Bladder cancer, a review of the environmental risk factors

<p>Abstract</p> <p>Background</p> <p>Many epidemiological studies and reviews have been performed to identify the causes of bladder cancer. The aim of this review is to investigate the links between various environmental risk factors and cancer of the bladder.</p> <p>Methods</p> <p>A systematic literature search was performed using PubMed, Science Direct, Scopus, Scholar Google and Russian Google databases to identify reviews and epidemiological studies on bladder cancer risk factors associated with the environment published between 1998 and 2010. Only literature discussing human studies was considered.</p> <p>Results</p> <p>Smoking, mainly cigarette smoking, is a well known risk factor for various diseases, including bladder cancer. Another factor strongly associated with bladder cancer is exposure to arsenic in drinking water at concentrations higher than 300 µg/l. The most notable risk factor for development of bladder cancer is occupational exposure to aromatic amines (2-naphthylamine, 4-aminobiphenyl and benzidine) and 4,4'-methylenebis(2-chloroaniline), which can be found in the products of the chemical, dye and rubber industries as well as in hair dyes, paints, fungicides, cigarette smoke, plastics, metals and motor vehicle exhaust. There are also data suggesting an effect from of other types of smoking besides cigarettes (cigar, pipe, Egyptian waterpipe, smokeless tobacco and environmental tobacco smoking), and other sources of arsenic exposure such as air, food, occupational hazards, and tobacco. Other studies show that hairdressers and barbers with occupational exposure to hair dyes experience enhanced risk of bladder cancer. For example, a study related to personal use of hair dyes demonstrates an elevated bladder cancer risk for people who used permanent hair dyes at least once a month, for one year or longer.</p> <p>Conclusion</p> <p>Smoking, in particular from cigarettes, exposure to arsenic in drinking water, and occupational exposure to aromatic amines and 4,4'-methylenebis(2-chloroaniline) are well known risk factors for various diseases including bladder cancer. Although the number of chemicals related to occupational exposure is still growing, it is worth noting that it may take several years or decades between exposure and the subsequent cancer.</p

Berberine enhances inhibition of glioma tumor cell migration and invasiveness mediated by arsenic trioxide

<p>Abstract</p> <p>Background</p> <p>Arsenic trioxide (As₂O₃) exhibits promising anticarcinogenic activity in acute promyelocytic leukemic patients and induces apoptosis in various tumor cells <it>in vitro</it>. Here, we investigated the effect of the natural alkaloid berberine on As₂O₃-mediated inhibition of cancer cell migration using rat and human glioma cell lines.</p> <p>Methods</p> <p>The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to determine the viability of rat C6 and human U-87 glioma cells after treatment with As₂O₃or berberine, and after co-treatment with As₂O₃and berberine. The wound scratch and Boyden chamber assays were applied to determine the effect of As₂O₃and berberine on the migration capacity and invasiveness of glioma cancer cells. Zymography and Western blot analyses provided information on the effect of As₂O₃and berberine on the intracellular translocation and activation of protein kinase C (PKC), and some PKC-related downstream factors. Most assays were performed three times, independently, and data were analyzed using ANOVA.</p> <p>Results</p> <p>The cell viability studies demonstrated that berberine enhances As₂O₃-mediated inhibition of glioma cell growth after 24 h incubation. Untreated control cells formed a confluent layer, the formation of which was inhibited upon incubation with 5 μM As₂O₃. The latter effect was even more pronounced in the presence of 10 μM berberine. The As₂O₃-mediated reduction in motility and invasion of glioma cells was enhanced upon co-treatment with berberine. Furthermore, it has been reported that PKC isoforms influence the morphology of the actin cytoskeleton, as well as the activation of metalloproteases MT1-MMP and MMP-2, reported to be involved in cancer cell migration. Treatment of glioma cells with As₂O₃and berberine significantly decreased the activation of PKC α and ε and led to actin cytoskeleton rearrangements. The levels of two downstream transcription factors, myc and jun, and MT1-MMP and MMP-2 were also significantly reduced.</p> <p>Conclusion</p> <p>Upon co-treatment of glioma cells with As₂O₃and berberine, cancer cell metastasis can be significantly inhibited, most likely by blocking the PKC-mediated signaling pathway involved in cancer cell migration. This study is potentially interesting for the development of novel chemotherapeutic approaches in the treatment of malignant gliomas and cancer development in general.</p

Vplyv vône na dopyt po občerstvení v Slovenskom národnom divadle

Letašiová, L. The influence of smell on demand for refreshments in The Slovak National Theatre. Bachelor thesis. Brno: Mendel University, 2017. In this thesis the influence of smell is examined using a sensory marketing in the attempt to sway the consumers' decision making in relation to choosing the refreshments in this cultural environment. The goal is also to identify other factors apart from the sense of smell that can be influential for the visitor in buying and to create a recommendation leading into higher sales and profit based on identified information. The research was held during two performances, when the visitors to The Slovak National Theatre were exposed to the influence of the scent and the purchase of selected refreshments was tracked. The outcome values were then compared to values gained during normal duty without the scent influence and analysed. The sale was increased in two out of three tracked items, a coffee and a strudel to be exact. Other factors that could have possibly influenced the outcome are mostly the limited time for sales or other scents indoors, as more of the people stated

Vplyv vône ako nástroja zmyslového marketingu na rozhodovanie spotrebiteľa

In this master’s thesis, the effect of smell as a tool of sensory marketing on consumer decision making is examined. The aim of the thesis is to describe the functioning of smell in a consumer decision making context and based on gathered data suggest possible recommendations applicable for selected culinary establishments that would serve to meet the needs of consumers as well as operators of these establishments. The case is demonstrated on an empirical study carried out in the Slovak National Theatre, whereby visitors were exposed to purposefully released smells over the period of two weeks. Consumer behaviour and revenues attributable to three selected items were observed over the studied timeframe. The collected data was subsequently compared to that of a counterfactual period in which no smells were being released. A statistically significant difference was observed in the sales of all three items examined, whereby the revenues stemming from coffee and strudel saw an increase, while the revenue from savoury pastry saw a decline. At the same time, it is necessary to identify potential factors that may have skewed the obtained data. Visitors have in their consumption process felt restricted primarily by a time constraint, which is necessary to take into account for long-term application of smell as a tool of sensory marketing, as well as for future research purposes

Miejsce fizjoterapii w zapobieganiu i leczeniu osteoporozy

Osteoporoza w ostatnich latach stała się ważnym problemem zdrowotnym i społeczno-ekonomicznym porównalnym z innymi chorobami cywilizacyjnymi. Jest to choroba należąca do osteologii i najważniejszym powikłaniem jest złamanie proksymalnej części kości udowej, kręgu kręgosłupa lub przedramienia. Osteologia jest nauką, która zajmuje się rozwojem i chorobami kości i dziedziną, która w ostatnich latach bardzo się rozwija. Osteoporoza nie jest nieuchronną konsekwencją starzenia, wręcz odwrotnie – jest to schorzenie spełniające kryteria choroby: 1. Osteoporoza jest jednoznacznie zdefiniowana jako choroba i jej kryteriami już nie są złamania. 2. Udało się dobrze objaśnić mechanizmy patofizjologiczne utraty masy kostnej przy osteoporozie. 3. Zwiększone ryzyko złamań można wcześnie zdiagnozować poprzez pomiar masy kostnej. 4. Są znane skuteczne środki zapobiegania i leczenia osteoporozy. Fizjoterapia i odpowiednia aktywność fizyczna mają niezastąpioną rolę w prewencji i leczeniu osteoporozy i złamań osteoporotycznych. Mechanizmy aktywności fizycznej w prewencji konsekwencji osteoporozy są następujące: w młodym wieku odpowiednia aktywność fizyczna zwiększa szczytową masę kostną (peak bone mass), w okresie menopauzy zwalnia zwiększoną utratę masy kostnej i w starszym wieku poprawia siłę mięśni, koordynacyjne zdolności i stabilność, dzięki czemu może zmniejszyć częstość występowania i powagę upadkówIn the recent years osteoporosis has become a substantial health and social-economic problem reaching the level of other civilization diseases. The most significant complication of this osteology illness is the fracture of a thigh bone proximal part, vertebra or forearm. Osteology, a field of study remarkably evolving nowadays, is the science exploring development of bone mass and bone diseases. Osteoporosis is not an inevitable consequence of aging, on the contrary it is a physical disorder that meets all criteria of an illness: 1. Osteoporosis is clearly defined as an illness and its criteria are not only fractures. 2. Science clarified pathophysiological processes of osteoporosis bone mass reduction. 3. Increased peril of fractures can be early diagnosed by measuring bone mass content. 4. There are well known measures for prevention and therapy of osteoporosis. Physiotherapy and appropriate physical activity have their unique place in prevention and treatment of osteoporosis and osteoporotic fractures. Mechanisms of physical activity in prevention of osteoporosis consequences are as follows: physical activity increases the peak bone mass in young age and it slows down the increased loss of bone mass during the menopause and in older age it improves muscle strength, coordination capabilities and stability whereby it can decrease the incidence and severity of fall

Comparison of murine fibroblast cell response to fluor-hydroxyapatite composite, fluorapatite and hydroxyapatite by eluate assay

Fluorapatite (FA) is one of the inorganic constituents of bone or teeth used for hard tissue repairs and replacements. Fluor-hydroxyapatite (FHA) is a new synthetic composite that contains the same molec- ular concentration of OH – groups and F – ions. The aim of this experiment was to evaluate the cellular responses of murine fibroblast NIH-3T3 cells in vitro to solid solutions of FHA and FA and to compare them with the effect of hydroxyapatite (HA). We studied 24, 48 and 72 h effects of biomaterials on cell morphology, proliferation and cell cycle of NIH-3T3 cells by eluate assay. Furthermore, we examined the ability of FHA, FA and HA to induce cell death and DNA damage. Our cytotoxic/antiproliferative studies indicated that any of tested biomaterials did not cause the total inhibition of cell division. Biomaterials induced different antiproliferative effects increasing in the order HA<FHA<FA which were time- and concentration-dependent. None of the tested biomaterials induced necrotic/apoptotic death of NIH-3T3 cells. On the other hand, after 72 h we found that FHA and FA induced G 0 /G 1 arrest of NIH-3T3 cells, while HA did not affect any cell cycle phases. Comet assay showed that while HA demonstrated weaker genotoxicity, DNA damage induced by FHA and FA caused G 0 /G 1 arrest of NIH- 3T3 cells. Fluoridation of hydroxyapatite and different FHA and FA structure caused different cell response of NIH-3T3 cells to biomaterials

Arylamine N-acetyltransferases: from drug metabolism and pharmacogenetics to drug discovery.

Arylamine N-acetyltransferases (NATs) are polymorphic drug-metabolizing enzymes, acetylating arylamine carcinogens and drugs including hydralazine and sulphonamides. The slow NAT phenotype increases susceptibility to hydralazine and isoniazid toxicity and to occupational bladder cancer. The two polymorphic human NAT loci show linkage disequilibrium. All mammalian Nat genes have an intronless open reading frame and non-coding exons. The human gene products NAT1 and NAT2 have distinct substrate specificities: NAT2 acetylates hydralazine and human NAT1 acetylates p-aminosalicylate (p-AS) and the folate catabolite para-aminobenzoylglutamate (p-abaglu). Human NAT2 is mainly in liver and gut. Human NAT1 and its murine homologue are in many adult tissues and in early embryos. Human NAT1 is strongly expressed in oestrogen receptor-positive breast cancer and may contribute to folate and acetyl CoA homeostasis. NAT enzymes act through a catalytic triad of Cys, His and Asp with the architecture of the active site-modulating specificity. Polymorphisms may cause unfolded protein. The C-terminus helps bind acetyl CoA and differs among NATs including prokaryotic homologues. NAT in Salmonella typhimurium supports carcinogen activation and NAT in mycobacteria metabolizes isoniazid with polymorphism a minor factor in isoniazid resistance. Importantly, nat is in a gene cluster essential for Mycobacterium tuberculosis survival inside macrophages. NAT inhibitors are a starting point for novel anti-tuberculosis drugs. Human NAT1-specific inhibitors may act in biomarker detection in breast cancer and in cancer therapy. NAT inhibitors for co-administration with 5-aminosalicylate (5-AS) in inflammatory bowel disease has prompted ongoing investigations of azoreductases in gut bacteria which release 5-AS from prodrugs including balsalazide