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Objectives Chronic obstructive pulmonary disease (COPD) is a risk factor for osteoporosis. Nevertheless, much remains unclear regarding the bone metabolism dynamics associated with COPD. The present study focuses on the associations between the COPD severity and serum bone metabolism biomarkers. Methods We enrolled 40 patients who visited the orthopedics departments at our institutions and underwent dual-energy X-ray absorptiometry between September 2015 and December 2017. Only male osteoporosis patients over 45 years of age were included, and 5 patients were excluded due to disease or use of internal medicines affecting bone metabolism. All subjects underwent lung function testing, spine radiography, and blood tests. We measured percent forced expiratory volume in 1 second (%FEV1), which reflects COPD severity, and we examined the relationships between %FEV1 and serum levels of bone metabolism biomarkers. Results All subjects were diagnosed with osteoporosis based on T-scores. %FEV1 correlated with body weight, body mass index (BMI), and Z-score/T-scores. %FEV1 moderately correlated with serum levels of alkaline phosphatase (ALP), procollagen type 1 N-terminal propeptide (P1NP), and tartrate-resistant acid phosphatase 5b in the partial correlation analysis adjusted for BMI or T-score in the lumbar vertebrae. We performed a hierarchical multiple regression analysis to identify that serum ALP and P1NP were the independent explanatory variables to %FEV1 independent of other factors. Conclusions The data suggest that the COPD severity in middle-aged and older men with osteoporosis associates with decreased bone formation. COPD patients may exhibit bone metabolism dynamics characterized by low bone turnover with osteogenesis dysfunction as COPD becomes severe.

The Beidabate deposit is a porphyry Cu-Mo deposit located in the West Tianshan Orogenic Belt , Xinjiang Uygur Autonomous Region. The fluid evolution path and Cu-Mo mineralization mechanism remain obscured by multiple hydrothermal pulses. Systematic fluid inclusion and H-O-C-S isotope analyses were performed on five identifiable mineralization stages. Variations in fluid composition, temperature, and pressure record the fluid evolution path: (1) During the formation of barren quartz veins (stage I), fluid inclusions were trapped under single- to two-phase transitional conditions, as evidenced by the presence of intermediate-density inclusions as well as coexisting daughter mineral-bearing inclusions and vapor-rich inclusions (boiling FIAs). Fluid phase separation occurred at temperatures of 387–412 °C and pressures of 180–300 bar. (2) Fluid inclusions in K-feldspar-quartz veins (stage II) and molybdenite-quartz veins (stage III) were trapped under two-phase conditions. Boiling FIAs were also recognized, with homogenization temperatures of 306–368 °C and entrapment pressures of 80–200 bar. Fluid boiling is the main precipitation mechanism of molybdenite . (3) Fluid inclusions in pyrite-chalcopyrite-quartz veins (stage IV) and fluorite-chalcopyrite veins (stage V) are predominantly liquid-rich and CO 2 -bearing inclusions, which represent extraneous fluids. These inclusions homogenized at temperatures of 192° to 285 °C, and minimum entrapment pressures of 40–50 bar. Fluid mixing is the main precipitation mechanism of chalcopyrite . H-O-C-S isotope data (δ 18O = 3.2 to 15.2‰, δD = −103.6 to −75.1‰, δ13C = −24.2 to −9.7‰ and δ34 S = 4.6 to 7.0‰) indicate that the ore-forming fluids have a predominantly magmatic signature with subsequent dilution by late meteoric water and intense water–rock interaction. We established a genetic model of the Beidabate porphyry Cu-Mo deposit with the aim of providing insight into prospecting at a regional scale.

We demonstrated an extremely unusual case of an 83-year-old male's sudden death secondary to characteristic myocardial necrosis and fibrosis with calcification and multinucleated giant cells infiltration, possibly due to sepsis and Stage IV pulmonary pleomorphic carcinoma-induced cachexia after postmortem study. We propose that this calcifying giant cell cardiomyopathy (CGC) would be a new entity especially from the pathological viewpoints and should be considered in the classification of noninfectious myocarditis. Further prospective studies are needed to validate the presence and significance of CGC and the association with any triggers of somewhat microvascular dysfunction and/or toxic agents, after collecting and investigating a larger number of CGC cases examined.

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that plays a crucial role in stress-induced apoptosis. Recently, we have reported that suppressed macrophage apoptosis in ASK1 and apolipoprotein E double-knockout mice accelerates atheromatous plaques in the hyperlipidemia-induced atherosclerotic model. However, the pathogenic role of smooth muscle cell (SMC) apoptosis in atherosclerosis still remains unclear. We investigated neointimal remodeling in ligated carotid arteries of ASK1-deficient mice (ASK1(-/-)) for 3 weeks. ASK1(-/-) mice had significantly more suppressed intimal formation, inversely manifesting as potential anti-atherogenic aspects of ASK1 deficiency, characterized by fewer SMCs and less collagen synthesis; and fewer apoptotic SMCs, infiltrating T lymphocytes, and microvessels, associated with decreased apoptosis of luminal endothelial cells, compared with those of wild-type mice. Injured arteries of ASK1(-/-) mice also showed significantly down-regulated expression of pro-apoptotic markers, adhesion molecules, and pro-inflammatory signaling factors. Moreover, tumor necrosis factor-α-induced apoptosis was markedly suppressed in cultured aortic SMCs from ASK1(-/-) mice. These findings suggest that ASK1 accelerates mechanical injury-induced vascular remodeling with activated SMC migration via increased neovascularization and/or enhanced SMC and endothelial cell apoptosis. ASK1 expression, especially in the SMCs, might be crucial, and reciprocally responsible for various pro-atherogenic functions, and SMC apoptosis seems to be detrimental in this model.

A case of non-functioning adrenocortical adenoma combined with myelolipoma and endothelial cysts is reported. A 72-year-old Japanese female was noticed to have right renal and left adrenal tumors by an abdominal CT scan. At surgery, the mildly enlarged left adrenal gland contained a well-demarcated tumor. Macroscopically, it was yellowish to dark red or grayish in color, and was characterized by geographic appearance on the cut surface. Histopathological examination revealed a solid proliferation of clear or compact cells and a normal rim of adrenal gland, coexisting with vascular multiple cysts and myelolipomas. The cysts were filled with clotted blood, fibrinous material, or thrombi, and were partially lined with flattened endothelial cells with focal papillary hyperplasia, which were immunohistochemically positive for CD31 and CD34. These cystic walls were often thickened with hyalinized fibrosis and calcification, and were connected to myelolipomatous elements. To our knowledge, this is the first case report of adrenocortical adenoma associated with myelolipoma and endothelial cysts. It is probable that the extensive degeneration in adenoma might induce myelolipomatous metaplasia and cystic vascular formation.

Histamine has been proposed to be an important regulator of energy intake and expenditure. The aim of this study was to evaluate histamine regulation of glucose and lipid metabolism and development of nonalcoholic steatohepatitis (NASH) with a hyperlipidemic diet. Histamine regulation of glucose and lipid metabolism, adipocytokine production, and development of hyperlipidemia-induced hepatic injury were studied in histamine H1 (H1R−/−) and H2 (H2R−/−) receptor knockout and wild-type mice. H1R−/− mice showed mildly increased insulin resistance. In contrast, H2R−/− mice manifested profound insulin resistance and glucose intolerance. High-fat/high-cholesterol feeding enhanced insulin resistance and glucose intolerance. Studies with two-deoxy-2-[18F]-fluoro-d-glucose and positron emission tomography showed a brain glucose allocation in H1R−/− mice. In addition, severe NASH with hypoadiponectinemia as well as hepatic triglyceride and free cholesterol accumulation and increased blood hepatic enzymes were observed in H2R−/− mice. H1R−/− mice showed an obese phenotype with visceral adiposity, hyperleptinemia, and less severe hepatic steatosis and inflammation with increased hepatic triglyceride. These data suggest that H1R and H2R signaling may regulate glucose and lipid metabolism and development of hyperlipidemia-induced NASH.

Whether fatty streaks are directly followed by fibrous plaque formation in atherosclerosis remains controversial. Disruption of the basement membrane and elastic layers is thought to be essential for this process. Matrix metalloproteinase 12 (MMP-12) can degrade a broad spectrum of substrates, but the role of MMP-12 in the early stage of atherosclerosis is unclear. To investigate MMP-12 function in the initiation and progression of atherosclerosis, we investigated macrophage migration and elastolysis in relation to fatty streaks in human MMP-12 transgenic (hMMP-12 Tg) rabbits. Fatty streaks in hMMP-12 Tg rabbits fed a 1% cholesterol diet for 6 weeks (cholesterol-induced model of atherosclerosis) were more pronounced and were associated with more significant degradation of the internal elastic layer compared with wild-type (WT) animals. Numbers of infiltrating macrophages and smooth muscle cells in the lesions were increased in hMMP-12 Tg compared with WT animals. In both cuff- and ligation-induced models of atherosclerosis, smooth muscle cell-predominant atherosclerotic lesions were elevated with significant elastolysis of the internal elastic lamina in Tg compared with WT animals; "microelastolytic sites" were recognized before formation of the neointima in the cuff model only. These results indicate that MMP-12 may be critical to the initiation and progression of atherosclerosis via degradation of the elastic layers and/or basement membrane. Therefore, a specific MMP-12 inhibitor might prove useful for the treatment of progressive atherosclerosis.

This work presents a reliable and efficient technique for displaying color mapping of data for post-processing of the Hybrid-Trefftz (HT) finite element method (FEM). The isoparametric mapping fill method developed in conventional FE models is generalized to HT FE models. Several steps of the procedure for HT FEM are demonstrated, as well as the aspects to be modified. For illustration purposes, a computer program has been written in VC++ and two 2D examples discretized by HT FEM are provided. The results are found to agree well with the analytical solutions although there are some discrepancies. Finally, conclusions are inferred and extension of this work to the 3D case is discussed.