Objctive:To find an effective clinical method for caleaneal pain .Methods: 68 Cases of caleaneal pain in clinic service were collected from August 2006 to August 2008, and were treated with radix decoctum and Biqi Capsule. Tracing observation was used to evaluate the curative effect. Results: 41 Cases were healing well, 24 cases were improving, 3 cases were useless. The total effective rate was 95.6%. Conclusion: Radix decoctum with Biqi Capsule was an effective method for caleaneal pain.

Objective To investigate the positive rates and susceptibility of Ureaplasma urealyticum(Uu) and Mycoplasma hominis(Mh) in urogenital mycoplasma infection under three years.Methods Culture,identification and susceptibility test were performed on 4 414 specimens collected from suspected patients with mycoplasma infection by using Antu mycoplasma kits.Results In the 4 414 patients,2 295 cases with mycoplasma infection were detected and the positive rate was 51.99％.The infection rates of Uu and Mh respectively were 40.69％ and 2.08％,and the both infection rate was 9.22％.Antibiotic sensitive rates of josamycin(JOX),doxycycline(DOX),clarithromycin(CLA),gatifloxacin(GAT) and erythromycin(ERY) were 96.03％,95.51 ％,78.69 ％％,77.21 ％ and 72.55 ％.Drug resistant rates of roxithromycin(RXT),thiamphenicol (THI),clindamycin (CLI) and clarithromycin(CLA) were 16.90％,22.27％,41.96％ and 17.60％.Conclusion Uu is the predominant mycoplasma in urogenital tract infection in the study.DOX,JOS,GAT and ERY can be chosen as the fist line drugs for the treatment of urogenital tract infection.RXT,THI,CLI and CLA with high drug resistant rates are not recommended to be used.

Objective To explore the effect of expression of protein kinase C receptor 1(RACK1) induced by lipopolysaccharide (LPS) on Sonic hedgehog(SHH) signaling pathway in rat puhnonary microvascular endothelial cells (RPMVEC).Methods The healthy male SPF grade SD rat with 100-120 g body weight were gotten from the laboratory animal center of Anhui province.Using immunocytochemistry method,the expression of RACK1 protein in RPMVECs was detected,cultured RPMVECs were randomly divided into different groups as LPS dose-dependent group,SAG(smoothened Agonist,a SHH signaling pathway specific agonist) dose-dependent group,LPS time-dependent group,SAG time-dependent group and LPS+SAG group.In LPS dose-dependent groups,RPMVECs were cultured with 0.1,1,10 mg/L LPS for 8 h.In LPS time-dependent groups,RPMVECs were cultured with 10 mg/L LPS for 0,2,4,8,12,24 h.In SAG dose-dependent groups,RPMVECs were cultured with 0.1,1,10 μ mol/L for 8 h.In SAG time-dependent groups,RPMVECs were cultured with 1 μ mol/L SAG for 0,2,4,8,12,24 h.In LPS+SAG group,RPMVECs were cultured with 1 μ mol/L SAG 8 h after 10 mg/L LPS treatment for 1 h.In addition,blank group,LPS group and SAG group were set for control.Western blot were used to detect the level of RACK1 and RT-PCR were used to detect the expression of GLI-1 mRNA after intervention.Results Immunocytochemistry revealed that RACK1 were present in RPMVEC.1.In LPS dose-dependent groups (0,0.1,1,10 mg/L),the level of RACK1 elevated as LPS dose increased correspondingly with inter-group difference (P＜0.05);the relative expression levels of GLI-1 mRNA were (1.109 + 0.063),(1.039 + 0.135),(0.813 ± 0.066),(0.770 + 0.105),(1 mg/L vs.10 mg/L,P＞0.05;the rest P＜0.05).In LPS time-dependent groups,the relative expression level of RACK1 at 2 h (0.370 + 0.010) was higher than that at 0 h (0.329 ± 0.008),peaked at 12 h (1.296 ± 0.048),and compared with 0 h,there was significant differences (F=1 272.204,P＜0.05).The relative expression level of GLI-1 mRNA was decreased at 2 h (0.929 ±-0.007),and compared with 0 h(1.089 ± 0.042),there was significant differences (F=306.609,P＜0.05).2.In SAG dose-dependent groups,there was no significant difference in level of RACK1 between groups(all P＞0.05).The relative expression levels ofGLI-1 mRNA were (1.109 ± 0.063),(1.169 ± 0.052),(3.468 ± 0.128),(3.434 ± 0.054),(0 μ mol/L vs.0.1 μ mol/L and 1 μ mol/L vs.10 μ mol/L,P＞0.05,the rest P＜0.05).Among SAG time-dependent groups,there was no significant difference in levels of RACK1 protein(P＞0.05).The relative expression level of GLI-1 mRNA increased at 2 h (3.027 ± 0.065),and compared with 0 h (2.651 + 0.123),there was significant differences (F=132.841,P＜0.05).3.In LPS+SAG intervention groups,the expression of RACKI was lower than that in LPS group (0.831 ±0.040 vs.1.189 ± 0.149,P＜0.05),and the expression of GLI-1 mRNA was higher than that in LPS group (2.720 + 0.130 vs.0.796-4-0.082,P＜0.05).Conclusions The LPS up-regulates the expression of RACK1 in RPMVECs,and the activated SHH signaling pathway can down-regulate the expression of RACK1 induced by LPS in RPMVECs.

Objective:To explore the effect of intelligent chronic disease management system for rheumatoid arthritis patients under mobile terminal APP.Methods:From June 2018 to June 2021, 100 patients with rheumatoid arthritis treated in Mianyang Central Hospital were selected by convenience sampling. The 50 patients admitted from June 2018 to November 2019 were in the control group, and the 50 patients admitted from December 2019 to June 2021 were in the observation group. The control group received routine nursing, while the observation group implemented intelligent chronic disease management under mobile terminal APP on the basis of the control group. Six months after intervention, the awareness of disease health knowledge, self-management ability and rehabilitation indicators were compared between the two groups.Results:Six months after intervention, the awareness of disease health knowledge and self-management ability of the observation group were higher than those of the control group, and the differences were statistically significant ( P<0.05) . Six months after intervention, the rehabilitation indicators of the observation group were lower than those of the control group, with statistically significant differences ( P<0.05) . Conclusions:The intelligent chronic disease management system under mobile terminal APP can increase the recognition of disease health knowledge and self-management ability of rheumatoid arthritis patients, improve various rehabilitation indicators, and promote enhanced recovery of diseases.

Objective To investigate the genetic causes of auditory neuropathy with optic atrophy in a family.Methods The proband's medical history and family history were inquired in detail,and relevant clinical examina-tions were performed to confirm the diagnosis of auditory neuropathy with optic atrophy,and the genetic pedigree of the family was drawn.Peripheral blood of proband(Ⅲ-7)was collected for whole exome sequencing,and the patho-genicity of the detected mutations were interpreted.Blood samples of proband's wife(Ⅲ-8),eldest daughter(Ⅳ-7),second daughter(Ⅳ-9)and son(Ⅳ-10)were tested for mutation sites by Sanger sequencing.Combined with clinical manifestations and examination results,the family was studied.Results The genetic pattern of this family was autosomal dominant.The proband showed decreased visual acuity at the age of 19,bilateral sensorineural deaf-ness at the age of 30,and decreased speech recognition rate.Among 20 members of the family of 5 generations,10(2 deceased)showed similar symptoms of hearing and visual impairment.Proband(Ⅲ-7),eldest daughter(Ⅳ-7)and son(Ⅳ-10)underwent relevant examination.Pure tone audiometry showed bilateral sensorineural deafness.ABR showed no response bilaterally.The 40 Hz AERP showed no response in both ears.OAE showed responses in some or all of the frequencies.No stapedial reflex was detected.The eye movement of Ⅲ-7 and Ⅳ-10 were reasona-ble in all directions,and color vision was normal.Ocular papilla atrophy was observed in different degrees in fundus examination.OCT showed thinning of optic disc nerve fibers in both eyes,and visual evoked potential showed pro-longed P100 wave peak.They were diagnosed as hereditary auditory neuropathy with optic atrophy.A mutation of the OPA1 gene c.1334G＞A(p.Arg445His,NM_015560.2)at a pathogenic locus on chromosome 3 was detected by whole exon detection in Ⅲ-7.The results of generation sequencing analysis showed that the OPA1 gene c.1334G＞A(p.Arg445His,NM_015560.2)mutation of chromosome 3 was also found in Ⅳ-7 and Ⅳ-10.Meanwhile,the gen-otypes of Ⅲ-8 and Ⅳ-9 were wild homozygous,that is,no mutation occurred.Conclusion The OPA1 c.1334G＞A(p.Arg445His,NM_015560.2)mutation site might be the pathogenic mutation in this family.