RESUMO
The cerebellum is conceptualized as a processor of complex movements and is also endowed with roles in cognitive and emotional behaviors. Although the axons of deep cerebellar nuclei are known to project to primary thalamic nuclei, macroscopic investigation of the characteristics of these projections, such as the spatial distribution of recipient zones, is lacking. Here, we studied the output of the cerebellar interposed nucleus (IpN) to the ventrolateral (VL) and centrolateral (CL) thalamic nuclei using electrophysiological recording in vivo and trans-synaptic viral tracing. We found that IpN stimulation induced mono-synaptic evoked potentials (EPs) in the VL but not the CL region. Furthermore, both the EPs induced by the IpN and the innervation of IpN projections displayed substantial heterogeneity across the VL region in three-dimensional space. These findings indicate that the recipient zones of IpN inputs vary between and within thalamic nuclei and may differentially control thalamo-cortical networks.
RESUMO
The cerebellum is conceptualized as a processor of complex movements and is also endowed with roles in cognitive and emotional behaviors. Although the axons of deep cerebellar nuclei are known to project to primary thalamic nuclei, macroscopic investigation of the characteristics of these projections, such as the spatial distribution of recipient zones, is lacking. Here, we studied the output of the cerebellar interposed nucleus (IpN) to the ventrolateral (VL) and centrolateral (CL) thalamic nuclei using electrophysiological recording in vivo and trans-synaptic viral tracing. We found that IpN stimulation induced mono-synaptic evoked potentials (EPs) in the VL but not the CL region. Furthermore, both the EPs induced by the IpN and the innervation of IpN projections displayed substantial heterogeneity across the VL region in three-dimensional space. These findings indicate that the recipient zones of IpN inputs vary between and within thalamic nuclei and may differentially control thalamo-cortical networks.
Assuntos
Axônios , Núcleos Cerebelares , Cerebelo , Núcleos TalâmicosRESUMO
BACKGROUND: Opportunistic infection of Candida albicans (C. albicans) has become a serious problem in immunocompromised patients. The study aimed to explore the mechanism of enterogenous infection of C. albicans in immunocompromised rats under severe acute pancreatitis (SAP). METHODS: Sprague Dawley (SD) rats (n=100) were randomly assigned into 5 groups as the following: blank group, cyclophosphamide+ceftriaxone+SAP group, cyclophosphamide+ceftriaxone group, cyclophosphamide+SAP group, and cyclophosphamide group. The rats were sacrificed at 5 and 10 days, and their jejunum, colon, mesenteric lymph nodes, pancreas, intestinal content, and blood were quickly collected to detect C. albicans. A region of the 25S rRNA gene was chosen and amplified by polymerase chain reaction (PCR) to differentiate C. albicans genotypes. The amplified products were further sequenced and compared to judge their homology. RESULTS: Compared with the Cyclophosphamide group, the combination of immunosuppressants and broad-spectrum antibiotics significantly increased the colonization of C. albicans in intestine in 5 and 10 days. Pure SAP stress did not increase the opportunistic infection of C. albicans. The PCR products of C. albicans isolates all belonged to the genotype A family, and sequence alignment showed that the amplified fragments were homologous. CONCLUSION: The damage of immune system and broad-spectrum antimicrobial agents are important risk factors for opportunistic fungal infection. Intestinal tract is an important source for genotype-A C. albicans to translocate and invade into bloodstream.
RESUMO
This study examined the effect of Notch-1 signaling on malignant behaviors of breast cancer cells by regulating breast cancer stem cells (BCSCs). BCSCs were enriched by using serum-free medium and knocked out of Notch-1 by using a lentiviral vector. Real-time polymerase chain reaction (RT-PCR) and Western blotting were used to detect the Notch-1 expression levels in breast cancer cell lines and BCSCs, and flow cytometry to detect the proportion of BCSCs in BCSC spheres. The BCSC self-renewal, migration, invasion, and tumorigenicity were examined by the tumor microsphere-forming assay and transwell assay and after xenotransplantation. The results showed that the Notch-1 silencing reduced the number of BCSC spheres, the proportion of BCSCs, and the number of cells penetrating through the transwell membrane. It also decreased the size of tumors that were implanted in the nude mice. These results suggest that Notch-1 signaling is intimately linked to the behaviors of BCSCs. Blocking Notch-1 signaling can inhibit the malignant behaviors of BCSCs, which may provide a promising therapeutical approach for breast cancer.
