[Experimental study on Dendrobium candidum polysaccharides on promotion of hair growth].

OBJECTIVE: To observe the effect and mechanism of Dendrobium candidum polysaccharides (DCP) in promoting hair growth, in order to lay a foundation for the development and utilization of D. candidum. METHOD: The water-extraction and alcohol-precipitation method was adopted to extract DCP, and the phenol-sulphuric acid method was used to determine its content. Thirty C57BL6J mice were collected to establish the hair loss model with hair removal cream. They were randomly divided into the control group, the positive control group and the DCP group, and given 0.2 mL of ultra-pure water, minoxidil tincture and DCP (5.0 g x L(-1)) 21 days. The mice hair growth scoring standard was adopted to evaluate the hair growth of C57BL/6J mice at 7, 14 d. The hairs in unit hair-losing areas of treated C57BL/6J mice at 21 d were weighed to evaluate the effect of DCP on the promotion of hair growth. MTT assay and RT-PCR method were used to evaluate the effect of DCP on the proliferatin of HaCaT cells and the mRNA expression of VEGF in HaCaT cells. RESULT: The extraction percent of DCP was 29.87%, and its content was 79.65%. The average scores for the hair growth and weight of C57BL/6J mice of DCP group were much higher than the control group. The survival rate and mRNA expression of VEGF of HaCaT cells were much higher than the control group. CONCLUSION: DCP has the effect in promoting hair growth. Its mechanism may be related to the up-regulation of the mRNA expression of VEGF.

Apathy is associated with striatal atrophy and cognitive impairment in cerebral small vessel disease.

BACKGROUND: Apathy has been considered a common neuropsychiatric symptom and an important contributor to cognitive impairment in cerebral small vessel disease (SVD). However, the mechanism leading to apathy in SVD and the process whereby apathy promotes cognitive impairments remain largely unknown. We aimed to explore the relationship between apathy, cognition, and structural changes of deep grey matter (DGM) in SVD patients. METHODS: Participants were screened for SVD, completed assessments of apathy cognition, underwent magnetic resonance imaging (MRI) scanning, and then stratified into apathy and non-apathy groups. We used region of interest (ROI)-based, voxel-based volume, and vertex-based shape analyses to compare DGM structures between study groups. Using linear regression analysis, we examined the association between apathy, structural changes, and cognition, followed by a mediation analysis of these factors. RESULTS: A total of sixty-four SVD participants were included, with thirty in the apathy group and thirty-four in the non-apathy group. Intergroup comparison showed significantly lower volumes in bilateral caudate, right putamen, and pallidum and smaller vertex-based shapes in the right caudate and pallidum in participants with apathy compared to those without apathy. Apathy was associated with the striatal atrophy (i.e., lower volumes and smaller shape) and independently contributed to cognitive impairments in SVD. However, the above structural differences did not mediate the association between apathy and cognitive impairments. CONCLUSION: These results highlight the important role of striatal atrophy in apathy in SVD and call for additional studies to explore the relationship between apathy, cognition, and DGM.

Altered cerebellar gray matter and cerebellar-cortex resting-state functional connectivity in patients with bipolar disorder â .

BACKGROUND: Bipolar disorder (BP) is a common psychiatric disorder characterized by extreme fluctuations in mood. Recent studies have indicated the involvement of cerebellum in the pathogenesis of BP. However, no study has focused on the precise role of cerebellum exclusively in patients with bipolar I disorder (BP-I). METHODS: Forty-five patients with BP-I and 40 healthy controls were recruited. All subjects underwent clinical evaluation and Magnetic Resonance diffusion Tension Imaging scans. For structural images, we used a spatially unbiased infratentorial template toolbox to isolate the cerebellum and then preformed voxel-based morphometry (VBM) analyses to assess the difference in cerebellar gray matter volume (GMV) between the two groups. For the functional images, we chose the clusters that survived from VBM analysis as seeds and performed functional connectivity (FC) analysis. Between-group differences were assessed using the independent Students t test or the nonparametric Mann-Whitney U Test. For multiple comparisons, the results were further corrected with Gaussian random field (GRF) approach (voxel-level P < 0.001, cluster-level P < 0.05). RESULTS: Compared with healthy controls, BP-I patients showed significantly decreased GMV in left lobule V and left lobule VI (P < 0.05, GRF corrected). The FC of cerebellum with bilateral superior temporal gyrus, bilateral insula, bilateral rolandic operculum, right putamen, and left precentral gyrus was disrupted in BP-I patients (P < 0.05, GRF corrected). CONCLUSIONS: BP-I patients showed decreased cerebellar GMV and disrupted cerebellar-cortex resting-state FC. This suggests that cerebellar abnormalities may play an important role in the pathogenesis of BP-I.

A GRIP-1-EZH2 switch binding to GATA-4 is linked to the genesis of rhabdomyosarcoma through miR-29a.

Terminal differentiation failure is an important cause of rhabdomyosarcoma genesis, however, little is known about the epigenetic regulation of aberrant myogenic differentiation. Here, we show that GATA-4 recruits polycomb group proteins such as EZH2 to negatively regulate miR-29a in undifferentiated C2C12 myoblast cells, whereas recruitment of GRIP-1 to GATA-4 proteins displaces EZH2, resulting in the activation of miR-29a during myogenic differentiation of C2C12 cells. Moreover, in poorly differentiated rhabdomyosarcoma cells, EZH2 still binds to the miR-29a promoter with GATA-4 to mediate transcriptional repression of miR-29a. Interestingly, once re-differentiation of rhabdomyosarcoma cells toward skeletal muscle, EZH2 was dispelled from miR-29a promoter which is similar to that in myogenic differentiation of C2C12 cells. Eventually, this expression of miR-29a results in limited rhabdomyosarcoma cell proliferation and promotes myogenic differentiation. We thus establish that GATA-4 can function as a molecular switch in the up- and downregulation of miR-29a expression. We also demonstrate that GATA-4 acts as a tumor suppressor in rhabdomyosarcoma partly via miR-29a, which thus provides a potential therapeutic target for rhabdomyosarcoma.