A Delayed Postoperative Anastomotic Submucosal Abscess.

Delayed anastomotic submucosal abscess is a rare complication of rectal tumor resection. A submucosal tumor-like lesion near the anastomotic site was detected in a 57-year-old woman, and pus and sutures were found through spontaneously formed fistulas. Endoscopic ultrasound confirmed the presence of hyperechoic pus flowing out from the fistulas on compression of the lesion.

Mechanism of the G/M ratio and zein in enhancing the mechanical and hydrophobic properties of sodium alginate films.

This study developed an edible film based on calcium-crosslinked sodium alginate (SA) using the casting method. The investigation assessed how the α-L-guluronic acid/β-D-mannuronic acid (G/M ratio) and zein addition influence the film's physicochemical properties. Fourier transform infrared spectroscopy and scanning electron microscopy findings suggest that the G/M ratio modulates the film's physicochemical characteristics by altering SA molecular cross-linking strength and the film's network structure density.

SHMT2 Mediates Small-Molecule-Induced Alleviation of Alzheimer Pathology Via the 5'UTR-dependent ADAM10 Translation Initiation.

It is long been suggested that one-carbon metabolism (OCM) is associated with Alzheimer's disease (AD), whereas the potential mechanisms remain poorly understood. Taking advantage of chemical biology, that mitochondrial serine hydroxymethyltransferase (SHMT2) directly regulated the translation of ADAM metallopeptidase domain 10 (ADAM10), a therapeutic target for AD is reported. That the small-molecule kenpaullone (KEN) promoted ADAM10 translation via the 5' untranslated region (5'UTR) and improved cognitive functions in APP/PS1 mice is found.

Circulating antibodies to Helicobacter pylori are associated with biomarkers of neurodegeneration in cognitively intact adults.

Helicobacter pylori (H. pylori) infection confers risk for Alzheimer's Disease (AD), with the mechanisms unknown. Infections are linked to the etiology of AD partly through modulating the humoral immunity post-infection.

Apicidin attenuates memory deficits by reducing the Aβ load in APP/PS1 mice.

Aims: Amyloid beta (Aβ) is an important pathological feature of Alzheimer's disease (AD). A disintegrin and metalloproteinase 10 (ADAM10) can reduce the production of toxic Aβ by activating the nonamyloidogenic pathway of amyloid precursor protein (APP). We previously found that apicidin, which is a histone deacetylase (HDAC) inhibitor, can promote the expression of ADAM10 and reduce the production of Aβ in vitro.

Discovery of novel thiophene derivatives as potent neuraminidase inhibitors.

Neuraminidase (NA) is an important target for the treatment of influenza. In this study, a new lead NA inhibitor, 4 (ZINC01121127), was discovered by pharmacophore-based virtual screening and molecular dynamic (MD) simulation. Some novel NA inhibitors containing thiophene ring were synthesized by optimizing the skeleton of the lead compound 4.

Influenza infection elicits an expansion of gut population of endogenous Bifidobacterium animalis which protects mice against infection.

Background: Influenza is a severe respiratory illness that continually threatens global health. It has been widely known that gut microbiota modulates the host response to protect against influenza infection, but mechanistic details remain largely unknown. Here, we took advantage of the phenomenon of lethal dose 50 (LD) and metagenomic sequencing analysis to identify specific anti-influenza gut microbes and analyze the underlying mechanism.

Estrogen receptor α promotes Cav1.2 ubiquitination and degradation in neuronal cells and in APP/PS1 mice.

Cav1.2 is the pore-forming subunit of L-type voltage-gated calcium channel (LTCC) that plays an important role in calcium overload and cell death in Alzheimer's disease. LTCC activity can be regulated by estrogen, a sex steroid hormone that is neuroprotective.

Cosmosiin Increases ADAM10 Expression via Mechanisms Involving 5'UTR and PI3K Signaling.

The α-secretase "a disintegrin and metalloproteinase domain-containing protein" (ADAM10) is involved in the processing of amyloid precursor protein (APP). Upregulation of ADAM10 precludes the generation of neurotoxic β-amyloid protein (Aβ) and represents a plausible therapeutic strategy for Alzheimer's disease (AD). In this study, we explored compounds that can potentially promote the expression of ADAM10.

Phorbol esters dPPA/dPA promote furin expression involving transcription factor CEBPβ in neuronal cells.

Using high-throughput small molecule screening targeting furin gene, we identified that phorbol esters dPPA (12-Deoxyphorbol 13-phenylacetate 20-acetate) and dPA (12-Deoxyphorbol 13-acetate) significantly increased furin protein and mRNA expression in SH-SY5Y cells. This effect was prevented by PKC (protein kinase C) inhibitor calphostin C but not Ro318220, suggesting that the C1 domain, rather than the catalytic domain of PKC plays an important role. Luciferase assay revealed that nucleotides -7925 to -7426 were sufficient to mediate dPPA/dPA enhancement of P1 promoter activity.

HMGCS2 promotes autophagic degradation of the amyloid-β precursor protein through ketone body-mediated mechanisms.

HMGCS2 (mitochondrial 3-hydroxy-3-methylglutaryl-COA synthase 2) is a control enzyme in ketogenesis. The mitochondrial localization and interaction with APP (β-amyloid precursor protein) suggest that HMGCS2 may play a role in the pathophysiology of AD (Alzheimer's disease). Here we report that overexpression of HMGCS2 decreased levels of APP and related CTFs (carboxy-terminal fragments), which was largely prevented by an autophagic inhibitor chloroquine.

Estrogen Modulates ubc9 Expression and Synaptic Redistribution in the Brain of APP/PS1 Mice and Cortical Neurons.

Estrogen exerts multiple actions in the brain and is an important neuroprotective factor in a number of neuronal disorders. However, the underlying mechanism remains unknown. Studies demonstrate that ubiquitin-conjugating enzyme 9 (ubc9) has an integral role in synaptic plasticity and may contribute to the pathology of neuronal disorders.

Inhibition of iNOS alleviates cognitive deficits and depression in diabetic mice through downregulating the NO/sGC/cGMP/PKG signal pathway.

Diabetes mellitus often results in a number of complications involving impaired brain function, including cognitive deficits and depression. However, the potential mechanisms for diabetes-related cognitive deficits and depression are not fully understood. Neurons in the hippocampal, cortical and amygdala functional regions are more susceptible to damage during hyperglycemia.

Depression can be prevented by astaxanthin through inhibition of hippocampal inflammation in diabetic mice.

The critical factor considered in a depression induced by diabetes is the inflammation eliciting hippocampal, amygdala and thalamic neuronal injury. Therefore, inhibiting inflammatory reactions in the brain and reducing neuronal injury can alleviate depression in rodents suffering from diabetes mellitus. The oral administration of astaxanthin has been employed in emotional disorders and diabetic complications due to its anti-depressant, anti-inflammatory and anti-apoptotic functions.

Histone deacetylase inhibitor apicidin increases expression of the α-secretase ADAM10 through transcription factor USF1-mediated mechanisms.

ADAM10 (a disintegrin and metalloproteinase domain-containing protein 10) is the α-secretase that is involved in APP (β-amyloid precursor protein) processing. Enhancement of the nonamyloidogenic APP pathway by ADAM10 provides therapeutic potential for Alzheimer's disease (AD). By using high-throughput screening that targeted ADAM10, we determined that apicidin-an inhibitor of HDACs (histone deacetylases)-significantly increased mRNA and protein levels of ADAM10 in SH-SY5Y cells.

Regulation and the Mechanism of Estrogen on Cav1.2 Gene in Rat-Cultured Cortical Astrocytes.

L-type calcium channel (LTCC) gene Cav1.2 is believed to play an important role in the alteration of Ca(2+) homeostasis in brain astrocytes. Increasing evidence shows that alteration of intracellular Ca(2+) concentration is related to the effect of 17β-estradiol (E2) in a variety of neurophysiological and neuropathological conditions.

Anti-inflammatory Effect of Astaxanthin on the Sickness Behavior Induced by Diabetes Mellitus.

Chronic inflammation appears to play a critical role in sickness behavior caused by diabetes mellitus. Astaxanthin has been used in treating diabetes mellitus and diabetic complications because of its neuroprotective and anti-inflammatory actions. However, whether astaxanthin can improve sickness behavior induced by diabetes and its potential mechanisms are still unknown.

Advances in epigenetic biomarker research in colorectal cancer.

Colorectal cancer (CRC) causes approximately 600000 deaths annually and is the third leading cause of cancer mortality worldwide. Despite significant advancements in treatment options, CRC patient survival is still poor owing to a lack of effective tools for early diagnosis and a limited capacity for optimal therapeutic decision making. Since there exists a need to find new biomarkers to improve diagnosis of CRC, the research on epigenetic biomarkers for molecular diagnostics encourages the translation of this field from the bench to clinical practice.

Mechanisms involved in biological behavior changes associated with Angptl4 expression in colon cancer cell lines.

Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths throughout the world. Angiopoietin-like-4 (Angptl4), a member of the angiopoietin family of secreted proteins, is frequently expressed in the perinecrotic areas of different human tumors, yet its role is still unclear in colorectal cancer. Angptl4 mRNA expression in primary colorectal cancer tissue and seven colon cancer cell lines was measured by semi-quantitative RT-PCR; the influence of Angptl4 expression on the colon cancer cell lines was investigated by either overexpression or knockdown of Angptl4 in colon cancer cell lines HCT116 and HT29, respectively.

Chemically-induced cancers do not originate from bone marrow-derived cells.

Background: The identification and characterization of cancer stem cells (CSCs) is imperative to understanding the mechanism of cancer pathogenesis. Growing evidence suggests that CSCs play critical roles in the development and progression of cancer. However, controversy exists as to whether CSCs arise from bone marrow-derived cells (BMDCs).

Recent progress in the study of methylated tumor suppressor genes in gastric cancer.

Gastric cancer is one of the most common malignancies and a leading cause of cancer mortality worldwide. The pathogenesis mechanisms of gastric cancer are still not fully clear. Inactivation of tumor suppressor genes and activation of oncogenes caused by genetic and epigenetic alterations are known to play significant roles in carcinogenesis.

[ANGPTL4 gene silencing by short-hairpin RNA inhibits the migration of human colorectal cancer cell line HT29].

Objective: To investigate the effect of ANGPTL4 gene silencing on the migration of human colon cancer cells in vitro.

Methods: The expression of ANGPTL4 in human colorectal cancer cell lines was detected by semi-quantitative RT-PCR. Following stable transfection with a short-hairpin RNA (shRNA) targeting ANGPTL4 gene in HT29 cells, ANGPTL4 mRNA and protein expressions were detected by semi-quantitative RT-PCR and direct ELISA, respectively, and the changes in cell migration ability and cell morphology were observed with transwell and immunofluorescence assays.

[Silencing of Adrm1 by RNA interference suppresses proliferation of colorectal cancer cells].

Objective: To investigate the effects of the novel proteasome subunit Adrm1 knockdown by RNA interference on proliferation of colorectal cancer cells.

Methods: The shRNA eukaryotic expression vector against Adrm1 was constructed and transfected into colon cancer RKO cells. The Adrm1-shRNA stable transfected clones were selected.

CD44 activation in mature B-cell malignancies by a novel recurrent IGH translocation.

Using inverse polymerase chain reaction, we identified CD44, located on chromosome 11p13, as a novel translocation partner of IGH in 9 of 114 cases of gastric, nongastric extranodal, follicular, and nodal diffuse large B-cell lymphoma (DLBCL). Notably, these translocations involving IGHSmu were detected in follicular lymphomas and exclusively in germinal center B cell-ike (GCB)-DLBCLs. CD44 is not expressed in reactive GC B cells.