Acupuncture treatment of chronic pain combined with depression (CPDC) is the result of a multi-target, multi-pathway approach. Acupuncture can treat CPDC by inhibiting the activation of glial cells, regulating the release of inflammatory mediators, regulating the expressions of neurotransmitters, changing the plasticity of neural synapses, regulating related epigenetic effects, regulating the microbiota-brain-gut axis, inhibiting nerve cell apoptosis, and antagonizing oxidative stress. The mechanism of its effect mainly involves anti-inflammatory related signaling pathways, regulation of neural synapse-related signaling pathways, and exerts its therapeutic effect through hippocampus, cerebral cortex, and amygdala.

The regulatory processes in developmental biology research are significantly influenced by long non-coding RNAs (lncRNAs). However, the dynamics of lncRNA expression during human tooth development remain poorly understood. In this research, we examined the lncRNAs present in the dental epithelium (DE) and dental mesenchyme (DM) at the late bud, cap, and early bell stages of human fetal tooth development through bulk RNA sequencing. Developmental regulators co-expressed with neighboring lncRNAs were significantly enriched in odontogenesis. Specific lncRNAs expressed in the DE and DM, such as PANCR, MIR205HG, DLX6-AS1, and DNM3OS, were identified through a combination of bulk RNA sequencing and single-cell analysis. Further subcluster analysis revealed lncRNAs specifically expressed in important regions of the tooth germ, such as the inner enamel epithelium and coronal dental papilla (CDP). Functionally, we demonstrated that CDP-specific DLX6-AS1 enhanced odontoblastic differentiation in human tooth germ mesenchymal cells and dental pulp stem cells. These findings suggest that lncRNAs could serve as valuable cell markers for tooth development and potential therapeutic targets for tooth regeneration.
Humans ; RNA, Long Noncoding/metabolism* ; Odontogenesis/genetics* ; Tooth Germ/embryology* ; Cell Differentiation ; Gene Expression Regulation, Developmental ; Mesoderm/metabolism* ; Tooth/embryology* ; Gene Expression Profiling ; Sequence Analysis, RNA ; Dental Pulp/cytology*

Micrognathia is a severe craniofacial deformity affecting appearance and survival. Previous studies revealed that multiple factors involved in the osteogenesis of mandibular bone have contributed to micrognathia, but concerned little on factors other than osteogenesis. In the current study, we found that ectopic activation of Fgf8 by Osr2-cre in the presumptive mesenchyme for masseter tendon in mice led to micrognathia, masseter regression, and the disrupted patterning and differentiation of masseter tendon. Since Myf5-cre;Rosa26R-Fgf8 mice exhibited the normal masseter and mandibular bone, the possibility that the micrognathia and masseter regression resulted directly from the over-expressed Fgf8 was excluded. Further investigation disclosed that a series of chondrogenic markers were ectopically activated in the developing Osr2-cre;Rosa26R-Fgf8 masseter tendon, while the mechanical sensing in the masseter and mandibular bone was obviously reduced. Thus, it suggested that the micrognathia in Osr2-cre;Rosa26R-Fgf8 mice resulted secondarily from the reduced mechanical force transmitted to mandibular bone. Consistently, when tenogenic or myogenic components were deleted from the developing mandibles, both the micrognathia and masseter degeneration took place with the decreased mechanical sensing in mandibular bone, which verified that the loss of mechanical force transmitted by masseter tendon could result in micrognathia. Furthermore, it appeared that the micrognathia resulting from the disrupted tenogenesis was attributed to the impaired osteogenic specification, instead of the differentiation in the periosteal progenitors. Our findings disclose a novel mechanism for mandibular morphogenesis, and shed light on the prevention and treatment for micrognathia.
Mice ; Animals ; Micrognathism ; Masseter Muscle ; Mandible ; Osteogenesis

Objective:To evaluate thrombo-pretreatment in AngioJet mechanical thrombectomy.Methods:68 acute DVT patients were randomized into two groups: thrombo-pretreatment with low-dose urokinase via popliteal vein before operation (experimental group)comparing with those undergoing upfront surgery.Results:After pretreatment, the immediate thrombus clearance grade in the experimental group was higher than that in the control group( Z=2.446, P=0.014), the procedure time was shorter [(289.1±57.9) s vs. (342.3±75.2) s] and less hemoglobin decreased after operation [(7.2±2.4) g/L vs. (11.4±2.1) g/L]. There was no difference in the deep vein patency and the incidence of PTS between the two groups at 3 , 12 and 24 months after operation. Conclusion:Pre-treatment with low dose urokinase before operation can improve the efficiency of PMT, effectively reduce the time of AngioJet activation and the destruction of red blood cells.

Objective To evaluate the therapeutic effect of catheter-directed thrombolysis (CDT) for the treatment of acute deep venous thrombosis (DVT) of the lower extremity.Methods Clinical data of 195 patients of acute DVT treated by CDT and adjunctive angioplasty and stenting from August 2010 to February 2014 were analyzed retrospectively.CDT by antegrade puncture of popliteal vein,CDT by great saphenous vein and CDT by retrograde puncture of contralateral femoral vein were used in these cases.Venous recanalization was graded by a thrombus score based on pre-and post-treatment venography.Results Technique success rate,clinical success rate,in popliteal vein group,great saphenous vein group and contralateral femoral vein group were 94.6％,72.2％ and 90.3％,97.3％,83.3％,and 90.0％.Patent rate of deep venous,patent rate of stenting and mild post-thrombotic syndrome (PTS) rate were 88.6％,66.7％ and 75.0％,83.3％,57.1％ and 88.9％,8.3％,26.7％ and 20.8％.Conclusion CDT by antegrade puncture of popliteal vein group combined with adjunctive angioplasty and stenting is safe and effective with higher clinical success rate and better long term results than other approaches for the treatment of DVT patients.

The levels of the products of RNA polymerase Ⅲ-dependent genes(Pol Ⅲ genes),including tRNAs and 5S rRNA,are elevated in transformed and tumor cells,which potentiate tumorigenesis.TFIIB-related factor 1(Brf1)is a key transcription factor and specifically regulates the transcription of Pol Ⅲ genes.In vivo and in vitro studies have demonstrated that a decrease in Brf1 reduces Pol Ⅲ gene transcription and is suf-ficient for inhibiting cell transformation and tumor formation.Emerging evidence indicates that dys-regulation of Brf1 and Pol Ⅲ genes is linked to the development of hepatocellular carcinoma(HCC)in humans and animals.We have reported that Brf1 is overexpressed in human liver cancer patients and that those with high Brf1 levels have shorter survivals.This review summarizes the effects of dysregu-lation of these genes on HCC and their regulation by signaling pathways and epigenetics.These novel data should help us determine the molecular mechanisms of HCC from a different perspective and guide the development of therapeutic approaches for HCC patients.