferation and invasion of human umbilical cord vascular endothelial cells (HUVECs). In HUVECs JQ1 partially suppressed c-MYC levels, but dramatically reduced AP-1 levels and activity through suppression of the AP-1 associated protein FOSL1. Our data suggest that the antitumor activity of JQ1 in these sarcoma models is largely a consequence of its anti-angiogenic activity.

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Systematic review with meta-analysis: diagnostic overlap of microscopic colitis and functional bowel disorders

Summary

Background

Microscopic colitis shares certain common clinical manifestations with functional bowel disorders, especially diarrhoea-dominant irritable bowel syndrome (IBS) and functional diarrhoea. However, the exact relationship between microscopic colitis and functional bowel disorders has not been systematically assessed.

Aim

To conduct a systematic review and meta-analysis on the diagnostic overlap between functional bowel disorders and microscopic colitis.

Methods

We searched MEDLINE, EMBASE and SCOPUS databases, as well as the abstract books of the major gastroenterology meetings, to investigate the prevalence of microscopic colitis among patients with functional bowel disorders (considering all subtypes of both disorders) and vice versa. Data were pooled with a random-effects model.

Results

Of 227 references identified, data were collected from 26 studies and a total of 5,099 adult patients. The pooled prevalence any type of functional bowel disorders in patients who present diagnostic criteria of microscopic colitis was 39.1% (95% CI: 22.8–56.6%; I²: 97%) and was higher for lymphocytic colitis than for collagenous colitis (40.7% vs. 28.4%, respectively; P = 0.58). The prevalence of microscopic colitis in functional bowel disorders patients was 7% (95% CI: 3.6–11.4%), reaching 9.8% (95% CI: 4.4–17.1%; I²: 95%) in patients exhibiting diarrhoea-dominant IBS, nonsignificantly higher than microscopic colitis rates among patients with constipation-dominant IBS (1.3%) or mixed-dominant IBS (1.9%).

Conclusions

There is a significant overlap of symptoms between microscopic colitis and functional bowel disorders, especially in diarrhoeal subtypes. The high proportion of microscopic colitis among diarrhoea-dominant functional syndromes should serve as a call for more active diagnosis in selected patients.

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Review article: bile acid diarrhoea – pathogenesis, diagnosis and management

Summary

Background

Bile acid diarrhoea results from imbalances in the homoeostasis of bile acids in the enterohepatic circulation. It can be a consequence of ileal disease/dysfunction, associated with other GI pathology or can be idiopathic.

Aims

To summarise the different types of bile acid diarrhoea and discuss the currently available diagnostic methods and treatments.

Results

Bile acid diarrhoea is found in up to 40% of patients diagnosed as having functional diarrhoea/IBS-D, and in up to 80% of patients who have undergone ileal resection. It is likely under-diagnosed and under-treated. In idiopathic disease, errors in regulation feedback of fibroblast growth factor 19 contribute to the development of the condition. Clinical therapeutic trials for bile acid diarrhoea have been used to diagnose it, but the ⁷⁵SeHCAT test is the primary current method. It is sensitive, specific and widely available, though not in the USA. Other diagnostic methods (such as serum measurement of the bile acid intermediate 7α-hydroxy-4-cholesten-3-one, or C4) have less widespread availability and documentation, and some (such as faecal measurement of bile acids) are significantly more complex and costly. First-line treatment of bile acid diarrhoea is with the bile acid sequestrant cholestyramine, which can be difficult to administer and dose due to gastrointestinal side effects. These side effects are less prominent in newer agents such as colesevelam, which may provide higher efficacy, tolerability and compliance.

Conclusion

Bile acid diarrhoea is common, and likely under-diagnosed. Bile acid diarrhoea should be considered relatively early in the differential diagnosis of chronic diarrhoea.

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Kidney-specific knockout of Sav1 in the mouse promotes hyper-proliferation of renal tubular epithelium through suppression of the Hippo pathway

Abstract

Previously, we have reported that Salvador homolog 1 (SAV1), a component of the Hippo pathway, is significantly downregulated in high-grade clear cell renal cell carcinoma (ccRCC) due to 14q copy number loss, and that this downregulation contributes to the proliferation and survival of renal tubular epithelial cells through activation of Yes-associated protein 1 (YAP1), a downstream target of the Hippo pathway. However, the impact of SAV1 loss on the proliferation and survival of kidney cells in vivo remained to be determined. To address this issue, we generated kidney-specific Sav1-knockout (Cdh16-Cre;Sav1^fl/fl) mice. Sav1 deficiency enhanced the proliferation of renal tubular epithelial cells in Cdh16-Cre;Sav1^fl/fl mice accompanied by nuclear localization of Yap1, suggesting suppression of the Hippo pathway. Sav1 deficiency in renal tubules also caused structural and cellular abnormalities of the epithelial cells, including significant enlargement of their nuclei. Furthermore, Cdh16-Cre;Sav1^fl/fl mice developed both glomerular and tubular cysts. Although lining cells of the glomerular cysts showed no atypia, those of the tubular cysts showed variations in cell size and nuclear shape, which became more severe as mice aged. In aged Cdh16-Cre;Sav1^fl/fl mice, we observed focal disruption of proximal tubules and perivascular lymphocytic infiltration. In conclusion, Sav1 is required for maintenance of growth, nuclear size and structure of renal tubules under physiological conditions, and its deficiency leads to acquisition of enhanced proliferation of renal epithelial cells through suppression of Hippo signalling.

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