Background Despite a recent upsurge of HIV/AIDS epidemic among young people in China, youth-specific HIV data were limited. Methods Altogether 56621 HIV/AIDS cases, aged 15–24, registered in the Case Reporting System of China between 2005 and 2012 and having complete spatial information were included in the present analysis. Spatial autocorrelation (general and local) and space-time scanning were performed using ArcGIS10.2 and SaTScan 9.3 software, respectively. Results During 2005–2012, the number of reported HIV/AIDS cases and proportion of HIV cases increased while proportion of AIDS cases decreased. Sexual contact evolved as the pre-dominant route of transmission in later years. Spatial analysis showed marked geographic variations of HIV infection among young people throughout China during 2005–2012. The number of new hotspots increased over years. They were mainly localized in southeast coastal areas and southwest bordering provinces or autonomous regions of Guangxi, Yunnan and Sichuan and Beijing municipality. Later these hotspots shifted towards northeastern part. Significant clusters of HIV positive cases were identified in three different time-periods, which indicated high HIV transmission among young Chinese in the recent past. The risk of HIV was highest in the first cluster (2009–2012, largest in size) covering Guizhou and Yunnan province, Chongqing municipality, Guangxi and Sichuan province. The second cluster (2010–2012) was mostly located in Shanghai, South Jiangsu, Zhejiang and South Anhui area while the third cluster (2010–2012) was in Beijing and Tianjin. Conclusions Target-specific comprehensive behavioral interventions were urgently needed to contain further spread of HIV epidemic among young people.

The Usher syndrome type IC {USHIC} and familial hyperinsulinism [HI) loci have been assigned to chromosome Ilpl4-15.1, within the interval DIIS419-DI1SI310. We have constructed a yeast artificial chromosome {YAC} contig, extending from D11S926 to DIIS899, which encompasses the critical regions for both USHIC and HI and spans an estimated genetic distance of ---4 cM. A minimal set of six YAC clones constitute the contig, with another 22 YACs confirming the order of sequence-tagged sites [STSs) and position of YACs on the contig. A total of 40 STSs, including 10 new STSs generated from YAC insert-end sequences and inter-A/u PCR products, were used to order the clones within the contig. This physical map provides a resource for identification of gene transcripts associated with USHIC, HI, and other genetic disorders that map to the DllS?26-DIIS899 interval.

Background: Epirubicin is a potent chemotherapeutic agent for the treatment of breast cancer. However, it may lead to cardiotoxicity and cardiomyopathy, and no reliable biomarker was available for the early prediction of epirubicin-induced cardiomyopathy. Methods: Global gene expression changes of peripheral blood cells were studied using high-throughput RNA sequencing in three pair-matched breast cancer patients (patients who developed symptomatic cardiomyopathy paired with patients who did not) before and after the full session of epirubicin-based chemotherapy. Functional analysis was conducted using gene ontology and pathway enrichment analysis. Results: We identified 13 significantly differentially expressed genes between patients who developed symptomatic epirubicin-induced cardiomyopathy and their paired control who did not. Among them, the upregulated Bcl-associated X protein was related to “apoptosis,” while the downregulated 5′-aminolevulinate synthase 2 (ALAS2) was related to both “glycine, serine, and threonine metabolism” and “porphyrin and chlorophyll metabolism” in pathway enrichment analysis. Conclusions: ALAS2 and the metabolic pathways which were involved may play an important role in the development of epirubicin-induced cardiomyopathy. ALAS2 may be useful as an early biomarker for epirubicin-induced cardiotoxicity detection.

Our findings expand the spectrum of ALMS1 gene mutations causing Alström syndrome and further confirm the role of ALMS1 gene in the pathogenesis of Alström syndrome.