Personal non-commercial use only

ABSTRACT. Objective. To investigate whether development of systemic lupus erythematosus (SLE), its clinical manifestations, and autoantibody production are associated with polymorphisms of the mannose-binding lectin Conclusion. A significantly increased prevalence of anti-Smith antibody was associated with the heterozygous genotypes A/B and A/C. Although MBL structural gene polymorphism was not a risk factor for SLE development in this study population, homozygosity of MBL variant alleles may be a weak disease-modifying factor, particularly for renal involvement, in North American patients with SLE

Central nervous system (CNS)–resident natural killer cells suppress Th17 responses and CNS autoimmune pathology

Natural killer (NK) cells of the innate immune system can profoundly impact the development of adaptive immune responses. Inflammatory and autoimmune responses in anatomical locations such as the central nervous system (CNS) differ substantially from those found in peripheral organs. We show in a mouse model of multiple sclerosis that NK cell enrichment results in disease amelioration, whereas selective blockade of NK cell homing to the CNS results in disease exacerbation. Importantly, the effects of NK cells on CNS pathology were dependent on the activity of CNS-resident, but not peripheral, NK cells. This activity of CNS-resident NK cells involved interactions with microglia and suppression of myelin-reactive Th17 cells. Our studies suggest an organ-specific activity of NK cells on the magnitude of CNS inflammation, providing potential new targets for therapeutic intervention

Analysis of the Degradation Characteristics of Chlorpyrifos in an Electrochemically Constructed Wetland Coupled System under Different Pesticide Exposure Conditions and Microbial Community Analysis

This study investigates the degradation characteristics of chlorpyrifos under individual exposure and compound exposure to multiple pesticides in both traditional constructed wetlands and electrochemically constructed wetland coupled systems, while also analyzing the microbial communities within the systems using high-throughput sequencing technology. The results show that the electric field can enhance the degradation performance of the system. The degradation effect of the coupled electrochemically constructed wetland coupled system is better than that of the traditional constructed wetland, while the compound exposure to multiple pesticides inhibits the degradation efficiency. Under the influence of pesticides, the diversity of microbial communities decreases towards the end of the system operation, and the electrochemically constructed wetland coupled system exhibits lower diversity compared to the traditional constructed wetland. Proteobacteria is the dominant phylum under compound exposure to multiple pesticides, while Firmicutes, Fusobacteria, Verrucomicrobia, Aeromonas, and Methylophilus are the dominant electrochemically active phyla and genera in the electrochemically constructed wetland coupled system. The impact of pesticides and the electric field results in a decrease in amino acid metabolism and carbohydrate metabolism functions, while membrane transport functions increase. The compound exposure to multiple pesticides has a more significant impact on the microbial community structure and functionality than the electric field. The results also lay a theoretical foundation for the expansion of pesticide degradation technology and constructed wetland treatment technology to new fields, which is of great significance in realizing the “zero direct discharge” of agricultural production wastewater, solving the problem of agricultural non-point source pollution and ensuring the availability of agricultural production

Changes in Biochemical Properties and Activity of Trypsin-like Protease (Litopenaeus vannamei) Treated by Atmospheric Cold Plasma (ACP)

The changes in the functional properties of trypsin from shrimps (Litopenaeus vannamei) after, Atmospheric Cold Plasma (ACP) treatments, have been evaluated in terms of enzyme inactivation, surface hydrophobicity, secondary structure, fluorescence intensity, and particle size distribution. Different exposure voltages of 10, 20, 30, 40, and 50 kV at various treatment times (1, 2, 3, and 4 min) have been employed, in a separate assay. The results showed that trypsin-like protease activity decreased (by about 50%), and the kinetic constants Km value increased, while the kcat value decreased. Surface hydrophobicity and fluorescence intensity revealed a significant increase compared to the control sample. A high degree of protein degradation has been noticed by SDS-PAGE analysis. In addition, circular dichroism indicated that random coil and α-helix contents declined while β-turn and β-sheet contents have raised. A sharp drop in the particle size was observed with increasing the treatment voltage from 0 to 40 kV for 4 min, and the corresponding peak reached the minimum of 531.2 nm. Summing up the results, it can be concluded that the ACP technique effectively affects the activity of trypsin-like protease, which in terms enhances the quality of dietary protein

Enhancement of surimi gel properties through the synergetic effect of fucoidan and oligochitosan

For the first time, two common marine-derived dietary fibres (MDFs), fucoidan (FU) and oligochitosan (OCS), were introduced as textural and nutritional enhancers in hairtail surimi gels. The MDFs could assist with inhabiting the endogenous proteolytic enzyme activity, unfolding the myosin to expose more reactive domains, inducing favorable protein conformational transition, and thus, promoting gelation. The highly hydrophilic MDFs rich in –OH groups can bind water molecules via strong hydrogen bonds, facilitating water redistribution within the gel network. Driven by the enhanced chemical forces, a stable protein-FU-OCS gel is obtained, which improves the hardness by almost 100% and the water holding capacity from 86.25% to 92.25%. Collectively, this study demonstrates that MDFs are a group of effective additives to improve gel characteristics and nutritional profiles of surimi-based seafood products. The proposed MDF-protein interaction model would guide the application of MDFs as novel additives in the food industry.</p

Central nervous system (CNS)-resident natural killer cells suppress Th17 responses and CNS autoimmune pathology.

Natural killer (NK) cells of the innate immune system can profoundly impact the development of adaptive immune responses. Inflammatory and autoimmune responses in anatomical locations such as the central nervous system (CNS) differ substantially from those found in peripheral organs. We show in a mouse model of multiple sclerosis that NK cell enrichment results in disease amelioration, whereas selective blockade of NK cell homing to the CNS results in disease exacerbation. Importantly, the effects of NK cells on CNS pathology were dependent on the activity of CNS-resident, but not peripheral, NK cells. This activity of CNS-resident NK cells involved interactions with microglia and suppression of myelin-reactive Th17 cells. Our studies suggest an organ-specific activity of NK cells on the magnitude of CNS inflammation, providing potential new targets for therapeutic intervention

Insulin-like growth factor-I receptor blockade reduces the invasiveness of gastrointestinal cancers via blocking production of matrilysin

Insulin-like growth factor-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal (GI) cancers. We have previously shown significant therapeutic activity for recombinant adenoviruses expressing dominant-negative insulin-like growth factor-I receptor (IGF-IR/dn), including suppression of tumor invasion. In this study, we sought to evaluate the mechanism of inhibition of invasion and the relationship between IGF-IR and matrix metalloproteinase (MMP) activity in GI carcinomas. We analyzed the role of IGF-IR on invasion in three GI cancer cell lines, colorectal adenocarcinoma, HT29; pancreatic adenocarcinoma, BxPC3 and gastric adenocarcinoma, MKN45, using a modified Boyden chamber method and subcutaneous xenografts in nude mice. The impact of IGF-IR signaling on the expression of MMPs and the effects of blockade of matrilysin or IGF-IR on invasiveness were assessed using recombinant adenoviruses, a tyrosine kinase inhibitor NVP-AEW541 and antisense matrilysin. Invasive subcutaneous tumors expressed several MMPs. IGF-IR/dn reduced the expression of these MMPs but especially matrilysin (MMP-7). Insulin-like growth factor (IGF) stimulated secretion of matrilysin and IGF-IR/dn blocked IGF-mediated matrilysin induction in three GI cancers. Both IGF-IR/dn and inhibition of matrilysin reduced in vitro invasion to the same degree. NVP-AEW541 also reduced cancer cell invasion both in vitro and in murine xenograft tumors via suppression of matrilysin. Thus, blockade of IGF-IR is involved in the suppression of cancer cell invasion through downregulation of matrilysin. Strategies of targeting IGF-IR may have significant therapeutic utility to prevent invasion and progression of human GI carcinomas.Piao WH, 2008, MOL CANCER THER, V7, P1483, DOI 10.1158/1535-7163.MCT-07-2395Miyamoto S, 2007, CANCER SCI, V98, P685Imsumran A, 2007, CARCINOGENESIS, V28, P947, DOI 10.1093/carcin/bgl247Mitsui Y, 2006, CANCER RES, V66, P9913, DOI 10.1158/0008-5472.CAN-06-0377Girnita A, 2006, CLIN CANCER RES, V12, P1383, DOI 10.1158/1078-0432.CCR-05-1106Harper J, 2006, CANCER RES, V66, P1940, DOI 10.1158/0008-5472.CAN-05-2036ADACHI Y, 2006, DIGEST ENDOSC, V18, P245Shimizu M, 2005, BIOCHEM BIOPH RES CO, V334, P947, DOI 10.1016/j.bbrc.2005.06.182Nakamura M, 2005, BIOCHEM BIOPH RES CO, V333, P1011, DOI 10.1016/j.bbrc.2005.06.010Min Y, 2005, GUT, V54, P591, DOI 10.1136/gut.2004.048926Nosho K, 2005, BRIT J CANCER, V92, P1193, DOI 10.1038/sj.bjc.6602442Foulstone E, 2005, J PATHOL, V205, P145, DOI 10.1002/path.1712Nosho K, 2004, CLIN CANCER RES, V10, P7950Garcia-Echeverria C, 2004, CANCER CELL, V5, P231Mochizuki S, 2004, BIOCHEM BIOPH RES CO, V315, P79, DOI 10.1016/j.bbrc.2004.01.022Miyamoto S, 2004, CANCER RES, V64, P665Burtrum D, 2003, CANCER RES, V63, P8912Pavelic K, 2003, J PATHOL, V201, P430, DOI 10.1002/path.1465Min YF, 2003, CANCER RES, V63, P6432Zhang DL, 2003, ONCOGENE, V22, P974, DOI 10.1038/sj.onc.1206197Adachi Y, 2002, GASTROENTEROLOGY, V123, P1191, DOI 10.1053/gast.2002.36023Adachi Y, 2001, TUMOR BIOL, V22, P247Dunn SE, 2001, CANCER RES, V61, P1367Yu H, 2000, J NATL CANCER I, V92, P1472Adachi Y, 1999, GUT, V45, P252Yamamoto H, 1999, CANCER RES, V59, P3313Freier S, 1999, GUT, V44, P704Ma J, 1999, J NATL CANCER I, V91, P620Simmons JG, 1999, AM J PHYSIOL-GASTR L, V276, pG817Mira E, 1999, ENDOCRINOLOGY, V140, P1657Yamamoto H, 1999, JPN J CLIN ONCOL, V29, P58Adachi Y, 1998, INT J ONCOL, V13, P1031Long L, 1998, CANCER RES, V58, P3243Yamamoto H, 1997, GASTROENTEROLOGY, V112, P1290Wilson CL, 1997, P NATL ACAD SCI USA, V94, P1402StetlerStevenson WG, 1996, SEMIN CANCER BIOL, V7, P147Crawford HC, 1996, ENZYME PROTEIN, V49, P20BERGMANN U, 1995, CANCER RES, V55, P2007YAMAMOTO H, 1995, INT J CANCER, V61, P218BASERGA R, 1995, CANCER RES, V55, P249BASERGA R, 1994, CELL, V79, P927SELL C, 1993, P NATL ACAD SCI USA, V90, P11217LIU JP, 1993, CELL, V75, P59YOSHIMOTO M, 1993, INT J CANCER, V54, P614REMACLEBONNET M, 1992, INT J CANCER, V52, P910MIYAZAKI K, 1990, CANCER RES, V50, P7758THOMPSON MA, 1990, ENDOCRINOLOGY, V126, P3033WOESSNER JF, 1988, J BIOL CHEM, V263, P16918ULLRICH A, 1986, EMBO J, V5, P2503LIOTTA LA, 1986, CANCER RES, V46, P1