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Objective To investigate whether the process of primary gingival keratinocytes culture obtained from normal human gingiva modifies the expression of keratins (K) 10, K14, and K19. Design Human gingival fragments were collected from healthy individuals in the same oral site. One part of the samples underwent an immunohistochemistry assay for K10, K14, and K19. The labeling in the epithelium was quantified using a semiautomated method. Another part was used for primary gingival keratinocytes isolation and growth in two-dimensional culture. These cells were also stained for K10, K14, and K19 using immunofluorescence and immunocytochemistry. Positive cells were counted, and the nuclei and cytoplasmatic labeling areas were quantified. Results In the gingival tissue, a higher expression was found for K14 versus K10 (p less then 0.001); K19 was negative in all samples. In gingival keratinocytes culture, K14 (89.6 %) had the highest expression with significant differences in relation to K10 (76.9 %, p less then 0.01) and K19 (9.9 %, p less then 0.01). The cells positive for K14 exhibited larger nuclei in comparison with K10 (p less then 0.05) and K19 (p less then 0.05), suggesting a more undifferentiated phenotype. K19 cells showed the largest cytoplasmatic labeling in relation to K10- (p less then 0.05) and K14-positive (p less then 0.05) cells. Conclusion The process of growth in culture of gingival keratinocytes maintained the expression pattern of K10 and K14 observed in gingival tissues. However, this method induces the expression of K19, suggesting a potential transformation of the keratin network presented in the gingival keratinocytes during the formation of a monolayer in vitro. This reflects the dynamics of cell differentiation.Objective Low-level laser therapy is a method for osteogenesis since it stimulates cell proliferation, vascularization and osteoblastic activity. Various protocols applying low-level laser with different outcomes exist. The aim of the present study was to review the result of different methods on bone formation in critical-size defects of in vivo studies. Design According to PRISMA statement, electronic search of PubMed, google scholar, Scopus and Web of Science and a hand search limited to in vivo English language studies until December 2019. Studies used low-level laser therapy in bone regeneration of critical-size defects met the inclusion criteria and which used high power lasers or a defect size smaller than 5 mm, were excluded. Results Finally, 18 studies were included. Fourteen studies utilized low-level laser with a wavelength ranging from 606 to 980 nm and 53 % of studies applied low-level laser in a single session. Ten studies utilized continuous wave mode of laser. Highest and lowest values of power density were 1.5 W/cm2 and 0.1 W/cm2 in order. Eleven studies evaluated low-lever laser therapy on defects of 5 mm in calvaria. Glycyrrhizin manufacturer Meta-analysis showed the positive effect of low-level laser therapy on osteogenesis after 30 days compared to control group and no significant difference after 60 days. Conclusions New bone formation can be increased in early stage by applying low-level laser therapy through stimulating osteoblasts and fibroblasts' proliferation. This effect would be more remarkable by combining with bone substitutes. Hence, for each case, protocol selection should be performed according defect's properties, attentively.Objective The Ehlers-Danlos syndromes (EDS) and Hypermobility Spectrum Disorders (HSD) have profound and life-threatening consequences in childbearing as they affect connective tissues throughout the body. Hypermobile EDS (hEDS) and HSD are estimated here for the first time to affect 6 million (4.6%) pregnancies globally per year. The aim of this study was to arrive at a deeper biopsychosocial understanding of childbearing in the context of hEDS/HSD. Methods English speaking women aged over 18 years who had previously given birth and had a confirmed medical diagnosis of hEDS/HSD or equivalent diagnosis under a preceding nosology were included in this study (n=40). Narrative interviews were used to collect qualitative data from this international sample of participants. Thematic narrative analysis was used to understand how participants made sense of their experiences. Findings Participants were aged between 25 and 55. Births (n= 52) between 1981 and 2018 were captured across United Kingdom=29 (73%), United Stacknowledge and respond to women with hEDS/HSD appropriately throughout their childbearing journey. Dismissal can lead to trauma and needless morbidity.Inflammation is an important part of the fracture repair process which requires osteogenic cells to interact with innate immune cells such as macrophages. All murine macrophages express the F4/80 cell surface marker but they may be further subdivided into two main phenotypes M1 (proinflammatory) or M2 (anti-inflammatory) based on surface marker expression and function. Macrophages polarize between these two main classes in response to inflammation while differentially regulating the healing process. Studies have shown that F4/80+ cell ablation impairs fracture healing, however, the distinct phenotypes that participate in the early healing process is unclear. We hypothesized that the M1 subtype is essential for the early steps of fracture healing and their depletion would impair fracture repair. To test this hypothesis, M1 (F4/80+/MHCII+/CD86+/CDllb+) macrophages were depleted using a saporin conjugated Mac-1 antibody (Mac1SAP) in vitro using primary macrophages and in vivo using a mouse femur fracture model. -2 and TNFα. M1 depletion was also found to reduced callus properties at day 14 via microCT analysis. link2 Overall, the data suggests that depletion of M1 macrophages by Mac1SAP treatment alters the cytokine expression profiles during early bone repair which ultimately impairs bone healing.Osteoporosis is the most common bone disorder worldwide and is associated with a reduced quality of life with important clinical and economic consequences. The most widely accepted etiopathogenic hypothesis on the origin of osteoporosis and its complications is that they are a consequence of the synergic action of environmental and genetic factors. Bone is constantly being remodelled through anabolic and catabolic pathways in which inflammation, the NF-kB pathway and the renin-angiotensin-aldosterone system (RAAS) are crucial. The aim of our study was to determine whether polymorphisms in genes implicated in inflammation, the NF-kB pathway and RAAS modified the risk of osteoporotic fracture. We analysed 221 patients with osteoporotic fracture and 354 controls without fracture from the HORTEGA sample after 12-14 years of follow up. In addition, we studied the genotypic distribution of 230 single nucleotide polymorphisms (SNPs) in genes involved in inflammation, NF-kB pathway and RAAS. Our results showed that be carrier of the C allele of the rs2228145 IL6R polymorphism was the principal genetic risk factor associated with osteoporotic fracture. The results also showed that variant genotypes of the rs4762 AGT, rs4073 IL8, rs2070699 END1 and rs4291 ACE polymorphisms were important genetic risk factors for fracture. The study provides information about the genetic factors associated with inflammation, the NF-kB pathway and RAAS, which are involved in the risk of osteoporotic fracture and reinforces the hypothesis that genetic factors are crucial in the etiopathogenesis of osteoporosis and its complications. Contrary to previous findings, new Ocn-/- mice revealed that osteocalcin has no function in the regulation of bone quantity, but instead, functions to direct the parallel alignment of the c-axis of apatite crystals with collagen fibrils. Moreover, it has no physiological function as a hormone that regulates glucose metabolism, testosterone synthesis, or muscle mass. These controversial phenotypes require further investigation. The relationship of serum osteocalcin with glucose metabolism or cardiovascular risk suggests the importance of exercise for their improvement.Background Extracellular vesicles (EVs) have come into the spotlight as messengers, delivering cargo for cell-cell communication. Concomitantly, increasing attention has been focused on microRNAs (miRNAs) as EV cargo. Besides their well-known role in extracellular matrix mineralization, whether matrix vesicles (MVs) - which are in a broad sense a class of EV - also deliver miRNAs to regulate the function of recipient cells remains unclear. Highlight We recently found that MVs budding from osteoblasts contain many miRNAs that can be transferred to the bone matrix. Of these, miR-125b was released into the bone marrow microenvironment during bone resorption, where it targeted the transcriptional repressor Prdm1 in osteoclast precursors, resulting in increased expression of anti-osteoclastogenic factors and suppression of osteoclastogenesis, thereby increasing bone mass in mice. Conclusion Beyond their well-established action in bone mineralization, MVs play a role in the transport of miRNAs from osteoblasts into the bone matrix. Similar to the miR-125b axis in osteoclastogenesis, it seems likely that other miRNAs that accumulate in bone via MV transport may also act as mediators of cell-cell communication in the skeletal system.The development of analytical methods for the detection and accurate quantification of algal toxins is of importance to assess the health risk of exposure to algal toxins in freshwater sources. This study established a sensitive and accurate analytical method for the quantification of 13 algal toxins (microcystins and nodularin) based on solid phase extraction (SPE) coupled with UPLC-MS/MS, in which 15N-microcystins were used as surrogate/internal standards. SPE method was optimized to extract the target algal toxins in freshwater samples. Good SPE efficiencies (84-96%) were achieved for the overwhelming majority of the investigated algal toxins when SPE was performed using HLB (500 mg, 6 mL) under alkaline conditions (pH 11). An accurate quantitative analysis of the algal toxins in real freshwater samples was performed by using 15N-labelled microcystins as isotopically labelled internal standards (ILISs), which compensated for the loss of target toxins during the whole analytical process. In addition, ILISs also helped to correct the effects of environmental matrices and instrument fluctuation in UPLC-MS/MS analysis. The limit of method quantification (MQL) for the algal toxins was less then 2.0 ng/L that is sensitive enough to quantify extremely low levels of target toxins in freshwater samples.Whether carbon emissions trading system promotes green development is important, especially from the land supply perspective. This paper investigates the effects of the carbon emissions trading pilot program on the land supply of the energy-intensive industries using the difference-in-difference approach, based on a big land-transaction dataset for the Chinese land market from 2007 to 2017. This paper finds that the carbon emissions trading program decreases the supply of energy-intensive industries' land by 25%, suggesting that it promotes the green development. Local governments' behavior affects the supply of energy-intensive industrial land. Industry structure dependence reinforce the effects of the carbon emissions trading program. link3 The impacts of the carbon emissions trading program on the supply of energy-intensive industrial land would be less in cities with stronger regional competition, higher fiscal pressure or during political cycles. This study implies that the supply of energy-intensive industrial land can be used as an indicator for evaluating the effects of the carbon emissions trading system from the factor input perspective.

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