Multimodal Assessments of Altered Sensation after Transoral Endoscopic Thyroidectomy.

Background: Transoral endoscopic thyroidectomy, a novel technique, uses oral vestibule as the entry point and leaves no scar on the body surface. However, because the incisions are close to the mental nerve, nerve damage and the associated sensory impairment are concerning. Herein, we evaluated sensory alteration after transoral endoscopic thyroidectomy and determined factors associated with the prolonged sensory alteration.

Indocyanine Green Angiography for Parathyroid Gland Evaluation during Transoral Endoscopic Thyroidectomy.

Indocyanine green (ICG) angiography, a real-time intraoperative imaging technique, is associated with better parathyroid identification and functional evaluation during open thyroidectomy. However, the benefits of ICG fluorescence imaging application in transoral endoscopic thyroidectomy are not well-documented. Consecutive patients who underwent transoral endoscopic thyroidectomy were retrospectively reviewed.

Aberrant DNA Hypermethylation Silenced LncRNA Expression in Gastric Cancer.

Background/aim: Long noncoding RNAs (lncRNAs) are noncoding transcripts that are >200 nucleotides in length. However, the biological functions and regulation mechanisms of lncRNAs in gastric carcinogenesis remain unknown.

Materials And Methods: The expression levels of Linc00472 were analyzed by real-time PCR.

MiR-193a-5p and -3p Play a Distinct Role in Gastric Cancer: miR-193a-3p Suppresses Gastric Cancer Cell Growth by Targeting ETS1 and CCND1.

Background/aim: MicroRNAs (miRNAs) are small non-protein-coding RNAs, that can be generated from the 5p or 3p arm of precursor miRNA (pre-miRNA). Differential miRNA arm selection has been reported between tumor and normal tissue in many cancer types; however, the biological function and mechanism of miRNA arm switching in gastric cancer remain unclear.

Materials And Methods: Profiles of miRNA expression in gastric cancer were obtained from The Cancer Genome Atlas (TCGA).

Targeting DTL induces cell cycle arrest and senescence and suppresses cell growth and colony formation through TPX2 inhibition in human hepatocellular carcinoma cells.

Background: Hepatocellular carcinoma (HCC) has an increasing incidence and high mortality. Surgical operation is not a comprehensive strategy for liver cancer. Moreover, tolerating systemic chemotherapy is difficult for patients with HCC because hepatic function is often impaired due to underlying cirrhosis.

Ten-eleven translocation 1 dysfunction reduces 5-hydroxymethylcytosine expression levels in gastric cancer cells.

A sixth base, 5-hydroxymethylcytosine (5hmC), is formed by the oxidation of 5-methylcytosine (5mC) via the catalysis of the ten-eleven translocation (TET) protein family in cells. Expression levels of 5hmC are frequently depleted during carcinogenesis. However, the detailed mechanisms underlying the depletion of 5hmC expression in gastric cancer cells remains unclear, and further research is required.

Isocitrate Dehydrogenase 2 Dysfunction Contributes to 5-hydroxymethylcytosine Depletion in Gastric Cancer Cells.

The isocitrate dehydrogenase (IDH) family of enzymes comprises of the key functional metabolic enzymes in the Krebs cycle that catalyze the conversion of isocitrate to α-ketoglutarate (α-KG). α-KG acts as a cofactor in the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). However, the relationship between 5hmC and IDH in gastric cancer remains unclear.

Link between DYRK1A overexpression and several-fold enhancement of neurofibrillary degeneration with 3-repeat tau protein in Down syndrome.

Triplication of chromosome 21 in Down syndrome (DS) results in overexpression of the minibrain kinase/dual-specificity tyrosine phosphorylated and regulated kinase 1A gene (DYRK1A). DYRK1A phosphorylates cytoplasmic tau protein and appears in intraneuronal neurofibrillary tangles (NFTs). We have previously shown significantly more DYRK1A-positive NFTs in DS brains than in sporadic Alzheimer disease (AD) brains.

Cells of monocyte/microglial lineage are involved in both microvessel amyloidosis and fibrillar plaque formation in APPsw tg mice.

Ultrastructural three-dimensional reconstruction indicates that deposition of amyloid in the wall of capillaries and in perivascular plaques in APP(SW) transgenic mice (Tg2576) represents two steps of one pathological process associated with inflammation of the vascular wall and perivascular space with cells of monocyte/microglia lineage and fibrillar amyloid-beta deposition. Plaque growth is associated with an increase in the number of microglial cells from two in the smallest plaque to 113 in the largest plaque; however, the growth in the number of microglial cells does not result in amyloid deposit degradation. On the contrary, an increase in the number and volume of microglial cells correlates with the growth of amyloid star from 62 to 34,460 microm(3), and an increase of the plaque volume from 1555 to 284,497 microm(3) (r=0.

Contribution of glial cells to the development of amyloid plaques in Alzheimer's disease.

Amyloid plaques appear early during Alzheimer's disease (AD), and their development is intimately linked to activated astrocytes and microglia. Astrocytes are capable of accumulating substantial amounts of neuron-derived, amyloid beta(1-42) (Abeta42)-positive material and other neuron-specific proteins as a consequence of their debris-clearing role in response to local neurodegeneration. Immunohistochemical analyses have suggested that astrocytes overburdened with these internalized materials can eventually undergo lysis, and radial dispersal of their cytoplasmic contents, including Abeta42, can lead to the deposition of a persistent residue in the form of small, GFAP-rich, astrocytic amyloid plaques, first appearing in the molecular layer of the cerebral cortex.

Origin and turnover of microglial cells in fibrillar plaques of APPsw transgenic mice.

Activated microglial cells are an integral component of fibrillar plaques in brains of subjects with Alzheimer's disease (AD) and in brains of transgenic mice overexpressing amyloidogenic fragments of human amyloid precursor protein (APP). The aim of this ultrastructural study of fibrillar plaques was to characterize the origin of microglial cells involved in cored plaque formation. Computer-aided three-dimensional reconstruction of plaques and microvessels in APPsw transgenic mice shows perivascular development of cored plaques.