To clarify the effect of the sympathetic nerves on the body's physiopathological changes and acupuncture effect by the alphal-AR mediation in the past 30 years.The paper has referred to the database of CNKI and Pubmed,and systematically reviewed the publications in the past 30 years about the research of the alphal-AR mediation of the sympathetic nerves to the body's physiological andpathological changes and acupuncture effect.Alphal-AR not only mediated the sympathetic nerves on the inotropic change of the heart,and the contraction of the vascular smooth muscles,bladder sphincter,and uterine smooth muscles and other physiological effect,but also mediated cardiac arrhythmia,myocardial hypertrophy and other pathological process.In addition,Alphal-AR also mediated the acupuncture signal transmission,and acupuncture was able to adjust the sympathetic nervous tension.The body's physiopathological changes are closely related to alpha1-AR and subtype alteration.The in-depth study of alphal-AR helps to explain physiopathological mechanism of the body,as well as provide theoretical basis and the corresponding pharmacological models for better selective drugs.Studying Alpha1-AR on meridians contributes to the discovery of meridian essence and the substantial basis of acupuncture effects.

Objective To observe over-time changes in rat blood flow in the skins of related meridian points during physiological status, the pathological state of ischemic myocardial injury and low or high frequency electroacupuncture intervention and explore the post effect of different frequency electroacupuncture on related meridian points after treating ischemic myocardial injury. Method Fifty male Wister rats were randomized into five groups: blank control, sham operation, model, low frequency electroacupuncture (meridian point A) and high frequency electroacupuncture (meridian point B), 10 rats each. Blood flow in the skins of bilateral points Neiguan (PC6), Ximen (PC4) and Tianquan (PC2), and non-meridian and non-acupoint control points was measured by laser speckle contrast imaging in every group immediately and at 30 and 60 min after the end of three treatments. Statistical analysis was made. Result Blood flow in the skins of bilateral points Neiguan, Ximen and Tianquan was significantly lower in the blank control group than in the model group (P<0.01,P<0.05). Blood flow in the skin of every acupoint increased in varing degrees after low or high frequency electroacupuncture treatment. Blood flow in bilateral points Neiguan, Ximen and Tianquan regions in meridian point group A was closer to that in the blank control group immediately after treatment. Blood flow in three left-side and three right-side acupoint regions in meridian point group B was closer to that in the blank control group at 30 and 60 min, respectively, after treatment. Conclusion The immediate effect of low frequency electroacupuncture on blood flow in acupoint regions is better than high frequency electroacupuncture during intervention in ischemic myocardial injury. The post effect of high frequency electroacupuncture on blood flow in acupoint regions is better than low frequency electroacupuncture during intervention in ischemic myocardial injury.

OBJECTIVETo study the clinical and histopathologic features of metanephric adenoma (MA).

METHODSEight cases of recently diagnosed MA were retrieved from archival file. Immunohistochemical study was carried out. The clinical characteristics, pathologic parameters, differential diagnosis, treatment options and prognosis of MA were analyzed, with literature review.

RESULTSThe patients included 6 females and 2 males. The age of patients ranged from 12 to 70 years (mean=43.6 years). Eight cases were located in renal cortex and showed well-defined borders. Histologically, the tumor was composed of tubules lined by small basophilic cells and embedded in an edematous stroma. Papillary structures and psammoma bodies were focally seen. Immunohistochemical study showed that the tumor cells were positive for PAX2 and vimentin in all the 8 cases. WT-1 was positive in 2 cases, focal and weak in 5 cases, and negative in 1 case. CK-Pan was positive in 3 cases. CK7 staining was mostly negative, with focal and weak positivity only in 1 case. The proliferative index, as highlighted by Ki-67 staining, was less than 2% in 7 cases and focally around 5% in 1 case. The expressions of CK20, CD10, RCC, epithelial membrane antigen, CD56, synaptophysin and chromogranin A were negative. Follow-up information from 7 to 57 months was available in all patients; and none of them developed local recurrence or distant metastasis.

CONCLUSIONSThe diagnosis of MA relies primarily on thorough histologic examination and immunohistochemical study (vimentin and PAX2 positive, WT-1 focally and weakly positive in some cases, and low proliferative index). Correlation with clinical and radiologic findings would also be helpful.

Adenoma ; diagnostic imaging ; metabolism ; pathology ; surgery ; Adolescent ; Adult ; Aged ; Biomarkers, Tumor ; metabolism ; Carcinoma, Renal Cell ; metabolism ; pathology ; Child ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Kidney Neoplasms ; diagnostic imaging ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Nephrectomy ; methods ; PAX2 Transcription Factor ; metabolism ; Tomography, X-Ray Computed ; Vimentin ; metabolism ; WT1 Proteins ; metabolism ; Wilms Tumor ; pathology ; Young Adult

Peripheral bacterial infections without impaired blood-brain barrier integrity have been attributed to the pathogenesis of Parkinson's disease (PD). Peripheral infection promotes innate immune training in microglia and exacerbates neuroinflammation. However, how changes in the peripheral environment mediate microglial training and exacerbation of infection-related PD is unknown. In this study, we demonstrate that GSDMD activation was enhanced in the spleen but not in the CNS of mice primed with low-dose LPS. GSDMD in peripheral myeloid cells promoted microglial immune training, thus exacerbating neuroinflammation and neurodegeneration during PD in an IL-1R-dependent manner. Furthermore, pharmacological inhibition of GSDMD alleviated the symptoms of PD in experimental PD models. Collectively, these findings demonstrate that GSDMD-induced pyroptosis in myeloid cells initiates neuroinflammation by regulating microglial training during infection-related PD. Based on these findings, GSDMD may serve as a therapeutic target for patients with PD.