A postmortem case control study of asbestos burden in lungs of malignant mesothelioma cases.

BACKGROUND: Asbestos lung content is regarded as the most reliable tool for causal attribution of malignant mesothelioma (MM) to previous asbestos exposures. However, there is a lack of studies on asbestos burden in lungs of MM patients in comparison with healthy individuals. This study aims to provide such a comparison, investigating, as well, differences in asbestos lung burden with sex and time trends. METHODS: Asbestos lung content has been assessed on formalin-fixed lung fragments using scanning electron microscopy coupled with energy dispersion spectroscopy (SEM-EDS) on individuals deceased from MM (cases) and healthy subjects without any lung disease who died from violent causes (controls) between 2005 and 2023. RESULTS: Asbestos and asbestos bodies (ABs) were found, respectively, in 73.7% and 43.2% of cases and in 28 and 22% of controls; in MM cases the most represented asbestos types were crocidolite and amosite, whereas in controls it was tremolite-actinolite asbestos. The concentration of both asbestos fibers and ABs was statistically significantly higher in MM cases compared to controls. The mean asbestos fibers width was also significantly higher in cases than controls. Males and females with MM showed similar asbestos and ABs concentrations, but females had higher concentrations of chrysotile, and significantly lower fibers width compared to males. Time trends show that MM lung asbestos concentrations decreased starting in 2011. DISCUSSION: The results suggest a correlation between asbestos burden in lungs and MM risk. The different concentration of chrysotile, as well as the different width of asbestos fibers in MM males and females might reflect a sex difference in response of the lung microenvironment to inhaled asbestos. Finally, this study provides the first pathological evidence of the effect of the ban of asbestos use, demonstrating a significant decrease of asbestos lung content after 2011.

Building dampness and mold in European homes in relation to climate, building characteristics and socio-economic status: The European Community Respiratory Health Survey ECRHS II.

We studied dampness and mold in homes in relation to climate, building characteristics and socio-economic status (SES) across Europe, for 7127 homes in 22 centers. A subsample of 3118 homes was inspected. Multilevel analysis was applied, including age, gender, center, SES, climate, and building factors. Self-reported water damage (10%), damp spots (21%), and mold (16%) in past year were similar as observed data (19% dampness and 14% mold). Ambient temperature was associated with self-reported water damage (OR=1.63 per 10°C; 95% CI 1.02-2.63), damp spots (OR=2.95; 95% CI 1.98-4.39), and mold (OR=2.28; 95% CI 1.04-4.67). Precipitation was associated with water damage (OR=1.12 per 100 mm; 95% CI 1.02-1.23) and damp spots (OR=1.11; 95% CI 1.02-1.20). Ambient relative air humidity was not associated with indoor dampness and mold. Older buildings had more dampness and mold (P<.001). Manual workers reported less water damage (OR=0.69; 95% CI 0.53-0.89) but more mold (OR=1.27; 95% CI 1.03-1.55) as compared to managerial/professional workers. There were correlations between reported and observed data at center level (Spearman rho 0.61 for dampness and 0.73 for mold). In conclusion, high ambient temperature and precipitation and high building age can be risk factors for dampness and mold in homes in Europe.

The risk of respiratory symptoms on allergen exposure increases with increasing specific IgE levels.

BACKGROUND: The relation between IgE sensitization and allergic respiratory symptoms has usually been evaluated by dichotomizing specific IgE levels. The aim of this study was to evaluate the association between specific IgE levels and risk of symptoms on allergen-related exposure, with special reference to allergen-related asthma-rhinitis comorbidity. METHODS: We considered 6391 subjects enrolled within the European Community Respiratory Health Survey 2, having information on cat/grass/D. pteronyssinus IgE levels and symptoms on exposure to animals/pollen/dust. The risk of oculonasal/asthmalike/both symptoms was evaluated by a multinomial logistic model. RESULTS: A clear positive association was observed between specific IgE levels to cat/grass/mite and the risk of symptoms on each allergen-related exposure (test for trend with P < 0.001). This trend was particularly pronounced when considering the coexistence of asthmalike and oculonasal symptoms. Compared to non-sensitized subjects, subjects with specific IgE to cat >= 3.5 kU/l presented relative risk ratios of 11.4 (95% CI 6.7-19.2), 18.8 (8.2-42.8), and 55.3 (30.5-100.2) when considering, respectively, only oculonasal symptoms, only asthmalike symptoms, or both. A similar pattern was observed when considering specific IgE to grass/mite and symptoms on exposure to pollen/dust. Also the proportion of people using inhaled medicines or visiting a general practitioner for breathing problems in the previous year increased with increasing sum of specific IgE to cat/grass/mite. CONCLUSION: Specific IgE level is the most important predictor of allergen-related symptoms. The risk of both oculonasal/asthmalike symptoms increases with specific IgE levels, suggesting that specific IgE contributes to the 'united airways disease'.

Prevalence of Streptomycin-Resistant Erwinia amylovora in New York Apple Orchards.

Resistance to streptomycin in Erwinia amylovora was first observed in the United States in the 1970s but was not found in New York until 2002, when streptomycin-resistant (SmR) E. amylovora was isolated from orchards in Wayne County. From 2011 to 2014, in total, 591 fire blight samples representing shoot blight, blossom blight, and rootstock blight were collected from 80 apple orchards in New York. From these samples, 1,280 isolates of E. amylovora were obtained and assessed for streptomycin resistance. In all, 34 SmR E. amylovora isolates were obtained from 19 individual commercial orchards. The majority of the resistant isolates were collected from orchards in Wayne County, and the remaining were from other counties in western New York. Of the 34 resistant isolates, 32 contained the streptomycin resistance gene pair strA/strB in the transposon Tn5393 on the nonconjugative plasmid pEA29. This determinant of streptomycin resistance has only been found in SmR E. amylovora isolates from Michigan and the SmR E. amylovora isolates discovered in Wayne County, NY in 2002. Currently, our data indicate that SmR E. amylovora is restricted to counties in western New York and is concentrated in the county with the original outbreak. Because the resistance is primarily present on the nonconjugative plasmid, it is possible that SmR has been present in Wayne County since the introduction in 2002, and has spread within and out of Wayne County to additional commercial growers over the past decade. However, research is still needed to provide in-depth understanding of the origin and spread of the newly discovered SmR E. amylovora to reduce the spread of streptomycin resistance into other apple-growing regions, and address the sustainability of streptomycin use for fire blight management in New York.

Adult eczema in Italy: prevalence and associations with environmental factors.

BACKGROUND: Studies on the prevalence of eczema and atopic dermatitis (AD), and on the factors associated with these diseases, have been mostly performed in children, whereas studies on adult populations are lacking. OBJECTIVES: To determine the prevalence of eczema and AD in the Italian adult population, and to investigate risk factors associated with the disease. METHODS: A postal screening questionnaire was administered to 18 357 randomly selected subjects aged 20-44 years in the Gene-Environment Interaction in Respiratory Diseases study, which involved seven centres distributed across northern, central and southern Italy. The questionnaire included items on the occurrence of doctor-diagnosed eczema, asthma and hay fever, socio-demographic characteristics and environmental exposures. RESULTS: In all, 10 464 (57.0%) subjects responded to the questionnaire. The prevalence of current eczema was 8.1% (95% CI: 7.6-8.7%), while the prevalence of eczema with asthma and/or hay fever (EAH), which was adopted as proxy of AD, was 3.4% (95% CI: 3.1-3.8%). About 60% of the subjects with current eczema reported the onset of the disease in adulthood. In multi-variable models, the prevalence of eczema was significantly associated with female sex, older age, living close to industrial plants, high levels of heavy traffic near home and living in central-southern Italy. CONCLUSIONS: Eczema and EAH are highly prevalent in Italian young adults, especially in women. Our results suggest that adult onset is not unusual, and that environmental factors may influence the occurrence of eczema and EAH.

Asthma incidence can be influenced by climate change in Italy: findings from the GEIRD study-a climatological and epidemiological assessment.

An association between climatic conditions and asthma incidence has been widely assumed. However, it is unclear whether climatic variations have a fingerprint on asthma dynamics over long time intervals. The aim of this study is to detect a possible correlation of the Summer North Atlantic Oscillation (S-NAO) index and the self-calibrated palmer drought severity index (scPDSI) with asthma incidence over the period from 1957 to 2006 in Italy. To this aim, an analysis of non-stationary and non-linear signals was performed on the time series of the Italian databases on respiratory health (ISAYA and GEIRD) including 36,255 individuals overall, S-NAO, and scPDSI indices to search for characteristic periodicities. The ISAYA (Italian Study on Asthma in Young Adults) and GEIRD (Gene Environment Interactions in Respiratory Diseases) studies collected information on respiratory health in general population samples, born between 1925 and 1989 and aged 20-84 years at the time of the interview, from 13 Italian centres. We found that annual asthma total incidence shared the same periodicity throughout the 1957-2006 time interval. Asthma incidence turned out to be correlated with the dynamics of the scPDSI, modulated by the S-NAO, sharing the same averaged 6 year-periodicity. Since climate patterns appear to influence asthma incidence, future studies aimed at elucidating the complex relationships between climate and asthma incidence are warranted.

Trends in the prevalence of asthma and allergic rhinitis in Italy between 1991 and 2010.

The prevalence of asthma increased worldwide until the 1990s, but since then there has been no clear temporal pattern. The present study aimed to assess time trends in the prevalence of current asthma, asthma-like symptoms and allergic rhinitis in Italian adults from 1990 to 2010. The same screening questionnaire was administered by mail or phone to random samples of the general population (age 20-44 yrs) in Italy, in the frame of three multicentre studies: the European Community Respiratory Health Survey (ECRHS) (1991-1993; n = 6,031); the Italian Study on Asthma in Young Adults (ISAYA) (1998-2000; n = 18,873); and the Gene Environment Interactions in Respiratory Diseases (GEIRD) study (2007-2010; n = 10,494). Time trends in prevalence were estimated using Poisson regression models in the centres that repeated the survey at different points in time. From 1991 to 2010, the median prevalence of current asthma, wheezing and allergic rhinitis increased from 4.1% to 6.6%, from 10.1% to 13.9% and from 16.8% to 25.8%, respectively. The prevalence of current asthma was stable during the 1990s and increased (relative risk 1.38, 95% CI 1.19-1.59) from 1998-2000 to 2007-2010, mainly in subjects who did not report allergic rhinitis. The prevalence of allergic rhinitis has increased continuously since 1991. The asthma epidemic is not over in Italy. During the past 20 yrs, asthma prevalence has increased by 38%, in parallel with a similar increase in asthma-like symptoms and allergic rhinitis.

Geographical variation and the determinants of domestic endotoxin levels in mattress dust in Europe.

UNLABELLED: Endotoxin exposures have manifold effects on human health. The geographical variation and determinants of domestic endotoxin levels in Europe have not yet been extensively described. To investigate the geographical variation and determinants of domestic endotoxin concentrations in mattress dust in Europe using data collected in the European Community Respiratory Health Survey follow-up (ECRHS II). Endotoxin levels were measured in mattress dust from 974 ECRHS II participants from 22 study centers using an immunoassay. Information on demographic, lifestyle, and housing characteristics of the participants was obtained in face-to-face interviews. The median endotoxin concentration in mattress dust ranged from 772 endotoxin units per gram (EU/g) dust in Reykjavik, Iceland, to 4806 EU/g in Turin, Italy. High average outdoor summer temperature of study center, cat or dog keeping, a high household crowding index, and visible damp patches in the bedroom were significantly associated with a higher endotoxin concentrations in mattress dust. There is a large variability in domestic endotoxin levels across Europe. Average outdoor summer temperature of study center, which explains only 10% of the variation in domestic endotoxin level by center, is the strongest meteorological determinant. The observed variation needs to be taken into account when evaluating the health effects of endotoxin exposures in international contexts. PRACTICAL IMPLICATIONS: The incoherent observations of the health effects of endotoxin may be partly owing to the geographical heterogeneity of endotoxin exposure. Therefore, the observed variation should be considered in further studies. Measurements of indoor endotoxin are recommended as an indicator for the level of exposures of individual domestic environments.

First Report of White Pine Blister Rust Caused by Cronartium ribicola on Immune Black Currant Ribes nigrum Cv. Titania in Preston, Connecticut.

Since the relaxation of federal sanctions on the planting of Ribes crops because of the development of white pine blister rust (WPBR) immune Ribes cultivars (3), a small industry for the production of Ribes fruit for fresh and processing markets was established in New York and surrounding New England states. The majority of Ribes acreage in the region is planted to a WPBR immune black currant R. nigrum cv. Titania. From 2008 to June 2011, symptoms resembling those caused by WPBR pathogen Cronartium ribicola were observed at a large (>12 ha) R. nigrum cv. Titania planting in Preston, CT. In 2008, infection was restricted to a single field (100% incidence), but in 2009, all fields suffered from premature defoliation by late July. In 2010 and 2011, there was considerable incidence (>85%), but premature defoliation was kept in check by chemical management. Symptoms began as chlorotic lesions (0.5 to 4.3 mm in diameter) on both sides of the leaf. These chlorotic lesions had margins delineated by leaf veins and many developed necrotic (0.3 to 0.9 mm in diameter) centers on the upper surface of leaves within 2 to 3 weeks. The undersides of lesions developed blisters containing orange uredinia (0.1 to 0.33 mm in diameter) with smooth peridia that broke with the production of yellow-orange urediniospores (30 × 15 to 25 µm). Symptoms and signs were consistent with published descriptions of C. ribicola (1) and with WPBR infections on highly susceptible R. nigrum cv. Ben Alder planted at the New York State Agricultural Experiment Station in Geneva. Additional confirmation was provided by sequencing the two internal transcribed spacer (ITS) regions and the 5.8S gene (GenBank Accession No. JN587805; 98% identity with No. DQ533975) in the nuclear ribosomal repeat using primers ITS1-F and ITS4 as described previously (2,4). Furthermore, an attempt was made to confirm pathogenicity in the greenhouse by inoculating shoots of potted nursery stock of R. nigrum cv. Titania. Shoots were inoculated by rubbing leaves with either an uninfected currant leaf or a currant leaf from Preston, CT sporulating with urediniospores. Plants were subsequently misted with dH20 and covered with plastic bags for 24 h. Plants were watered biweekly and kept in a greenhouse with 39 to 65% relative humidity at 21 to 26°C. Shoots were monitored for symptom development on a weekly basis. After 3 weeks, 2 of the 10 plants inoculated with infected leaves developed chlorotic lesions and uredinia identical to those on leaves from Preston, CT, while all others remained healthy. Although not easily reproducible in a greenhouse, the breakdown of immunity in R. nigrum cv. Titania was observed for the last 4 years in Connecticut. Given that WPBR immunity was one of the conditions for legalized planting of Ribes, the breakdown of immunity has potentially deleterious implications particularly for nearby states like Massachusetts and New York, in which the Ribes industries are expanding. Moreover, Ribes growers may need to rely on chemical management programs to manage WPBR in the future. References: (1) G. B. Cummins. Illustrated Genera of Rust Fungi. Burgess Publishing Company, Minneapolis, MN, 1959. (2) M. Gardes and T. D. Bruns. Mol. Ecol. 2:113, 1993. (3) S. McKay. Hortic. Technol. 10:562, 2000. (4) T. J. White et al. PCR Protocols: A Guide to Methods and Applications. Academic Press, Inc., San Diego, CA, 1990.

First Reports of Brown Fruit Rot on Sweet Cherry (Prunus avium) and Plum (P. domestica) and Shoot Blight on Apricot (P. armeniaca), Kwanzan Cherry (P. serrulata), and Sweet Cherry (P. avium) Caused by Monilinia laxa in New York, Rhode Island, and Massachusetts.

In the eastern United States, Monilinia laxa (Aderh. & Ruhl.) Honey has only been reported on tart cherry in New York (NY) (1). As a result of considerable rain in May of 2009 and 2011, an ornamental planting of Kwanzan cherries in Middletown, Rhode Island (RI), a planting of sweet cherry cvs. Ulster, Hedelfingen, Sam, and Lapins in Lanesboro, Massachusetts (MA), and plantings of apricot cvs. Harcot and Hargrande in Albion, Aurora, and Geneva, NY, and Harogem in Lanesboro, MA developed severe shoot blight (>15 to 100% of first-year shoots). Blighted shoots were wilted with the blight encompassing the distal end and often extending into second-year tissue with a distinct sunken margin. Leaves on symptomatic shoots had flushed, but were blighted and light brown. Blossom spurs were often blighted and gummosis was frequently observed at the base. In these same years, sweet cherry cv. Black Gold in Walworth, NY and plum cv. Stanley in Olcott, NY developed severe fruit rot (35 to 70% incidence). Plantings suffering from fruit rot had fruit lesions that began as pale brown, soft lesions with indiscriminant margins that covered 15 to 85% of the fruit surface area. Many blighted spurs, shoot tissues, and infected fruit were sporulating with tan-to-buff colored conidia produced in chains. From each planting with shoot blight, shoot tips were removed for pathogen isolation. Sections of symptomatic shoots (5 cm long) were surface sterilized in 0.6% NaOCl for 1 min and rinsed in sterile dH20. From plantings displaying blighted spurs or fruit rot, isolation was attempted directly from sporulating tissue. Cross sections of sterilized shoot tissue (3 mm thick) or tufts of sporulation from fruit and spurs were placed on potato dextrose agar amended with 50 µg/ml of streptomycin sulfate. After incubation at 24°C for 5 days, colonies with lobed margins, commonly described for M. laxa (4), were obtained. Several colonies resembling M. fructicola were isolated from all locations, but the majority of isolates from spurs and shoots resembled M. laxa. Conidia from both colony morphotypes were lemon shaped, but as expected, those from putative M. laxa isolates were smaller (10.75 × 12.0 µm) compared with those from putative M. fructicola isolates (15.75 × 18.25 µm) (4). Confirmation of M. laxa was further achieved by PCR amplification of the ß-tubulin gene using M. laxa-specific primers as previously described (3). Pathogenicity of M. laxa isolates was proven by inoculating fruit of the stone fruit crop from which they were isolated as previously described (2). Fruit inoculated with M. laxa developed brown, soft sporulating lesions identical to the original observations, while those inoculated with water remained healthy. M. laxa was reisolated from symptomatic shoots and spurs, but not from water-inoculated tissues. The presence of M. laxa has been reported on tart cherries in NY (1), but to our knowledge, this is the first instance of economically devastating shoot blight on apricot in NY and MA, ornamental cherry in RI, and sweet cherry in MA and fruit rot on sweet cherry and plum in NY caused by M. laxa. In wet seasons, stone fruit growers may need to revise their chemical management programs to better prepare for M. laxa epidemics on several stone fruit species. References: (1) K. D. Cox and S. M. Villani. Plant Dis. 94:783, 2010. (2) K. D. Cox and S. M. Villani. Plant Dis. 95:828, 2011. (3) Z. Ma et al. Pest Manag. Sci. 61:449, 2005. J.M. (4) G. C. M. van Leeuwen and H. A. van Kesteren. Can. J. Bot. 76:2042, 1998.

Early life origins of chronic obstructive pulmonary disease.

BACKGROUND: Early life development may influence subsequent respiratory morbidity. The impact of factors determined in childhood on adult lung function, decline in lung function and chronic obstructive pulmonary disease (COPD) was investigated. METHODS: European Community Respiratory Health Survey participants aged 20-45 years randomly selected from general populations in 29 centres underwent spirometry in 1991-3 (n = 13 359) and 9 years later (n = 7738). Associations of early life factors with adult forced expiratory volume in 1 s (FEV(1)), FEV(1) decline and COPD (FEV(1)/FVC ratio <70% and FEV(1) <80% predicted) were analysed with generalised estimating equation models and random effects linear models. RESULTS: Maternal asthma, paternal asthma, childhood asthma, maternal smoking and childhood respiratory infections were significantly associated with lower FEV(1) and defined as "childhood disadvantage factors"; 40% had one or more childhood disadvantage factors which were associated with lower FEV(1) (men: adjusted difference 95 ml (95% CI 67 to 124); women: adjusted difference 60 ml (95% CI 40 to 80)). FEV(1) decreased with increasing number of childhood disadvantage factors (> or =3 factors, men: 274 ml (95% CI 154 to 395), women: 208 ml (95% CI 124 to 292)). Childhood disadvantage was associated with a larger FEV(1) decline (1 factor: 2.0 ml (95% CI 0.4 to 3.6) per year; 2 factors: 3.8 ml (95% CI 1.0 to 6.6); > or =3 factors: 2.2 ml (95% CI -4.8 to 9.2)). COPD increased with increasing childhood disadvantage (1 factor, men: OR 1.7 (95% CI 1.1 to 2.6), women: OR 1.6 (95% CI 1.01 to 2.6); > or =3 factors, men: OR 6.3 (95% CI 2.4 to 17), women: OR 7.2 (95% CI 2.8 to 19)). These findings were consistent between centres and when subjects with asthma were excluded. CONCLUSIONS: People with early life disadvantage have permanently lower lung function, no catch-up with age but a slightly larger decline in lung function and a substantially increased COPD risk. The impact of childhood disadvantage was as large as that of heavy smoking. Increased focus on the early life environment may contribute to the prevention of COPD.

Healthy hire effect, job selection and inhalation exposure among young adults with asthma.

The aim of the present study was to assess whether asthma onset prior to entering the workforce influences whether a person holds a subsequent job with asthma-related inhalation exposures. The data of 19,784 adults from the European Community Respiratory Health Survey were analysed. For each respondent, a current or previously held job was linked to a job exposure matrix assigning high, low or no exposure to dust, gases or fumes. Jobs were also categorised according to the risk of exposures related to occupational asthma. Associations between asthma and subsequent occupational exposures were assessed using logistic regression models, with a random intercept for study centre and fixed adjustment for age, sex, type of study sample and smoking status. Of the respondents, 8% (n = 1,619) reported asthma with onset before completion of full-time education. This population was at decreased risk of having a job with high (odds ratio 0.79; 95% confidence interval 0.68-0.92) or low (0.91; 0.80-1.03) exposure to dust, gases or fumes. The associations were consistent across exposure types (dusts, gases or fumes) and for jobs with a high risk of occupational asthma. Adults with asthma onset prior to entering the workforce may be less likely to hold jobs involving inhalation exposures.

The occupational contribution to severe exacerbation of asthma.

The goal of this study was to identify occupational risk factors for severe exacerbation of asthma and estimate the extent to which occupation contributes to these events. The 966 participants were working adults with current asthma who participated in the follow-up phase of the European Community Respiratory Health Survey. Severe exacerbation of asthma was defined as self-reported unplanned care for asthma in the past 12 months. Occupations held in the same period were combined with a general population job-exposure matrix to assess occupational exposures. 74 participants reported having had at least one severe exacerbation event, for a 1-yr cumulative incidence of 7.7%. From regression models that controlled for confounders, the relative risk (RR) was statistically significant for low (RR 1.7, 95% CI 1.1-2.6) and high (RR 3.6, 95% CI 2.2-5.8) biological dust exposure, high mineral dust exposure (RR 1.8, 95% CI 1.02-3.2), and high gas and fumes exposure (RR 2.5, 95% CI 1.2-5.5). The summary category of high dust, gas, or fumes exposure had RR 3.1 (95% CI 1.9-5.1). Based on this RR, the population attributable risk was 14.7% among workers with current asthma. These results suggest occupation contributes to approximately one in seven cases of severe exacerbation of asthma in a working population, and various agents play a role.

The Gene-Environment Interactions in Respiratory Diseases (GEIRD) Project.

The role of genetic and environmental factors, as well as their interaction, in the natural history of asthma, allergic rhinitis and chronic obstructive pulmonary disease (COPD) is largely unknown. This is mainly due to the lack of large-scale analytical epidemiological/genetic studies aimed at investigating these 3 respiratory conditions simultaneously. The GEIRD project is a collaborative initiative designed to collect information on biomarkers of inflammation and oxidative stress, individual and ecological exposures, diet, early-life factors, smoking habits, genetic traits and medication use in large and accurately defined series of asthma, allergic rhinitis and COPD phenotypes. It is a population-based multicase-control design, where cases and controls are identified through a 2-stage screening process (postal questionnaire and clinical examination) in pre-existing cohorts or new samples of subjects. It is aimed at elucidating the role that modifiable and genetic factors play in the occurrence, persistence, severity and control of inflammatory airway diseases, by way of the establishment of a historical multicentre standardized databank of phenotypes, contributed by and openly available to international epidemiologists. Researchers conducting population-based surveys with standardized methods may contribute to the public-domain case-control database, and use the resulting increased power to answer their own scientific questions.

Homocysteine, vitamin B12 and folic acid levels in psoriatic patients and correlation with disease severity.

Hyperhomocysteinaemia represents an independent risk factor for atherosclerotic cardiovascular disease, stroke, peripheral arterial occlusive disease and venous thrombosis. Psoriasis is a chronic inflammatory skin disease associated with increased atherothrombosis and cardiovascular risk profile. The aim of this study is to investigate homocysteine, folic acid and vitamin B12 levels in a cohort of psoriatic patients and its relationship with the severity of the disease. A retrospective observational study in 98 patients with chronic plaque psoriasis and 98 healthy controls was performed. Total plasma homocysteine level, folic acid, vitamin B12 and PASI index were assessed in every patient. Patients with psoriasis had plasma homocysteine levels higher than controls (57% of cases and 25% of controls; p<0.0001). Folic acid and vitamin B12 plasma levels were lower in psoriatic patients than in controls (p = NS), lower levels of vitamin B12 were found in patients with hyperhomocysteinaemia compared to patients with a normal value of homocysteine (p = 0.0009). The severity of psoriasis assessed according to PASI (19.51+/-16.26) did not directly correlate either with higher levels of homocysteine or with vitamin B12 and folic acid plasma levels. In conclusion, a significantly higher prevalence of hyperhomocysteinaemia was found in psoriatic patients compared to healthy controls. A significant correlation between hyperhomocysteinaemia and lower vitamin B12 levels, but not folic acid, was evidenced. On the contrary, our data do not correlate the high level of homocysteine with higher PASI scores or psoriasis type, suggesting that homocysteine level can be considered an independent risk factor in psoriatic patients.

Boar sperm encapsulation reduces in vitro polyspermy.

A boar sperm encapsulation technology in barium alginate has been developed to enhance reproductive performances and spermatozoa preservation time; aim of this work was to evaluate the effect of in vitro sperm encapsulation on polyspermy as a function of storage time at 18 degrees C. A total number of 40 in vitro fertilization (IVF) tests were performed using encapsulated or diluted spermatozoa (20 IVF each treatment). Overall, 1288 in vitro matured oocytes were fertilized with spermatozoa stored at 24, 48 or 72 h at 18 degrees C for both treatments polyspermy and normospermy, and the non-penetration rates were assessed by optical microscopy. Results indicate a significant reduction in risk of polyspermic oocytes when spermatozoa are preserved in barium alginate membranes (incidence risk ratio: 0.766 with respect to diluted); such enhancement could be explained by lesser damage of sperm membranes achieved by encapsulation technology.

Confirmation of European Brown Rot Caused by Monilinia laxa on Tart Cherry, Prunus cerasus, in Western New York.

Monilinia fructicola (G. Wint.) Honey and M. laxa (Aderh. & Ruhl.) Honey are two pathogens causing brown rot in the United States. While the presence of M. fructicola has been confirmed in all major stone-fruit-production regions in the United States, M. laxa has yet to be detected in much of the eastern production regions. In July 2008, a planting of tart cherries cv. Surefire in Appleton, NY developed severe shoot blight. Blighted shoots (>15% of first-year shoots) were wilted and light brown with the blight encompassing the distal end and often extending into second-year tissue with a distinct sunken margin. Leaves on symptomatic shoots had flushed, but were blighted. Blossom spurs were either blighted at bloom or bore fruit, which were subsequently blighted. Gummosis was commonly observed from cankers at the base of spurs. Both mature and immature mummified fruit in addition to spurs and shoot tissue were sporulating in a manner characteristic of Monilinia (2). Eleven branches displaying symptoms were removed for isolation. Sections of symptomatic shoots (5 cm long) were surface sterilized in 0.6% NaOCl for 1 min and rinsed in sterile dH2O. Cross sections of shoot tissue (3 mm thick), in addition to spores from fruit and spurs, were placed on potato dextrose agar amended with 50 µg/ml of streptomycin sulfate. Following incubation at 24°C for 5 days, 24 colonies exhibiting morphology consistent with that of M. fructicola (uniform colony margin) were obtained, along with nine colonies exhibiting lobed colony margins, commonly associated with M. laxa (3). All colonies resembling M. fructicola were isolated from fruit, whereas those resembling M. laxa were isolated from spurs and shoots. Conidia from both colony morphotypes were lemon-shaped, but those from putative M. laxa isolates were smaller on average (10.75 × 12.0 µm) compared with those from putative M. fructicola isolates (15.75 × 18.25 µm). Confirmation of M. laxa was also accomplished by inoculation of mature green pear (2). Pears inoculated with 104 putative M. laxa conidia per ml produced a region of white-buff colored mycelium but no spores within the inoculated area, while M. fructicola-inoculated pears sporulated abundantly. Identity was further confirmed by PCR amplification of the ß-tubulin gene using M. laxa specific primers as previously described (1). Pathogenicity was proven by inoculating flowering shoots of tart cherry trees (cv. Montmorency) in spring 2009. Twenty shoots were spray inoculated with either 104 M. laxa conidia per ml or sterile dH2O and covered with plastic bags for 24 h. Shoots were monitored for symptom development on a weekly basis. Shoots inoculated with M. laxa developed characteristic shoot blight symptoms, while those inoculated with water remained healthy. M. laxa was reisolated from symptomatic shoots and spurs, but not water-inoculated tissues. The presence of M. laxa is reported for the Great Lakes region, which includes New York, but to our knowledge, this report is the first confirmed instance of economically devastating brown rot caused by M. laxa in New York. In the coming seasons, tart cherry growers must consider revising chemical management programs to protect against European brown rot infection during bloom. References: (1) Z. Ma et al. Pest Manag. Sci. 61:449, 2005. (2) J. M. Ogawa et al. Compendium of Stone Fruit Diseases. The American Phytopathological Society. St. Paul, MN, 1995. (3) G. C. M. van Leeuwen and H. A. van Kesteren. Can. J. Bot. 76:2042, 1998.

Crtap and p3h1 knock out zebrafish support defective collagen chaperoning as the cause of their osteogenesis imperfecta phenotype.

Prolyl 3-hydroxylation is a rare collagen type I post translational modification in fibrillar collagens. The primary 3Hyp substrate sites in type I collagen are targeted by an endoplasmic reticulum (ER) complex composed by cartilage associated protein (CRTAP), prolyl 3-hydroxylase 1 (P3H1) and prolyl cis/trans isomerase B, whose mutations cause recessive forms of osteogenesis imperfecta with impaired levels of α1(I)3Hyp986. The absence of collagen type I 3Hyp in wild type zebrafish provides the unique opportunity to clarify the role of the complex in vertebrate. Zebrafish knock outs for crtap and p3h1 were generated by CRISPR/Cas9. Mutant fish have the typical OI patients' reduced size, body disproportion and altered mineralization. Vertebral body fusions, deformities and fractures are accompanied to reduced size, thickness and bone volume. Intracellularly, collagen type I is overmodified, and partially retained causing enlarged ER cisternae. In the extracellular matrix the abnormal collagen type I assembles in disorganized fibers characterized by altered diameter. The data support the defective chaperone role of the 3-hydroxylation complex as the primary cause of the skeletal phenotype.

A survey on Prader-Willi syndrome in the Italian population: prevalence of historical and clinical signs.

Clinical criteria for the diagnosis of Prader-Willi Syndrome (PWS) were established by consensus in 1993 (Holm et al.). Specific molecular testing is now available and the purpose of diagnostic criteria has shifted to identify individuals to test, thus avoiding the expense of unnecessary analysis. The aim of this study was to find clinical indicators to select patients with suspected PWS for laboratory testing. We analyzed the prevalence of clinical signs and symptoms in 147 genetically diagnosed Italian patients with PWS (67 males and 80 females), aged from 9 months to 34.6 years (13.6 +/- 8.3 years), using the consensus diagnostic criteria, and according to age, sex and type of genetic abnormality. The prevalence of several clinical features changed significantly with age, but very few with sex. According to genetic subtypes (deletion vs UPD), only hypopigmentation and acromicria were more frequent in patients with deletion. Some criteria considered as minor or supportive by Holm et al. have higher prevalence than some major criteria. In conclusion, in order to identify patients with suspected PWS to submit to laboratory testing, we recommend a classification of clinical criteria according to age, giving more attention to those so-called minor or supportive criteria.

Statistical approach in alginate membrane formulation for cell encapsulation in a GMP-based cell factory.

A cell encapsulation technology in alginate has been developed with the aim of obtaining cell controlled release or three-dimensional cultures. The aim of this work is to verify the predictability of alginate capsules for large-scale production by Good Manufacturing Practice (GMP) standardized procedures in a cell factory. A cell-free capsule model was performed following the GMP guidelines: an opaque agent suspension in a bivalent cation solution (Ca(2+), Ba(2+), Sr(2+)) was dropped in a sodium alginate solution, obtaining capsules presenting a liquid core surrounded by a gel alginate membrane. The concentration of the ion, and the treatment with protamine, can considerably vary the characteristics of the capsules (weight, whole diameter, core diameter, gel capsule thickness, capsule strength). It is therefore possible to optimize the performance of the capsules, relating the molecular structure and size of the polymeric membrane to the desired functional properties. Technological resources are available for large-scale cell encapsulation intended for advanced therapies (gene therapy, somatic cell therapy and tissue engineering) in a cell factory, following GMP guidelines.