The autoimmune regulator (Aire) controls iNKT cell development and maturation.

The mechanism underlying the autoimmune polyglandular syndrome type-1 (APS1) has been attributed to defective T-cell negative selection resulting from reduced expression and presentation of autoantigens in thymic medullary epithelial cells (MECs). It has also been postulated that Aire is involved in development of regulatory T cells, although supporting evidence is lacking. Here we show that expression of Aire in MECs is required for development of iNKT cells, suggesting a role for iNKT cells in APS1.

Characterization of PAF-AH Ib1 in NOD mice: PAF-AH may not be a candidate gene of the diabetes susceptibility Idd4.1 locus.

We recently mapped Idd4 to a 5.2 cM interval on chromosome 11 with two subloci, Idd4.1 and Idd4.2, in nonobese diabetic (NOD) mice. Based on the localization of platelet-activating factor acetylhydrolase Ib1 (PAF-AHIb1) and the decreased activity of PAF-AH in type 1 diabetes (T1D) patients, we hypothesized that PAF-AHIb1 in Idd4.1 is a candidate gene. The PAF-AHIb1 gene in NOD mice was cloned and sequenced, and its expression and function were studied. No polymorphisms were detected in PAF-AHIb1 cDNA between NOD and B6 mice. The expression of PAF-AH Ib1 at the mRNA and protein levels was found to be similar in different tissues between NOD and B6 mice. PAF-AH activity does not differ in the pancreatic islets or spleen between NOD and B6 mice. Our findings suggest that PAF-AH Ib1 may not be a diabetes-susceptibility gene in the Idd4.1 sublocus.

[Community structure of phytoplankton and its relationships with environmental factors in surface water of Ankang Reservoir, Northwest China].

To evaluate trophic state and biotic community as well as the relationship between phytoplankton community composition and environmental factors in surface water of Ankang Reservoir, the water and phytoplankton were sampled monthly from January to December in 2012. The phytoplankton distribution and the physical and chemical indicators were analyzed. The characteristics of phytoplankton community were studied via Shannon diversity index (H) and Pielou evenness index (J). The trophic level was assessed via physical and chemical indicators, and trophic state index (TSI). One hundred and ten genera belonging to seven phyla were identified. The abundance of phytoplankton ranged from 0.11 x 10(4) to 2.08x10(4) cells . L-1. The composition of phytoplankton and distribution of pollution indicator species, biodiversity and TSI indicated that surface water of Ankang Reservoir belonged to the ecological middling pollution type and was at a mesotrophic level. High-density feeding aquaculture and direct discharge of domestic wastewater had adverse effects on water quality. The water quality of Lanhe River, a tributary of Hanjiang River, was poor. Canonical correspondence analysis (CCA) showed that the impacts of the eight tested environmental factors on phytoplankton community composition and distribution varied in different seasons. Moreover, nitrogen was the main nutrient factor affecting the community composition of the phytoplankton. The physical and chemical indicators showed that the water quality of surface water of Ankang Reservoir was generally good and satisfied the standard of class II water. However, the quality of total nitrogen poorer than the standard of class II water in several sampling sites suggested that the water quality of Ankang Reservoir had the trend to be deteriorated.

[Cloning and analysis of three genes encoding type II CHH family neuropeptides from Fennropenaeus chinensis].

On the basis of sequence similarity, the crustean hyperglycemic hormone (CHH) family peptides have been classified into two types of hormones: type I and type II. Molt-inhibiting hormone (MIH) is a neuropeptide member of type II CHH family. Molting in shrimp is controlled by MIH and ecdysone. By inhibiting the synthesis of ecdysone in the Y-organ, MIH indirectly suppresses the molting activity of shrimp. In this study, we reported the cloning and characterization of 3 gene fragments encoding type II CHH family neuropeptides of the shrimp Fennropenaeus chinensis. According to the complementary DNA sequence of the mult-inhibiting hormone of Fennropenaeus chinensis, 3 primers were designed and synthesized. MP1 and MP2 are sense primers, and MP3 is anti-sense primer. Polymerase chain reaction was performed using genomic DNA of Fennropenaeus chinensis as template. Three PCR products were obtained using primers MP1 and MP3. Their sizes are about 600 bp, 850 bp, 1050 bp, respectively. A 580 bp PCR product was obtained using primers MP2 and MP3. All the 4 PCR products were cloned into pMD18-T vector. The recombinant clones were sequenced using ABI 310 Genetic Analyzer. After sequencing, all the DNA sequences were searched in the GenBank by Blast program to find similar gene sequences. The searching results revealed 3 DNA fragment sequences were of high similarity with CHH family neuropeptide genes from various crustean species. The 3 DNA fragments were named as NP1, NP2, and NP3. Their sizes were 540 bp, 601 bp, and 826 bp, respectively. Using the mRNA sequences with the most similarity to the 3 sequence fragments as reference, the gene structure of the 3 DNA fragment sequences was analyzed. The exons of 3 sequence fragments were aligned with their similar sequences by Clustal W program. Both NP1 and NP2 consisted of 1 intron and 2 exons. NP3 consisted of 2 introns and 3 exons. Sequence analysis suggested that these 3 products belonged to sequence fragments of neuropeptide gene of type II crustacean hyperglycemic hormone family. The exons of NP1, NP2, and NP3 had highest similarity respectively with mRNA of Pem-SCP-C2 and Pem-SGP-C1 both from Penaeus monodon, and FenchMIH from Fennropenaeus chinensis. The identities were 91.5%, 92.8%, 88.9%, respectively. The results suggest NP3 is a fragment of molt-inhibiting hormone gene of Fennropenaeus chinensis NP1 and NP2 are two fragments of neuropeptide genes of type II crustacean hyperglycemic hormone family, which were found in Fennropenaeus chinensis for the first time.

[Molecular cloning and sequence analysis of full length cDNA encoding molt-inhibiting hormone from Fennropenaeus chinensis].

Molt-inhibiting hormone (MIH) is a neuropeptide member belonging to the eyestalk CHH family. Molting in shrimp is controlled by MIH and ecdysone. By inhibiting the synthesis of ecdysone in the Y-organ, MIH indirectly suppress the molting activity of shrimp. A 697 bp full-length encoding molt-inhibiting hormone precursor cDNA, which has been accepted by GenBank (accession number: AF469187), was firstly amplified from the total RNA of eyestalk from Fennropenaeus chinensis by the 3' and 5' rapid amplification of cDNA ends (RACE) method. The 697 bp full-length cDNA encoding MIH precursor was assembled with a 320 bp 3' RACE product and 468 bp 5' RACE product. Results derived from searching by Blast revealed the 697 bp cDNA had high similarity with MIH gene of crustacean. By using Clustal X program, alignment of the amino acid sequence deduced from the 697 bp cDNA with amino acid sequences of 7 MIHs revealed that the deduced amino acid sequence had very high identity with amino acid sequences of MIHs of shrimps. The identities between the deduced amino acid sequence with that of MIH of Marsupenaeus japonicus, Penaeus monodon and Metapenaeus ensis were respectively 95.1%, 83.1% and 79.1%. On the base of all the data, we concluded that the 697 bp full-length cDNA was the cDNA encoding MIH precursor of F. chinensis. Sequence analysis of the 697 bp cDNA revealed a 312 bp open reading frame, and 81 bp 5' untranslated region, and a 302 bp 3' untranslated region. The deduced 103 amino acid polypeptide consisted of a 28 amino acid region of signal peptide and a 75 amino acid region of mature peptide. The six cysteine residues were very conserved in the mature peptide.

Disordered osteoclast formation in RAGE-deficient mouse establishes an essential role for RAGE in diabetes related bone loss.

The mechanisms underlying diabetes-mediated bone loss are not well defined. It has been reported that the advanced glycation endproducts (AGEs) and receptor for AGEs (RAGEs) are involved in diabetic complications. Here, mice deficient in RAGE were used as a model for investigating the effects of RAGE on bone mass. We found that RAGE-/- mice have a significantly increased bone mass and bone biomechanical strength and a decreased number of osteoclasts compared to wild-type mice. The serum levels of IL-6 and bone breakdown marker pyridinoline were significantly decreased in RAGE-/- mice. RAGE-/- mice maintain bone mass following ovariectomy, whereas wild-type mice lose bone mass. Furthermore, osteoclast-like cells do express RAGE mRNA. Our data therefore indicate that RAGE serves as a positive factor to regulate the osteoclast formation, directly implicates a role for RAGE in diabetes-promoted bone destruction, and documents that the AGE-RAGE interaction may account for diabetes associated bone loss.