Evaluation of MHOST analysis capabilities for a plate element

Results of the evaluation of the static, buckling, and free vibration analyses capabilities of MHOST for the plate elements are presented. Two large scale, general purpose finite element codes (MARC and MSC/NASTRAN) are used to validate MHOST. Comparisons of MHOST results with those from MARC and MSC/NASTRAN show good agreement and indicate that MHOST can be used with confidence to perform the aforementioned analyses using the plate element

Sleep duration and patterns in Chinese older adults: A comprehensive meta-analysis

This meta-analysis examined the mean sleep duration and patterns in Chinese older adult population. A literature search was systematically conducted covering major English (PubMed, Embase and PsycINFO) and Chinese (Chinese National Knowledge Infrastructure (CNKI), WanFang and SinoMed) databases. Data in studies with the mean and standard deviation of sleep duration and/or the proportion of short and long sleep durations in Chinese older adults were extracted and pooled using random-effects models. Subgroup analyses were conducted according to gender, region, area, survey time and sample size. A total of 36 studies with 150,616 subjects were included for analyses. The pooled mean sleep duration of 21 studies with available data was 6.82 hours/day (95% CI: 6.59–7.05 hours/day). The estimated proportions of sleep duration \u3c5 hours/day, \u3c6 hours/day, \u3c7 hours/day were 18.8% (95% CI: 1.7%–35.9%), 26.7% (95% CI: 19.7%–33.7%) and 42.3% (95% CI: 34.8%–49.8%), respectively. The pooled proportions for long sleepers were 22.6% (95% CI: 13.9%–31.4%) (\u3e8 hours/day) and 17.6% (95% CI: 12.4%–22.9%) (\u3e9 hours/day). Given the adverse effects of unhealthy sleep patterns, health professionals should pay more attention to sleep patterns in this population in China

Teknik Proteksi Silang Untuk Pengendalian CMV Pada Krisan

. Rahardjo, I.B., E. Diningsih, and Y. Sulyo. 2008. Cross Protection Technique for Controlling CMV on Chrysanthemum. One of viru s attack chry santhemum is CMV. The alternative to control CMV is the use of vacc ine CARNA 5. The objective of the experiment was to test the cr oss protection tech nique for controlling of CMV on several chry santhemum varieties. The experiment was conduc ted in Virology Laboratory of Indonesian Ornamental Plant Research Institute (IOPRI) in Segu nung, Pacet, Cianjur , West Java, from Augu st to December 2004, using a RC BD split-plot design with 3 replications. The main plot was 5 chry santhemum varieties of White Reagent, Town Talk, Dark Fiji, Stroika, and Revert. The subplot was treatments of vacc ine and CMV, i.e. without vacc ine and CMV, CMV only, vacc ine only, and both vacc ine and CMV. The results of the experiment showed that CARNA 5 vacc ine was able to protect chry santhemum varieties of White Reagent, Town Talk, Dark Fiji, Stroika, and Revert from CMV with normal plant growth and produced good flower quality

Analisis Struktur Daerah Integral dari Himpunan Polinomial Berdasarkan Struktur Polinomial Gelanggang

Himpunan R[x] polinomial dengan koefisien dari gelanggang R juga merupakan sebuah gelanggang dengan berbagai operasi polinomial jumlahan dan perkalian, dan bahwa R merupakan gelanggang bagian dari R[x]. Oleh karena itu akan ditunjukkan bahwa jika D adalah sebuah daerah integral maka demikian juga dengan himpunan polinomial dengan koefisien di dalam D, yaitu D[X]

Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats Through Enhanced Apoptosis

Periodontal disease is the most common osteolytic disease in humans and is significantly increased by diabetes mellitus. We tested the hypothesis that bacterial infection induces bone loss in diabetic animals through a mechanism that involves enhanced apoptosis. Type II diabetic rats were inoculated with Aggregatibacter actinomycetemcomitans and treated with a caspase-3 inhibitor, ZDEVD-FMK, or vehicle alone. Apoptotic cells were measured with TUNEL; osteoblasts and bone area were measured in H&E sections. New bone formation was assessed by labeling with fluorescent dyes and by osteocalcin mRNA levels. Osteoclast number, eroded bone surface, and new bone formation were measured by tartrate-resistant acid phosphatase staining. Immunohistochemistry was performed with an antibody against tumor necrosis factor-α. Bacterial infection doubled the number of tumor necrosis factor-α–expressing cells and increased apoptotic cells adjacent to bone 10-fold (P \u3c 0.05). Treatment with caspase inhibitor blocked apoptosis, increased the number of osteoclasts, and eroded bone surface (P \u3c 0.05); yet, inhibition of apoptosis resulted in significantly greater net bone area because of an increase in new bone formation, osteoblast numbers, and an increase in bone coupling. Thus, bacterial infection in diabetic rats stimulates periodontitis, in part through enhanced apoptosis of osteoblastic cells that reduces osseous coupling through a caspase-3–dependent mechanism. Diabetes is a chronic inflammatory disease characterized by hyperglycemia that affects 26 million Americans.1 Diabetes has several complications, such as cardiovascular, renal, microvascular, and periodontal diseases. Periodontal disease is one of the most common forms of osteolytic bone disease and one of the most frequent complications of the diabetes.2 Recent research suggests that the relationship between periodontitis and diabetes is reciprocal.3, 4 People with diabetes are more susceptible to periodontitis, and periodontitis may affect serum glucose levels and contribute to progression of diabetes.5 Diabetes may contribute to periodontitis because of its effect on inflammation.6, 7 Despite being triggered by bacterial infection, periodontal bone loss is tied to the inflammatory host response, which leads to the generation of prostaglandins and cytokines that stimulate osteoclastogenesis and periodontal bone loss.8 Several of the detrimental aspects of periodontal disease have recently been shown to be mediated by elevated levels of tumor necrosis factor-α (TNF-α).9, 10 TNF-α is a proinflammatory cytokine produced by leukocytes and other cell types.11 Enhanced TNF-α levels have been directly linked to cellular changes in diabetic retinopathy, deficits in wound healing, and diabetes-enhanced periodontitis.12, 13, 14 Some of the detrimental effects of diabetes-enhanced TNF-α levels may be because of the induction of cell death by triggering caspase activity. Caspases are a family of cysteine proteases that can act as either initiators (caspases 2, 8, and 9) or executioners (caspases 3, 6, and 7) of apoptosis.15 Caspase-3 appears to play a central role in bacteria and lipopolysaccharide-mediated apoptosis.16, 17 In addition, it has been shown that TNF-α can stimulate the expression of several pro-apoptotic genes, many of which are regulated by the pro-apoptotic transcription factor, forkhead box-O1 (FOXO1).18 The functional role of apoptosis in pathological processes can be studied with caspase inhibitors, which are small peptides that block the activity of well-defined caspases.19 These inhibitors have been used in animal models to attenuate cell death and diminish tissue damage in ischemic conditions, sepsis, and other pathological processes.20, 21 Other studies using caspase inhibitors have shown that part of the detrimental effect of diabetes on healing after infection is the result of increased fibroblast or osteoblast apoptosis.16, 22 To understand how diabetes may affect periodontal bone loss through apoptosis, we used a caspase-3/7 inhibitor in a type 2 Goto-Kakizaki (GK) diabetic rat model of periodontal disease induced by bacterial infection. The aim of this study was to determine how apoptosis of osteoblasts contributed to periodontal bone loss by its effect on bone formation in diabetic animals

A.Actinomycetemcomitans‐Induced Periodontal Disease Promotes Systemic and Local Responses in Rat Periodontium

Aim To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. Material & Methods Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF‐α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. Results An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p \u3c 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p \u3c 0.05). TNF‐α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF‐α expression in the connective tissue (p \u3c 0.05). PMN recruitment significantly increased after Aa infection (p \u3c 0.05). Aa also increased the number of CD8+ T cells (p \u3c 0.05), but not CD4+ T cells or regulatory T cells (Tregs) (p \u3e 0.05). Conclusion Aa infection stimulated a local response that increased numbers of PMNs and TNF‐α expression in the junctional epithelium and loss of attachment. Both TNF‐α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF‐α in the connective tissue, osteoclast numbers and CD8+ T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction

Mass Changes of the Greenland and Antarctic Ice Sheets and Shelves and Contributions to Sea-level Rise: 1992-2002

Changes in ice mass are estimated from elevation changes derived from 10.5 years (Greenland) and 9 years (Antarctica) of satellite radar altimetry data from the European Remote-sensing Satellites ERS-1 and -2. For the first time, the dH/dt values are adjusted for changes in surface elevation resulting from temperature-driven variations in the rate of fun compaction. The Greenland ice sheet is thinning at the margins (-42 plus or minus 2 Gta(sup -1) below the equilibrium line altitude (ELA)) and growing inland (+53 plus or minus 2 Gt a(sup -1)above the ELA) with a small overall mass gain (+11 plus or minus 3 Gt a(sup -1); -0.03 mm a(sup -1) SLE (sea level equivalent)). The ice sheet in West Antarctica (WA) is losing mass (-47 (dot) 4 GT a(sup -1) and the ice sheet in East Antarctica (EA) shows a small mass gain (+16 plus or minus 11 Gt a(sup -1) for a combined net change of -31 plus or minus 12 Gt a(sup -1) (+0.08 mm a(sup -1) SLE)). The contribution of the three ice sheets to sea level is +0.05 plus or minus 0.03 mm a(sup -1). The Antarctic ice shelves show corresponding mass changes of -95 (dot) 11 Gt a(sup -1) in WA and +142 plus or minus 10 Gt a(sup -1) in EA. Thinning at the margins of the Greenland ice sheet and growth at higher elevations is an expected response to increasing temperatures and precipitation in a warming climate. The marked thinnings in the Pine Island and Thwaites Glacier basins of WA and the Totten Glacier basin in EA are probably ice-dynamic responses to long-term climate change and perhaps past removal of their adjacent ice shelves. The ice growth in the southern Antarctic Peninsula and parts of EA may be due to increasing precipitation during the last century

Greenland Ice Sheet Mass Balance: Distribution of Increased Mass Loss with Climate Warming; 2003-07 Versus 1992-2002

We derive mass changes of the Greenland ice sheet (GIS) for 2003-07 from ICESat laser altimetry and compare them with results for 1992-2002 from ERS radar and airborne laser altimetry. The GIS continued to grow inland and thin at the margins during 2003 07, but surface melting and accelerated flow significantly increased the marginal thinning compared with the 1990s. The net balance changed from a small loss of 7 plus or minus 3 Gt a 1(sup -1) in the 1990s to 171 plus or minus 4 Gt a (sup -1) for 2003-07, contributing 0.5 mm a(sup -1) to recent global sea-level rise. We divide the derived mass changes into two components: (1) from changes in melting and ice dynamics and (2) from changes in precipitation and accumulation rate. We use our firn compaction model to calculate the elevation changes driven by changes in both temperature and accumulation rate and to calculate the appropriate density to convert the accumulation-driven changes to mass changes. Increased losses from melting and ice dynamics (17-206 Gt a(sup-1) are over seven times larger than increased gains from precipitation (10 35 Gt a(sup-1) during a warming period of approximately 2 K (10 a)(sup -1) over the GIS. Above 2000m elevation, the rate of gain decreased from 44 to 28 Gt a(sup-1), while below 2000m the rate of loss increased from 51 to 198 Gt a(sup-1). Enhanced thinning below the equilibrium line on outlet glaciers indicates that increased melting has a significant impact on outlet glaciers, as well as accelerating ice flow. Increased thinning at higher elevations appears to be induced by dynamic coupling to thinning at the margins on decadal timescales

Kindlin-1 promotes pulmonary breast cancer metastasis

Abstract In breast cancer, increased expression of the cytoskeletal adaptor protein Kindlin-1 has been linked to increased risks of lung metastasis, but the functional basis is unknown. Here, we show that in a mouse model of polyomavirus middle T antigen–induced mammary tumorigenesis, loss of Kindlin-1 reduced early pulmonary arrest and later development of lung metastasis. This phenotype relied on the ability of Kindlin-1 to bind and activate β integrin heterodimers. Kindlin-1 loss reduced α4 integrin–mediated adhesion of mammary tumor cells to the adhesion molecule VCAM-1 on endothelial cells. Treating mice with an anti–VCAM-1 blocking antibody prevented early pulmonary arrest. Kindlin-1 loss also resulted in reduced secretion of several factors linked to metastatic spread, including the lung metastasis regulator tenascin-C, showing that Kindlin-1 regulated metastatic dissemination by an additional mechanism in the tumor microenvironment. Overall, our results show that Kindlin-1 contributes functionally to early pulmonary metastasis of breast cancer. Significance: These findings provide a mechanistic proof in mice that Kindin-1, an integrin-binding adaptor protein, is a critical mediator of early lung metastasis of breast cancer. Cancer Res; 78(6); 1484–96. ©2018 AACR.</jats:p

Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'.

Innate immune cells must be able to distinguish between direct binding to microbes and detection of components shed from the surface of microbes located at a distance. Dectin-1 (also known as CLEC7A) is a pattern-recognition receptor expressed by myeloid phagocytes (macrophages, dendritic cells and neutrophils) that detects β-glucans in fungal cell walls and triggers direct cellular antimicrobial activity, including phagocytosis and production of reactive oxygen species (ROS). In contrast to inflammatory responses stimulated upon detection of soluble ligands by other pattern-recognition receptors, such as Toll-like receptors (TLRs), these responses are only useful when a cell comes into direct contact with a microbe and must not be spuriously activated by soluble stimuli. In this study we show that, despite its ability to bind both soluble and particulate β-glucan polymers, Dectin-1 signalling is only activated by particulate β-glucans, which cluster the receptor in synapse-like structures from which regulatory tyrosine phosphatases CD45 and CD148 (also known as PTPRC and PTPRJ, respectively) are excluded (Supplementary Fig. 1). The 'phagocytic synapse' now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular antimicrobial responses only when they are required