Objective To understand the infection status and gene types of Cryptosporidium among HIV/AIDS patients in Guangxi Zhuang Autonomous Region. Methods The fecal samples were collected from 285 HIV/AIDS cases in Nanning,Gui?lin,Qinzhou,Baise,Hechi cities of Guangxi and 150 HIV negative persons in Nanning City. The modified acid?fast staining and nested?PCR based on 18S rRNA were employed to detect the infection status of Cryptosporidium. The nested PCR products were sequenced,and the homology searches and identification for the gene types of Cryptosporidium were done by DNAStar soft?ware. Results The infection rate of Cryptosporidium in HIV/AIDS patients was 0.70%(2/285),and the rate of those with chronic diarrhea was 6.67%(2/30),the latter was significantly higher than that of the HIV negative persons(0,0/150)(P=0.002). Both the two HIV/AIDS patients infected with Cryptosporidium were from Guilin City. By molecular identification,the Cryptosporidium strains which the above 2 patients were infected with were Cryptosporidium andersoni and Cryptosporidium hominis respectively. Conclusions Cryptosporidium co?infection can be found in HIV/AIDS patients in Guangxi. The geno?types of the infection strains include Cryptosporidium andersoni and Cryptosporidium hominis.

Unlike healthy, non-transformed cells, the proteostasis network of cancer cells is taxed to produce proteins involved in tumor development. Cancer cells have a higher dependency on molecular chaperones to maintain proteostasis. The chaperonin T-complex protein ring complex (TRiC) contains eight paralogous subunits (CCT1-8), and assists the folding of as many as 10% of cytosolic proteome. TRiC is essential for the progression of some cancers, but the roles of TRiC subunits in osteosarcoma remain to be explored. Here, we show that CCT4/TRiC is significantly correlated in human osteosarcoma, and plays a critical role in osteosarcoma cell survival. We identify a compound anticarin-β that can specifically bind to and inhibit CCT4. Anticarin-β shows higher selectivity in cancer cells than in normal cells. Mechanistically, anticarin-β potently impedes CCT4-mediated STAT3 maturation. Anticarin-β displays remarkable antitumor efficacy in orthotopic and patient-derived xenograft models of osteosarcoma. Collectively, our data uncover a key role of CCT4 in osteosarcoma, and propose a promising treatment strategy for osteosarcoma by disrupting CCT4 and proteostasis.