Effect of Gradually Decreasing Photoperiod on Immune Function in Siberian Hamsters

Animals usually use photoperiod as an important environmental cue to time the year. In terms of the winter immunocompetence enhancement hypothesis, animals in the non-tropical zone would actively enhance their immune function to decrease the negative influence of stressors such as low temperature and food shortage in winter. In the present study, we mimicked the transition from summer to winter by decreasing photoperiod gradually and examined the variations of immune repsonses in Siberian hamsters (Phodopus sungorus)  to test this hypothesis. Twenty two female adult hamsters were randomly divided into the control (12h light: 12h dark, Control, n=11) and the gradually decreasing photoperiod group (Experiment, n=11). In the experiment group, day length was decreased from 12 h: 12 h light-dark cycle to 8 h: 16 h light-dark cycle at the pace of half an hour per week. We found that gradually decreasing photoperiod had no effect on body composition (wet carcass mass, subcutaneous, retroperitoneal, mesenteric and total body fat mass) and the masses of the organs detected such as brain, heart, liver and so on in hamsters. Similarly, immunological parameters including immune organs (thymus and spleen), white blood cells and serum bacteria killing capacity indicative of innate immunity were also not influenced by gradually decreasing photoperiod, which did not support the winter immunocompetence enhancement hypothesis. However, gradually decreasing photoperiod increased phytohaemagglutinin response post-24h of PHA challenge, which supported this hypothesis. There was no correlation between cellular, innate immunity and body fat mass, suggesting that body fat was not the reasons of the changes of cellular immunity. In summary, distinct components of immune system respond to gradually decreasing photoperiod differently in Siberian hamsters

Model to predict cause‐specific mortality in patients with olfactory neuroblastoma: a competing risk analysis

Abstract Purpose The main objective of this study was to evaluate the cumulative incidence of cause-specific mortality and other causes of mortality for patients with olfactory neuroblastoma (ONB). The secondary aim was to model the probability of cause-specific death and build a competing risk nomogram to predict cause-specific mortality for this disease. Methods Patients with ONB from 1975 to 2016 were identified from the Surveillance, Epidemiology, and End Results database. We estimated the cumulative incidence function (CIF) for cause-specific mortality and other causes of mortality, and constructed the Fine and Gray’s proportional subdistribution hazard model, as well as a competing-risk nomogram based on Fine and Gray’s model, to predict the probability of cause-specific mortality for patients with ONB. Results After data selection, 826 cases were included for analysis. Five-year cumulative incidence of cause-specific mortality was 19.5% and cumulative incidence of other causes of mortality was 11.3%. Predictors of cause-specific mortality for ONB included tumor stage, surgery and chemotherapy. Age was most strongly predictive of other causes of mortality: patients aged > 60 years exhibited subdistribution hazard ratios of 1.063 (95 % confidence interval [CI] 1.05–1.08; p = 0.001). The competing risk nomogram for cause-specific mortality was well-calibrated, and had good discriminative ability (concordance index = 0.79). Conclusions We calculated the CIF of cause-specific mortality and other causes of mortality in patients with the rare malignancy ONB. We also built the first competing risk nomogram to provide useful individualized predictive information for patients with ONB

Enzyme-Antibody-Modified Gold Nanoparticle Probes for the Ultrasensitive Detection of Nucleocapsid Protein in SFTSV

As humans and climate change continue to alter the landscape, novel disease risk scenarios have emerged. Sever fever with thrombocytopenia syndrome (SFTS), an emerging tick-borne infectious disease first discovered in rural areas of central China in 2009, is caused by a novel bunyavirus (SFTSV). The potential for SFTS to spread to other countries in combination with its high fatality rate, possible human-to-human transmission, and extensive prevalence among residents and domesticated animals in endemic regions make the disease a severe threat to public health. Because of the lack of preventive vaccines or useful antiviral drugs, diagnosis of SFTS is the key to prevention and control of the SFTSV infection. The development of serological detection methods will greatly improve our understanding of SFTSV ecology and host tropism. We describe a highly sensitive protein detection method based on gold nanoparticles (AuNPs) and enzyme-linked immunosorbent assay (ELISA)—AuNP-based ELISA. The optical sensitivity enhancement of this method is due to the high loading efficiency of AuNPs to McAb. This enhances the concentration of the HRP enzyme in each immune sandwich structure. The detection limit of this method to the nucleocapsid protein (NP) of SFTSV was 0.9 pg mL−1 with good specificity and reproducibility. The sensitivity of AuNP-based ELISA was higher than that of traditional ELISA and was comparable to real-time quantitative polymerase chain reaction (qRT-PCR). The probes are stable for 120 days at 4 °C. This can be applied to diagnosis and hopefully can be developed into a commercial ELISA kit. The ultrasensitive detection of SFTSV will increase our understanding of the distribution and spread of SFTSV, thus helping to monitor the changes in tick-borne pathogen SFTSV risk in the environment

H10Nx avian influenza viruses detected in wild birds in China pose potential threat to mammals

H10 subtype avian influenza viruses (AIVs) have been isolated from wild and domestic avian species worldwide and have occasionally crossed the species barrier to mammalian hosts. Fatal human cases of H10N8 infections and the recent detection of human H10N3 infections have drawn widespread public attention. In this study, 25 H10Nx viruses were isolated from wild waterfowl in China during a long-term surveillance of AIVs. We conducted phylogenetic and phylogeographic studies of the hemagglutinin (HA) genes of global H10 viruses to determine the spatiotemporal patterns of spread and the roles of different hosts in viral transmission. We found the pattern of AIV transmission from wild birds to poultry to humans, and Anatidae have acted as the seeding population in the spread of the virus. Phylogenetic incongruence indicated complex reassortment events and our isolates were divided into eight genotypes (G1–8). We also found that the HA genes of the G8 viruses belonged to the North American lineage, indicating that intercontinental gene flow has occurred. Their receptor-binding specificity showed that the G1/4/5/6/7/8 viruses bind to both human-type α2,6-linked sialic acid receptors and avian-type α2,3-linked sialic acid receptors. Mouse studies indicated that the H10Nx isolates replicated efficiently in the respiratory system without preadaptation, but showed low pathogenicity in mice. The H10Nx isolates showed no (G2/4/7) or low pathogenicity (G1/3/5/6/8) in chickens, and the G6 and G8 viruses could be transmitted to chickens through direct contact. The asymptomatic shedding of these wild-bird-origin H10Nx isolates in chickens and their good adaptation in mice should increase the ease of their transmission to humans, and they therefore pose a threat to public health. Our findings demonstrate a further understanding of wild bird-origin H10 viruses and provide information for the continuous surveillance of H10 subtype viruses