Efficacy of combined orthodontic-periodontic treatment for patients with periodontitis and its effect on inflammatory cytokines: A comparative study.

INTRODUCTION: In this study, we aimed to investigate the efficacy of combined orthodontic-periodontic treatment in the treatment of patients with periodontitis and its effects on the levels of inflammatory cytokines. METHODS: A total of 117 patients with periodontitis were randomly assigned to the basic group (receiving basic periodontic treatment, n = 58) and the combined group (receiving combined orthodontic-periodontic treatment, n = 59). In addition, 52 healthy people without periodontal disease were selected as the normal group. Probing depth, tooth mobility, plaque index, clinical attachment level, and sulcus bleeding index were recorded. ELISA was applied to detect gingival crevicular fluid (GCF) and serum levels of inflammatory cytokines. A 2-year clinical follow-up was conducted. RESULTS: Before treatment, the periodontal parameters (probing depth, tooth mobility, plaque index, clinical attachement level, and sulcus bleeding index) and GCF and serum levels of inflammatory cytokines (high-sensitivity C-reactive protein, interleukin-1ß, interleukin-5, interleukin-6, interleukin-8, tumor necrosis factor-α, and prostaglandin E2) in the combined and basic groups were higher than those in the normal group. After 6 and 18 months of treatment, the periodontal parameters and GCF and serum levels of inflammatory cytokines decreased in the combined and basic groups. The periodontal parameters and the GCF and serum levels of inflammatory cytokines in the combined group were significantly lower than those in the basic group after 18 months of treatment. The combined group had a lower recurrence rate compared with the basic group. CONCLUSIONS: Combined orthodontic-periodontic treatment had good clinical efficacy in the treatment of periodontitis and could effectively decrease the levels of inflammatory cytokines.

[Monitoring of farmland drought based on LST-LAI spectral feature space].

Farmland drought has the characteristics of wide range and seriously affecting on agricultural production, so real-time dynamic monitored has been a challenging problem. By using MODIS land products, and constructing the spectral space of LST and LAI, the temperature LAI drought index (TLDI) was put forward and validated using ground-measured 0-10 cm averaged soil moisture of Ningxia farmland. The results show that the coefficient of determination (R2) of both them varies from 0.43 to 0.86. Compared to TVDI, the TLDI has higher accuracy for farmland moisture monitoring, and solves the saturation of NDVI during the late development phases of the crop. Furthermore, directly using MODIS land products LST and LAI and avoiding the complicated process of using the original MODIS data provide a new technical process to the regular operation of farmland drought monitoring.

[New index for soil moisture monitoring based on deltaT(s)-albedo spectral information].

Monitoring soil moisture by remote sensing has been an important problem for both agricultural drought monitoring and water resources management. In the present paper, we acquire the land surface temperature difference (deltaT(s)) and broadband albedo using MODIS Terra reflectance and land surface temperature products to construct the deltaT(s)-albedo spectral feature space. According to the soil moisture variation in spectral feature space, we put forward a simple and practical temperature difference albedo drought index (TDADI) and validate it using ground-measured 0-10 cm averaged soil moisture of Ningxia plain The results show that the coefficient of determination (R2) of both them varies from 0.36 to 0.52, and TDADI has higher accuracy than temperature albedo drought index (TADI) for soil moisture retrieval. The good agreement of TDADI, Albedo/LST, LST/ NDVI and TVDI for analyzing the trends of soil moisture change supports the reliability of TDADI. However, TDADI has been designed only at Ningxia plain and still needs further validation in other regions.

Mineralocorticoid receptor expression in human venous smooth muscle cells: a potential role for aldosterone signaling in vein graft arterialization.

Experimental studies have suggested a role for the local renin-angiotensin-aldosterone system in the response to vascular injury. Clinical data support that aldosterone, via activation of the mineralocorticoid receptor (MR), is an important mediator of vascular damage in humans with cardiovascular disease. In mineralocorticoid-sensitive target tissue, aldosterone specificity for MR is conferred enzymatically by the cortisol-inactivating enzyme 11ß-hydroxysteroid-dehydrogenase-2 (11ßHSD2). However, the role of MR/aldosterone signaling in the venous system has not been explored. We hypothesized that MR expression and signaling in venous smooth muscle cells contributes to the arterialization of venous conduits and the injury response in vein bypass grafts. MR immunostaining was observed in all samples of excised human peripheral vein graft lesions and in explanted experimental rabbit carotid interposition vein grafts, with minimal staining in control greater saphenous vein. We also found upregulated transcriptional expression of both MR and 11ßHSD2 in human vein graft and rabbit vein graft, whereas control greater saphenous vein expressed minimal MR and no detectable 11ßHSD2. The expression of MR and 11ßHSD2 was confirmed in cultured human saphenous venous smooth muscle cells (hSVSMCs). Using an adenovirus containing a MR response element-driven reporter gene, we demonstrate that MR in hSVSMCs is capable of mediating aldosterone-induced gene activation. The functional significance for MR signaling in hSVSMCs is supported by the aldosterone-induced increase of angiotensin II type-1 receptor gene expression that was inhibited by the MR antagonist spironolactone. The upregulation of MR and 11ßHSD2 suggests that aldosterone-mediated tissue injury plays a role in vein graft arterialization.

Angiotensin II and tumor necrosis factor-alpha upregulate survivin and Kruppel-like factor 5 in smooth muscle cells: Potential relevance to vein graft hyperplasia.

BACKGROUND: Survivin (SVV) is a unique inhibitor of apoptosis protein (IAP) that regulates both apoptosis and mitosis. Recent work suggests that SVV plays a critical role in the vascular injury response, but the molecular pathways remain unclear. METHODS: We examined the expression of SVV and the transcription factor, KLF5, in human venous smooth muscle cells (VSMC) by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis after treatment with angiotensin II (Ang II) or tumor necrosis factor-alpha (TNF-alpha). An adenoviral construct expressing SVV or GFP was also employed to assess effects on KLF5 expression. A rabbit carotid interposition vein graft model was used to assess the relevance of KLF5 to bypass graft healing. RESULTS: Stimulation of VSMC with Ang II and TNF-alpha led to a rapid upregulation of KLF5 expression, and a later increase in SVV, which was cell-cycle independent. Overexpression of SVV in VSMC led to an early and persistent induction of KLF5. KLF5 was upregulated in rabbit vein grafts early (1 day) after grafting. CONCLUSIONS: We speculate that SVV is a central point of convergence of multiple signaling pathways in vascular injury, and that it regulates the local amplification of these pathways in the vessel wall.

Regulation of vein graft hyperplasia by survivin, an inhibitor of apoptosis protein.

OBJECTIVE: Survivin (SVV) is an inhibitor of apoptosis protein (IAP) that is upregulated in cancer and has recently been implicated in vascular injury. We sought to investigate the role of SVV in vein graft hyperplasia. METHODS AND RESULTS: Adenoviral constructs expressing a dominant-negative (AdT34A) and wild-type (AdWT) SVV were used. Proliferation and apoptosis were assayed on endothelial cells (ECs) and smooth muscle cells (SMCs) from human saphenous vein. A rabbit carotid interposition vein graft model (N=31) was used, with adventitial gene transfer of SVV constructs. In vitro, overexpression of SVV was associated with protection from cytokine-induced apoptosis in ECs and SMCs; conversely, AdT34A directly induced apoptosis in these cells. SMC proliferation was increased by AdWT infection, whereas AdT34A reduced proliferation; both effects were serum-dependent. Expression of platelet-derived growth factor (PDGF) in SMCs was regulated by functional SVV expression in analogous fashion. In vivo, proliferation and apoptosis (7 days), as well as wall thickness (30 days), were modified by adenoviral-mediated SVV expression. Adventitial angiogenesis was regulated by the SVV-expressing constructs in a fashion parallel to wall thickness changes. CONCLUSIONS: SVV is a critical regulator of multiple processes, including proliferation, apoptosis, and angiogenesis, that determine the remodeling response of vein grafts following arterialization.