Exposure of the Hidden Anti-Ferromagnetism in Paramagnetic CdSe:Mn Nanocrystals

We present theoretical and experimental investigations of the magnetism of paramagnetic semiconductor CdSe:Mn nanocrystals and propose an efficient approach to the exposure and analysis of the underlying anti-ferromagnetic interactions between magnetic ions therein. A key advance made here is the build-up of an analysis method with the exploitation of group theory technique that allows us to distinguish the anti-ferromagnetic interactions between aggregative Mn2+ ions from the overall pronounced paramagnetism of magnetic ion doped semiconductor nanocrystals. By using the method, we clearly reveal and identify the signatures of anti-ferromagnetism from the measured temperature dependent magnetisms, and furthermore determine the average number of Mn2+ ions and the fraction of aggregative ones in the measured CdSe:Mn nanocrystals.Comment: 26 pages, 5 figure

Digging deeper into the intronic sequences of the SPINK1 gene [Letter]

We read with great interest the recent paper by Beer and Sahin-Tóth1 addressing the ‘missing heritability’ observed in approximately 60% of German cases of chronic pancreatitis.2 These authors opined that ‘discovery studies tend to focus on exons and exon–intron boundaries and may thus miss many intronic variants’.1 This premise seems eminently reasonable, given the generally much larger size of intronic sequences as compared with the coding sequences of protein-coding genes. However, there is a trade-off here. On the one hand, larger sequence size means larger target size for mutation, and hence the greater the number of mutations that could be missed if intronic sequences were not screened. On the other hand, to be of pathological significance, an intronic mutation must either create a new functional splicing donor or acceptor site or alternatively impact a functional sequence motif responsible for regulating splicing (eg, an intronic splicing enhancer), which depends upon many additional factors other than just sequence length. As yet, it is unclear what the ratio of pathological intronic:exonic variants will turn out to be, although intronic mutations are

In silico prioritization and further functional characterization of SPINK1 intronic variants

Background SPINK1 (serine protease inhibitor, kazal-type, 1), which encodes human pancreatic secretory trypsin inhibitor, is one of the most extensively studied genes underlying chronic pancreatitis. Recently, based upon data from qualitative reverse transcription-PCR (RT-PCR) analyses of transfected HEK293T cells, we concluded that 24 studied SPINK1 intronic variants were not of pathological significance, the sole exceptions being two canonical splice site variants (i.e., c.87 + 1G > A and c.194 + 2T > C). Herein, we employed the splicing prediction tools included within the Alamut software suite to prioritize the ‘non-pathological’ SPINK1 intronic variants for further quantitative RT-PCR analysis. Results Although our results demonstrated the utility of in silico prediction in classifying and prioritizing intronic variants, we made two observations worth noting. First, we established that most of the prediction tools employed ignored the general rule that GC is a weaker donor splice site than the canonical GT site. This finding is potentially important because for a given disease gene, a GC variant donor splice site may be associated with a milder clinical manifestation. Second, the non-pathological c.194 + 13T > G variant was consistently predicted by different programs to generate a new and viable donor splice site, the prediction scores being comparable to those for the physiological c.194 + 2T donor splice site and even higher than those for the physiological c.87 + 1G donor splice site. We do however provide convincing in vitro evidence that the predicted donor splice site was not entirely spurious. Conclusions Our findings, taken together, serve to emphasize the importance of functional analysis in helping to establish or refute the pathogenicity of specific intronic variants

Toxoplasma gondii infection in farmed wild boars (Sus scrofa) in three cities of northeast China

The apicomplexan protozoan parasite Toxoplasma gondii is a widely distributed etiological agent of foodborne illness. This parasite can cause production losses in livestock and serious disease in humans through consumption of contaminated meat. Pig meat is the most likely source of human infection, and wild boars may play a role in the transmission of T. gondii by serving as a reservoir host. This study aimed to investigate the seroprevalence of antibodies to T. gondii among farmed wild boars in China. In an 11-month survey, a total of 882 serum samples were obtained from farmed wild boars from three cities (Jilin City, Siping City, and Baishan City) in Jilin province, Northeast China and were tested for antibodies specific for T. gondii. Using modified agglutination test and a cutoff titer of 1:25, the prevalence of T. gondii infection in the examined samples was 10.0% (88 of 882). The highest seroprevalence was observed in animals from Jilin city (15.3%, 43/281) and followed by Siping (11.4%, 30/263) and Baishan (4.4%, 15/338). Logistic regression analysis revealed a significant correlation between the investigated geographic region and T. gondii infection. In addition, prevalence was higher in females compared to males, and the highest prevalence was detected in piglets. These findings indicate that farmed wild boars may become a source of foodborne toxoplasmosis, posing a food safety threat to the public health in the investigated areas. Implementation of effective measures to control T. gondii infection in farmed wild boars in China may be warranted

Diaqua­bis­(5-carb­oxy-2-propyl-1H-imidazole-4-carboxyl­ato-κ2 N 3,O 4)cadmium(II) 3.5-hydrate

In the title complex, [Cd(C8H9N2O4)2(H2O)2]·3.5H2O, the CdII is coordinated by two water mol­ecules and N,O-chelated by two 5-carb­oxy-2-propyl-1H-imidazole-4-carboxyl­ate anions in a distorted octa­hedral geometry. The two imidazole rings are oriented to each other with a dihedral angle of 75.1 (2)°. Strong O—H⋯O hydrogen bonds between protonated and deprotonated carboxyl­ate groups occur in the mol­ecular structure. In the crystal structure extensive O—H⋯O and N—H⋯O hydrogen bonds help to stabilize the three-dimensional supra­molecular framework. The propyl groups of anions are disordered over two sites with refined occupancies of 0.768 (6):0.232 (6) and 0.642 (8):0.358 (8)

Toxocara canis Infection Alters lncRNA and mRNA Expression Profiles of Dog Bone Marrow

Bone marrow is the main hematopoietic organ that produces red blood cells, granulocytes, monocyte/macrophages, megakaryocytes, lymphocytes, and myeloid dendritic cells. Many of these cells play roles in the pathogenesis of Toxocara canis infection, and understanding how infection alters the dynamics of transcription regulation in bone marrow is therefore critical for deciphering the global changes in the dog transcriptional signatures during T. canis infection. In this study, long non-coding RNA (lncRNA) and messenger RNA (mRNA) expression profiles in the bone marrow of Beagle dogs infected with T. canis were determined at 12 h post-infection (hpi), 24 hpi, 96 hpi, and 36 days post-infection (dpi). RNA-sequencing and bioinformatics analysis identified 1,098, 984, 1,120, and 1,305 differentially expressed lncRNAs (DElncRNAs), and 196, 253, 223, and 328 differentially expressed mRNAs (DEmRNAs) at 12 h, 24 h, 96 h, and 36 days after infection, respectively. We also identified 29, 36, 38, and 68 DEmRNAs potentially cis-regulated by 44, 44, 51, and 80 DElncRNAs at 12 hpi, 24 hpi, 96 hpi, and 36 dpi, respectively. To validate the sequencing findings, qRT-PCR was performed on 10 randomly selected transcripts. Many altered genes were involved in the differentiation of bone marrow cells. GO of DElncRNAs and GO and KEGG pathway analyses of DEmRNAs revealed alterations in several signaling pathways, including pathways involved in energy metabolism, amino acid biosynthesis and metabolism, Wnt signaling pathway, Huntington's disease, HIF-1 signaling pathway, cGMP–PKG signaling pathway, dilated cardiomyopathy, and adrenergic signaling in cardiomyocytes. These findings revealed that bone marrow of T. canis-infected dogs exhibits distinct lncRNA and mRNA expression patterns compared to healthy control dogs. Our data provide novel insights into T. canis interaction with the definitive host and shed light on the significance of the non-coding portion of the dog genome in the pathogenesis of toxocariasis