Effect of Electroacupuncture on the Pathomorphology of the Sciatic Nerve and the Sensitization of P2X_3 Receptors in the Dorsal Root Ganglion in Rats with Chronic Constrictive Injury

Objective： To explore the effect of electroacupuncture （EA） on the pathomorphology of the sciatic nerve and the role of P2X3 receptors in EA analgesia. Methods： The chronic constriction injury （CCI） model was adopted in this study. A total of 32 rats were randomly divided into four groups： sham CCI, CCI, CCI plus contralateral EA （CCI ＋ conEA） and CCI plus ipsilateral EA （CCI ＋ ipsEA）. Mechanical withdrawal threshold （MWT） and thermal withdrawal latency OWL） were measured. EA began at day 7 after the CCI operation and was applied to the Zusanli （ST 36） and Yanglingquan acupoints （GB 34）. At day 14, the pathomorphologic changes of the operated sciatic nerve were demonstrated by hematoxylin and eosin staining. In addition, dorsal root ganglion （DRG） neurons isolated from rats were examined by electrophysiological recording to determine if the P2X3 receptor agonists, adenosine 5＇-tdphosphate disodium （ATP） and α, 13 -methylen-ATP （or, 13 -meATP） evoked inward currents. Results： Pain thresholds in the CCI group were obviously decreased post CCI surgery （P〈0.01）. In the EA groups, thermal and mechanical threshold values were increased after the last EA treatment （P〈0.05, P〈0.01）. There was no significant difference in light microscopic examination among the four groups （P〉0.05）. Current amplitude after application of ATP and or, 13 -meATP in DRG neurons were much larger in the CCI group compared to those obtained in sham CCI （P〈0.05）. ATP and α, 13 -meATP invoked amplitudes in the CCI ＋ EA groups were reduced. There was no significant difference between the CCI ＋ conEA group and the CCI ＋ ipsEA group （P〉0.05）. Conclusion： EA analgesia may be mediated by decreasing the response of P2X8 receptors to the agonists ATP and or, 13 -meATP in the DRG of rats with CCI. No pathological changes of the sciatic nerve of rats were observed after EA treatment.

Mass screening of prostate cancer in a Chinese population:the relationship between pathological features of prostate cancer and serum prostate specific antigen

Aim:To investigate the pathological features of the prostate biopsy through mass screening for prostate cancer in a Chinese cohort and their association with serum prostate specific antigen (PSA).Methods:A total of 12 027 Chinese men in Changchun were screened for prostate cancer by means of the serum total prostate specific antigen (tPSA) test (by Elisa assay).Transrectal ultrasound-guided systematic six-sextant biopsies were performed on those whose serum tPSA value was >4.0 ng/mL and those who had obstructive symptoms (despite their tPSA value) and were subject to subse- quent pathological analysis with the aid of the statistic software SPSS 10.0 (SPSS.Inc.,Chicago.USA).Results:Of the 12 027 cases,158 (including 137 patients whose serum tPSA values were >4.0 ng/mL and 21 patients [serum tPSA <4. 0 ng/mL] who had obstructive symptoms) undertook prostate biopsy.Of the 158 biopsies,41 cases of prostatic carci- noma were found (25.9 %,41/158).The moderately differentiated carcinoma and poorly differentiated carcinoma ac- counted for 61% and 34 %,respectively.A significant linear positive correlation between the serum tPSA and the Gleason scores in the 41 cases of prostatic carcinoma (r=0.312,P<0.01) was established.A significant linear positive correlation between the serum tPSA value of the 41 prostatic carcinoma and the positive counts of carcinoma in sextant biopsies was established (r=0.406,P<0.01),indicating a significant linear relationship between serum tPSA and the size of tumor. Condusion:This study was the first to conduct mass screening for prostate cancer by testing for serum tPSA values and the first to investigate the pathological features of prostate cancer in a cohort of Chinese men.Our results reveal that the moderately differentiated carcinoma is the most common type of prostate cancer.This study also has shown that the serum tPSA value in prostate cancer is associated with the Gleason score and the size of tumor.

In the Basis of Hashimoto’s Thyroiditis, to Form Papillary Thyroid Carcinoma, Metastasized and Then to De-Differentiate into Poorly Differentiated Squamous Cell Carcinoma

Thyroid squamous cell carcinoma is very rare. At present, it is limited to case reports. Since the thyroid follicular epithelium is the non-squamous epithelium, how primary squamous cell carcinoma (SCC) of the thyroid occurs is still a controversial issue. Hashimoto’s thyroiditis (HT) is considered to be an independent risk factor for thyroid cancer, under the basis of HT, how tumor cells evolve and develop to papillary thyroid carcinoma (PTC), and particularly to de-differentiate into SCC is elusive. We report a 72-year-old female patient who developed multiple subtypes of PTC on a basis of HT, and finally to de-differentiate into SCC within the local foci of lymph node metastasis. We found that there was a variety of sub-types of PTC in this patient in the background of HT. SCC was found within local lymph node metastasis. Pathomorphology, immunohistochemistry, and molecular pathology have confirmed that the SCC was derived from PTC, and then developed into poorly differentiated SCC and/or anaplastic carcinoma. We also conducted a comprehensive literature review.

Effect of Electro-acupuncture on Rat Joint Pathomorpnology of Chronic Adjuvant Arthritis Model

Objective:To study the effect of electro-acupuncture (EA) on pathomorphological changes of joints in rat model of chronic adjuvant arthritis. Methods: The rat chronic adjuvant arthritis model was established by subcutaneous injection of 0.1 ml of complete Freund’s adjuvant to the left hind sole. Forty Wistar rats were randomly divided into the model group, the low frequency (2 Hz) EA group, the high frequency EA (100 Hz) group and the body acupuncture group. After being modeled except the model group, the other three groups were treated with EA or body acupuncture in Yanglingquan points (bilateral) for 3 weeks, the left ankle joints and metatarsal joints of rats were taken for pathological examination by fixing with 10% formalin and embedding in paraffin, sectioning and staining with HE. Results: Obvious inflammatory cell infiltration, loosened synovial tissue, damage of articular cartilage and proliferation of synovial cells and granulation tissue were observed in the sections of joints in model rats.

A preliminary study of the mechanism of compound hearing loss caused by ototoxic drugs combined with impulse noise

Background:Hearing loss(HL)is becoming increasingly common and is more commonly caused by noise,ototoxic substances,or a combination of ototoxic factors.However,so far,few studies have examined the mechanism by which compound factors cause HL.The only relevant study is about occupational ototoxic substances combined with environmental noise at 85-110 dB SPL.In this study,to address the shortcomings of existing research,we innovatively focused on HL induced by loud noise(impulse noise,>160 dB SPL)combined with common ototoxic drugs.The aim of this study was to establish and validate a mature animal model,and then to compare the characteristics of audiology,pathomorphology and molecular features,and to preliminarily predict pathogenesis in compound HL.Materials and Methods:We selected guinea pigs to construct in vivo HL model groups for different extents of exposure,including a blank control group,a single-drug group,a single-impulse noise group,and a compound group.The animal model of the mature compound HL group was established using gentamicin combined with impulse noise.We then performed audio-logical and pathological verification.We analyzed the auditory brainstem response(ABR),pathological morphology of the cochlea,and molecules(including important self-radicals,cytokines,and apoptosis signal trans-duction pathway proteins in the pathogenesis of drug-and noise-induced HL),compared the effect of different extents of exposure on HL,and preliminarily predict the pathogenic mechanism of compound HL.Results:Four groups of animal models were established successfully and verified by audiology and pathology.Regarding audiology,there were no sig-nificant differences in the ABR thresholds before exposure(p>0.05),but differences emerged among the groups after exposure.Notably,after 3,7,and 14 days of exposure,there were significant differences in the ABR thresholds between the compound group and both the drug and noise groups(p<0.01),and after 14 days,the HL of the compound group was much more severe(greater than the linear sum of single-factor HL group).Regarding the patho-morphology,compared with the control group,the cochleae were damaged to different degrees in the factor exposure groups.The drug group had the least severe HL,the noise group had serious HL(p<0.05),and the compound group had the most severe HL(p<0.01).The compound group's damage was greater than the linear sum of the single-factor group in many ways,such as the loss and damage of hair cells and cilia,disturbed morphology and arrangement of hair cells,protein metabolism,cell function,and structural defects on the epidermal plate(p<0.01).From a molecular perspective,the trend was similar to pathology and audiology,and the synergistic effect of ototoxic drugs and impulse noise significantly increased cytokine levels(IL-6,ICAM-1,8-OHDG,IL-1,and TNF-α),free radicals Malondialdehyde([MDA],▪OH,LPO,O•2ˉ),and the apoptosis signal transduction pathway protein.There were significant differences between the compound group and single-factor groups(p<0.05).Conclusion:Gentamicin,impulse noise,and compound factors were used to induce HL in animal models,which were verified by audiology and pathology,laying a foundation for future studies.After constructing the animal models,we found that 50 mg/kg of gentamicin for 10 days was a subinjury dose,and 50�impulse noise caused partial HL,but the two factors combined had a significant synergistic ototoxicity effect,which increased the level of oxidative stress and the waterfall response of inflammatory cytokines in the cochleae and enhanced the expression of apoptosis-related proteins,resulting in syn-ergistic pathomorphological and audiological injury.We preliminarily analyzed the pathogenic mechanism of compound HL,establishing the basis for further study of the mechanism,prevention,and treatment of this increasing global problem.