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Sequencing the human genome has shown unexpectedly that the human genome contains a surprisingly small number of protein-coding genes [40] purchase discount super avana online thyroid causes erectile dysfunction. Clearly the protein coding gene content of animal chromosomes does not change dramatically with vertebrate and mammalian evolution discount 160mg super avana free shipping erectile dysfunction protocol pdf. These apparently contradictory data suggest that Myc-mediated epigenetic programming is complex, but taken as a whole, prevents cell cycle arrest. Some genes that are moderately methylated during stem cell renewal, become hypomethylated, while others exhibit increased methylation. Collectively, these factors contribute to Myc-mediated epigenetic control over stem cell renewal and maintenance of pluripotency. Myc also directly binds to, and strongly represses, the transcription of Gata6, a transcription factor that promotes endoderm differen- tiation of stem cells. Other members of the pluripotency network are also subject to epigenetic regulatory programs. The human genome contains six pseudogenes for Oct3/4 and ten pseudogenes for Nanog, compared to a relative paucity of psuedogenes for other non-pluripotency-related transcription factors [64]. The Oct4 pseudo- gene family has been recently found to exert complex and mutually interdependent epigenetic regulation of the Oct4 promoter. Imprinted gene loci play an important role in tissue growth in mammals and therefore an analysis of how they control stem cell differentiation is particularly important for the thera- peutic use of stem cells. The Mest/Peg (Paternally-Expressed Gene)-1 locus is a good example of the role of epigenetics in stem cell maturation. Inter- estingly, these regions, particularly at the second CpG island also coincide with a high density of activation acetylation (H3K27Ac) and methylation (H3K4me3 and H3K4Me1) marks on histones, suggesting differential activation of maternal and paternal alleles. We previously discussed evidence, for example, that Wnt signaling directs mesenchymal stem cells towards osteoblast-specic differentiation and inhibits adipocyte differentiation. However, miR335 also acts as a direct negative regulator of Runx2, a factor required for osteogenic differentiation [73]. For example, researchers have reported the loss of X-chromosome inactivation in well-established human embryonic stem cell lines [80] suggesting that stem cells can experience epigenetic drift. This suggests that the environment can reprogram epigenetic controls over stem cell renewal and maturation. Most epigenetic changes do not lead to alterations in the primary sequence of genes and are potentially reversible. However, some epigenetic mutations do lead to genetic mosaicism in somatic stem cells, potentially leading to permanent alterations in differentiation. The retro- transposon genes, which constitute approximately 45% of the sequence of the human genome [82] are a good example of how mutations in the epigenome may produce genetic drift among somatic cells, and perhaps even among stem cells. However, epigenetic mutations may contribute to senescence of adult tissue stem cells, compromising their regenerative capacity [22]. Moreover, epigenetically driven genetic diversi- cation of somatic cells means that these cells may not be equipped to recapitulate native pluripotency states of embryonic stem cells derived from the blastocyst. The authors were able to show vascularization, osteogenesis, and successful functional engraftment of the engineered mandible into a patient. A clearer understanding of the epigenetic landscape of the stem cell during renewal and through successive stages of maturation will be a critical requirement for the development of effective stem cell therapy. A reserve stem cell population in small intestine renders Lgr5-positive cells dispensable. Reprogramming with dened factors: from induced pluripotency to induced transdifferentiation. Sprouty1 Regulates Neural and Endothelial Differentiation of Mouse Embryonic Stem Cells. Induction of chondro-, osteo- and adipogenesis in embryonic stem cells by bone morphogenetic protein-2: effect of cofactors on differentiating lineages. Downregulation of Dlx5 and Dlx6 expression by Hand2 is essential for initiation of tongue morphogenesis. Comparison of human stem cells derived from various mesenchymal tissues: superiority of synovium as a cell source. Luminal and systemic signals trigger intestinal adap- tation in the juvenile python. Epigenetic proling at mouse imprinted gene clusters reveals novel epigenetic and genetic features at differentially methylated regions. The Angelman syndrome ubiquitin ligase localizes to the synapse and nucleus, and maternal deciency results in abnormal dendritic spine morphology. Multiple retropseudogenes from pluripotent cell-specic gene expression indicates a potential signature for novel gene identication. Transcriptional and post-transcriptional regulation of Sprouty1, a receptor tyrosine kinase inhibitor in prostate cancer. Epigenetic memory and preferential lineage-specic differentiation in induced pluripotent stem cells derived from human pancreatic islet Beta cells. Generation, purication and transplantation of photoreceptors derived from human induced pluripotent stem cells. Platelets generated from human embryonic stem cells are functional in vitro and in the microcirculation of living mice. At that time, the biochemical nature of genes was unknown as well as their role as repositories and transmitters of the genetic information. Waddington imagined the epigenetics as a conceptual model to explain his theory sustaining that different interac- tions between the genes and their surroundings (or, we could say their environment) could result in different phenotypes, starting from the same genetic material. He used the metaphor of the epigenetic landscape to explain the biological development. Waddington stated that cell fates were established during the development similarly to a stone (a marble) that rolls down from high places to the point of lowest local elevation; the increasing irreversibility associated with cell-type differentiation was imagined as due to ridges, rising along the slope where the stone is rolling down, directing the marble into different valleys [1]. More recently, Holliday dened epigenetics in a more formal way as the study of the mechan- isms of temporal and spatial control of gene activity during the development of complex organisms [2]. Specic combinations of epigenetic modications determine the conformation of the chro- matin ber, thereby having the possibility to regulate the transcriptional potential of the associated genes. Despite the advances in our knowledge about cell differentiation and epigenetic phenomena, and with the unavoidable adjustments and corrections, Waddingtons model still represents a nice visualization of the epigenetics. As a matter of fact, it appears really useful to suggest that aging processes are particularly prone to epigenetic mechanisms. The notion Waddington could not know, indeed, was that once differentiation has been completed (i. To resume and apply Waddingtons model to the aging, we can imagine that erosive processes can change the shape of the slope and of the surroundings of the stone, causing the reprise of its rolling down through new ridges and valleys. According to this view, the terminally differentiated cell is subjected to environ- mental stimuli (originated either from the organism itself or from the external environment) able to induce changes in gene expression through epigenetic mechanisms. The higher the mountain, the longer the slope; consequently, the stone encounters many more possibilities to be subjected to changes of directions and shape.

These studies provide evidence that the early environment can cause epigenetic alterations at imprinted loci buy cheap super avana on line erectile dysfunction enlarged prostate, leading to human disorders that include obesity as a clinical characteristic cheap super avana online mastercard erectile dysfunction oral treatment. A number of factors during early life alter the epigenome of the fetus, producing long-term changes in gene expression. In an elegant study of the effect of maternal behavior during suckling on the development of stress response in the offspring, Weaver et al. These changes were reversed in the brains of the adults by intracranial administration of the histone deacetylase inhibitor Trichostatin A and L-methionine [91]. In the Epigenetics in Human Disease agouti mouse variations in the maternal intake during pregnancy of nutrients involved in vy 1-carbon metabolism induces differences in the coat color of the offspring. Supplementation of the mothers diet with methyl donors such as betaine, choline, folic acid, and vitamin B12 shifted the distribution of coat color of the offspring from yellow (agouti) to brown (pseudo-agouti) [93]. These studies showed for the rst time that, in contrast to modifying the maternal intake of nutrients directly involved 1-carbon metabolism [44], stable changes to the epigenetic regulation of the expression of transcription factors can be induced in the offspring by modest changes to maternal macronutrient balance during pregnancy. This is consistent with raised plasma b-hydroxybutyrate and glucose concentrations in the fasting offspring [97]. The mechanisms involved are not known but by regulating effects of transcription factors on expression they may have important effects on phenotype. Together, these results indicate that modest dietary protein restriction during pregnancy induces an altered phenotype through epigenetic changes in specic genes. One explanation may lie in the differences in severity of nutritional restriction between these two dietary regimens. If the induction of altered phenotypes is predictive, then it may be anticipated that induced changes in the epigenome would differ according to dietary regimen, in order to match the phenotype to the predicted future environment. In contrast more severe global undernutrition induces conservation of energy substrates. These interpretations are consistent with the phenotypes induced in the offspring [52,55,95]. There is also evidence that an excessive early nutritional environment can alter the epigenetic regulation of genes. This suggests that overfeeding during early postnatal life when the appetite circuitry within the hypothalamus is still developing can alter the methylation of genes critical for bodyweight regulation, resulting in the altered programming of this system and an increased tendency towards obesity in later life. These ndings raise the important issue that assessment of true non-genomic transmission between gener- ations requires studies which continue to at least the F3 generation [110]. There is substantial evidence for transgenerational epigenetic inheritance in non-mammalian species and its role in evolutionary biology has been reviewed [111,112]. Although epidemi- ological and experimental studies have shown transmission of induced phenotypes between generations, to date only one study has reported transmission of nutritionally induced vy epigenetic marks between generations [96]. The tendency towards obesity in A mice is exacerbated thorough successive generations [113]. Transmission of the obese phenotype was prevented by supplementation of females with a methyl donors and cofactors, although this vy was not associated with a change in the methylation status of the A locus. The mechanism by which induced epigenetic marks are transmitted to subsequent generations is not known, although studies have begun to unpick the mechanisms involved [114]. When the transmission is only to the F2 generation, a direct effect of the diet fed to the F0 dams on Epigenetics in Human Disease germ cells which gave rise to the F2 offspring cannot be ruled out. An alternative possibility is that prenatal nutritional constraint induces physical or physiological changes in the female which, in turn, restrict the intrauterine environment in which her offspring develop. In this case, transmission of an altered phenotype between generations would involve induction of changes in gene methylation de novo in each generation. If so, the magnitude of the induced effect, epigenetic or phenotypic, might differ between generations. However, studies in vitro show loss of Dnmt1-induced demethyla- tion of only a subset of genes [116,117]. Dnmt1 activity is also required for progression through mitosis [118] and its expression is substantially reduced in non-proliferating cells [119]. Thus, suppression of Dnmt1 activity in the preim- plantation period could also account for the changes in the number of cell types during early embryonic development in this model [120]. Tet1, is an enzyme which catalyzes the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine [121,122] and has therefore been considered as a promising candidate for demethylation. Studies have shown that 5hmC levels across the genome are low, consistent with the hypothesis that these may be short-lived. Alternatively, 5hmC may be an epigenetic modication in its own right, attracting its own chromatin or transcriptional modications. The mark is signicantly enriched in CpG dinucleotides within genes, particularly at exons and this has been found to be associated with gene expression as well as polycomb-mediated silencing [125]. Genome-wide proling methods have also shown that the distribution of 5hmC is distinct to that of 5mC [125]. High levels of Tet1 in primordial germ cells have also been observed [126] suggesting that Tet1 is associated with the pluripotent state. It is difcult to identify those individuals most at risk and those who would most benet from individualized monitoring and care. In the worst instances preferential accumulation of fat occurs in visceral adipose tissue and ectopic fat deposition in insulin-sensitive tissues such as muscle, liver, and pancreas, which correlates strongly with severe generalized insulin resistance due to the development of a chronic inammatory state partly due to inltration of adipose tissue by macrophages. A more detailed analysis of the promoters of these genes showed that an increase in maternal folic acid intake induced subtle changes in gene regula- tion and altered the methylation of individual CpGs dependent on the supplementation given [95]. Folic acid supplementation of the diet of rats during their juvenile-pubertal period [129] was found to induce impaired lipid homeostasis in addition to increased weight gain. These effects were seen irrespective of the maternal diet given and were associated with altered methylation status of specic genes in the liver. These observations are supportive of the view that puberty is a time of increased instability of the epigenome. However, this study highlights the ability to alter effects of prenatal nutrition with interventions during puberty. Studies carried out by Waterland and colleagues on a mouse model of obesity [113] were also able to demonstrate that obesity in offspring could be prevented by appropriate vy supplementation of the maternal diet. The mouse A allele results from a transposition of a murine intracisternal A particle retrotransposon upstream of the agouti gene. The agouti 311 signaling molecule induces yellow pigmentation in the hair follicles as well as antagonizing satiety signaling at the melanocortin 4 receptor in the hypothalamus; as a result the mice have v/y yellow coats and are prone to hyperphagic obesity. In these studies the altered A allele was vy passed through three successive generations of A /a females and a cumulative effect on coat color and obesity was observed. The work found that maternal obesity could cause transgenerational amplication of increased body weight and that a methyl-supplemented diet was able to prevent this effect. This conrms that epigenetic mechanisms such as meth- ylation play a role in the transgenerational increases in mammalian obesity, but also provides evidence that dietary intervention during pregnancy to prevent obesity is possible. These initial studies point to the need for further work to determine whether increased adiposity occurs as a result of increased energy intake, decreased energy expenditure, or both. Having an understanding of the epigenetic mechanisms which underlie the observed increase in obesity presents the opportunity to prevent or reverse further increases in obesity. Among the best-characterized of the animal models of intervention is neonatal leptin treat- ment. Leptin is produced by white adipose tissue and plays a key role in maintaining body weight homeostasis [130].

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The rates in women appear to be According to the Healthcare Cost and Utilization relatively constant across age groups purchase super avana online from canada erectile dysfunction jacksonville doctor. The steady decline in the rate of hospitalization the true prevalence of stone disease purchase super avana now erectile dysfunction nerve. In addition, for patients with upper tract stones between 1994 these new data cannot be used to determine incidence and 2000 likely refects the greater effciency and or recurrence rates. The include temporizing procedures prior to defnitive high rate of inpatient hospitalization for the older stone treatment such as placement of a ureteral stent age groups likely refects the lower threshold for or percutaneous nephrostomy to relieve obstruction, admission for an acute stone event or after surgical especially in an infected kidney. National rates of inpatient and ambulatory surgery visits for urolithiasis by age group, 2000. Admission group than in the <65 age group, peaking in the 75- to rates for Hispanics were one-half to two-thirds those 84-year group in each year of study. Age-adjustment did not affect regional age-unadjusted and the age-adjusted data, the male- differences in admission rates, but it did slightly to-female ratios also fell slightly over time. Although the total number of procedures increased from 1994 to 1998, the rate decreased (from 14 15 Urologic Diseases in America Urolithiasis Table 9. In all years of study, the rates highest in the 85+ age group, although they increased of procedures increased with age to a maximum in the substantially after age 64by 2. Beyond that age, procedure refecting the higher prevalence of bladder stones counts in this database were too small to be reliable. Inpatient procedures for individuals having commercial health insurance with urolithiasis listed as primary diagnosis, counta, rateb 1994 1996 1998 2000 Count Rate Count Rate Count Rate Count Rate Total 272 25 375 24 539 22 682 25 Age < 3 1 * 1 * 3 * 4 * 310 2 * 0 0. Geographic steadily over time, decreasing by 15% from a mean variation was also evident, with rates highest in the of 3. National trends in mean length of stay (days) for Outpatient Care individuals hospitalized with lower tract urolithiasis listed An individual may be seen in the outpatient as primary diagnosis setting as part of the diagnosis of urolithiasis, during Length of Stay urologic treatment (pre- and/or post-procedure), 1994 1996 1998 2000 or for medical evaluation and prevention. Overall, the absolute Asian/Pacifc Islander * * * * number of hospital outpatient visits during this Hispanic 3. Other * * * * Information on hospital outpatient visits is also Region available from Medicare data for 1992, 1995, and 1998 Midwest 3. There were also regional differences, with the from National Ambulatory Medical Care Survey highest rates occurring in the South. The visit visit rate for a primary diagnosis of bladder stones rate was 43% higher in 2000 than it was in 1992. The rates peaked in the 65-to 74-year nearly 2 million visits in 2000 by patients with age group and then declined. In 1995 and 1998, the rates were higher for translates into a rate of 731 per 100,000 population. Thus, the vast majority offce visit rates slightly widened in all three years of of visits for urolithiasis (74%) are for urolithiasis as study, but the relative differences in geographic and the primary diagnosis (Tables 15 and 17). However, the data do not represent all decreased between 1999 and 2001 (Table 19). This outpatient procedures performed in a population, 24 25 Urologic Diseases in America Urolithiasis 24 25 Urologic Diseases in America Urolithiasis Table 19. The available data regarding ambulatory surgery During the years studied, the male-to-female for urolithiasis in children are too scant to provide ratio varied from 1. Regional differences were apparent: the highest rates were consistently seen in the Southeast; 28 29 Urologic Diseases in America Urolithiasis Table 22. Ureteroscopy of the Holmium laser in 1995 rendered virtually all remained stable over time and comprised 40% to stones amenable to fragmentation if they could be 42% of the procedures. Open stone surgery made up accessed endoscopically (14); however, this new only 2% of the total procedures in 1994 and dropped technology may have not yet reached widespread use to less than 1% in 2000. In database of commercially insured patients (Table both 1995 and 1998, the rates were highest among 24). Each inpatient or outpatient encounter determine whether this represented a sharp increase involves a variety of cost sources, including physician or simply year-to-year variability. In general, the professional fees, radiographic studies, room and rate for males was twice that for females. It is noted board, laboratory, pharmacy, and operating room that the confdence intervals for these estimates are costs. Among Medicare benefciaries, the rate always be easily arrived at or consistently applied. There were clear regional variations, for those without a claim relating to urolithiasis (Table with rates highest in the South. Hence, a $4,472 difference per covered individual 32 33 Urologic Diseases in America Urolithiasis 32 33 Urologic Diseases in America Urolithiasis Table 27. Expenditures for urolithiasis and share of costs, by type of service (in millions of $) Year 1994 1996 1998 2000 Totala 1,373. Average drug spending for urolithiasis-related conditions is estimated at $4 million to $14 million annually for the period 1996 to 1998. Evaluation 100% of regional differences in medical expenditures 90% suggests that overall higher expenditures for the 80% group without urolithiasis-related claims were found 70% in the South and West, whereas in the urolithiasis 60% group, expenditures were highest in the Midwest 50% and South. As prescription drug costs showed 40% little regional variation, the geographic differences 30% 20% in expenditures are likely related to direct medical 10% expenditures or possibly due to differences in the age 0% distributions of the regions. Percent share of costs for urolithiasis by type was spent on treating urolithiasis in 2000, based solely of service, 19942000. That these fgures are somewhat should be accounted for by expenditures either lower than the $1. Total expenditures (excluding as primary hyperparathyroidism, chronic diarrheal outpatient prescription drug costs) increased by syndrome due to bowel disease, etc. During that time period, non-inpatient differences (such as comorbidities) between those services (including physician offce visits, emergency with and without stone disease. When stratifed by of total expenditures for emergency room services age, the expenditures of those without a urolithiasis- also increased, from 15% in 1992 to 24% in 2000. In contrast, the peak total Medicare population also increased signifcantly over medical expenditure for the group with a urolithiasis- time. However, given the higher incidence of stone on outpatient prescription drugs for the treatment disease in men (a factor of 2 to 3), one might expect of urolithiasis in 19961998 ranged from $4 million a greater impact of gender in the group with stones. Expenditures for Medicare benefciaries age 65 and over for treatment of urolithiasis (in millions of $) Year 1992 1995 1998 Total 613. Expenditures In addition to the direct medical costs of in 2001 were nearly twice as high among infants (0 treatment, the economic effects of urolithiasis include to 2 years of age) as they were among children ages labor market outcomes such as absenteeism and work 3 to 10 or 11 to 17 and twice as high among African limitations. The setting for urolithiasis are diffcult to estimate, largely because of both the acute care and the surgical management of the paucity of data. However, some data are available patients with stones has changed over time: inpatient in the medical and fnancial records of the National admissions and length of stay have decreased as Table 30. Annual use of outpatient prescription drugs for the treatment of urolithiasis, 19961998 All Persons with Urolithiasis Conditional on Rx Use Number with % with Rx Claim Mean Number of Mean Rx Gender Urolithiasis for Urolithiasis Prescriptions Expenditures (in $) Male 676,144 29. Work loss is based on reported absences contiguous to the admission and discharge dates of each hospitalization or the date of the outpatient visit. The trends medical evaluation to determine the etiology of in distribution of surgical treatment modalities stone formation? How frequently are preventive measures however, shock wave lithotripsy remains the most recommended?

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Later she developed a productive cough and breathing problems order super avana no prescription erectile dysfunction johns hopkins, and a medical specialist diagnosed her with asthma discount 160mg super avana otc erectile dysfunction from adderall. The Committee in particular took into consideration that the operator had been working with glue with acrylate compounds, which is known as a potential cause of asthma. Example 4: Recognition of irritated mucous membranes of nose and throat (coolants and oil) A machine engineer worked for many years in a shipyard. The machine used coolants and lubricants for cooling stones and unit for transporting away the dust. Normally the system was closed, but towards the end of the working period a defect occurred in the machine so that the suction system blew the coolant and vaporised oil into his face. He developed complaints from skin, eyes and mucous membranes, and a medical specialist diagnosed him with dry mucous membranes of nose and throat. The Committee found that working with the defective grinding machine mainly had caused irritated mucous membranes in nose and throat. The Committee took into consideration that the machine engineer for 2 months had been exposed to direct contact with coolant and vaporised oil on his face. Example 5: Recognition of chronically irritated mucous membranes of nose and sinuses and perforation of the nasal septum (process operator exposed to dust from minerals and vitamins) A 55-year-old man worked for well over 12 years as a process operator in a business manufacturing mixtures of vitamins and minerals as additives to food. For the longest period of time, his work consisted in weighing out raw materials and producing and weighing out mixtures. Despite having an exhaust system and mechanical ventilation he was unable to avoid dust from i. After some time he developed dryness and irritation in his nose, which typically became evident during the weighing-out work. A medical specialist found that he had developed a hole in the nasal septum as well as chronically irritated mucous membranes of nose and sinuses. The Committee found that the process operator mainly had developed chronically irritated mucous membranes in his nose and sinuses with subsequent perforation of the nasal septum due to his work, where he had been exposed to dust from various minerals and vitamins. Example 6: Recognition of asthma welder with exposure to welding smoke) A 33-year-old man worked for 2 years in a steel factory. His work consisted in welding steel constructions for the building sector and he worked in a big hall together with about 12 welders. The Working Environment Authority had inspected the factory and found problems with the exhaust system. There was respiratory protection equipment available, but filtrating respiratory protection was not sufficiently effective in connection with welding. It also appeared, however, that on the day of the inspection there were only four welders present in the hall and not 12. After one year the welder began to develop an increasingly dry, irritated cough and wheezing. He had some allergy tests made, and these showed hypersensitivity to birch pollen, grass pollen and dust mites. The Committee found that due to exposure to welding smoke the welder mainly had developed considerable aggravation of a private, pre-existing asthma. It was included in the assessment that heavy welding smoke can trigger asthma in a person who is sensitive beforehand and has a private disposition for developing asthma. When calculating the compensation for permanent injury and loss of earning capacity, the National Board of Industrial Injuries may make a deduction in the compensation to the 37 extent that the private disposition for asthma can be deemed to be a contributory cause of part of the asthma disease. Example 7: Claim turned down lung fibrosis (grinding dust from metal and grinding agents) A man worked for many years as a metal grinder. For 10 years he worked with hand grinding of fittings for kitchen sinks and bathrooms. Here he was exposed to grinding dust from brass and stainless steel and various grinding agents. He developed reduced lung function and a medical specialist diagnosed him with lung fibrosis. The Committee found that the lung fibrosis had not, mainly or solely, been caused by the described exposure to grinding dust and grinding agents. The Committee took into consideration that the cause of the lung fibrosis in the concrete case was unknown, and that the rather sudden onset and quick progression of the disease made it unlikely that there should be any correlation with the many years of exposure to metal dust. The lung disease you would typically see after many years of exposure to metal dust is pneumoconiosis, and x-rays and tissue microscopy showed no signs of that disease. Example 8: Claim turned down indoor air quality symptoms (poor ventilation and micro fungi in school A woman worked as a school teacher for more than 20 years. She furthermore experienced immunodeficiency and had an increasing number of sickness periods. There was no general improvement after the school moved to other premises 15 years after she started work there. The Committee found that the work as a teacher in the buildings in question had not, mainly or solely, caused a disease related to indoor air quality. The Committee found that it was not a specific disease caused by indoor air quality exposures, including micro fungi exposure. Scientific surveys have shown an increased frequency of these symptoms in relation to certain indoor air quality conditions, i. There is uncertainty as to the significance of micro fungi, but a few reports raise the suspicion that massive growth of micro fungi may be a contributing factor. In the teachers case there was no evidence of any physical, pathological changes that might form the basis for the diagnosis of indoor air quality symptoms, and it was not possible to document any allergic or equivalent reaction to fungi or other exposures. Example 9: Claim turned down chronic obstructive lung disease/bronchitis (waiter exposed to passive smoking) For 23 years a 42-year-old man had worked as a waiter and occasionally as a cook in several hotels. About half of the 23-year-period he was exposed to extensive passive smoking in restaurants and bars with poor ventilation. It appeared that the waiter was a never smoker and that the spouse was a no smoker as well. In childhood he was exposed to passive smoking through his father, who smoked 15 cigarettes per day. Towards the end of the period he developed coughing and shortness of breath and in a lung function examination was diagnosed with chronic obstructive lung disease (bronchitis) with a certain asthma element. The Committee took into consideration that there is no known medical correlation between exposure to passive smoking and the development of chronic, obstructive lung disease (bronchitis), and that there was no description of any concrete circumstances in the workplace that might be regarded as significantly increasing the risk of developing the disease in question. Read more about the practice of the Occupational Diseases Committee with regard to chronic bronchitis after exposure to passive smoking. Diseases of other organs Example 1: Recognition of benign bladder polyp/bladder papilloma (dyes, printing work) A man worked for well over 30 years as a printer for a newspaper. His primary task was to look after the printing works that produced coloured prints. For well over 20 years the work was done at a high pressure machine which gave off a lot of dye dust to the surroundings. He was diagnosed with a growth at the left side of his bladder, and a detailed cystoscopic examination showed that there was a bladder tumour without ingrowth, a benign bladder polyp (bladder papilloma).