Parkinson's disease （PD） is a complex neurodegenerative disease involving multiple systems and neurotransmitters. Due to the high clinical heterogeneity of PD，it is urgent to establish a comprehensive and long-term traditional Chinese medicine （TCM） management model. In this paper，the conceptual framework of full-cycle management of PD is preliminarily constructed：based on the evolution of the pathophysiological mechanisms of protein deposition and neurotransmitter disorder in PD，the three-stage syndrome characteristics of the prodromal stage （predominant healthy Qi with subtle pathogenic factors），the early clinical stage （declining healthy Qi with growing pathogenic factors） and the middle and late stages （overwhelming pathogenic factors with deficient healthy Qi） are longitudinally described. Through the syndrome differentiation of visceral manifestations，the etiology and pathogenesis of PD motor and non-motor symptoms were comprehensively analyzed，while the matching treatment methods and prescriptions were inferred，and the modular scheme of the combining main symptoms，accompanying symptoms and secondary symptoms was proposed. The conceptual gap of TCM regarding motor complications （'variable syndrome'） and PD-related hyperpyrexia syndrome （'critical syndrome'） was explained. This framework reflects the characteristics of combination of disease and syndrome and overall constant motion，and provides new theories and research ideas for individualized and whole-process management of PD in TCM.

Parkinson's disease （PD） is a complex neurodegenerative disease involving multiple systems and neurotransmitters. Due to the high clinical heterogeneity of PD，it is urgent to establish a comprehensive and long-term traditional Chinese medicine （TCM） management model. In this paper，the conceptual framework of full-cycle management of PD is preliminarily constructed：based on the evolution of the pathophysiological mechanisms of protein deposition and neurotransmitter disorder in PD，the three-stage syndrome characteristics of the prodromal stage （predominant healthy Qi with subtle pathogenic factors），the early clinical stage （declining healthy Qi with growing pathogenic factors） and the middle and late stages （overwhelming pathogenic factors with deficient healthy Qi） are longitudinally described. Through the syndrome differentiation of visceral manifestations，the etiology and pathogenesis of PD motor and non-motor symptoms were comprehensively analyzed，while the matching treatment methods and prescriptions were inferred，and the modular scheme of the combining main symptoms，accompanying symptoms and secondary symptoms was proposed. The conceptual gap of TCM regarding motor complications （'variable syndrome'） and PD-related hyperpyrexia syndrome （'critical syndrome'） was explained. This framework reflects the characteristics of combination of disease and syndrome and overall constant motion，and provides new theories and research ideas for individualized and whole-process management of PD in TCM.

Objective To investigate the effect of autophagy response on neurological functions and the role of mitogen-activated protein kinases (MAPKs) signaling pathway in rats after traumatic brain injury (TBI).Methods Fifty-four healthy male SD rats were randomly divided into sham-operated group,TBI group and TBI+autophagy inhibitor 3-methyladenine (3-MA) group (n=18).TBI animal models of the later two groups were established using Feeney's method.Rats in the sham-operated group were only performed bone window opening without knock;rats in the TBI+3-MA group were given intraperitoneal injection of 3-MA(5 mg/kg) 30 min after modeling and rats in the other two groups were given the same volume of normal saline.Three and 7 d after modeling,the protein levels of S100B and neuron specific enolase (NSE) in serum were tested with enzyme linked immunosorbent assay (ELISA);modified neurologic severity scale (mNSS) was used to detect the movement,sense and reflex functions;brain water content was measured with wet-dry weight method.The autophagy related factors (LC3-Ⅱ and Beclin-1) and MAPKs signaling pathway related factors (c-Jun N-terminal kinase [JNK],phosphorylated [p]-JNK,extracellular signal-regulated kinase [ERK]1/2,p-ERK1/2,p38MAPK and p-p38MAPK) protein expressions in TBI cerebral cortex were determined by Western blotting.Results As compared with those in the sham-operated group,the brain edema level,mNSS scores,and S100B and NSE protein levels in the TBI group and TBI+3-MA group were significantly increased (P＜0.05);TBI+3-MA group had significantly lower brain edema level,mNSS scores,and S100B and NSE protein levels than TBI group (P＜0.05).The expression levels of autophagy and MAPKs signaling pathway related factors in the TBI group and TBI+3-MA group were significantly higher as compared with those in the sham-operated group (P＜0.05).As compared with the TBI group,TBI+3-MA group had significantly decreased levels of LC3-Ⅱ,Beclin-1 and activation of JNK and p-p38MAPK signaling pathways (P＜0.05).Conclusion Suppressing autophagy response markedly improves neurological outcomes after TBI,possibly mediated by inhibiting activation of JNK and p38MAPK signaling pathways.

Congenital clubfoot(CCF), which is also known as equines deformity, is a common congenital malformation that affect children′s life quality. However, its cause is still to be elucidated. Currently, polygenetic and environmental fac?tors are both believed to play important roles in CCF pathogenesis. Several genes including HOX, PITX1, NAT2, P63, DTDS and COL9A were shown to contribute to congenital clubfoot, but which is the most critical gene remains unclear. Several re?ports have revealed that Hox genes are closely related to the cause of CCF. Hox genes are regulators of body morphogenesis, and its mutation result in limbs and trunk deformity in human. Here, we systematically reviewed the latest literature that stud?ied the role of Hox genes in pathogenesis of Congenital clubfoot, with the prospect of laying a foundation for its future clinic treatment.