This study was aimed to verify the effects of staged sequential therapy on expressions of matrix metalloproteinase-9 (MMP-9) and its inhibitor TIMP-1 within lung tissues in asthmatic rats with the airway remodeling, by applying a series of tests such as the immunohistochemistry, western blot and real-time fluorescent quantitative PCR. SD rats were randomly divided into 7 groups, which were the asthmatic group (Group X), the normal group (Group Z), the No. 1 sequential therapy group (Group A1), the No. 2 sequential therapy group (Group A2), the No. 3 sequential therapy group (Group A3), the montelukast group (Group M), and the budesonide group (Group B). The asthmatic model was established in each group except Group Z, by sensitization with both ovalbumin (OVA) and aluminium hydroxide via injection at the 1st, 8th and 15th day in a 22-day duration, followed by OVA aerosol inhalation every other day for 8 weeks for asthma activation. At the 8th day after the asthmatic model was established, Group A1 was orally given Ma-Xing Er-Chen Tang (MXECT) during acute phase while given normal saline (NS) during catabasis and stable phase; Group A2 was given MXECT during acute phase, and given modified Jin-Shui Liu-Jun Jian (JSLJJ) during catabasis as well as given NS during stable phase; Group A3 was given MXECT during acute phase, and given modified JSLJJ during catabasis as well as given Liu-Wei Di-Huang (LWDH) Powders during stable phase;Group M was given salbutamol via aerosol inhalation after stimulation, while orally given montelukast during catabasis and stable phase; Group B was given salbutamol via aerosol inhalation after stimulation, while given inhaled budesonide during catabasis and stable phase; Group X was given NS. After the 7-week intervention, the immunohistochemistry, western blot and real-time quantitative PCR were applied to analyze the location and quantitative expression of MMP-9 and TIMP-1, so as to find out the biological mechanism on expressions of MMP-9 and TIMP-1 in lung tissues of asthmatic rats from molecular levels to gene levels. The results of immunohistochemistry, western blot and real-time fluorescent quantitative PCR showed as follows. Compared with Group Z, the contents of MMP-9 and TIMP-1 increased significantly within lung tissues in Group X. Compared with Group X, the contents of MMP-9 and TIMP-1 decreased within lung tissues of asthmatic rats in each treatment group. It was concluded that the expression of MMP-9 and TIMP-1 elevated during asthma. TCM staged sequential therapy can regulate the ratio between MMP-9 and its inhibitor so as to block the airway remodeling, by decreasing the expression of MMP-9 and its inhibitor within lung tissues in asthmatic rats. This is one of the important action mechanisms.

Objective To explore the effect of cigarette smoke exposure on testis structure and nitric oxide (NO) level in testis of rats.Methods A total of 160 adult male SD rats were divided into control group and low,medium,high dose groups.The smoke-exposed rats were respectively exposed to the smog for the periods of 2,4,6,8 and 12 weeks,10 rats in each group.The smoke-exposed rats were exposed to cigarette smoke for 0.5 h per day.The testicular tissue structure was observed and the body mass and the NO level of testis were measured.Results Compared with the control group and low dose group,the body mass of the rats was significantly lower in the medium and high dose groups exposed for 4,6,8,12 weeks (P<0.05).Compared with the medium dose groups,the body mass of the rats was significantly lower in the high dose group exposed for 8 weeks and 12 weeks (P<0.05).And with the increase of exposure dose,the reducing was even more obvious.Compared with the control group and low and medium dose groups,NO level in testis of rats was significantly increased in the high dose groups exposed for 2,4,6,8 weeks (P<0.05).Compared with the control group,NO level in testis of rats was significantly increased in the medium dose groups exposed for 8 weeks (P<0.05).Compared with the control group,NO level in testis of rats was significantly increased in the low,medium and high dose groups exposed for 12 weeks (P<0.05);and compared with the low dose group,NO level in testis of rats was significantly increased in the medium and high dose groups(P<0.05).Conclusion Cigarette smoke exposure may have impacts on testis tissue and lead to the increase of NO level in testis of male rats.

Objectives To explore the expression of HER4 and VEGF in NSCLC and elucidate the relationship between their expression and the characteristic of clinical pathology. Methods 82 cases of paraffin-embedded tissues from informative NSCLC were used to detect the expression of HER4 and VEGF by means of immunohistochemical assay. Results HER4 is overexpressed in 65;9%of NSCLC cases. The overexpression of HER4 is correlated with the lymph node metastasis and TNM staging. VEGF is expressed in 53.7%of NSCLC cases. The expression of VEGF is also correlated with the lymph node metastasis and TNM staging, and the expression of VEGF is correlated with the overexpression of HER4.Conclusions HER4 and VEGF are the protein to regulate the growth of NSCLC and it might be a good way for the treatment of NSCLC by suppressing the overexpression of HER4 and VEGF.

ObjectiveTo construct a mouse model for studying pathophysiology and mechanism of human Chlamydia trachomatis genital infection.MethodsInnate immunity-deficient C3H/HeJ female mice were infected intravaginally with human C.trachomatis serovar D urogenital isolates for screening the highest violent clinical strain.The clinical strain UT0603 as well as standard strain D/UW-3/CX were then used to reinfect na(i)ve mice,the lower genital tract shedding were monitored by swabbing every 3-7 day over the entire infection period by culture.Some mice were sacrificed at early infection stage to detection of in site Chlamydia growth by immunofluorescence assay,then all the mice were sacrificed at later infection stage to evaluate upper genital tract gross pathology and histopathological characterization.ResuIts In the lower genital tract,Chlamydia shedding time course were significantly prolonged in clinical strain infected mice.Chlamydia not only growth in the lower genital tract,the live organism also ascending and growth in the upper genital tissue.The gross appearance under naked eyes and dilation and inflammation scores under microscope all showed that the genital tract pathology from the clinical strain infected mice were much more severe than standard strain infected control mice.Conclusion Together,all these results demonstrated that a mouse model for Chlamydia genital infection was constructed.

Objective To investigate the immune injury in genital tract of BALB/c mice induced by plasmid protein pORF5 of Chlamydia trachomatis and its possible mechanism.Methods GST(glutathione-S-transferases)-pORF5 fusion protein was expressed and digested with PreScission Protease to obtain the target protein without GST tag.After further purification and endotoxin removal,pORF5 protein was injected into the posterior fornix of BALB/c mice on day 1,3 and 6,while the control groups were injected with PBS or GST protein respectively,and then all the mice were sacrificed on day 7 to evaluate genital tract gross pathology and histopathological characterization.The levels of TNF-α,IL-1β and IL-6 in serum,splenocytes culture supernatant and vaginal douche were detected by ELISA.Results Mice in pORF5 group developed different degrees of swelling in isthmic portion and ampulla of uterine tube,connective tissue adhesion and hydrosalpinx in the genital tract tissues,while the PBS group and the GST group did not show any obvious change.The inflammatory score showed that the genital tract pathology in pORF5 group was much more severe than PBS and GST control groups (P＜0.O1).The levels of TNF-α,IL-1β and IL-6 in vaginal douche and splenocytes culture supernatants in pORF5 group were obviously higher than those of PBS and GST groups (P＜0.05).The levels of TNF-α and IL-1β in serum were also higher than those of GST and PBS groups (P＜0.01).Conclusion pORF5 plasmid protein could induce pathological immune response in the genital tract of BALB/c mice,which may be associated with the increase of the production of the inflammatory cytokines TNF-α,IL-1β and IL-6 in BALB/c mice.

BACKGROUND: Perioperative treatment has become an increasingly important aspect of the management of patients with non-small cell lung cancer (NSCLC). Small-scale clinical studies performed in recent years have shown improvements in the major pathological remission rate after neoadjuvant therapy, suggesting that it will soon become an important part of NSCLC treatment. Nevertheless, neoadjuvant immunotherapy may be accompanied by serious adverse reactions that lead to delay or cancelation of surgery, additional illness, and even death, and have therefore attracted much attention. The purpose of the clinical recommendations is to form a diagnosis and treatment plan suitable for the current domestic medical situation for the immune-related adverse event (irAE). METHODS: This recommendation is composed of experts in thoracic surgery, oncologists, thoracic medicine and irAE related departments (gastroenterology, respirology, cardiology, infectious medicine, hematology, endocrinology, rheumatology, neurology, dermatology, emergency section) to jointly complete the formulation. Experts make full reference to the irAE guidelines, large-scale clinical research data published by thoracic surgery, and the clinical experience of domestic doctors and publicly published cases, and repeated discussions in multiple disciplines to form this recommendation for perioperative irAE. RESULTS: This clinical recommendation covers the whole process of prevention, evaluation, examination, treatment and monitoring related to irAE, so as to guide the clinical work comprehensively and effectively. CONCLUSIONS Perioperative irAE management is an important part of immune perioperative treatment of lung cancer. With the continuous development of immune perioperative treatment, more research is needed in the future to optimize the diagnosis and treatment of perioperative irAE.