[Goblet cell adenocarcinoma in the digestive system: a clinicopathological analysis of 22 cases].

Objective: To investigate the clinical features, morphological characteristics, immunophenotype, and differential diagnosis of goblet cell adenocarcinoma (GCA) in the digestive system. Methods: The clinicopathological data, morphological characteristics, immunophenotypes of 22 cases of GCA in the digestive system diagnosed from January 2010 to January 2021 were collected. Meanwhile, 25 cases of neuroendocrine neoplasm (NEN) and 24 cases of adenocarcinoma were used as controls. Relevant literature was also reviewed. Results: There were 16 males and 6 females, aged from 36 to 79 years with an average of 56 years. The anatomical sites of the 22 GCA were mostly appendix (17 cases) and occasionally extra-appendix (5 cases), including 3 cases in stomach, 1 case in duodenum and 1 case in anal. All 17 cases of appendiceal GCA were pure GCA. Among the 5 cases of extra-appendiceal GCA, One case of gastric GCA was pure, two cases of gastric GCA with NEN or adenocarcinoma, duodenal GCA with NEN and adenocarcinoma, anal GCA with NEN.Low-grade GCAs were composed of goblet, Paneth and neuroendocrine cells, which were arranged in intestinal crypt tubular or cluster structures and distributed in the wall of digestive system. The tubular and cluster structures lacked adhesion. Goblet cells were columnar, located in the base, with clear cytoplasm, small nuclei, inconspicuous atypia, and uncommon mitoses. Extracellular mucus and signet-ring cells with nuclear variations could be seen in some cases. Nerve fiber bundle invasion and tumor thrombus in vessels were often present. High-grade GCAs lacked tubular and cluster structures, and their histological structures were more complex. Tumor cells expressed mixed neuroendocrine and glandular epithelial markers. Similar to the expression patterns of synaptophysin and chromogranin A, CD200 and INSM1 were also dot-like or patch-positive in GCA. Conclusions: GCA is an infrequent tumor of the digestive system and shows the bi-directional differentiation characteristics of neuroendocrine and glandular epithelium. Accurate diagnosis and staging are related to its prognosis.

Dephasing time in graphene due to interaction with flexural phonons.

We investigate decoherence of an electron in graphene caused by electron-flexural phonon interaction. We find out that flexural phonons can produce a dephasing rate comparable to the electron-electron one. The problem appears to be quite special because there is a large interval of temperature where the dephasing induced by phonons cannot be obtained using the golden rule. We evaluate this rate for a wide range of density (n) and temperature (T) and determine several asymptotic regions with the temperature dependence crossing over from τ_{ϕ}^{-1}∼T^{2} to τ_{ϕ}^{-1}∼T when temperature increases. We also find τ_{ϕ}^{-1} to be a nonmonotonic function of n. These distinctive features of the new contribution can provide an effective way to identify flexural phonons in graphene through the electronic transport by measuring the weak-localization corrections in magnetoresistance.

Retraction Note: Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal.

The article "Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal", by K. Zhao, J.-Y. Tan, Q.-D. Mao, K.-Y. Ren, B.-G. He, C.-P. Zhang, L.-Z. Wei published in Eur Rev Med Pharmacol Sci 2019; 23 (1): 312-320-DOI: 10.26355/eurrev_201901_16778-PMID: 30657572 has been retracted by the authors for the following reasons: We are still conducting research in the effect of long non-codingRNA TUG1 in interstitial cells of Cajal recently. It turned out that some of the current experimental results are inconsistent with the previous results. Some data cannot be repeated by further research. We need to further confirm the effect of long non-coding RNA TUG1 on alleviating TNF-α-induced inflammatory injury in interstitial cells of Cajal and for this reason, the authors all agreed to withdraw the manuscript. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16778.

Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal.

OBJECTIVE: Irritable bowel syndrome (IBS) is a common functional disorder in the gastrointestinal tract. Inflammatory response has been found to participate in the pathogenesis of IBS. This study aimed to explore the effects of long non-coding RNA taurine upregulated gene 1 (TUG1) on tumor necrosis factor alpha (TNF-α)-induced interstitial cells of Cajal (ICC) inflammatory injury, which was relevant to the pathogenesis of IBS. PATIENTS AND METHODS: The expression levels of TUG1 and microRNA-127 (miR-127) were analyzed by qRT-PCR. Viability, apoptosis and the expression of apoptosis-associated factors were analyzed by CCK-8 assay, flow cytometry and Western blot, respectively. The mRNA and protein levels of pro-inflammatory cytokines were detected by qRT-PCR and Western blot, respectively. Finally, activations of nuclear factor kappa-B (NF-κB) and Notch pathways were evaluated by Western blot. RESULTS: TNF-α treatment inhibited ICC viability, induced ICC apoptosis and promoted an inflammatory response in ICC. TUG1 was downregulated in TNF-α-treated ICC. TUG1 overexpression protected ICC from TNF-α-induced apoptosis and pro-inflammatory cytokines expression. TUG1 suppression showed opposite effects. MiR-127 was negatively regulated by TUG1 and implicated in the action of TUG1 in ICC. MiR-127 up-regulation largely reversed the effects of TUG1 on TNF-α-treated ICC. Mechanistically, TUG1 inhibited TNF-α-induced activation of NF-κB and Notch pathways in ICC by down-regulating miR-127. CONCLUSIONS: TUG1 attenuated TNF-α-caused apoptosis and inflammatory response in ICC by down-regulating miR-127 and then inactivating NF-κB and Notch pathways.

Clostridium butyricum promotes intestinal motility by regulation of TLR2 in interstitial cells of Cajal.

OBJECTIVE: Clostridium butyricum (C. butyricum) as a probiotic has been reported to have an important role in the pathogenesis of gastrointestinal diseases. However, the effects of C. butyricum on regulation of intestinal motility of ulcerative colitis (UC) remain unclear. Our study aimed to explore the cross-regulation effect of C. butyricum and toll-like receptor 2 (TLR-2) on UC. MATERIALS AND METHODS: Interstitial cells of Cajal (ICCs) were treated by C. butyricum for 2 h, the mRNA and protein levels of TLR-2, IL-6, and IL-8 were detected by RT-qPCR and Western blot. Then, TLR2-specific small interfering RNA (si-TLR2) was transfected into ICCs, and the relative expressions of IL-6 and IL-8, SCF, cell viability, ghrelin, SP, and ET were measured by RT-qPCR, Western blot, CCK-8, and ELISA. Besides, the signal pathways of NF-κB and JNK were determined by Western blot. RESULTS: C. butyricum significantly increased TLR2, IL-6, and IL-8 expressions in ICCs. However, TLR2 silence alleviated C. butyricum-induced IL-6 and IL-8 expressions. Moreover, TLR2 silence significantly inhibited C. butyricum-induced cell viability in ICCs. Additionally, C. butyricum significantly increased SCF expression and promoted the secretion of ghrelin and SP. However, a significant reduction in the levels of SCF, ghrelin, and SP was evident in the silence of TLR2 expression. Besides, TLR2 silence reduced C. butyricum-activation NF-κB and JNK signal pathways in ICCs. CONCLUSIONS: These findings revealed that C. butyricum promoted intestinal motility by regulation of TLR2 in ICCs, which contributed to understand the molecular mechanisms of C. butyricum on UC.

Flexural phonons in supported graphene: from pinning to localization.

We identify graphene layer on a disordered substrate as a system where localization of phonons can be observed. Generally, observation of localization for scattering waves is not simple, because the Rayleigh scattering is inversely proportional to a high power of wavelength. The situation is radically different for the out of plane vibrations, so-called flexural phonons, scattered by pinning centers induced by a substrate. In this case, the scattering time for vanishing wave vector tends to a finite limit. One may, therefore, expect that physics of the flexural phonons exhibits features characteristic for electron localization in two dimensions, albeit without complications caused by the electron-electron interactions. We confirm this idea by calculating statistical properties of the Anderson localization of flexural phonons for a model of elastic sheet in the presence of the pinning centers. Finally, we discuss possible manifestations of the flexural phonons, including the localized ones, in the electronic thermal conductance.

MicroRNA-455 suppresses the oncogenic function of HDAC2 in human colorectal cancer.

Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3'UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (P<0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (P<0.01). Moreover, miR-455 decreased the expression of HDAC2 (P<0.01). miR-455 remarkably decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after transfection while inducing cell apoptosis (P<0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.