Activity

As the manual creation and maintenance of biomedical ontologies are labor-intensive, automatic aids are desirable in the lifecycle of ontology development.

Provided with a set of concept names in the Foundational Model of Anatomy (FMA), we propose an innovative method for automatically generating the taxonomy and the partonomy structures among them, respectively.

Our approach comprises 2 main tasks The first task is predicting the direct relation between 2 given concept names by utilizing word embedding methods and training 2 machine learning models, Convolutional Neural Networks (CNN) and Bidirectional Long Short-term Memory Networks (Bi-LSTM). The second task is the introduction of an original granularity-based method to identify the semantic structures among a group of given concept names by leveraging these trained models.

Results show that both CNN and Bi-LSTM perform well on the first task, with F1 measures above 0.91. For the second task, our approach achieves an average F1 measure of 0.79 on 100 case studies in the FMA using Bi-LSTM, which outperforms the primitive pairwise-based method.

We have investigated an automatic way of predicting a hierarchical relationship between 2 concept names; based on this, we have further invented a methodology to structure a group of concept names automatically. selleck compound This study is an initial investigation that will shed light on further work on the automatic creation and enrichment of biomedical ontologies.

We have investigated an automatic way of predicting a hierarchical relationship between 2 concept names; based on this, we have further invented a methodology to structure a group of concept names automatically. This study is an initial investigation that will shed light on further work on the automatic creation and enrichment of biomedical ontologies.Corneal stromal wound healing is a complex event that occurs to restore the transparency of an injured cornea. It involves immediate apoptosis of keratocytes followed by their activation, proliferation, migration, and trans-differentiation to myofibroblasts. Myofibroblasts contract to close the wound and secrete extracellular matrix and proteinases to remodel it. Released proteinases may degenerate the basement membrane allowing an influx of cytokines from overlying epithelium. Immune cells infiltrate the wound to clear cellular debris and prevent infections. Gradually basement membrane regenerates, myofibroblasts and immune cells disappear, abnormal matrix is resorbed, and transparency of the cornea is restored. Often this cascade deregulates and corneal opacity results. Factors that prevent corneal opacity after an injury have always intrigued the researchers. They hold clinical relevance as they can guide the outcomes of corneal surgeries. Studies in the past have shed light on the role of various factors in stromal healing. TGFβ (transforming growth factor-beta) signaling is the central player guiding stromal responses. Other major regulators include myofibroblasts, basement membrane, collagen fibrils, small leucine-rich proteoglycans, biophysical cues, proteins derived from extracellular matrix, and membrane channels. The knowledge about their roles helped to develop novel therapies to prevent corneal opacity. This article reviews the role of major regulators that determine the outcome of stromal healing. It also discusses emerging therapies that modulate the role of these regulators to prevent stromal opacity.

To evaluate the role of transient receptor potential melastatin 8 (TRPM8) activity in menthol-induced cold sensitivity and its qualitative perception in patients with dry eye (DE).

This prospective, cross-sectional, comparative study included 52 eyes of 52 subjects (mean age 66.8±9.2 years; range 44-86) with a tear break-up time (TBUT) of ≤5s. The participants were classified into three groups 17 patients with DE symptoms and keratoconjunctival (KC) staining scores of ≥3 points (positive KC-DE group), 18 patients with DE symptoms and KC staining scores of <3 points (negative KC-DE group), and 17 individuals with KC staining scores of <3 points and no symptoms (non-DE control group). The menthol-induced cool sensation (M-cool) and TBUT were measured after administration of 2μl of 1.0mM menthol eye drops. Furthermore, participants answered a questionnaire regarding their stimulus perception (pleasant, unpleasant, or neither).

M-cool values were similar in the three groups. TBUT significantly increased in the negative KC-DE and control groups (P<0.05) and remained unchanged in the positive KC-DE group (P>0.05) after menthol administration. DE patients reported the sensation as pleasant or unpleasant, whereas most control participants were indifferent (P<0.05).

While M-cold sensitivity was similar in DE and control groups, its qualitative perception differed between these groups. Thus, TRPM8 activation at the peripheral level alone may not be sufficient to account for the manifestation of discomfort symptoms associated with DE.

While M-cold sensitivity was similar in DE and control groups, its qualitative perception differed between these groups. Thus, TRPM8 activation at the peripheral level alone may not be sufficient to account for the manifestation of discomfort symptoms associated with DE.

Tofacitinib is an oral, small molecule Janus kinase inhibitor for the treatment of ulcerative colitis (UC). The efficacy and safety of tofacitinib were demonstrated in a dose-ranging phase 2 induction trial, 3 phase 3 randomized, placebo-controlled trials (OCTAVE Induction 1 and 2; and OCTAVE Sustain), and an ongoing, open-label, long-term extension trial (OCTAVE Open) in patients with moderately to severely active UC. Here, we assessed short- and long-term efficacy and safety of extended induction (16 weeks) with tofacitinib 10 mg twice daily (BID) in patients who failed to respond to initial induction (8 weeks) treatment.

In patients who achieved a clinical response following extended induction (delayed responders), the efficacy and safety of tofacitinib were evaluated up to Month 36 of OCTAVE Open.

52.2% of patients who did not achieve clinical response to 8 weeks’ treatment with tofacitinib 10 mg BID in the induction studies achieved a clinical response following extended induction (delayed responders).