This paper summarized that the treatments of nourishing lung yin and Tonifying Qi, promoting blood circulation and removing blood stasis and the method of Chinese medicine iontophoresis could work on lung function of the patients with idiopathic pulmonary fibrosis. The review suggested that traditional Chinese medicine compound for treating pulmonary fibrosis mainly by Nourishing Yin, Qi and promoting blood circulation. In the treatment of IPF, the combination of traditional Chinese medicine and Western medicine showed more benefit than western medicine treatment alone.

Objective To observe the safety of midazolam and fentanyl in coronary intervention and its effect on haemodynamics. Methods 150 cases undergoing coronary intervention were randomly divided into three groups(n=50 for each):the control group were given injection of 5 ml saline,midazolam group were given 0.04 mg/kg midazolam and combined fentanyl group were given injection of 0.02 mg/kg midazolam with 1.2μg/kg fent-anyl intravenously. Heart rate(HR),mean blood pressure(MAP),SpO<,2>,OAA/S and BIS were observed during the intervention and the patients' satisfaction and the incidence of complications were investigated. Results There was no significant difference among the three groups in MAP and HR (F=3.34,2.98,P>0.05). MAP increased from (95.7±14.5) mm Hg to (85.4±15.3) mm Hg after treatment (t=4.34,P<0.01) and HR increased from (83.3±23.4) times/min to (78.4±22.7) times/min in control group (t=3.37,P<0.01). BIS score was (90.5±7.2),(75.5±12.8) and (72.3±14.1) during intervention and 24 hVAS score was (53.5±25.4),(58.8±18.2) and (71.9±16.8) in control group,midazolam group and combined fentanyl group,with significant difference between groups (F=10.89,8.56,P<0.01). Conclusion Low dose of midazolam and fentanyl can make the patients calm,which relieves the tensity and anxiety and enhance the tolerance and safety of intervention but has no remarkable effect on bemodynamics.

BACKGROUND:Wear particles-induced osteoblasts apoptosis in vitro has been documented in many studies. However, the apoptosis of osteoblasts in osteolytic bone tissue and the selective mechanisms involved in the pathogenesis of osteolysis have been studied rarely.
OBJECTIVE:To investigate the influence of endoplasmic reticulum (ER) stress on the apoptosis of osteoblasts in osteolytic bone tissue and osteolysis progression.
METHODS:The mouse model of osteolysis was induced with wear particles placed onto the calvaria. The experiment was divided into four groups:blank control group (PBS stimulation);wear particle group (nano-al oy powder suspension stimulation);ER stress positive control group (nano-al oy powder+thapsin stimulation);and ER stress inhibitor group (nano-al oy powder+sodium 4-phenylbutyrate stimulation). The histopathologic change of osteolysis was assessed by hematoxylin-eosin, toluidine blue and alkaline phosphatase staining. Osteoblast proliferation and differentiation in osteolytic craniums were measured. The expression of ER stress markers in osteolytic craniums was examined by western blot analysis. Osteoblast apoptosis was analyzed by TUNEL staining and immunohistochemistry of Caspase-3 in osteolytic craniums.
RESULTS AND CONCLUSION:Wear particles were capable of inducing osteolysis, aggravating the infiltration of inflammatory cells, and inhibiting the differentiation of osteoblasts in osteolytic craniums. Meanwhile wear particles upregulated the ER stress markers and promote the apoptosis in osteolytic craniums. Blocking ER stress with sodium 4-phenylbutyrate dramatical y reduced the severity of osteolysis, significantly reduced bone invasion and inflammatory infiltration, promoted the differentiation of osteoblasts, and dramatical y reduced the apoptosis. Along with apoptosis, the expression of ER stress marker was decreased. The present study suggests that the ER stress may be crucial for osteolysis and represent a potential therapeutic target in the prevention and treatment of patients with total joint replacement who are at high risk of early aseptic loosening development.

Objective To observe the changes of cerebral inflammation-related markers in brain of a transgenic mouse model of Alzheimer's disease (AD) ,and to determine the causative factor to the development of cerebral inflammation in AD. Methods 3- and 12-month-old β-amyloid protein precursor ( APP)/presenilin (PSI) transgenic mice and age-matched wild-type mice (WT) were used in the study. The changes of amyloid plaques, inflammatory factors ( interleukin 1β ( IL-1β ); interleukin 6( IL-6 ); tumor necrosis factor α (TNFα) ;prostaglandin E2 (PGE2)) in the brains among these mice were measured by immunohistochemistry and ELISA. Results Immunohistochemical analysis revealed that no amyloid plaques and activated astrocytes as well as microglia were observed in the 3-month-old APP/PS1 mice. There were no significant differences in the levels of inflammatory factors (IL-1β, IL-6 ,TNFα,and PGE2) between the 3-month-old APP/PS1 and WT mice ( Ps ＞ 0. 05 ). However, abundant amyloid plaques accompanied by a remarkable increase of activated astrocytes and microglia were found in the brain of the 12-month-old APP/PS1 mice. The levels of inflammatory factors (IL-1β,IL-6,TNFα, and PGE2 ) were significantly increased in the 12-month-old APP/PS1 mice ([56. 02 ±9. 04] ng/g, [8. 66 ±0.83] ng/g, [97.48 ±26.58] ng/g, [72. 18 ±21.01] ng/g) than in the WT mice ([29. 18 ± 6. 03] ng/g, [7. 73 ± 0. 74] ng/g, [61.98 ±11.11] ng/g, [37. 23 ± 10. 96] ng/g) and the 3-month-old APP/PS1 mice ( [30. 05 ± 3.53] ng/g, [7.43 ± 1.17] ng/g, [59.34 ± 10. 07] ng/g, [42. 56 ±5.93] ng/g) (P＜0.05,or P＜0.01,respectively). Conclusion This study demonstrates that the APP/PS1mice did not show cerebral inflammation before the appearance of amyloid plaques, and exhibited remarkable inflammation after amyloid plaque deposition. These findings suggest that the induction of cerebral inflammation is tightly associated with amyloid plaque formation, and deposition of amyloid-beta protein (Aβ) may be the direct causative factor to the development of cerebral inflammation in AD.

Objective To investigate the clinical features and the possible pathogenesis of rhythmic movement disorder (RMD) by analyzing 2 patients with RMD and reviewing the literature. Methods By using overnight polysomnogram (PSG) and sleeping video monitoring, the movement patterns, sleep architecture, and sleep quality of 2 patients who met the RMD diagnostic criteria were examined. Results Two male patients were 15-years old. The onset age of patient 1 was 3-years old, and patient 2 was 10-years old. All abnormal movements occurred in sleep, which presented with repetitive, stereotyping and rhythmical movements. Multiple patterns of abnormal sleeping movement were observed in 2 patients: head hypsokinesis, thoracic and waist hyperextension, and pendular movement of bilateral upper extremities. In the sitting position, the patient exhibited kneeling position, and fore-and-aft or lateral rhythmical swing of the upper body accompanied with head-banging. In the prone position, the patient behaved head backward hyperextension, and horizontal and fluctuating pendular movement of the body, which was just like the auto-erotic situation. In the lateral sleep position, the patient supported their head by using the right hand accompanied with fore-and-aft pendular movement of the head and the upper body. These symptoms mentioned above emerged immediately when the patient fell asleep, and continuously existed in all sleep period including non-rapid eye movement and rapid eye movement. All of the symptoms disappeared once the patient woke. The abnormal movement frequency was 0.1-2.0 Hz. In addition, the sleep architecture and quality were severely influenced by RMD in patient 2. Clonazepam might markedly ameliorate the symptoms and sleep quality. Conclusions Multiple abnormal movement patterns may exist in the RMD patients, and these abnormal movements could last during the whole sleep period. PSG and sleeping video monitoring should be undertaken for the suspected RMD patients, which are very useful for the definite diagnosis of RMD.

Objective To investigate the inhibitory effect of IN5 from chlamydiaphage phiCPG1 capsid protein Vp1 on Chlamydia trachomatis (Ct).Methods PCR was used to amplify IN5 gene from Vp1 DNA of phiCPG1, then the recombinant plasmid pET28a/IN5 was constructed.After transformation, the fusion protein IN5 was induced,identified and purified.Ct was incubated with the purified IN5 protein or Vp1 protein.After 48 h of incubation, the inclusion bodies were counted with iodine staining and indirect immunofluorescence.One-way ANOVA was used to compare the difference of inclusion bodies among groups.If the difference among the groups was statistically significant, the Bonferroni method was used to compare any two mean values.Finally, the inhibitory rate of IN5 protein and Vp1 protein to Ct was calculated.Results IN5 protein from chlamydiaphage phiCPG1 capsid protein Vp1 was successfully obtained.At the same concentration of 53μg/mL,the inhibitory rates of Ct growth in IN5 and in Vp1 groups were 52.42% and 78.04%, respectively.Conclusion IN5 protein has inhibitory effect on the growth of Ct,but the inhibitory rate is lower than that of Vp1, which provides a preliminary clue for searching the dominant region of Vp1 protein inhibiting the growth of Ct.

Objective:To compare the analgesic effect between living rhino horn and rhino horn in mice and rats,and to explore the possibility of living rhino horn used as a substitute of rhino horn. Methods:The analgesic effect was compared using the body tor-sion method and the formaldehyde method in mice,and the hot plate method and the thermal sting imager method in rats. Results:Compared with the control group,the living rhino horn at the dose of 0. 35,0. 7 and 1. 4 g·kg - 1 could significantly prolong the incu-bation period of body torsion induced by acetic acid(P < 0. 05 or P < 0. 01),and significantly reduce the number of body torsion(P <0. 05 or P < 0. 01). The three dose groups(0. 35,0. 7,1. 4 g·kg - 1 )of rhino horn could significantly reduce the number of body tor-sion(P < 0. 05 or P < 0. 01). After the second dose and compared with the control group,the pain threshold of high dose group(1. 4 g·kg - 1 )of living rhino horn,high and middle dose groups(0. 7,1. 4 g·kg - 1 )of rhino horn was significantly prolonged(P < 0. 05 or P < 0. 01). Compared with the control group,three dose groups(0. 175,0. 35,0. 7 g·kg - 1 )of living rhino horn and rhino horn could significantly reduce the analgesic effect in mice induced by formaldehyde in the second phase(P < 0. 01). Compared with the control group,the changes of pain threshold before and after the administration in three dose groups(110,220,440 mg·kg - 1 )of liv-ing rhino horn and high dose group(440 mg·kg - 1 )of rhino horn was significantly increased(P < 0. 05 or P < 0. 01). Conclusion:Living rhino horn can be used as a substitute of rhino horn with promising analgesia effect.

Objective To clone and express the polymorphic membrane protein I(PmpI)gene of Chlamydia trachomatis(Ct), and to assess the immunogenicity and biological characteristics of PmpI. Methods A bioinformatic software was used to analyze the sequence of the PmpI gene of Ct, and to predict B cell epitopes in PmpI. With Ct serovar D DNA as the template, PCR was performed to amplify the N?terminal region(from position 90 to 1464)of the PmpI gene, which was cloned into a prokaryotic expression vector pET28a to express the recombinant protein PmpI. A Ni?ion affinity chromatography column was used to purify the recombinant protein, which was used to immunize New Zealand rabbits for preparation of polyclonal antibodies. Western blot analysis was conducted to evaluate the immunogenicity of this protein. Results A comprehensive analysis was carried out on the secondary structure, flexible regions, hydrophilicity plot, antigenic index and surface probability plot of the protein, which suggested that PmpI had 8 dominant B?cell epitopes. The product of PCR targeting the PmpI gene of Ct serovar D showed a total length of 1 375 bp. The recombinant prokaryotic expression vector pET28a?PmpI was successfully constructed. A recombi?nant protein with a relative molecular mass of approximately 50 000 was successfully expressed after isopropylβ?d?1?thiogalactopyranoside (IPTG) induction, and purified by affinity chromatography. Polyclonal antibodies against the recombinant protein were successfully prepared. Conclusion The N?PmpI protein of Ct serovar D is cloned and expressed successfully, laying a foundation for further studies on its biological functions.

Objective To evaluate the clinical efficacy of Compound Sophorae Flavescentis Radix (Kushen) Injection combined with gamma knife for treatment of locally advanced pancreatic carcinoma. Methods Totally 65 patients of locally advanced pancreatic cancer were randomly divided into two groups:32 cases of simple gamma knife group (group A), 33 cases of Compound Kushen Injection combined with gamma knife treatment (group B). Patients received enhancement computed tomography scanning and CA199 review at 1, 3, 6, 9, 12 months after treatment, and once every six months, a total of 36 months of follow-up. Short-term and long-term efficacy was observed after treatment, and survival curve analysis was carried out. Results Clinical benefit response was 53.13% in group A and 84.85% in group B (P=0.006);median survival time of two groups was 11.00 months in group A and 23.00 months in group B;the average survival time in group A was 16.37 months, and 22.28 months in group B (P=0.017). In the two groups, treatment of the 65 patients was completed smoothly as planned, and no one had serious complications, such as pancreatic leakage, skin burns, viscera perforation and radioactive enteritis. Conclusion Compound Kushen Injection combined with gamma knife can treat locally advanced pancreatic carcinoma safely and efficiently, which can improve patients’ life quality, especially in cancer pain control.

OBJECTIVETo investigate the effects of hydrogen sulfide (H₂S) on oxidative stress and endoplasmic reticulum stress (ERS) in a rat model of diabetic cardiomyopathy (DCM).

METHODSThirty male SD rats were randomly divided into control group, diabetes group and treatment group( n = 10). Intraperitoneal injection of streptozotocin was utilized to establish a rat model of DCM. The rats with DCM in treatment group were intraperitoneally injected with NaHS solution. After treated for 12 weeks, the hearts isolated from rats were perfused on a langendorff apparatus. The ventricular hemodynamic parameters were measured. The ultrastructures of myocardium were observed using electron microscopy. The content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in myocardial tissue were determined by spectrophotometry. The expressions of C/EBP homologous protein( CHOP), glucose-regulated protein 78 (GRP78) and Caspase 12 at mRNA level in myocardium were detected using RT-PCR.

RESULTSCompared with control group, the cardiac function and myocardial ultrastructure were damaged obviously in diabetic rats. In myocardial tissue, the content of MDA was increased, while the activities of SOD and GSH-Px were decreased. CHOP, GRP78 and Caspase 12 mRNA expressions were increased significantly. Compared with diabetes group, cardiac function and myocardial ultrastructure damage were improved in treatment group. The content of MDA was decreased, while the activities of SOD and GSH-Px were increased significantly. The mRNA levels of CHOP, GRP78 and Caspase 12 were increased.

CONCLUSIONH2S can protect myocardium in diabetic rats, maybe it is related to reduce oxidative stress damage and inhibition of the ERS-induced apoptosis pathway.

Animals ; Apoptosis ; Caspase 12 ; metabolism ; Diabetes Mellitus, Experimental ; drug therapy ; Diabetic Cardiomyopathies ; drug therapy ; Endoplasmic Reticulum Stress ; Glutathione Peroxidase ; metabolism ; Heat-Shock Proteins ; metabolism ; Hydrogen Sulfide ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Myocardium ; ultrastructure ; Oxidative Stress ; Rats ; Streptozocin ; Superoxide Dismutase ; metabolism ; Transcription Factor CHOP ; metabolism