Abnormal hypothalamic functional connectivity associated with cognitive impairment in craniopharyngiomas.

OBJECTIVE: This study sought to characterize resting-state functional connectivity (rsFC) patterns of the hypothalamic and extrahypothalamic nuclei in craniopharyngioma (CP) patients, and to investigate potential correlations between hypothalamic and extrahypothalamic rsFC maps and neurocognitive performance. METHODS: Ninety-two CP patients and 40 demographically-matched healthy controls were included. Whole-brain seed-to-voxel analyses were used to test for between-group rsFC differences, and regression analyses were used to correlate neurocognitive performance with voxel-wise hypothalamic and extrahypothalamic rsFC maps for CP patients. Finally, spectral DCM analysis was used to explore the hypothalamus circuit associated with neurocognitive performance. RESULTS: The seed-to-voxel analyses demonstrated that the hypothalamic nuclei showed mainly significant rsFC reduction in brain areas overlayed with the cortical regions of default mode network (DMN), notably in the bilateral anterior cingulate cortices and posterior cingulate cortices. The extrahypothalamic nuclei showed significant rsFC reduction in the limbic system of bilateral caudate nuclei, corpus callosum, fornix, and thalamus. Regression analyses revealed that worse cognitive performance was correlated with abnormal hypothalamic rsFC with brain areas in DMN, and DCM analysis revealed a hypothalamus-DMN circuit responsible for functional modulation of cognitive impairment in CP patients. CONCLUSIONS: Our study demonstrated that CPs invading into hypothalamus impacted hypothalamic and extrahypothalamic rsFC with brain areas of DMN and limbic system, the severity of which was parallel with the grading system of hypothalamus involvement. In addition to the CP-induced structural damage to the hypothalamus alone, abnormal functional connectivity within the hypothalamus-DMN circuit might be a functional mechanism leading to the cognitive impairment in CP patients.

[Effects of pathogenic wind-dampness on lung tissue cytokines in rats with syndrome due to pathogenic cold invading lung].

OBJECTIVE: To explore the effects of wind and dampness pathogens on cytokines in the lung tissue of rats with cold syndrome due to different gradient cold pathogens. METHODS: One hundred and four Wistar rats of SPF grade were randomly divided into 13 groups: normal temperature group, six cold pathogen groups and six cold plus wind-dampness pathogen (wind of grade 5 and 90%-100% relative humidity) groups. The cold pathogens were constant low temperature (including 10 degrees C, 0 degree C, -10 degrees C) and temperature change (including 20 to 10 degrees C, 20 to 0 degrees C, and 20 to -10 degrees C). The rats in different groups were kept in a temperature-controlled box under the corresponding condition for 2 hours on the first day of experiment. Then, the rats were all raised in normal temperature for 4 days and the rats' behaviors were observed. The contents of tumor necrosis factor alpha (TNF-alpha), interleukin-6(IL-6) and interleukin-4 (IL-4) in lung homogenate were measured by radioimmunoassay and the content of interferon-gamma (IFN-gamma) was detected by enzyme-linked immunosorbent assay. RESULTS: In comparison with cold pathogen groups, contents of TNF-alpha, IL-6 and IL-4 were obviously increased in lung homogenate of rats in cold plus wind-dampness pathogen groups (P<0.01), and the content of IFN-gamma and IFN-gamma/IL-4 ratio were obviously decreased (P<0.01). CONCLUSION: Wind-dampness pathogen can seriously aggravate the injury to lung tissue caused by cold pathogen, and the unbalance of Th(1)/Th(2) in lung homogenate of rats.