Correlation Between Aspartate Aminotransferase to Platelet Ratio Index Score and the Degree of Esophageal Varices with Liver Cirrhosis

Background: Esophageal varices is the most common complication in liver cirrhosis. Bleeding varices is a serious complication causing increased mortality rate. In anticipation of those complications, the role of screening test is essential. Endoscopy is the standard method for assessing esophageal varices, but it carries certain risks for patients if it is contraindicated. Moreover, it is an invasive, expensive and uncomfortable procedure. Accordingly, a non-invasive method, aspartat aminotransferase to platelet ratio index (APRI) score, has been developed for evaluating esophageal varices. Method: An analytic cross-sectional observational study was conducted in patients with liver cirrhosis who underwent endoscopy between March 2011 and August 2012. Data were obtained from medical records of hospitalized patients in Mohammad Hoesin General Hospital. The degree of esophageal varices was assessed based on endoscopic findings and APRI score. Spearman test was performed to analyze the correlation between APRI score and the degree of esophageal varices.Results: There were 55 patients, 30 (54.5%) male and 25 (45.5%) female patients, with a range of age between 15-70 years and a mean value of age of 47.09 ± 12.8. APRI score < 0.5 was found in 21.81% subjects, APRI score of 0.5-1.5 was obtained in 41.81% subjects and APRI score > 1.5 was noted in 36.36% subjects with a mean value of 2.32 ± 3.92. There was a correlation between APRI score and degree of esophageal varices with p = 0.011 Conclusion: APRI score can indirectly predict esophageal varices in patients with liver cirrhosis

Additional file 1: Table S1. of Characteristics of human adipose derived stem cells in scleroderma in comparison to sex and age matched normal controls: implications for regenerative medicine

Table detailing the medications prescribed to each of the participants in this study. (DOCX 58 kb

Additional file 3: Figure S3. of Multiplex serum protein analysis reveals potential mechanisms and markers of response to hyperimmune caprine serum in systemic sclerosis

Unsupervised cluster analysis for change in serum proteins from baseline to 26 weeks comparing treatment with hyperimmune caprine serum (HICS) with placebo over 26 weeks and in extended dataset at 52 weeks. (A) Unsupervised cluster analysis of change in protein level during 26-week treatment phase of placebo-controlled trial reveals patterns of change that are reflected in the supervised analysis shown in Fig. 3. Thus, subjects receiving placebo show generally less treatment effect and those treated with HICS show the patterns consistent with the summary changes shown above. (B) Unsupervised cluster analysis is also performed for the extended 52-week dataset that includes subjects moving from placebo to active treatment (n = 7) in the second 26 weeks and three cases that have no active treatment and were previously on placebo. This complements the presentation of data for baseline and 26 weeks presented in Additional file 1: Figure S1 and shows close congruity for the two 26-week unsupervised heat maps in the extended dataset. (TIF 1444 kb

Additional file 4: Figure S4. of Multiplex serum protein analysis reveals potential mechanisms and markers of response to hyperimmune caprine serum in systemic sclerosis

Average change in serum proteins comparing treatment with hyperimmune caprine serum (HICS) or placebo and for MRSS responders versus non-responder at 26 weeks. (A) Average change in serum protein was calculated for each treatment arm over 26 weeks and ranked according to fold change average after HICS treatment. (B) Similar analysis was undertaken for average protein changes in the subjects showing significant improvement of four skin score units and 20% of baseline MRSS score during the trial (responders) or these that did not demonstrate clinical response. These were ranked for the most increased proteins in responder cases. Key proteins that emerged as upregulated (red) or downregulated (blue) for HICS treatment, shown in Fig. 4, are annotated with asterisks. (TIF 761 kb

Cognitive triggers of auditory hallucinations: An experimental investigation

It has proved difficult to establish the internal process by which mental events are transformed into auditory hallucinations. The earlier stages of the generation of hallucinations may prove more accessible to research. Cognitions have been reported by patients as a trigger of auditory hallucinations, but the role of these preceding thoughts has not been causally determined. Therefore, the role of cognition in triggering auditory hallucinations was tested in an experimental study. Thirty individuals who experienced auditory hallucinations in social situations entered a neutral social situation presented using virtual reality. Participants randomised to the experimental condition were instructed to think their hallucination-preceding thoughts, and those randomised to the control condition were instructed to think neutral thoughts. Twenty-seven participants (93%) were able to spontaneously identify a cognition which preceded a hallucination. There was no difference between the experimental and control groups in the occurrence or severity of auditory hallucinations in virtual reality. Virtual reality did not lead to physical side effects or an increase in anxiety. The relationship between antecedent cognitions and auditory hallucinations is likely to be more complex than the one tested. It is argued that the effect of cognition on auditory hallucinations may be mediated by affect but this needs to be investigated through further experimental research

Fibril diameters in the KO reticular dermis are smaller and more uniform than WT fibrils.

<p><b>A.</b> Representative micrographs of skin in deep dermal areas near subcutaneous fat. (Scale bar = 0.5 μm) <b>B.</b> Histogram of the frequency of collagen fibrils with a given diameter range from WT (white bars) and KO (black bars). At least 200 fibrils from 3 WT and 3 KO animals at 5 months of age were used for analysis. P<0.05.</p

Stiff surfaces and TGFβ induce MRTF-A nuclear accumulation.

<p>SSc and control dermal fibroblast lines (both N = 3) were cultured on 6 well plates with collagen type I coated soft substrates (5 kPa Softwell), or hard substrate (50 kPa). <b>B. Induction of collagen transcription on hard surfaces requires MRTF-A.</b> Mouse fibroblasts from wild type (WT) and loss-of-function (KO) mice with collagen promoter driving GFP were cultured on fibronectin coated soft and hard surfaces. Pictures taken 24 hours after plating. Fluorescence was quantified using ImageJ. The numbers of cells in each image was counted (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0126015#pone.0126015.s004" target="_blank">S4 Fig</a>) to determine the luminance per cell. <b>C.&D.</b> Normal control fibroblasts and SSc fibroblasts were cultured without serum for 16 hours then treated with TGFβ (4 ng/ml) for 0, 8 and 24 hours or treated with either saline or TGFβ (4 ng/ml) with or without CCG1423 (10μM) or NSC2376 (50 μM). Proteins (20 μg) from cytoplasm and nuclei were extracted using NE-PER Nuclear Protein Extraction Kit and separated on 4–12% gradient gel and visualized using MRTF-A antibody.</p

Increased expression of MRTF-A in the SSc epidermis and at the epidermal dermal junction in established SSc correlates with increased intracellular procollagen, and SMA.

<p>The expression of MRTF-A, procollagen type I, and SMA was detected by immunohistochemical staining in the epidermis and papillary dermis of early and established SSc patients and controls healthy control patients. Arrows point to staining in vascular cells (V), epidermis (e), and fibroblast (F).</p

Nuclear MRTF-A expression is more prominent in SSc skin then healthy control.

<p><b>A.</b> Representative pictures of healthy control and SSc sections of biopsy. Histological samples of human skin were stained with MRTF-A antibody (1:2000). Higher magnification of epithelium and small vessels (20X) in papillary dermis. Brown arrows = MRTF-A nuclei, Blue arrow = hematoxylin stained nuclei without MRTF-A. Graphical representations of % nuclei in epidermis, vasculature, and interstitial cells in papillary dermis. Histological samples of 5 healthy control and 9 scleroderma human skin were evaluated for nuclear staining. B. Total cells with MRTF-A nuclear localization in the epidermis, vasculature, and interstitial papillary dermal layers were counted and compared with the total amount of nuclei in the epidermal/papillary dermal layer. White bars = healthy controls, Black bars = SSc (* = p<0.01 using nonparametric Mann-Whitney U, two-tailed).</p

Mouse KO skin and lung are less stiff than WT skin and lung.

<p>A 3x1x1 mm strip of dorsal skin or lung tissue was placed longitudinally into a computer-controlled dual-mode lever arm force transducer system and stretched intermittently. <b>A.</b> Young’s module plotted at each strain. The Young’s module is the slope of the stress-strain curve. <b>B.</b> Dynamic stretch storage modulus describes the ability of the material to store elastic energy during the loading phase of a cyclic stretch <b>C</b>. Dynamic stretch loss modulus—The amount of energy lost (usually as heat) during a cycle. Vertical brackets denote the overall group differences using 2-way repeated measure ANOVA (*: <i>p</i><0.05, **: <i>p</i><0.01 and ***: <i>p</i><0.001) whereas horizontal brackets show Tukey’s post hoc differences between WT and KO at the same strain (Panel A) or frequency (Panels B and C). For the Young’s and loss moduli of lung tissue, there are also significant interactions between strain and group (panel A) as well as frequency and group (panel C, p<0.05). For the skin, there is a significant interaction between frequency and group only for the loss modulus (p<0.05).</p