自記式「健康チェック票THI」による健康に及ぼす喫煙の影響評価－地方都市と大都市の学生間の比較－

キャンパスが群馬県内（Ｉキャンパス）、東京都内（Ｔキャンパス）および愛知県内（Ｎキャンパス）にあるＡ私立大学の学生347人（男子121人、女子226人）を対象に、喫煙が健康に及ぼす影響について、自記式「健康チェック票THI」によって評価した。対象学生の喫煙率は全国平均と比較して、Ｉキャンパスの男子学生がやや高かったことを除くと、ほぼ同程度であった。健康状態は1.2万人の標準グループから得られた尺度得点の分布をもとに、パーセンタイル値で評価した。喫煙者の健康状態は非喫煙者と比較して、身体面およびメンタル面の両方において劣る傾向がみられ、特に、女子学生の方が男子学生より顕著であった。さらに、Ｉキャンパスの学生より、ＴキャンパスやＮキャンパスの学生の方が、メンタル面の症状レベルが高い傾向が認められた。これらの結果は、喫煙が身体面の健康状態に悪影響を及ぼすことを確認するとともに、その影響は地方都市より大都会で学ぶ学生に強く出やすい可能性を示している

Site selective reading of epigenetic markers by a dual-mode synthetic receptor array.

Variably functionalized self-folding deep cavitands form an arrayed, fluorescent indicator displacement assay system for the detection of post-translationally modified (PTM) histone peptides. The hosts bind trimethyllysine (KMe3) groups, and use secondary upper rim interactions to provide more sensitive discrimination between targets with identical KMe3 binding handles. The sensor array uses multiple different recognition modes to distinguish between miniscule differences in target, such as identical lysine modifications at different sites of histone peptides. In addition, the sensor is affected by global changes in structure, so it is capable of discriminating between identical PTMs, at identical positions on amino acid fragments that vary only in peptide backbone length, and can be applied to detect non-methylation modifications such as acetylation and phosphorylations located multiple residues away from the targeted binding site. The synergistic application of multiple variables allows dual-mode deep cavitands to approach levels of recognition selectivity usually only seen with antibodies

Molecular Profiling of Lymphatic Endothelial Cell Activation In Vitro

The lymphatic vascular system plays a key role in cancer progression. Indeed, the activation of lymphatic endothelial cells (LECs) through the lymphangiogenic process allows for the formation of new lymphatic vessels (LVs) that represent the major route for the dissemination of solid tumors. This process is governed by a plethora of cancer-derived and microevironmental mediators that strictly activate and control specific molecular pathways in LECs. In this work we used an in vitro model of LEC activation to trigger lymphangiogenesis using a mix of recombinant pro-lymphangiogenic factors (VFS) and a co-culture system with human melanoma cells. Both systems efficiently activated LECs, and under these experimental conditions, RNA sequencing was exploited to unveil the transcriptional profile of activated LECs. Our data demonstrate that both recombinant and tumor cell-mediated activation trigger significant molecular pathways associated with endothelial activation, morphogenesis, and cytokine-mediated signaling. In addition, this system provides information on new genes to be further investigated in the lymphangiogenesis process and open the possibility for further exploitation in other tumor contexts where lymphatic dissemination plays a relevant role

Knowledge sharing in the health scenario

The understanding of certain data often requires the collection of similar data from different places to be analysed and interpreted. Interoperability standards and ontologies, are facilitating data interchange around the world. However, beyond the existing networks and advances for data transfer, data sharing protocols to support multilateral agreements are useful to exploit the knowledge of distributed Data Warehouses. The access to a certain data set in a federated Data Warehouse may be constrained by the requirement to deliver another specific data set. When bilateral agreements between two nodes of a network are not enough to solve the constraints for accessing to a certain data set, multilateral agreements for data exchange are needed. We present the implementation of a Multi-Agent System for multilateral exchange agreements of clinical data, and evaluate how those multilateral agreements increase the percentage of data collected by a single node from the total amount of data available in the network. Different strategies to reduce the number of messages needed to achieve an agreement are also considered. The results show that with this collaborative sharing scenario the percentage of data collected dramaticaly improve from bilateral agreements to multilateral ones, up to reach almost all data available in the network.Peer ReviewedPostprint (published version

Concentrations of mephedrone in cases of fatal and non-fatal clinical intoxications

Peer reviewe

Carotid artery disease: Novel pathophysiological mechanisms identified by gene-expression profiling of peripheral blood

AbstractObjectThe pathogenesis of carotid artery stenosis (CAS) as well as the mechanisms underlying the different localisation of the atherosclerotic lesions remains poorly understood. We used microarray technology to identify novel systemic mediators that could contribute to CAS pathogenesis.Moreover, we compared gene-expression profile of CAS with that of patients affected by abdominal aortic aneurysm (AAA), previously published by our group.Methods and resultsBy global gene-expression profiling in a pool of 10 CAS patients and 10 matched controls, we found 82 genes differentially expressed. Validation study in pools used for profiling and replication study in larger numbers of CAS patients (n = 40) and controls (n = 40) of 14 genes by real-time polymerase chain reaction (RT-PCR) confirmed microarray results. Fourteen out of 82 genes were similarly expressed in AAA patients. Gene ontology analysis identified a statistically significant enrichment in CAS of differentially expressed transcripts involved in immune response and oxygen transport. Whereas alteration of oxygen transport is a common tract of the two localisations, alteration of immune response in CAS and of lipid metabolic process in AAA represents distinctive tracts of the two atherosclerotic diseases.ConclusionsWe describe the systemic gene-expression profile of CAS, which provides an extensive list of potential molecular markers

Red mark syndrome of trout (Oncorhynchus mykiss; Walbaum, 1792): Histopathological scoring and correlation with gross lesions

Red mark syndrome (RMS) is a skin disorder affecting rainbow trout (Oncorhynchus mykiss). The present work aimed to correlate the gross skin lesions affecting 46 fish sampled from farms surveyed for RMS with their microscopic features, identifying histological parameters that may be suggestive of disease progression. Skin lesions were grossly included in one of three categories (types I, II and III) according to the progressive degree of severity. Histological parameters and anti-proliferating cell nuclear antigen (PCNA) tissue immunoreactivity were semi-quantitatively assessed. In the dermis, PCNA-positive lymphocytes, fibroblasts and endothelial cells were indicative of active phlogosis. A significant increase in PCNA-immunoreactive lymphocytes, from gross type I to type III cases, was found only in the hypodermis. The histological parameters significantly associated with the gross lesion severity were progressive loss of the epithelium and scales, recruitment of inflammatory cells in the stratum compactum, loss of architecture of the stratum compactum, perivascular and perineural granulomatous inflammation and increase in lymphocyte infiltration of the muscular layer. In the type II and type III categories, inflammation in the hypodermis and muscle displayed a granulomatous pattern, reinforcing the hypothesis of an immunopathological mechanism. The morphological diagnosis of “deep chronic dermatitis associated to panniculitis and myositis, characterised by lympho-histiocytic and granulomatous reaction” is suggested

Apolipoprotein(a) kringle-IV type 2 copy number variation is associated with venous thromboembolism

In addition to the established association between high lipoprotein(a) [Lp(a)] concentrations and coronary artery disease, an association between Lp(a) and venous thromboembolism (VTE) has also been described. Lp(a) is controlled by genetic variants in LPA gene, coding for apolipoprotein(a), including the kringle-IV type 2 (KIV-2) size polymorphism. Aim of the study was to investigate the role of LPA gene KIV-2 size polymorphism and single nucleotide polymorphisms (SNPs) (rs1853021, rs1800769, rs3798220, rs10455872) in modulating VTE susceptibility. Five hundred and sixteen patients with VTE without hereditary and acquired thrombophilia and 1117 healthy control subjects, comparable for age and sex, were investigated. LPA KIV-2 polymorphism, rs3798220 and rs10455872 SNPs were genotyped by TaqMan technology. Concerning rs1853021 and rs1800769 SNPs, PCR-RFLP assay was used. LPA KIV-2 repeat number was significantly lower in patients than in controls [median (interquartile range) 11(6-17) vs 15(9-25), p<0.0001]. A significantly higher prevalence of KIV-2 repeat number ≤7 was observed in patients than in controls (33.5% vs 15.5%, p<0.0001). KIV-2 repeat number was independently associated with VTE (p = 4.36 x10-9), as evidenced by the general linear model analysis adjusted for transient risk factors. No significant difference in allele frequency for all SNPs investigated was observed. Haplotype analysis showed that LPA haplotypes rather than individual SNPs influenced disease susceptibility. Receiver operating characteristic curves analysis showed that a combined risk prediction model, including KIV-2 size polymorphism and clinical variables, had a higher performance in identifying subjects at VTE risk than a clinical-only model, also separately in men and women