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Pulmonary hypertension is a disease that impairs cardiopulmonary function and is characterised by the limitation of progressive physical activity and decline in health-related quality of life. Patients usually present with a range of severe symptoms, including dyspnoea, fatigue, chest pain and oedema, which affect their quality of life. Compared to the general population, patients usually have a lower health-related quality of life, with differences in several aspects such as physical functioning, mental health, social interactions and career. The aim of this review is to examine recent research advances in health-related quality of life in patients with pulmonary hypertension, including its influencing factors and improvement measures, in order to improve the understanding and management of this condition.

Objective: To investigate the effects of Porphyromonas gingivalis derived outer membrane vesicles (Pg OMV) on osteoclast differentiation of macrophages and its underlying mechanisms. Methods: The morphology and the size distribution of Pg OMV were analyzed by transmission electron microscopy and nanoparticle tracing analysis, respectively. The osteoclast precursors were treated with 1, 3 and 10 mg/L Pg OMV (1, 3 and 10 mg/L OMV treatment group) or phosphate buffer solution (PBS)(control group). The formation of osteoclasts was analyzed by tartrate-resistant acid phosphase (TRAP) staining and F-actin staining and real-time quantitative PCR (RT-qPCR) were used to detect the expression of Fos and matrix metallopeptidase 9 (MMP9). Polymyxin B (PMB) was used to block lipopolysaccharide (LPS) and then Pg OMV was used to treat osteoclast precursor (PMB-OMV treatment group), and OMV treatment group was used as control. TRAP and F-actin staining were used to observe the formation of osteoclasts and actin rings. The effect of Pg OMV on the expression of Toll-like receptor (TLR) 2 and TLR4 in preosteoclasts was detected by Western blotting. The osteoclast precursors were pretreated with 10, 50, 100 and 200 μmol/L C29, an inhibitor of TLR2, and then treated with Pg OMV(OMV+10, 50, 100 and 200 μmol/L C29 treatment group) and OMV treatment group without C29 pretreatment was control. TRAP and F-actin staining were used to observe the formation of osteoclasts and actin rings. The osteoclast precursor cells were treated with OMV (OMV treatment group) and OMV incubated with PMB (PMB-OMV treatment group) and the expression of TLR2 in osteoclast precursor was detected by Western blotting. Results: Pg OMV showed classical vesicular structures, and the average particle size of Pg OMV were 179.2 nm. A large number of actin rings were observed in the 3 and 10 mg/L OMV treatment groups. The percentages of TRAP-positive osteoclast area in 3 mg/L OMV treatment group [(22.6±2.1)%] and 10 mg/L OMV treatment group [(32.0±2.3)%] were significantly increased compared with control group [(4.9±0.5)%] ( P <0.001). Compared with the control group (1.000±0.029), the mRNA relative expression of Fos in 3 mg/L OMV treatment group (1.491±0.114) and 10 mg/L OMV treatment group (1.726±0.254) was significantly increased ( P =0.013, P =0.001). Compared with the control group (1.007±0.148), the mRNA relative expression of MMP9 in the group of 10 mg/L OMV (2.232±0.097) was significantly increased ( P <0.001). Actin ring formation was less in PMB-OMV treatment groups than in OMV treatment groups. The proportion of TRAP-positive osteoclasts area [(14.8±3.8)%] in PMB-OMV treatment group was significantly lower than OMV treatment group [(31.5±6.7) %] ( P =0.004). The relative expression of TLR2 in OMV treatment group (1.359±0.134) was significantly higher than that in the control group (1.000±0.000) ( t =4.62, P =0.044). Compared with the OMV treatment group [(29.4±1.7)%], 50, 100 and 200 μmol/L C29 significantly decreased the formation of osteoclasts [(24.0±1.7)%, (18.5±2.1)%, (9.1±1.3) %] ( P =0.026, P <0.001, P <0.001). TLR2 protein expression in PMB-OMV group (0.780±0.046) was significantly lower than that in OMV group (1.000±0.000)( t =8.32, P =0.001). Conclusions: Pg OMV can promote osteoclast differentiation by carrying LPS, TLR2 plays an important role in Pg OMV mediated osteoclast differentiation.

Periodontitis is the main cause of adult tooth loss, which seriously affects oral health and acts as a high-risk factor for varieties of systemic diseases. Gestational diabetes mellitus (GDM) is defined as glucose intolerance occurred or firstly identified during pregnancy. Prevalence of GDM is increasing over the past years worldwide. Besides adverse effects toward maternal and infant health in perinatal period, GDM also has long-term effects. Current studies have demonstrated that there is a bidirectional relationship between periodontitis and diabetes; however, the exact relationship between periodontitis and GDM remains elusive. In this paper, first reviewed the clinical association of periodontitis and GDM, and then discussed the underlying mechanisms of the two diseases, finally summarized the positive effect of periodontal therapy in controlling GDM. This paper will provide theoretical basis for the prevention diagnosis and therapy for the related diseases, promoting the maternal and infant health.

Objective: To investigate the effect of focal adhesional kinase (FAK) on tumor necrosis factor α (TNF-α)-induced MMP-2 and -9 activities in cornea epithelium., Methods: Experimental research. The human corneal epithelial cells (HCE) were cultured in vitro. HCEs were incubated with different concentrations of TNF-α for 24 h, including 1 µg/L (group B), 10 µg/L (group C) and 100 µg/L (group D). The control group (group A) was incubated with phosphate buffer solution. The activities of MMPs were examined by gelatin zymography and the phosphorylation of FAK was examined by western blot analysis. FAK was down regulated by FAK siRNA following lipofectamine-mediated transfection in corneal epithelial cells. Down-regulation was confirmed using western blot analysis. Cells cultured with different concentrations of TNF-α (Groups B to D) and the control group (group A) was at similar volumes of media. Then the activities of MMP-2 and -9 were examined by gelatin zymography and the phosphorylation of FAK by western blot analysis. Statistical methods adopted one-way ANOVA and Tukey's honestly significant test between each group., Results: Gelatin zymography: Activities of MMP-2 and -9 in TNF-α treated groups were greater than those of the control group. The activity of MMP-2 in A, B, C and D groups was 124.06 ± 4.06, 146.72 ± 5.51, 241.18 ± 5.65 and 389.95 ± 4.44, respectively with F = 2960.91, P = 0.000. The activity of MMP-9 in A, B, C and D groups was 122.78 ± 5.86, 165.70 ± 7.90, 479.49 ± 6.22 and 495.88 ± 5.03 (F = 4937.46, P = 0.000). Significant differences were found in each two groups (P = 0.000). Western blot analysis:the phosphorylation of FAK (p-FAK) in test groups (10-100 ng/ml) were significantly greater than that in control group (p-FAK of group C and D was 0.52 ± 0.03 and 0.61 ± 0.06, F = 431.03, P = 0.000). p-FAK levels in 100 ng/ml group were greater than that in 10 ng/ml group (P = 0.005). After down-regulating the protein FAK, TNF-α had no effect on the activity of MMP-2 (The data of MMP-2 were 55.13 ± 0.66, 55.67 ± 0.43, 55.49 ± 0.20 and 55.91 ± 0.37 in groups A, B, C and D, F = 2.73, P = 0.079). We detected the increasing activity of MMP-9 in group C, D and p-FAK in group D (The data of MMP-9's activity were 80.48 ± 0.39, 81.26 ± 0.62, 84.43 ± 0.47, 85.56 ± 0.61 in groups A, B, C and D, F = 105.80, P = 0.000). The activity of MMP-9 in group D was stronger than that from the group C (P = 0.019). We just only detected a small quantity of p-FAK in group D (0.47 ± 0.05), which was weaker than that before down regulating the protein FAK (t = 5.03, P = 0.001)., Conclusion: Our results demonstrate the critical role of FAK in TNF-α induced activity of MMP-2 and -9 in human corneal epithelium cells. Blocking the FAK signaling pathway can reduce the activity of MMP-2 and -9 which may play an important role in prevention and treatment of corneal diseases.

Objective: the reversibility of chronic obstructive pulmonary disease (COPD) is evaluated mainly by FEV(1) after bronchodilators. However, lung volumes also change significantly in COPD, but few studies addressed the characteristics of the changes in post bronchodilator airflow and lung volume in patients with COPD. This study was carried out to evaluate the difference of FEV(1) response and forced vital capacity (FVC) response to bronchodilators in patients with COPD as well as the impact of severity of COPD on the flow and volume reversibility., Methods: 465 patients with COPD (male 426, female 39), aged 67.1 +/- 8.3 (42 approximately 86) yrs were enrolled from Jan. 2006 to Aug. 2008. The severity of COPD was graded according to the GOLD criteria. The change and rate of change of FVC and FEV(1) 20 minutes after inhalation of salbutamol 400 microg via spacer were measured and compared. Positive response to the bronchodilator was determined as FEV(1) or FVC increased 12% as well as 200 ml or above. The impacts of severity on flow and volume response were also studied., Results: post-bronchodilator FEV(1) increased 117 ml with a 13.2% improvement on average compared with baseline. Post-bronchodilator FVC increased 258 ml and improved by 14.0% on average. The rate of positive reversibility in FEV(1) and FVC was 18.7% (87/465) and 44.1% (205/465), respectively. The improvement of FEV(1) decreased as a function of the severity of COPD. In contrast, the improvement of FVC was increased in those with more severe disease., Conclusion: the improvement of lung volume is more significant and maybe more important than airflow response in patients with COPD, especially in those with severe disease. In addition to FEV(1), the reversibility of COPD should also be evaluated by FVC.

Objective: To study the effect of macrophage inflammatory protein-1alpha(MIP-1alpha) and its mRNA on airway inflammation of mouse with induced asthma., Methods: Seventy male BALB/C mice were randomly divided into the control group and asthma group (including 7 subgroups, 10 mice each). The control group included group A(24) (the lavaging subgroup was sacrificed 24 h after the last challenge) and group A(0) (the non-lavaging subgroup was sacrificed from 18 h to 24 h after the last challenge); asthma group included group B(3) (the lavaging subgroup was sacrificed 3 h after the last challenge), group B(8) (the lavaging subgroup was sacrificed 8 h after the last challenge), group B(24) (the lavaging subgroup was sacrificed 24 h after the last challenge), group B(36) (the lavaging subgroup was sacrificed 36 h after the last challenge) and group B(0) (the non-lavaging subgroup was sacrificed from 18 h to 24 h after the last challenge). In the experiment, the mice model of asthma was established by the ovalbumin (OVA) challenge methods. Eosinophils (EOS) numbers and differentiated cell numbers in bronchoalveolar lavage fluid (BALF) were counted; the concentrations of MIP-1alpha in serum and BALF were measured by sandwich enzyme-linked immunosorbent assay (sandwich ELISA); the protein expressions of MIP-1alpha were detected by immunohistochemical techniques; the mRNA expressions of MIP-1alpha were determined by in situ hybridization technique., Results: (1) The concentrations of MIP-1alpha in BALF and serum of group B(3) [(30.2 +/- 4.2) pg/ml, (30.8 +/- 4.6) pg/ml], group B(8) [(35.3 +/- 4.9) pg/ml, (34.9 +/- 5.1) pg/ml], group B(24) [(42.9 +/- 5.8) pg/ml, (41.7 +/- 6.3) pg/ml] and group B(36) [(37.8 +/- 4.7) pg/ml, (35.7 +/- 4.9) pg/ml] were significantly higher than those of group A(24) [(20.9 +/- 3.8) pg/ml, (22.4 +/- 4.3) pg/ml] (P < 0.01); the concentrations of MIP-1alpha in BALF and serum went up at 3 h, reached peak at 24 h, and had descended at 36 h. (2) Immunohistochemistry showed that the protein expressions of MIP-1alpha around the bronchus of group B(0) [(26.4 +/- 6.2)%] were significantly elevated as compared to those of group A(0) [(10.3 +/- 2.5)%] (P < 0.01), the epithelial cell was the chief expression cell. (3) In situ hybridization showed that the mRNA expressions of MIP-1alpha around the bronchus of group B(0) [(23.9 +/- 4.2)%] were significantly increased when compared to those of group A(0) [(8.7 +/- 1.8)%] (P < 0.01), the epithelial cell was the chief expression cell. (4) There was a significant correlation between the concentrations of MIP-1alpha and the numbers of EOS in BALF and between the concentrations of MIP-1alpha and the percentage of EOS numbers in the total cell numbers (EOS%) in BALF., Conclusions: MIP-1alpha protein and MIP-1alpha mRNA were found strongly expressed in mouse asthma model, the epithelial cell was the chief expression cell; the kinetic characteristic of MIP-1alpha showed that its level increased at 3 h, reached peak at 24 h and declined at 36 h; MIP-1alpha and EOS gathering had a significant correlation.

Objective: Asthma is a chronic respiratory tract disorder characterized by airway hyperreaction (AHR), persistent airway inflammation, high serum IgE, overproduction of IL-4, IL-5 and IL-13 by allergen-specific Th2 cells. The morbidity and mortality of asthma have continued to increase despite the use of currently available therapeutic agents. The reputed effects of traditional Chinese medicines (TCMs) have led to increasing use of TCMs for treatment of asthma throughout the world. The aims of this study were to investigate in asthma model of young rat the mRNA expressions of apoptotic gene fas and bcl-2, eosinophils (EOS) apoptosis in airway, and effects of achyranthes bidentata polysaccharides (ABPS), a group of polysaccharides extracted from TCM Achyranthes bidentata blume, on treatment of asthma., Methods: Fifty Sprague-Dawley (SD) rats were divided into five groups, 10 rats per group. Asthma in rats was induced by intraperitioneal sensitization and challenge with nebulized ovalbumin (OVA). A pretreatment with ABPS [50 mg/(kg x d)] was done according to three different schedules: consecutively 3 days at sensitization (T1), at challenge (T2) or both of the two periods (T3). Sham-treated rats (A) and naive rats (C) served as controls. The animals were sacrificed 24 hours after the last challenge. The mRNA expression of bcl-2 and fas in eosinophils presenting in airway and the apoptosis of eosinophils in airway were assessed by using in situ hybridization with oligonucleotide probe and TUNEL methods, respectively., Results: (1) Twenty-four hours after the last antigen challenge, the mRNA expression of fas in eosinophils presenting in airway significantly decreased in group A [(43.4 +/- 10.0)%] compared with that in group C [(73.2 +/- 11.9)%] (P < 0.01). ABPS could increase the fas mRNA expression significantly in all the three groups [(59.0 +/- 8.1)%, (57.5 +/- 9.6)%, (76.2 +/- 2.7)%], compared with that in group A (P < 0.05, P < 0.05, P < 0.01, respectively). The expression of the bcl-2 mRNA in group C was (47.9 +/- 8.7)%, it was elevated to (67.4 +/- 7.3)% in group A (P < 0.01). The expression of the bcl-2 mRNA in ABPS treated T1 and T3 groups was significantly lowered [(57.7 +/- 12.7)%, (57.3 +/- 6.8)%, P < 0.05], but not in T2 group [(72.4 +/- 6.7)%]. (2) In group A, the EOS presenting in the airway increased significantly, but there were few apoptotic EOS; the percentage of apoptotic eosinophil was distinctly lower in group A than that in group C [(5.3 +/- 2.2)% vs. (15.9 +/- 2.4)%, P < 0.01]. Compared with that in group A, the eosinophil apoptosis ratio in those ABPS treated groups T1, T3 was evidently elevated [(8.7 +/- 2.9)%, (9.8 +/- 2.2)%, P < 0.05, P < 0.05], but ABPS treated at challenge (T2) could not change the eosinophil apoptosis ratio significantly (P > 0.05)., Conclusion: (1) In asthmatic rat, the expressions of the genes fas and bcl-2 mRNA in EOS were changed evidently and the ratio of EOS apoptotosis reduced greatly. (2) ABPS could enhance the apoptosis of EOS by upregulating the expression of the genes fas and bcl-2 mRNA.