2,3-Dicyano-5,6-dichlorobenzoquinone-Mediated and Selective C-O and C-C Cross-Couplings of Phenols and Porphyrins.

A selective C-O cross-coupling reaction between porphyrins and phenols has been developed through 2,3-dicyano-5,6-dichlorobenzoquinone (DDQ)/Sc(OTf)3 oxidation, efficiently delivering meso-etherified porphyrins in good yields (≤93%). The radical complex process was proposed and calculated as the rationalized mechanism to block the homocoupling process. In addition, the switchable selective C-C cross-coupling reaction was achieved by using bulky electron-rich phenols and naphthols under DDQ oxidation conditions.

Mitochondrial translocation of cofilin is required for allyl isothiocyanate-mediated cell death via ROCK1/PTEN/PI3K signaling pathway.

BACKGROUND: Cofilin is a member of the actin depolymerizing factor (ADF)/cofilin family, which regulates actin dynamics. Increasing evidence suggests that mitochondrial translocation of cofilin appears necessary for the regulation of apoptosis. RESULTS: We report that allyl isothiocyanate (AITC) potently induces mitochondria injury and apoptosis. These events were accompanied by a loss of polymerized filamentous actin (F-actin) and increase in unpolymerized globular actin (G-actin). AITC also induces dephosphorylation of cofilin through activation of PP1 and PP2A. Only dephosphorylated cofilin binds to G-actin and translocates to mitochondria during AITC-mediated apoptosis. Mechanistic study revealed that interruption of ROCK1/PTEN/PI3K signaling pathway plays a critical role in AITC-mediated dephosphorylation and mitochondrial translocation of cofilin and apoptosis. Our in vivo study also showed that AITC-mediated inhibition of tumor growth of mouse leukemia xenograft model is in association with dephosphorylation of cofilin. CONCLUSIONS: These findings support a model in which induction of apoptosis by AITC stems primarily from activation of ROCK1 and PTEN, and inactivation of PI3K, leading in turn to activation of PP1 and PP2A, resulting in dephosphorylation of cofilin, which binds to G-actin and translocates to mitochondria, culminating in the dysfunction of mitochondria, release of cytochrome c and apoptosis.

Expression of cellular phenotype switching markers-matrix protein Gla, mRNA and collagen I, III and V of human airway smooth muscle cells in vitro after TGF-beta1 stimulation / 中华儿科杂志

<p><b>OBJECTIVE</b>Bronchial asthma is a chronic inflammatory disorder. Long-term inflammation leads to varying degrees of structural changes in the airway wall known as airway reconstruction or remodeling. These structural changes are found in the airways of most patients with prolonged disease. After remodeling, the airway walls show the submucous membrane becomes thick with collagen deposition, and the smooth muscle cells show hyperplasia and hypertrophy. Smooth muscle cells are a vital component of the airway wall, and a major effector cell involved in the course of bronchial contraction. Smooth muscle cell hyperplasia and hypertrophy are important pathological changes in airway remodeling. This study investigated the expression of markers of human airway smooth muscle cells (ASMCs) phenotypic change, which were matrix Gla protein (MGP) and major fibrosis proteins, after in vitro treatment with transforming growth factor-beta(1) (TGF-beta(1)).</p><p><b>METHODS</b>Human ASMCs were subjected to primary culture in vitro. Ten groups of cells were treated with 100 microg/ml of TGF-beta(1), while the cells in the control groups were treated with 10% fetal bovine serum. After being cultured for 7 d, the cells of both groups were harvested. MGP mRNA expression was detected by RT-PCR. Protein levels of collagen I, III and V were determined by Western blot analysis.</p><p><b>RESULTS</b>Treated with TGF-beta(1), airway smooth muscle cells expressed MGP mRNA greater than controls [(62.3 +/- 13.1)% vs (27.4 +/- 11.4)%, P < 0.01]. Also, airway smooth muscle cells stimulated by TGF-beta(1) produced more collagen I, III and V than the control group (P < 0.01).</p><p><b>CONCLUSIONS</b>TGF-beta(1) induced expression of collagen III and V, which are early markers of the switch from a contractile to a synthetic phenotype in ASMCs. This induction is an indication that ASMCs have the potential to make this switch and that TGF-beta(1) is involved in airway remodeling.</p>

Effects of feeding intervention on development of eczema in atopy high-risk infants: an 18-month follow-up study / 中华儿科杂志

<p><b>OBJECTIVE</b>To assess the preventive effects of different dietary regimens on development of eczema and food allergy in infants at high-risk for allergy.</p><p><b>METHODS</b>Forty-six infants whose parents were atopic and umbilical cord IgE > 0.35 kU/L were enrolled in the study. The infants were randomly assigned at birth to one of 2 dietary regimen protocols: those in intervention group (23 cases) were breast fed till more than 4 months of age, then followed by feeding with partially hydrolyzed formula (pHF), combined solid foods avoidance until 4-month of age, egg, fish, shrimp avoidance until 12-month of age. The other 23 cases in non-intervention group were breast fed for less than 4 months, or bottle fed with cow's milk-based formula, egg yolk was introduced at 4-month of age, and egg white at 6-month of age, besides, no any other dietary avoidance was applied. All the infants were followed-up for 18 months. The primary end point was the presence of atopic eczema. Food allergy was detected by fresh food prick-to-prick tests or in vitro sIgE or Fx5E.</p><p><b>RESULTS</b>At 6 months, 12 months and 18 months, the incidence of eczema in intervention group was 4.3% (1/23), 8.7% (2/23), and 17.4% (4/23), respectively, which was significantly reduced as compared to that of the non-intervention group, which was 26.1% (6/23), 34.8% (8/23), and 39.1% (9/23), respectively. Food allergy was found in 13.0% (3/23) of intervention group and 34.8% (9/23) of non-intervention group by skin prick tests or sIgE. Egg white was the most common offending food.</p><p><b>CONCLUSION</b>Early life dietary interventions which included breastfeeding, delayed solid food introducing, pHF feeding, and high risk food avoidance could reduce the risk of atopic eczema and food allergy development, and was probably an effective primary intervention method for infants at high risk for atopy.</p>

Change of Helper T Lymphocyte Cell 1/Helper T Lymphocyte Cell 2 Cytokine in Food Allergy Animal Model / 实用儿科临床杂志

Objective To investigate the function of helper T lymphocyte cell(Th)1/Th2 cytokine in food allergy development.Methods A total 110 Balb/c mice were randomly divided into 2 groups:control group(40 mice)and food allergy group(70 mice).Food allergy animal models were established by ovalbumin,performed by skin prick test;in positive reaction mice,serum specific IgE,IL-4 and IFN-? were measured by enzyme linked immuosorbent assay(ELISA),and intestinal pathology were performed,and the mRNA expressions of IL-10,TGF-? in intestinal were measured by real-time PCR assay.Results In food allergy group,the mRNA expression of IL-10,TGF? in intestinal decreased(P