Interconnected Microdomain Structure of a Cross-Linked Cellulose Nanocomposite Revealed by Micro-Raman Imaging and Its Influence on Water Permeability of a Film.

Substantial adsorption of water vapor triggered by hydrogen-bonding interactions between water molecules and cellulose chains (or nanoplates) is hard to avoid in nanocomposite films, although the addition of nanoplates can improve the oxygen (or carbon dioxide) barrier property. In the present work, an effective strategy is raised to decline adsorption by weakening hydrogen-bonding interactions via chemical cross-linking by epichlorohydrin (ECH) without sacrificing the homogeneous dispersion of nanoplates. The generated microdomain structure of the chemical cross-linking reaction via ECH is explicitly revealed by micro-Raman imaging. Unambiguously, Raman maps of scanning elucidate the distribution and morphology of physical and chemical cross-linking domains quantitatively. The chemical cross-linking domains are nearly uniformly located in the matrix at a low degree of cross-linking, while the interconnected and assembled networks are formed at a high degree of cross-linking. ECH boosts the formation of chemical cross-linking microdomains, bringing out the terrific water vapor barrier property and alleviating the interfacial interactions in penetration, consequently magnifying the water contact angle and holding back the water vapor permeability. Our methodology confers an effective and convenient strategy to obtain remarkable water vapor-resistant cellulose-based films that meet the practical application in the packaging fields.

Concise asymmetric synthesis of (+)-CP-99,994 and (+)-L-733,060 via efficient construction of homochiral syn-1,2-diamines and syn-1,2-amino alcohols.

An efficient asymmetric synthesis of human NK-1 SP receptor antagonists (+)-CP-99,994 and (+)-L-733,060 was achieved starting from a common chiral intermediate (5). Our route featured the SmI2-induced reductive coupling of N-tert-butanesulfinyl imine (7) with aldehyde (6) as the key step as well as pivotal transformations of the anti-1,2-amino alcohol thus obtained to homochiral syn-1,2-amino alcohol and syn-1,2-diamine for the asymmetric synthesis of 2,3-disubstituted piperidines.

[Study on the relationship between microsatellite alterations of RASSF1A gene and the development of cervical carcinoma].

OBJECTIVE: To explore the relationship between microsatellite alterations of RASSF1A gene and the development of cervical carcinoma, and HPV16 infection. METHODS: Two sites of microsatellite polymorphism of RASSF1A gene were selected, we used polymerase chain reaction (PCR) technique to detect the LOH and MSI of cervical tissues, and to detect the infection state of HPV16. RESULTS: There were significant differences of LOH rates at the two sites between clinical stage and pathological grade (P < 0.05). Significant differences were noted between the cervical carcinomas with lymph node metastasis and those without lymph node metastasis in regard to their LOH and MSI at the two sites ( P < 0.05). The incidence of LOH of RASSF1A gene was higher in HPV16(+) than that in HPV16(-) ( P < 0.05). CONCLUSION: The change of RASSF1A gene is a relatively late event in cervical carcinomas. The detection of the LOH and MSI of RASSF1A gene might be helpful to the early diagnosis and the screening of cervical carcinoma. It might also be useful for predicting the prognosis of cervical carcinoma. Infection of HPV16 and LOH of RASSF1A gene had reacted together in the development of cervical carcinoma.

Effect of blockage of costimulatory signal on murine abortion-prone model.

BACKGROUND: Inhibition of the key costimulatory signals results in T cell anergy, indicating the alloantigen-specific immunologic unresponsiveness. In this study, the effect of blockage of costimulatory signal CD(86) on murine abortion-prone model was studied. METHODS: Thirty CBA/J female mice cohabitated with DBA/2 male or BALB/c male mice were investigated. CBA/J x DBA/2 matings were used as the abortion-prone model, and CBA/J x BALB/c matings were used as the normal pregnant model. The abortion-prone models were divided into experimental and control groups, and the normal pregnant models were set as a normal group (10 mice in each group). The mice in the experimental group were treated with anti-mouse CD(86) monoclonal antibody (mAb) (100 microg) on day 4.5 of gestation, while the controls received irrelevant-isotype matched rat IgG(2b). As for the normal group, nothing was given to the mice. The mice were killed on day 13.5 of gestation, embryo resorption rate and the expression of transforming growth factor beta(1) (TGF-beta(1)), plasminogen activator inhibitor 1 (PAI-1), and matrix metalloproteinase 9 (MMP-9) were detected. Then the data were analyzed by Chi-square test and Fisher's exact test. RESULTS: The embryo resorption rate in the experimental (8.2%) and normal groups (7.7%) was significantly lower than that of the control (23.5%, P < 0.05). No significant difference was detected between the experimental and normal groups (P > 0.05). The positive expression rates of TGF-beta(1) and PAI-1 proteins in the experimental and normal groups were significantly higher than those in the control group (P < 0.05). The positive expression rate of MMP-9 protein in the experimental and normal groups was significantly lower than that in the control group (P < 0.05). No significant difference in the positive expression rates of the three proteins was detected between the experimental and normal groups (P > 0.05). CONCLUSIONS: Blockage of costimulatory signal CD(86) at early pregnancy can treat uncertain recurrent spontaneous abortion by stimulating the expression of TGF-beta(1), MMP-9 and PAI-1 and reducing the embryo resorption rate.

A dinucleotide deletion in CD24 confers protection against autoimmune diseases.

It is generally believed that susceptibility to both organ-specific and systemic autoimmune diseases is under polygenic control. Although multiple genes have been implicated in each type of autoimmune disease, few are known to have a significant impact on both. Here, we investigated the significance of polymorphisms in the human gene CD24 and the susceptibility to multiple sclerosis (MS) and systemic lupus erythematosus (SLE). We used cases/control studies to determine the association between CD24 polymorphism and the risk of MS and SLE. In addition, we also considered transmission disequilibrium tests using family data from two cohorts consisting of a total of 150 pedigrees of MS families and 187 pedigrees of SLE families. Our analyses revealed that a dinucleotide deletion at position 1527 approximately 1528 (P1527(del)) from the CD24 mRNA translation start site is associated with a significantly reduced risk (odds ratio = 0.54 with 95% confidence interval = 0.34-0.82) and delayed progression (p = 0.0188) of MS. Among the SLE cohort, we found a similar reduction of risk with the same polymorphism (odds ratio = 0.38, confidence interval = 0.22-0.62). More importantly, using 150 pedigrees of MS families from two independent cohorts and the TRANSMIT software, we found that the P1527(del) allele was preferentially transmitted to unaffected individuals (p = 0.002). Likewise, an analysis of 187 SLE families revealed the dinucleotide-deleted allele was preferentially transmitted to unaffected individuals (p = 0.002). The mRNA levels for the dinucleotide-deletion allele were 2.5-fold less than that of the wild-type allele. The dinucleotide deletion significantly reduced the stability of CD24 mRNA. Our results demonstrate that a destabilizing dinucleotide deletion in the 3' UTR of CD24 mRNA conveys significant protection against both MS and SLE.

The expression and functional role of nicotinic acetylcholine receptors in rat adipocytes.

To clarify whether nicotine has a direct effect on the function of adipocytes, we evaluated nicotinic acetylcholine receptor (nAChR) expression in adipocytes by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry and the direct effects of nicotine on the production of adipocytokines by enzyme-linked immunosorbent assay and Western blot analysis. Receptor binding assays were performed using [3H]nicotine. RT-PCR studies revealed that alpha1-7, 9, 10, beta1-4, delta, and epsilon subunit mRNAs are expressed in adipocytes. Immunocytochemical experiments also suggested the presence of alpha7 and beta2 subunits. The receptor binding assay revealed a binding site for nicotine (Kd = 39.2 x 10(-9) M) on adipocytes. Adipocytes incubated with nicotine for 12 and 36 h released tumor necrosis factor-alpha (TNF-alpha), adiponectin, and free fatty acid (FFA) into the medium in a dose-dependent manner with increasing nicotine concentration from 6 x 10(-8) to 6 x 10(-4) M. However, TNF-alpha protein levels in adipocytes incubated for 12 and 36 h decreased in a dose-dependent manner with increasing nicotine concentration from 6 x 10(-8) to 6 x 10(-4) M. These results show that adipocytes have functional nAChRs and suggest that nicotine reduces TNF-alpha protein production in adipocytes through the activation of nAChRs. Nicotine may temporarily lower insulin sensitivity by stimulating the secretion of TNF-alpha and FFA, whereas long-term direct stimulation of nAChRs by nicotine in addition to autonomic nervous system stimulation may contribute to better insulin sensitivity in vivo through a modulated secretion of adipocytokines.

Long-term oral nicotine administration reduces insulin resistance in obese rats.

This study aimed to investigate the effect of long-term oral nicotine administration on insulin resistance in an animal model of obesity. Eight-week-old male Zucker fatty rats (ZFRs) were administered nicotine tartrate dihydrate (4.6 mg/kg/day) in the drinking water. The control group was pair-fed. The body weights and food intake over 8 weeks were similar in both groups. Plasma glucose levels at 3, 6, 9, 12, and 15 min after insulin administration (0.5 U/kg) in the nicotine group were significantly lower than those in the control group. The calculated K(ITT) value for the nicotine group was significantly higher than that for the control group. Wet weight of the liver in the nicotine group was significantly lower than that in the control group. Transaminases and histological examination of the liver revealed no alteration by nicotine administration. Glycogen, glycogen synthetase activity and gluconeogenesis in the liver in the nicotine group were significantly lower than those in the control group. Phosphorylase-a activity of the liver in the nicotine group was significantly higher than that in the control group. Glycogen, glycogen synthetase, and phosphorylase-a activity of skeletal muscle were similar in both groups. These results suggest that long-term oral nicotine administration may reduce insulin resistance in obese diabetic rats through a reduced hepatic glucose release and, in part, contribute to lowering blood glucose levels.