This review highlights the structural and functional features shared by polycystin-1 and the adhesion GPCRs and discusses the implications of such similarities for our further understanding of the functions of this complicated protein. BACKGROUND Smoking is known to affect all the phases of atherosclerosis, thus is considered as an independent and major risk factor. The underlying mechanism responsible for the atherogenic effects of smoking is still uncertain and a major concern. Recent evidence implicates NLRP3 inflammasome, an innate immunity component in the pathogenesis of atherosclerosis. Therefore, we hypothesized that NLRP3 inflammasome may be an associated pathway between smoking and atherosclerosis. METHODS AND RESULTS Differentiation in monocytes, macrophages and foam cells are the key stages in atherosclerotic plaque development, best mimicked by THP-1 cells. Therefore, to determine whether cigarette smoke condensate (CSC) could induce differentiation of THP-1 monocytes into macrophages, morphological changes and the expression levels of the inflammatory surface markers, i.e. CD11b, CD14 and CD36 were analyzed. The results showed that CD14 and CD36 levels were significantly increased in CSC-treated THP-1 monocytes. Further, we investigated the effect of CSC exposure on the status of NLRP3 inflammasome markers, i.e. NLRP3, pro-caspase-1, caspase-1, pro-IL-18, pro-IL-1β, IL-1β and IL-18 in a stage-specific manner. For this, THP-1 monocytes, PMA-differentiated macrophages and oxidized-low density lipoprotein (ox-LDL)-induced macrophage foam cells were exposed to 10 μg/ml of CSC for 6 h. CSC exposure significantly upregulated the expression of NLRP3 inflammasome in CSC-treated cells at both transcriptional and translational levels. Moreover, downstream pro-cytokines, i.e. IL-1β and IL-18 levels were also significantly increased in culture supernatants of CSC-exposed cells. CONCLUSION These observations suggest that CSC exposure may activate NLRP3 inflammasome in a stage-specific manner and may promote initiation and progression of atherosclerosis. This article examines how good governance and technological innovation complement foreign direct investment (FDI) to mitigate carbon emissions in twenty-three emerging economies for the period 1996-2014. Based on the Generalized Method of Moments (GMM) approach, we established the following results First, from the non-interactive regressions, FDI inflows have positive effects on the four indicators of carbon emissions while increasing governance quality and technological innovation have negative effects on these indicators. Second, from the interactive regressions, the interactions between FDI and both political and institutional governance decrease the level of CO2 emissions. Moreover, the interactions between technological innovation and FDI reduce CO2 emissions in all the estimated models, except in the model pertaining to CO2 emissions from electricity and heat production; as a result, environmental quality is improved. Policy implications and future research directions are also discussed. Air pollution is the second most important risk factor associated with noncommunicable diseases after smoking. The effects of pollution on health are commonly attributable to particulate matter (PM), a complex mixture of particles suspended in the air. PM can penetrate the lower respiratory tract and has harmful direct and indirect effects on different organs and tissues. Direct effects are caused by the ability of PM components to cross the respiratory membrane and enter the bloodstream; indirect effects are systemic consequences of the local airway response. https://www.selleckchem.com/products/agi-24512.html Recent work suggests that PM is an independent risk factor for low bone mineral density and osteoporosis-related fractures. Osteoporosis is a common age-related disease closely linked to bone fractures, with severe clinical consequences affecting quality of life, morbidity, and mortality. In this review, we discuss potential mechanisms behind the association between outdoor air pollution, especially PM, and bone damage. The discussion features four main mechanisms 1) several different atmospheric pollutants can induce low-grade systemic inflammation, which affects bone metabolism through a specific effect of cytokines such as TNFα, IL-1β, IL-6, and IL-17 on osteoblast and osteoclast differentiation and function; 2) some pollutants, particularly certain gas and metal compounds, can cause oxidative damage in the airway and bone cells; 3) different groups of pollutants can act as endocrine disruptors when binding to the receptors in bone cells, changing their functioning; and 4) air pollution can directly and indirectly cause vitamin D deficiency. Characterizing these mechanisms will better define the physiopathology of bone damage, and recognizing air pollution as a modifiable risk factor for osteoporosis will inform environmental policies. Such knowledge will also guide the prevention of fractures due to fragility and help reduce health-related costs. INTRODUCTION We report a case of late onset hyperplastic callus formation (HPC) in the right femur in type V osteogenesis imperfecta (OI) mimicking the occurrence of a malignant osteosarcoma. PRESENTATION OF CASE A 27-year-old female patient consulted us due to swelling in her right femur over 2-3 months without trauma. X-rays looked like an osteosarcoma, blood tests showed increased bone metabolism. A CT scan, a MRI and biopsy were performed, showing late onset HPC due to osteogenesis imperfecta type V. DISCUSSION OI shows a heterogeneous disease pattern due to a variety of clinical and radiographic findings. HPC is a rare complication of OI type V. Differential diagnosis range from cortical or periosteal osteosarcoma, periostitis, myositis ossificans, subperiosteal hematoma secondary to trauma or osteomyelitis. CONCLUSION Recognition of HPC as a form of this particular type of OI is important to avoid misdiagnosis like malignant transformation to osteosarcoma. A biopsy and advanced imaging modalities like CT, MRI and scintigraphy are recommended. BACKGROUND Pyoderma Gangrenosum (PG) is a rare auto-inflammatory disease, characterized by painful ulcerative skin-lesions often developing at sites of injury or surgery because of the typical pathergy phenomena. We describe an unusual case of PG after a caesarean section with excessive extra-cutaneous manifestation within internal organs. PRESENTATION OF CASE A 21-year-old Dutch primigravida developed signs of sepsis after a caesarean section. Despite antibiotic treatment, fast clinical deterioration occurred. Exploration of the wound showed necrosis of the uterus and surrounding tissues. Due to the progression of necrosis, consecutive debridement procedures were executed resulting in a substantial abdominal wall defect. The progressive clinical course of the necrosis combined with absence of positive wound cultures and histology of prominent interstitial neutrophilic infiltration, led to the diagnosis 'Pyoderma Gangrenosum'. Treatment with high dose corticosteroids led to rapid regression of the disease. After several weeks, the abdominal wall defect was surgically corrected under systemic corticosteroid therapy.