Press and Journal | Crowdfundung success for Aberdeen man battling cancer Press and Journal ... of pounds to cover the cost of his treatment for throat cancer. Mark Millsom, 55, who ran Bistro Verde, Moonfish Café and La Bonne Brasserie, was diagnosed in autumn 2015 with an inoperable tumor in his throat, as well as cancer in his tonsils and ... |
Illawarra Mercury | Cancer toll on Williamtown's Cabbage Tree Road near Newcastle Illawarra Mercury ... cases of breast cancer, eight of prostate cancer, five of bowel cancer, three of stomach cancer, three of non-Hodgkin's lymphoma, two leukemias and two liver cancers over the time period, as well as individual cases of melanoma, lung, pancreatic ... and more » |
This article is the second in a new series in this regular feature. The intention of the series is to look at important global developments in health science libraries. These articles will serve as a road map, describing the key changes in the field and exploring factors driving these changes. The present article by two Canadian librarians identifies important national developments which are shaping the profession such as the centralisation of health care services, the challenge of providing consumer health information in the absence of a national strategy, government recognition of the need to recognise and respond to the health needs of indigenous peoples and the growing emphasis on managing research data. Although their profession is strong, health science librarians must find ways of providing enhanced services with fewer staff and demonstrate value to organisations. JM
Medical care is obviously an important public service to ensure the health of a nation; however, medical resources are not always used appropriately. 'Convenience-store consultations' and inappropriate ambulan...
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Press and Journal | Crowdfundung success for Aberdeen man battling cancer Press and Journal ... of pounds to cover the cost of his treatment for throat cancer. Mark Millsom, 55, who ran Bistro Verde, Moonfish Café and La Bonne Brasserie, was diagnosed in autumn 2015 with an inoperable tumor in his throat, as well as cancer in his tonsils and ... |
Uterine cancer is one of the most common malignancies in women, especially in Western countries and Taiwan.1 Traditionally, uterine cancers, including endometrial cancer and sarcoma are managed and staged surgically and postoperative multiple-modality treatment might be needed in the high-risk population.2–5 Uterine cancer is further separated into two distinguished histological subtypes– type 1 endometrioid histology and type 2 non-endometrioid histology, such as serous, clear cell and carcinosarcoma.
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Obstetric hemorrhage is frequently noted in routine clinical obstetric practice and also a main cause of maternal death in the world, although the incidence of major obstetric hemorrhage-inducing maternal death is extremely low in Western countries, including Taiwan.1 There are some reasons to respond to the discrepancy between the frequent occurrence of obstetric hemorrhage (a worldwide prevalence of 6%) and rare subsequent maternal death presents (less than 0.1%), including an early identification of risk factors associated with obstetric hemorrhage (placental previa, placenta accreta and uterine atony), and an early intervention and prompt management of obstetric hemorrhage (message, the use of carbetocin, and so on) and of most of importance, a more effective therapy available, including improvements in anesthesia, medicine, surgery, and even radiology for obstetric hemorrhage.
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Vascular remodeling is an essential component of gestation. Endothelial progenitor cells (EPCs) play an important role in the regulation of vascular homeostasis. The results of studies measuring the number of EPCs in normal pregnancies and in preeclampsia have been highly controversial or even contradictory because of some variations in technical issues and different methodologies enumerating three distinct subsets of EPCs: circulating angiogenic cells (CAC), colony forming unit endothelial cells (CFU-ECs), and endothelial colony-forming cells (ECFCs).
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As the regeneration technologies developing, stem cell therapy has been a promising and attractive way to enhance tissue regeneration and problem wound healing. Stem cells are characterized by their multipotency and capacity for self-renewal, and their ability to secrete proregenerative cytokines, making them a promising choice for the tissue regeneration.1 Currently, stem cell therapy has been tested in preclinical and clinical trials in several different fields with positive clinical outcomes.
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Refractive error is the major cause of moderate and severe visual impairment. Visual impairment limits people's ability to perform daily tasks and affects their quality of life. Longitudinal data on the refractive status of the elderly was available only for whites and Africans. The purpose of this study was to report the 7-year incidence of myopia, hyperopia and refractive error change as well as their associated risk factors in a metropolitan elderly Chinese population.
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To assess the efficacy of neoadjuvant chemotherapy (NAC) in esophageal squamous cell carcinoma (ESCC) patients treated with definitive chemoradiotherapy (CRT).
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Health risk: an adverse event or negative health consequence due to a specific event, disease, or condition. For example, the health risks of obesity include diabetes, joint disease, increased likelihood of certain cancers, and cardiovascular disease. All of these consequences are related to obesity and are therefore health risks associated with obesity. A health risk may be related to genetic conditions, chronic diseases, certain occupations or sports, lifestyle factors, or any number of events or situations.
Publication date: Available online 14 July 2017
Source:Bioactive Carbohydrates and Dietary Fibre
Author(s): Asma Ashraf Khan, Adil Gani, F.A. Masoodi, Umar Mushtaq, Azza Silotry Naik
β-glucan was extracted from three edible mushroom varieties namely Agaricus bisporus, Pleurotus ostreatus and Coprinus attrimentarius using hot water extraction method. The extracted β-glucan was studied to investigate its structural, rheological, antioxidant and functional properties. The ATR-FTIR was used to elicit the structural conformations of the three β-glucan and SEM was used to study the surface topography. The rheological properties showed that with the increase in the concentration of β-glucan, the elastic behavior increased. The antioxidant activities were determined using different assays like DPPH (2, 2-diphenyl-1-picryl-hydrazyl), reducing power, metal chelating ability and ABTS (2,2-Azino-bis, 3-ethylbenzothiazoline-6- sulfonic acid) and all these activities varied significantly (p≤0.05) among all the β-glucan, however the β-glucan from Coprinus attrimentarius showed the highest values for all antioxidant activities. As far as the functional properties were concerned, Coprinus β-glucan also showed the highest swelling power, fat binding, emulsifying properties, bile acid binding capacity and viscosity, however foaming properties were the highest in Pleurotus β-glucan.
Publication date: Available online 14 July 2017
Source:Experimental Cell Research
Author(s): Ryan M. Troyer, Carl E. Ruby, Cheri P. Goodall, Liping Yang, Claudia S. Maier, Hassan A. Albarqi, Jacqueline V. Brady, Kallan Bathke, Oleh Taratula, Dan Mourich, Shay Bracha
BackgroundCanine osteosarcoma (OSA) is the most common cancer of the appendicular skeleton and is associated with high metastatic rate to the lungs and poor prognosis. Recent studies have shown the impact of malignant-derived exosomes on immune cells and the facilitation of immune evasion. In the current study, we have characterized the proteomic profile of exosomes derived from healthy osteoblasts and osteosarcoma cell lines. We investigated the direct impact of these exosomes on healthy T cells.ResultsProteomic cargo of the malignant exosomes was markedly different from osteoblastic exosomes and contained immunosuppressive proteins including TGF-β, α fetoprotein and heat shock proteins. OSA exosomes directly attenuated the rate of T cell proliferation, increased a regulatory (FoxP3+) CD4+ phenotype and diminished the expression of the activation marker CD25+ on CD8+ cells. Exosomes of osteoblasts also demonstrated a direct impact on T cells, but to a lesser degree.ConclusionsOsteosarcoma-derived exosomes compared to normal osteoblasts contain an immunomodulatory cargo, which reduced the rate of T cell proliferation and promoted T regulatory phenotype. Osteoblast-derived exosomes can also reduce T cell activity, but to lesser degree compared to OSA exosomes and without promoting a T regulatory phenotype.
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Publication date: Available online 14 July 2017
Source:Experimental Cell Research
Author(s): Naoki Takizawa, Naoto Okubo, Masaharu Kamo, Naoyuki Chosa, Toshinari Mikami, Keita Suzuki, Seiji Yokota, Miho Ibi, Masato Ohtsuka, Masayuki Taira, Takashi Yaegashi, Akira Ishisaki, Seiko Kyakumoto
Immunosuppressive/anti-inflammatory macrophage (Mφ), M2-Mφ that expressed the typical M2-Mφs marker, CD206, and anti-inflammatory cytokine, interleukin (IL)−10, is beneficial and expected tool for the cytotherapy against inflammatory diseases. Here, we demonstrated that bone marrow-derived lineage-positive (Lin+) blood cells proliferated and differentiated into M2-Mφs by cooperation with the bone marrow-derived mesenchymal stem cells (MSCs) under hypoxic condition: MSCs not only promoted proliferation of undifferentiated M2-Mφs, pre-M2-Mφs, in the Lin+ fraction via a proliferative effect of the MSCs-secreted macrophage colony-stimulating factor, but also promoted M2-Mφ polarization of the pre-M2-Mφs through cell-to-cell contact with the pre-M2-Mφs. Intriguingly, an inhibitor for intercellular adhesion molecule (ICAM)−1 receptor/lymphocyte function-associated antigen (LFA)−1, Rwj50271, partially suppressed expression of CD206 in the Lin+ blood cells but an inhibitor for VCAM-1 receptor/VLA-4, BIO5192, did not, suggesting that the cell-to-cell adhesion through LFA-1 on pre-M2-Mφs and ICAM-1 on MSCs was supposed to promoted the M2-Mφ polarization.Thus, the co-culture system consisting of bone marrow-derived Lin+ blood cells and MSCs under hypoxic condition was a beneficial supplier of a number of M2-Mφs, which could be clinically applicable to inflammatory diseases.
Publication date: Available online 14 July 2017
Source:Experimental Cell Research
Author(s): Rose Cairns, Anna Alvarez-Guaita, Inés Martínez-Saludes, Sundeep J. Wason, Jacky Hanh, Shilpa R. Nagarajan, Elham Hosseini-Beheshti, Katia Monastyrskaya, Andrew J. Hoy, Christa Buechler, Carlos Enrich, Carles Rentero, Thomas Grewal
Annexin A6 (AnxA6) has been implicated in the regulation of endo-/exocytic pathways, cholesterol transport, and the formation of multifactorial signaling complexes in many different cell types. More recently, AnxA6 has also been linked to triglyceride storage in adipocytes. Here we investigated the potential role of AnxA6 in fatty acid (FA) – induced lipid droplet (LD) formation in hepatocytes. AnxA6 was associated with LD from rat liver and HuH7 hepatocytes. In oleic acid (OA) -loaded HuH7 cells, substantial amounts of AnxA6 bound to LD in a Ca2+-independent manner. Remarkably, stable or transient AnxA6 overexpression in HuH7 cells led to elevated LD numbers/size and neutral lipid staining under control conditions as well as after OA loading compared to controls. In contrast, overexpression of AnxA1, AnxA2 and AnxA8 did not impact on OA-induced lipid accumulation. On the other hand, incubation of AnxA6-depleted HuH7 cells or primary hepatocytes from AnxA6 KO-mice with OA led to reduced FA accumulation and LD numbers. Furthermore, morphological analysis of liver sections from A6-KO mice revealed significantly lower LD numbers compared to wildtype animals. Interestingly, pharmacological inhibition of cytoplasmic phospholipase A2α (cPLA2α) -dependent LD formation was ineffective in AnxA6-depleted HuH7 cells. We conclude that cPLA2α-dependent pathways contribute to the novel regulatory role of hepatic AnxA6 in LD formation.
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Thyroid , Vol. 0, No. 0.
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Apoptosis resistance is an acquired hallmark of cancer cells and many factors can contribute to the tumor cell apoptosis resistance. In this study, we demonstrated that HECTD3, overexpressed in human esophageal squamous cell carcinoma (ESCC), confers cells resistance to cisplatin-induced apoptosis and promotes cancer cell survival. HECTD3 can bind and ubiquitinate caspase-9, which leads to inhibiting caspase-9 oligomerization and association with Apaf-1, and results in suppressing caspase-9 activation and inhibiting apoptosis.
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Fibroblasts have been reported to play an important role in hepatocellular carcinoma (HCC). However, the role of fibroblasts have not been fully understood. Conditioned medium collected from human peri-tumor tissue-derived fibroblasts (CM-pTAFs) showed high metastasis ability than human HCC tissues-derived fibroblasts (CM-TAFs). To determine what component was secreted from fibroblasts, we used Bio-Plex analysis system and compared the factors secreted from CM-pTAFs and CM-TAFs, found a series of up-regulated cytokines in the CM-pTAFs, including IL-6, CCL2, CXCL1, CXCL8, SCGF-β, HGF and VEGF.
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The ruthenium drug and GRP78 inhibitor KP1339/IT-139 has already demonstrated promising anticancer activity in a phase I clinical trial. This study aimed to identify mechanisms underlying increased sensitivity to KP1339 treatment. Based on a screen utilizing 23 cell lines, a small panel was selected to compare KP1339-sensitive and low-responsive models. KP1339 sensitivity was neither based on differences in ruthenium accumulation, nor sensitivity to oxidative stress or constituents of KP1339 (ruthenium chloride and indazole).
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To report on the post-tonsillectomy bleeding outcomes and factors associated with hemorrhage among children with pre- or post-operatively diagnosed bleeding disorders treated with an institutional protocol.
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Endogenous circadian clocks regulate 24 h rhythms of physiology and behavior. Circadian rhythm disruption (CRD) is suggested as a risk factor for inflammatory bowel disease. However, the underlying molecular mechanisms remain unknown. Intestinal biopsies from Per1/2 mutant and wild-type (WT) mice were investigated by electron microscopy, immunohistochemistry, and bromodeoxyuridine pulse–chase experiments. TNF-α was injected intraperitoneally, with or without necrostatin-1, into Per1/2 mice or rhythmic and externally desynchronized WT mice to study intestinal epithelial cell death. Experimental chronic colitis was induced by oral administration of dextran sodium sulfate. In vitro, caspase activity was assayed in Per1/2-specific small interfering RNA–transfected cells. Wee1 was overexpressed to study antiapoptosis and the cell cycle. Genetic ablation of circadian clock function or environmental CRD in mice increased susceptibility to severe intestinal inflammation and epithelial dysregulation, accompanied by excessive necroptotic cell death and a reduced number of secretory epithelial cells. Receptor-interacting serine/threonine-protein kinase (RIP)-3-mediated intestinal necroptosis was linked to increased mitotic cell cycle arrest via Per1/2-controlled Wee1, resulting in increased antiapoptosis via cellular inhibitor of apoptosis-2. Together, our data suggest that circadian rhythm stability is pivotal for the maintenance of mucosal barrier function. CRD increases intestinal necroptosis, thus rendering the gut epithelium more susceptible to inflammatory processes.—Pagel, R., Bär, F., Schröder, T., Sünderhauf, A., Künstner, A., Ibrahim, S. M., Autenrieth, S. E., Kalies, K., König, P., Tsang, A. H., Bettenworth, D., Divanovic, S., Lehnert, H., Fellermann, K., Oster, H., Derer, S., Sina, C. Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine.
Mitochondrial dysfunction causes renal tubular epithelial cell injury and promotes cell apoptosis and renal tubulointerstitial fibrosis (TIF) progression. TNF receptor-associated protein 1 (TRAP1) is a molecular chaperone protein that is localized in mitochondria. It plays an important role in cell apoptosis; however, its functional mechanism in TIF remains unclear. In this study, we observed the effects of TRAP1 in renal tubular epithelial cell mitochondria in mice with unilateral ureteral obstruction and its function in cell apoptosis and TIF. Results show that TRAP1 could protect the mitochondrial structure in renal tubular epithelial cells; maintain the levels of mitochondrial membrane potential, ATP, and mitochondrial DNA copy number; inhibit reactive oxygen species production; stabilize the expression of the mitochondrial inner membrane protein mitofilin; reduce renal tubular epithelial cell apoptosis; and inhibit TIF. These results provide new theoretical foundations for additional understanding of the antifibrotic mechanism of TRAP1 in the kidney.—Chen, J.-F., Wu, Q.-S., Xie, Y.-X., Si, B.-L., Yang, P.-P., Wang, W.-Y., Hua, Q., He, Q. TRAP1 ameliorates renal tubulointerstitial fibrosis in mice with unilateral ureteral obstruction by protecting renal tubular epithelial cell mitochondria.
Foreign body aspiration (FBA) could be a serious life-threatening condition in children. Patients usually underwent bronchoscopy with suspicious of FBA alone. In this study, we aimed to determine which patients need to go to bronchoscopy based on pre-operative findings.
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To report on the post-tonsillectomy bleeding outcomes and factors associated with hemorrhage among children with pre- or post-operatively diagnosed bleeding disorders treated with an institutional protocol.
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Telemedicine and e-Health , Vol. 0, No. 0.
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Acid mine drainage (AMD) represents a major source of water pollution in the small watershed of Xingren coalfield in southwestern Guizhou Province. A detailed geochemical study was performed to investigate the origin, distribution, and migration of REEs by determining the concentrations of REEs and major solutes in AMD samples, concentrations of REEs in coal, bedrocks, and sediment samples, and modeling REEs aqueous species. The results highlighted that all water samples collected in the mining area are identified as low pH, high concentrations of Fe, Al, SO42− and distinctive As and REEs. The spatial distributions of REEs showed a peak in where it is nearby the location of discharging of AMD, and then decrease significantly with distance away from the mining areas. Lots of labile REEs have an origin of coal and bedrocks, whereas the acid produced by the oxidation of pyrite is a prerequisite to cause the dissolution of coal and bedrocks, and then promoting REEs release in AMD. The North American Shale Composite (NASC)-normalized REE patterns of coal and bedrocks are enriched in light REEs (LREEs) and middle REEs (MREEs) relative to heavy REEs (HREEs). Contrary to these solid samples, AMD samples showed slightly enrichment of MREEs compared with LREEs and HREEs. This behavior implied that REEs probably fractionate during acid leaching, dissolution of bedrocks, and subsequent transport, so that the MREEs is primarily enriched in AMD samples. Calculation of REEs inorganic species for AMD demonstrated that sulfate complexes (Ln(SO4)+and Ln(SO4)2−) predominate in these species, accounting for most of proportions for the total REEs species. The high concentrations of dissolved SO42− and low pH play a decisive role in controlling the presence of REEs in AMD, as these conditions are necessary for formation of stable REEs-sulfate complexes in current study. The migration and transportation of REEs in AMD are more likely constrained by adsorption and co-precipitation of Fe-Al hydroxides/hydroxysulfate. In addition, the MREEs is preferentially captured by poorly crystalline Fe-Al hydroxides/hydroxysulfate, which favors that sediments also preserve NASC-normalized patterns with MREEs enrichment in the stream.
This study aims to shed light on the seasonal behavior of yttrium and rare earth elements (YREEs) in the Urmia Aquifer (UA), in the immediate vicinity of Urmia Lake (UL) in Iran. Samples of groundwater, collected under dry and wet conditions in coastal wells of UA, suggest a large degree of variability in both YREE abundance and normalized patterns. Although weathering or water-rock interactions (between the surface/groundwater and rock samples) were predicted to be the most probable source in explaining YREEs in groundwater samples, results to the contrary indicate that the groundwater do not inherit aquifer rock-like YREE signatures in the study area; this might be due to the relative stability of YREEs during the process of water-rock interactions, which suggest that methods based on YREEs can be beneficial in discrimination of water sources. Furthermore, findings demonstrated no significant relationship between Ce/Ce* and salinity (0.08 and 0.05 in wet and dry seasons, respectively), and between Eu/Eu* and salinity (0.1 and −0.04 in wet and dry seasons, respectively). Dissimilarity of patterns of YREEs in rock and water samples reveals YREEs as no conservative tracers in determining the UL saltwater intrusion into coastal groundwater. Therefore, the groundwater YREE concentrations and fractionation patterns in UA warrant controlling by coastal aquifer need to be controlled by other chemical weathering, adsorption, desorption, and solution complexation reactions. Finally, comparison of REE concentration values in groundwater samples with corresponding indicative admissible drinking water concentrations (IAC) demonstrated their suitability for drinking purposes.
In this work, a multi-class analytical method for determination of 22 frequently used pharmaceuticals was developed and validated. Analytes were from different classes for example macrolides, fluoroquinolones, tetracyclines, sulfonamides, anthelmintics, anesthetics, and others. Method was intended for analysis of aqueous samples so the sample preparation was done using solid-phase extraction (SPE). Different sorbents (C8, C18, polymeric, and ion exchange sorbents) combining different eluents (methanol, ethanol, acetonitrile, acetone, ethyl acetate) were investigated during development of sample preparation step. Samples were analyzed using HPLC-MS/MS, and therefore, chromatographic and mass spectrometer conditions were investigated. Optimal extraction efficiencies for most of the investigated analytes were obtained with Oasis HLB polymeric sorbents with acetonitrile as eluent. A study of matrix effect was carried out for wastewater treatment plant (WWTP) influent and effluent. The method was validated for linearity, detection limits and quantification limits, repeatability, and reproducibility. Method detection limits were in the range of 2.0–204.0 ng L−1 for WWTP influent except for sulfaguanidine and dexamethasone. Also, method detection limits for WWTP effluent were from 1.0 to 115.4 ng L−1. Method was successfully applied for analysis of real wastewater samples from municipal wastewater treatment plant. In the influent, pharmaceuticals from all investigated groups were present and the concentrations were from 50.0 to 4914.3 ng L−1 for influent and 26.9 to 1699.2 ng L−1 for effluent. It was also reported that some pharmaceuticals showed higher concentrations in the wastewater effluent than in the influent.
Gene fusions in cancer typically lead to the expression of a fusion protein or disrupt the expression of one of the parental genes. Here we report a new phenomenon whereby a fusion transcript functions as a long non-coding chimeric RNA (lnccRNA). This fusion RNA, SLC45A3-ELK4, generated by cis-splicing between neighboring genes, was found in prostate cancer. The fusion RNA encodes the same protein as ELK4. Intriguingly, we found that the fusion RNA level is less than 1% of wild type ELK4, unlikely to perturb the general pool of ELK4 protein.
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Fibroblasts have been reported to play an important role in hepatocellular carcinoma (HCC). However, the role of fibroblasts have not been fully understood. Conditioned medium collected from human peri-tumor tissue-derived fibroblasts (CM-pTAFs) showed high metastasis ability than human HCC tissues-derived fibroblasts (CM-TAFs). To determine what component was secreted from fibroblasts, we used Bio-Plex analysis system and compared the factors secreted from CM-pTAFs and CM-TAFs, found a series of up-regulated cytokines in the CM-pTAFs, including IL-6, CCL2, CXCL1, CXCL8, SCGF-β, HGF and VEGF.
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Apoptosis resistance is an acquired hallmark of cancer cells and many factors can contribute to the tumor cell apoptosis resistance. In this study, we demonstrated that HECTD3, overexpressed in human esophageal squamous cell carcinoma (ESCC), confers cells resistance to cisplatin-induced apoptosis and promotes cancer cell survival. HECTD3 can bind and ubiquitinate caspase-9, which leads to inhibiting caspase-9 oligomerization and association with Apaf-1, and results in suppressing caspase-9 activation and inhibiting apoptosis.
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The ruthenium drug and GRP78 inhibitor KP1339/IT-139 has already demonstrated promising anticancer activity in a phase I clinical trial. This study aimed to identify mechanisms underlying increased sensitivity to KP1339 treatment. Based on a screen utilizing 23 cell lines, a small panel was selected to compare KP1339-sensitive and low-responsive models. KP1339 sensitivity was neither based on differences in ruthenium accumulation, nor sensitivity to oxidative stress or constituents of KP1339 (ruthenium chloride and indazole).
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Intratumoral heterogeneity at the genetic, epigenetic, transcriptomic and morphologic levels is a commonly observed phenomenon in many aggressive cancer types. Clonal evolution during tumor formation as well as in response to therapeutic intervention, can be predicted utilizing reverse engineering approaches on detailed genomic snapshots of heterogeneous patient tumor samples. In this study, we developed an extensive dataset for a GBM case via the generation of polyclonal and monoclonal glioma stem cell lines from initial diagnosis, as well as from multiple sections of distant tumor locations of the deceased patient's brain following tumor recurrence. Our analyses revealed the tissue-wide expansion of a new clone in the recurrent tumor as well as chromosome 7 gain and chromosome 10 loss as repeated genomic events in primary and recurrent disease. Moreover, chromosome 7 gain and chromosome 10 loss produced similar alterations in mRNA expression profiles in primary and recurrent tumors despite possessing other highly heterogeneous and divergent genomic alterations between the tumors. We identified ETV1 and CDK6 as putative candidate genes, and NFKB (complex), IL1B, IL6, Akt and VEGF as potential signaling regulators, as potentially central downstream effectors of chr7 gain and chr10 loss. Finally, the differences caused by the transcriptomic shift following gain of chromosome 7 and loss of chromosome 10 were consistent with those generally seen in GBM samples compared to normal brain in large-scale patient-tumor data sets. This article is protected by copyright. All rights reserved.
The possible role of dietary fiber in the etiology of head and neck cancers (HNCs) is unclear. We used individual-level pooled data from 10 case-control studies (5959 cases and 12,248 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium, to examine the association between fiber intake and cancer of the oral cavity/pharynx and larynx. Odds Ratios (ORs) and their 95% Confidence Intervals (CIs) were estimated using unconditional multiple logistic regression applied to quintile categories of non-alcohol energy-adjusted fiber intake and adjusted for tobacco and alcohol use and other known or putative confounders.
Fiber intake was inversely associated with oral and pharyngeal cancer combined (OR for 5th vs. 1st quintile category = 0.49, 95% CI: 0.40-0.59; p for trend <0.001) and with laryngeal cancer (OR = 0.66, 95% CI: 0.54-0.82, p for trend <0.001). There was, however, appreciable heterogeneity of the estimated effect across studies for oral and pharyngeal cancer combined. Nonetheless, inverse associations were consistently observed for the subsites of oral and pharyngeal cancers and within most strata of the considered covariates, for both cancer sites.
Our findings from a multicenter large-scale pooled analysis suggest that, although in the presence of between-study heterogeneity, a greater intake of fiber may lower HNC risk. This article is protected by copyright. All rights reserved.
Mutation of KRAS in non-small cell lung cancer (NSCLC) shows a poor response to epidermal growth factor receptor (EGFR) inhibitors and chemotherapy. Currently, there are no direct anti-KRAS therapies available. Thus, new strategies have emerged for targeting KRAS downstream signaling. Panobinostat is a clinically available histone deacetylase inhibitor for treating myelomas and also shows potentiality in NSCLC. However, the therapeutic efficacy of panobinostat against gefitinib-resistant NSCLC is unclear. In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild type NSCLC. Combined panobinostat and gefitinib synergistically reduced tumor growth in vitro and in vivo. Mechanistically, we identified that panobinostat, but not gefitinib, inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Clinically, TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild type NSCLC. This article is protected by copyright. All rights reserved.
Star2.com | What are the early signs of throat cancer? Star2.com Finally, cancer of the hypopharynx usually involves symptoms such as pain when swallowing and difficulty swallowing solid food. It is most common in people with a long history of tobacco smoking and daily alcohol consumption. This cancer almost always ... |
TMPRSS13 is a member of the type II transmembrane serine protease (TTSP) family. While various TTSPs have been characterized in detail biochemically and functionally, the basic properties of TMPRSS13 remain unclear. Here, we investigate the activation, inhibition, posttranslational modification, and localization of TMPRSS13. We show that TMPRSS13 is a glycosylated, active protease and that its own proteolytic activity mediates zymogen cleavage. Full-length, active TMPRSS13 exhibits impaired cell-surface expression in the absence of the cognate Kunitz-type serine protease inhibitors, hepatocyte growth factor activator inhibitor (HAI)-1 or HAI-2. Concomitant presence of TMPRSS13 with either HAI-1 or -2 mediates phosphorylation of residues in the intracellular domain of the protease, and coincides with efficient transport of the protease to the cellsurface and its subsequent shedding. Cell-surface labeling experiments indicate that the dominant form of TMPRSS13 on the cell-surface is phosphorylated, whereas intracellular TMPRSS13 is predominantly nonphosphorylated. These data provide novel insight into the cellular properties of TMPRSS13 and highlight phosphorylation of TMPRSS13 as a novel post-translational modification of this TTSP family member and potentially other members of this family of proteases.
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The interaction between the renal water channel aquaporin-2 (AQP2) and the lysosomal trafficking regulator-interacting protein LIP5 targets AQP2 to multivesicular bodies and facilitates lysosomal degradation. This interaction is part of a process which controls AQP2 apical membrane abundance in a vasopressin-dependent manner, allowing for urine volume adjustment. Vasopressin regulates phosphorylation at four sites within the AQP2 C-terminus (S256, S261, S264, T269), of which S256 is crucial and sufficient for AQP2 translocation from storage vesicles to the apical membrane. However, whether AQP2 phosphorylation modulates AQP2-LIP5 complex affinity is unknown. Here using far-western blot analysis and microscale thermophoresis (MST) to show that the AQP2 binds LIP5 in a phosphorylation-dependent manner. We constructed five phospho-mimicking mutants (S256E, S261E, S264E, T269E, S256E/T269E) and a C-terminal truncation mutant (ΔP242) that lacked all phosphorylation sites but retained a previously suggested LIP5-binding site. CD-spectroscopy indicated that wild-type AQP2 and the phospho-mimicking mutants had similar overall structure but displayed differences in melting temperatures possibly arising from C-terminal conformational changes. Non-phosphorylated AQP2 bound LIP5 with the highest affinity while AQP2-ΔP242 had 20-fold lower affinity as determined by MST. AQP2-S256E, S261E, T269E and S256E/T269E all had reduced affinity. This effect was most prominent for AQP2-S256E, which fits well with its role in apical membrane targeting. AQP2-S264E had affinity similar to non-phoshorylated AQP2, possibly indicating a role in exosome excretion. Our data suggest that AQP2 phosphorylation allosterically controls its interaction with LIP5, illustrating how altered affinities to interacting proteins forms the basis for regulation of AQP2 trafficking by post-translational modifications.
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Using the energy of ATP hydrolysis ABC transporters catalyze the trans-membrane transport of molecules. In bacteria they partner with a high affinity substrate binding protein (SBP) to import essential micronutrients. ATP binding by Type-I ABC transporters (importers of amino acids, sugars, peptides, small ions) stabilizes the interaction between the transporter and the SBP, thus allowing transfer of the substrate from the latter to the former. In Type-II ABC transporters (importers of trace elements, e.g., vitamin B12, heme, iron-siderophores) the role of ATP remains debatable. Here we studied the interaction between the Yersinia pestis ABC heme importer (HmuUV) and its partner substrate binding protein (HmuT). Using real-time surface plasmon resonance experiments, and interaction studies in membrane vesicles, we find that in the absence of ATP the transporter and the SBP tightly bind. Substrate in excess inhibits this interaction, and ATP binding by the transporter completely abolishes it. To release the stable docked SBP from the transporter hydrolysis of ATP is required. Based on these results we propose a mechanism for heme acquisition by HmuUV-T where the substrate-loaded SBP docks to the nucleotide-free outward-facing conformation of the transporter. ATP binding leads to formation of an occluded state with the substrate trapped in the trans-membrane translocation cavity. Subsequent ATP hydrolysis leads to substrate delivery to the cytoplasm, release of the SBP, and resetting of the system. We propose that other Type-II ABC transporters likely share the fundamentals of this mechanism.
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Alpha-synuclein (αS) is the primary protein associated with Parkinson's disease, and undergoes aggregation from its intrinsically disordered monomeric form to a cross-β fibrillar form. The closely related homolog beta-synuclein (βS) is essentially fibril resistant under cytoplasmic physiological conditions. Toxic gain of function by βS has been linked to dysfunction, but the aggregation behavior of βS under altered pH is not well understood. In this work, we compare fibril formation of αS and βS at pH 7.3 and mildly acidic pH 5.8, and demonstrate that pH serves as an on/off switch for βS fibrillation. Using αS/βS domain-swapped chimera constructs and single residue substitutions in βS, we localize the switch to acidic residues in the N-terminal and NAC (non-amyloid component) domains of βS. Computational models of βS fibril structures indicate that key glutamate residues (E31, E61) in these domains may be sites of pH-sensitive interactions, and variants E31A and E61A show dramatically altered pH-sensitivity for fibril formation supporting the importance of these charged sidechains in fibril formation of βS. Our results demonstrate that relatively small changes in pH, which occur frequently in the cytoplasm and in secretory pathways, may induce the formation of βS fibrils and suggest a complex role for βS in synuclein cellular homeostasis and Parkinson's disease.
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Accurately predicting changes in protein stability upon amino acid substitution is a much sought after goal. Destabilizing mutations are often implicated in disease, while stabilizing mutations are of great value for industrial and therapeutic biotechnology. Increasing protein stability is an especially challenging task, with random substitution yielding stabilizing mutations in only ~2% of cases. To overcome this bottleneck, computational tools that aim to predict the effect of mutations have been developed; however, achieving accuracy and consistency remains challenging. Here, we combined 11 freely available tools into a meta-predictor (meieringlab.uwaterloo.ca). Validation against ~600 experimental mutations indicated that our meta-predictor has improved performance over any of the individual tools. The meta-predictor was then used to recommend 10 mutations in a previously designed protein of moderate thermodynamic stability, ThreeFoil. Experimental characterization showed that four mutations increased protein stability and could be amplified through ThreeFoil's structural symmetry to yield multi-mutants with >2 kcal/mol stabilization. By avoiding residues within functional ties, we could maintain ThreeFoil's glycan-binding capacity. Despite successfully achieving substantial stabilization, however, almost all mutations decreased protein solubility, the most common cause of protein design failure. Examination of the ~600-mutation dataset revealed that stabilizing mutations on the protein surface tend to increase hydrophobicity and that the individual tools favour this approach to gain stability. Thus, while currently available tools can increase protein stability and combining them into a meta-predictor yields enhanced reliability, improvements to the potentials/forcefields underlying these tools are needed to avoid gaining protein stability at the cost of solubility.
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Synaptic vesicles (SVs) form distinct pools at synaptic terminals, and this well-regulated separation is necessary for normal neuro-transmission. However, how SV cluster in particular synaptic compartments to maintain normal neurotransmitter release remains a mystery. The presynaptic protein Neurexin (NRX) plays a significant role in synaptic architecture and function, and some evidences suggest that NRX is associated with neurological disorders, including autism spectrum disorders. However, the role of NRX in SV clustering is unclear. Here, using the neuromuscular junction at the 2-3 instar stages of Drosophila larvae as a model and biochemical, imaging, and electrophysiology techniques, we demonstrate that Drosophila NRX (DNRX) plays critical roles in regulating synaptic terminal clustering and release of SVs. We found that DNRX controls the terminal clustering and release of SVs by stimulating presynaptic F-actin. Furthermore, our results indicate that DNRX functions through the scaffold protein Scribble and the GEF protein DPix to activate the small GTPase Ras-related C3 Botulinum toxin substrate 1 (Rac1). We observed a direct interaction between the C-terminal PDZ-binding motif of DNRX and the PDZ domains of Scribble and that Scribble bridges DNRX to DPix, forming a DNRX/Scribble/DPix complex that activates Rac1 and subsequently stimulates presynaptic F-actin assembly and SV clustering. Taken together, our work provides important insights into the function of DNRX in regulating SV clustering, which could help inform further research into pathological neurexin-mediated mechanisms in neurological disorders such as autism.
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Nonalcoholic fatty liver disease (steatosis) is the most prevalent liver disease in the Western world. One of the advanced pathologies is non Non-alcoholic steatohepatitis (NASH), which is associated with induction of the Unfolded protein response (UPR) and disruption of autophagic flux. However, the mechanisms by which these processes contribute to the pathogenesis of human diseases are unclear. Herein we identify the α isoform of the inhibitor of Brutons tyrosine kinase (IBTKα) as a member of the UPR whose expression is preferentially translated during endoplasmic reticulum (ER) stress. We found that IBTKα is located in the ER and associates with proteins LC3b, SEC16A, and SEC31A, and plays a previously unrecognized role in phagophore initiation from ER exit sites. Depletion of IBTKα helps prevent accumulation of autophagosome intermediates stemming from exposure to saturated free fatty acids and rescues hepatocytes from death. Of note, induction of IBTKα and the UPR, along with inhibition of autophagic flux, were associated with progression from steatosis to NASH in liver biopsies. These results indicate a function for IBTKα in NASH that links autophagy with activation of the UPR.
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The misfolding of proteins and their accumulation in extracellular tissue compartments as insoluble amyloid or amorphous protein aggregates is a hallmark feature of many debilitating protein deposition diseases such as Alzheimers disease, prion diseases and type II diabetes. The plasminogen activation system (PAS) is best known as an extracellular fibrinolytic system, but was previously reported to also be capable of degrading amyloid fibrils. Here we show that amorphous protein aggregates interact with tPA and plasminogen, via an exposed lysine dependent mechanism, to efficiently generate plasmin. The insoluble aggregate-bound plasmin is shielded from inhibition by α;2-antiplasmin and degrades amorphous protein aggregates to release smaller, soluble but relatively hydrophobic fragments of protein (plasmin-generated protein fragments, PGPFs) that are cytotoxic. In vitro, both endothelial and microglial cells bound and internalised PGPFs before trafficking them to lysosomes. Clusterin and α2-macroglobulin bound to PGPFs to significantly ameliorate their toxicity. On the basis of these findings we hypothesize that, as part of the in vivo extracellular proteostasis system, the PAS may work synergistically with extracellular chaperones to safely clear large and otherwise pathological protein aggregates from the body.
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Nitrate (NO3-) and nitrite (NO2-) are known to be cardioprotective and to alter energy metabolism in vivo. NO3- action results from its conversion to NO2- by salivary bacteria, but the mechanism(s) by which NO2- affects metabolism remains obscure. NO2- may act by S-nitrosating protein thiols, thereby altering protein activity. But how this occurs, and the functional importance of Snitrosation sites across the mammalian proteome remains largely uncharacterized. Here we analyzed protein thiols within mouse hearts in vivo using quantitative proteomics to determine S-nitrosation site occupancy. We extended the thiol-redox proteomic-labelling technique, ICAT (Isotope-Coded Affinity Tag), to quantify the extent of NO2- -dependent S-nitrosation of proteins thiols by in vivo. Using this approach, called SNOxICAT, we found that exposure to NO2- under normoxic conditions, or exposure to ischemia alone, results in minimal S-nitrosation of protein thiols. However, exposure to NO2- in conjunction with ischemia led to extensive Snitrosation of protein thiols across all cellular compartments. Several mitochondrial protein thiols exposed to the mitochondrial matrix were selectively S-nitrosated under these conditions, potentially contributing to the beneficial effects of NO2- on mitochondrial metabolism. The permeability of the mitochondrial inner membrane to HNO2, but not to NO2-, combined with the lack of S-nitrosation during anoxia alone, or by NO2- during normoxia place constraints on how S-nitrosation occurs in vivo and on its mechanisms of cardioprotection and modulation of energy metabolism. Quantifying S-nitrosated protein thiols now allows for determining modified cysteines across the proteome and for identifying those most likely responsible for the functional consequences of NO2- exposure.
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Urease is a ubiquitous nickel metalloenzyme. In plants, its activation requires three urease accessory proteins (UAPs), UreD, UreF, and UreG. In bacteria, the UAPs interact with urease and facilitate activation, which involves the channeling of two nickel ions into the active site. So far this process has not been investigated in eukaryotes. Using affinity pull-downs of Strep-tagged UAPs from Arabidopsis and rice transiently expressed in planta, we demonstrate that a urease:UreD:UreF:UreG complex exists in plants and show its stepwise assembly. UreG is crucial for nickel delivery because UreG-dependent urease activation in vitro was observed only with UreG obtained from nickel-sufficient plants. This activation competence could not be generated in vitro by incubation of UreG with nickel, bicarbonate, and GTP. Compared with their bacterial orthologs, plant UreGs possess an N-terminal extension containing a His and Asp/Glu-rich hypervariable region followed by a highly conserved sequence comprising two potential HXH metal-binding sites. Complementing the ureG-1 mutant of Arabidopsis with N-terminal deletion variants of UreG demonstrated that the hypervariable region has a minor impact on activation efficiency, whereas the conserved region up to the first HXH motif is highly beneficial and up to the second HXH motif strictly required for activation. We also show that urease reaches its full activity several days after nickel becomes available in the leaves, indicating that urease activation is limited by nickel accessibility in vivo. Our data uncover the crucial role of UreG for nickel delivery during eukaryotic urease activation, inciting further investigations of the details of this process.
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Management of type 2 diabetes mellitus aims to maintain a normal glycemic status, which if not, it may lead to acute and/or chronic diabetic complications. Earlier studies found Lipocalin-2 elevated in complic...
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In Bangladesh, each emergency physician faces amitriptyline overdose nearly a day. An acute cardiovascular complication, one of the worst complications is mainly responsible for the mortality in tricyclic over...
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This empirical study examines the short- and long-run relationship between GDP as an economic growth indicator and CO2 emissions as an environmental pollution indicator in Myanmar by using annual time series data over the period of 1970–2014. It also carefully considered other proxies, such as trade openness, financial openness and urbanization, and structural breaks in the country. The fundamental objective of this study is to test the validity of environmental Kuznets curve (EKC) in the context of Myanmar. The dynamic estimates of the long- and short-term relationship among greenhouse gases (CO2, CH4, N2O), GDP, trade intensity, financial openness, and urbanization growth are built through an autoregressive distributed lag (ARDL) model. The empirical findings indicate that there is positive short- and long-run relationship between CO2 and GDP and thus, no evidence of EKC hypothesis is found for CO2 in Myanmar. Nevertheless, the existence of the EKC is observed for CH4 and N2O. On the other hand, trade and financial openness have inverse relationship with CO2 emissions. These results demonstrate that trade liberalization and financial openness will improve the environment quality in Myanmar in the long run.
Bone tissue engineering combines biomaterials with biologically active factors and cells to hold promise for reconstructing craniofacial defects. In this study the biological activity of biphasic hydroxyapatite ceramics (HA; a bone substitute that is a mixture of hydroxyapatite and β-tricalcium phosphate in fixed ratios) was characterized (1) in vitro by assessing the growth of MC3T3 mouse osteoblast lineage cells, (2) in ovo by using the chick chorioallantoic membrane (CAM) assay and (3) in an in vivo pig animal model. Biocompatibility, bioactivity, bone formation and biomaterial degradation were detected microscopically and by radiology and histology. HA ceramics alone demonstrated great biocompatibility on the CAM as well as bioactivity by increased proliferation and alkaline phosphatase secretion of mouse osteoblasts. The in vivo implantation of HA ceramics with bone marrow mesenchymal stem cells (MMSCs) showed de novo intramembranous bone healing of critical-size bone defects in the right lateral side of pig mandibular bodies after 3 and 9 weeks post-implantation. Compared with the HA ceramics without MMSCs, the progress of bone formation was slower with less-developed features. This article highlights the clinical use of microporous biphasic HA ceramics despite the unusually shaped elongated micropores with a high length/width aspect ratio (up to 20) and absence of preferable macropores (>100 µm) in bone regenerative medicine.
Mounting evidence has showed that Tumor-associated calcium signal transducer 2 (Trop2) is upregulated in various kinds of human cancers and plays important roles in tumorigenesis. However, the expression statu...
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Greensboro News & Record | Hoppers dog Yogi's cancer diagnosed as inoperable Greensboro News & Record She said the tumor appears to have originated in one of the dog's salivary glands. "What we found today is the tumor is in an area where we can't remove it surgically, and it has spread into his chest," Scharf said. "... One potential option is trying ... and more » |
A laboratory-scale biodegradation and electron transfer based on the sulfur metabolism in the integrated (BESI®) process was used to treat a saline petrochemical nanofiltration concentrate (NFC). The integrated process consisted of activated sludge sulfate reduction (SR), and sulfide oxidation (SO) reactors, and a biofilm nitrification reactor. During the process, the total removal efficiencies of chemical oxygen demand (COD), ammonia nitrogen, and total nitrogen (TN) were 76.2, 83.8, and 73.1%, respectively. In the SR reactor, most of the organic degradation occurred and approximately 70% COD were removed by the sulfate-reducing bacteria (SRB). In the SO reactor, both the autotrophic and heterotrophic denitrifications were observed to take place. In parallel, batch experiments were conducted to detect the effects of different C/S and S/N ratios on COD removal and denitrification efficiency. The batch experiments were also conducted to detect the effects of salinity on COD and sulfate reduction. The composition of pollutants in the wastewater was complex, and some existing organics were not degraded by the SRB. The non-SRB groups also played important roles in the reactor. Under salinity-induced stress, the metabolisms of the SRBs and non-SRB groups were both inhibited. However, 6 g/L NaCl did not have much effect on the final COD removal efficiency. In the batch experiments, the added sulfide served as the electron donor for autotrophic denitrification. The added organics provided substance for heterotrophic denitrification.
The remediation of Cr(VI)-contaminated soil was investigated by electrokinetic (EK) and permeable-reactive-barrier assisted electrokinetic (EK-PRB). The medium of PRB was hydrocalumite (CaAl-LDH). The results showed that removal efficiency of hexavalent chromium (Cr(VI)) in EK-PRB and EK system was 96.49 and 85.50%, respectively. Simultaneously, the removal efficiency of total chromium (TCr) was 69.34 and 40.97% after 120-h treatment. The XRD, FTIR, and XPS analyses indicated that the reactive barrier media of CaAl-LDH successfully captured the chromium. Besides, the migration rate of chromium in EK-PRB was relatively faster than EK, since the media of PRB captured chromium in-time and reduced the influence of chromium accumulation on the migration of chromium. Moreover, the trivalent chromium (Cr(III)) was generated in EK/EK-PRB, and the chromium was stabilized in soil with the chemical speciations of oxidizable and residual fractions. Therefore, the treatment of EK-PRB and EK both increased the removal of chromium and decreased its environmental risks.
Star2.com | What are the early signs of throat cancer? Star2.com Most people discover cancer in the oropharynx when they notice a mass in their neck that's a result of the cancer spreading to a lymph node. Eighty percent of people with cancer that affects the tonsils and base of tongue are not diagnosed until the ... |
Publication date: Available online 14 July 2017
Source:Translational Research
Author(s): Mayra A. Carrillo, Anjie Zhen, Jerome A. Zack, Scott G. Kitchen
HIV infection continues to be a life-long chronic disease in spite of the success of antiretroviral therapy (ART) in controlling viral replication and preventing disease progression. However, because of the high cost of treatment, severe side effects, and inefficiency in curing the disease with ART therapy, there is a call for alternative therapies that will provide a functional cure for HIV. Cytotoxic T lymphocytes (CTLs) are vital in the control and clearance of viral infections and therefore immune-based therapies have attempted to engineer HIV-specific CTLs that would be able to clear the infection from the body. The development of chimeric antigen receptors (CAR) provides an opportunity to engineer superior HIV-specific CTLs that will be independent of MHC for target recognition. A CD4-based CAR has been previously tested in clinical trials to test the antiviral efficacy of peripheral T cells armed with this CD4-based CAR. The results from these clinical trials showed the safety and feasibility of CAR T cell therapy for HIV infection; however, minimal antiviral efficacy was seen. In this review, we will discuss the various strategies being developed to enhance the therapeutic potency of anti-HIV CARs with the goal of generating superior antiviral responses that will lead to life-long HIV immunity and clearance of the virus from the body.
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Publication date: Available online 14 July 2017
Source:Translational Research
Author(s): Michael Shaffer, Abigail J.S. Armstrong, Vanessa V. Phelan, Nichole Reisdorph, Catherine A. Lozupone
For much of our history, the most basic information about the microbial world has evaded characterization. Next-generation sequencing has led to a rapid increase in understanding of the structure and function of host-associated microbial communities in diverse diseases ranging from obesity to autism. Through experimental systems such as gnotobiotic mice only colonized with known microbes, a causal relationship between microbial communities and disease phenotypes has been supported. Now microbiome research must move beyond correlations and general demonstration of causality to develop mechanistic understandings of microbial influence, including through their metabolic activities. Similar to the microbiome field, advances in technologies for cataloguing small molecules have broadened our understanding of the metabolites that populate our bodies. Integration of microbial and metabolomics data paired with experimental validation has promise for identifying microbial influence on host physiology through production, modification or degradation of bioactive metabolites. Realization of microbial metabolic activities that affect health is hampered by gaps in our understanding of 1) biological properties of microbes and metabolites, 2) which microbial enzymes/pathways produce which metabolites and 3) the effects of metabolites on hosts. Capitalizing upon known mechanistic relationships and filling gaps in our understanding has the potential to enable translational microbiome research across disease contexts.
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Several lines of evidence suggest the consume of natural products for cancer prevention or treatment. In particular, isothiocyanates (ITCs) exerting anti-cancer properties, have received great interest as pote...
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In the treatment of functional dyspepsia, the placebo effect has been reported to be high, and the influence of the patient-practitioner relationship may be a major component of this effect. The specific and n...
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Il team di ricerca di Molecular Modeling & Drug Discovery di IIT –Istituto Italiano di Tecnologia, guidato da Marco De Vivo insieme ai gruppi di ricerca dell'Università di Padova...
| Myeloma Dispatches: Season Of Change The Myeloma Beacon Last month, a friend of mine lost his life to a rare form of salivary gland cancer, which he had battled for 20 years. He experienced several periods of remission, sometime for years. He was a powerful model of adapting to change and learning "to swim ... |
The use of acellular dermal matrices (ABDM) has become more common for breast reconstruction to improve postoperative outcomes. We evaluated the efficacy of breast reconstruction by the application of human ABDM in a sheep model.
The sheep in group I (GI) (N = 4) underwent the following procedures on the right side: (1) breast reconstruction using human ABDM after total mastectomy, (2) human ABDM under the skin, near the breast area and on the left side, (3) fat injection and human ABDM after partial mastectomy, and (4) replacement of ABDM in the abdominal wall far from the breast. Sheep in group II (GII) (N = 4) underwent the following procedures. On the right side: (1) breast reconstruction using ABDM after total mastectomy, (2) replacement of ABDM under the skin, near the breast area, and on the left side, (3) application of vicryl synthetic mesh after partial mastectomy and (4) replacement of mesh under the skin, near the breast area.
Histological evaluations of decellularized skin scaffolds demonstrated a collagen-based matrix with preserved ECM and complete nuclear removal. Histological evaluations of implanted ABDM demonstrated a viable matrix with fibroblast infiltration and revascularization in all follow-ups. The overall surgical complication rate was significantly lower in the ABDM implant under the skin and near the breast in both short- and long-term follow-ups.
The results of this study demonstrated that the application of novel prepared ABDMs has promising outcomes for breast reconstruction to provide total coverage without the need for breast expansion before implant placement.
This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors http://ift.tt/18t7xNj
Star2.com | What are the early signs of throat cancer? Star2.com Early voice box cancer is treated with surgery – often laser surgery – or radiation therapy. Both are highly effective. If left untreated, voice box cancer can grow and destroy more of the larynx. At that point, treatment usually includes major surgery ... |
[ Advance Publication ] [ Title ] A Heart-shaped Sleeve Simplifies Intramedullary Tibial Nail Insertion when Using the Suprapatellar Approach [ Author ] Kosuke Tajima,Chikako Shimizu,Soichiro Ohno,Yusho Nishida,Kazuhiko Udagawa,Junichi Sasaki [ Advance Pub. date ] 2017-07-15 [ DOI ] http://ift.tt/2t08fPW
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| Nivolumab improves quality of life for advanced head and neck cancer Healio Nivolumab led to greater stabilization of symptoms and functioning among patients with recurrent or metastatic head and neck squamous cell carcinoma than ... and more » |
The UK's healthcare system is the best out of 11 of the world's most developed countries, despite having one of the lowest levels of funding.The US health think tank the Commonwealth Fund ranked the...
