Cellular and Molecular Mechanisms of Hepatic Fibrosis

The occurrence of hepatic fibrosis is a multi-factor involved process. The key is the activation of hepatic stellate cells (HSC). Synthesis of extracellular matrix in the liver cells increases while degradation decreases. This paper reviews the tissue factors and the mechanism closely related to the forming of hepatic fibrosis

Size Effect on the Magnetic Phase in Sr\u3csub\u3e4\u3c/sub\u3eRu\u3csub\u3e3\u3c/sub\u3eO\u3csub\u3e10\u3c/sub\u3e

High quality Sr4Ru3O10 nanoflakes are obtained by the scotch tape-based micro-mechanical exfoliation method. The metamagnetic transition temperature Tmflake is found to decrease in line with the decrease of thickness, while the ferromagnetic (FM) phase, the ordinary, and anomalous Hall effects (OHE and AHE) are independent on the thickness of the flake. Analysis of the data demonstrates that the AHE reflects the FM nature of Sr4Ru3O10, and the decrease of thickness favors the Ru moments aligned in the ab-plane, which induces a decrease of the metamagnetic transition temperature compared with the bulk

One-Pot Regiospecific Synthesis of Imidazo[1,2‑<i>a</i>]pyridines: A Novel, Metal-Free, Three-Component Reaction for the Formation of C–N, C–O, and C–S Bonds

A novel transition-metal-free three-component reaction for the construction of imidazo­[1,2-<i>a</i>]­pyridines has been developed. It represents a facile approach for the formation of C–N, C–O, and C–S bonds from ynals, pyridin-2-amines, and alcohols or thiols

The Effects of Mycotoxins and Selenium Deficiency on Tissue-Engineered Cartilage

&lt;b&gt;&lt;i&gt;Objective:&lt;/i&gt;&lt;/b&gt; To investigate the effects of 3 mycotoxins, deoxynivalenol (DON), nivalenol (NIV) and T-2 toxin, in the presence and absence of selenium (Se) on the metabolism of tissue-engineered cartilage to mimic conditions found in Kashin-Beck disease (KBD) environments. &lt;b&gt;&lt;i&gt;Materials and Methods:&lt;/i&gt;&lt;/b&gt; Chondrocytes were seeded onto bone matrix gelatin (BMG) to construct engineered cartilage. The 3 toxins were added to the culture media for 3 weeks followed by immunhistochemical analyses of collagens type II and X, aggrecan, matrix metalloproteinases 1 and 3 (MMP-1 and MMP-3), MMP inhibitors 1 and 3 (TIMP-1 and TIMP-3) and α&lt;sub&gt;2&lt;/sub&gt; macroglobulin (α2M). &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; Type II collagen was decreased while type X collagen was increased in response to DON, NIV and T-2 toxin. Aggrecan was reduced by all 3 mycotoxins. Compared with the control, the 3 toxins decreased the expression of α2M, TIMP-1 and TIMP-3, and increased the expression of MMP-1 and MMP-3. Se could partially inhibit the effects of DON, NIV and T-2 toxins. &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Under the low Se condition, the 3 mycotoxins produced procatabolic changes in cartilage resulting in the loss of aggrecan and type II collagen and promoted a hypertrophic phenotype of chondrocytes characterized by increasing type-X-collagen expression, enhancing the expression of MMPs, while weakening the TIMPs. Se could partially block the effects mentioned above. These results support the hypothesis that the combination of mycotoxin stress and Se deficiency would be the causative factors for KBD.</jats:p