Ultrahangos hegesztés alkalmazástechnikai jellemzői

Az ultrahangos fémhegesztés alkalmazástechnikai előnyei: nem kell semmilyen hozaganyag; csekély elektromos átmeneti ellenállású kontaktusok készíthetők; vékony anyagok hegeszthetők vastag anyagokhoz is; hélium-tömör hegesztési varratot eredményez; a hegesztési paraméterek számítógépes beállítása egyszerűen megoldható; tiszta és biztonságos a munkafolyamat (nincs szikra, láng és füst); gyártósorba integrálható. Jelen cikk ezen hegesztési eljárás néhány további alkalmazástechnikai jellemzőjével foglalkozik

Lack of HIV testing and dissatisfaction with HIV testing and counselling among men having sex with men in Hungary.

Background: Using data from a large internet-based survey of European men having sex with men (MSM), we assessed factors associated with HIV testing and reasons for dissatisfaction with HIV testing and counselling among Hungarian MSM. Methods: A total of 2052 Hungarian MSM provided evaluable data for the European MSM Internet Survey (EMIS) in 2010. χ2 tests and Poisson regression with a robust variance estimator were used to assess factors associated with HIV testing and dissatisfaction with HIV testing and counselling. Results: A total of 42.1% of MSM reported never being testing for HIV. Over one-half of men (54.1%) who reported condomless anal intercourse (CAI) in the prior 12 months with a person of unknown or sero-discordant HIV status reported no lifetime HIV testing. The factor most strongly associated with dissatisfaction with HIV testing and counselling was test site with increased dissatisfaction with inpatient hospital settings vs. community-based organizations. Both lack of HIV testing and dissatisfaction with testing were independently associated with MSM who reported that no one, or only a few people, knew they were attracted to men. Conclusions: Lack of HIV testing was strongly associated with CAI. MSM reported that community-based organizations better supported confidentiality and were more respectful during HIV testing

A pathogenic PSEN1 Trp165Cys mutation associated with early-onset Alzheimers disease

Background Presenilin-1 (PSEN1) is one of the causative genes for early onset Alzheimers disease (EOAD). Recently, emerging studies reported several novel PSEN1 mutations among Asian. We describe a male with EOAD had a pathogenic PSEN1 mutation. Case presentation A 53-year-old male presented with memory decline, followed by difficulty in finding ways. Patient had positive family history, since his mother and one of his brother was also affected with dementia. Brain magnetic resonance imaging (MRI) scan showed mild degree of atrophy of bilateral hippocampus and parietal lobe. 18F-Florbetaben-PET (FBB-PET) revealed increased amyloid deposition in bilateral frontal, parietal, temporal lobe and precuneus. Whole exome analysis revealed a heterozygous, probably pathogenic PSEN1 (c.695G > T, p.W165C) mutation. Interestingly, Trp165Cys mutation is located in trans membrane (TM)-III region, which is conserved between PSEN1/PSEN2. In vitro studies revealed that PSEN1 Trp165Cys could result in disturbances in amyloid metabolism. This prediction was confirmed by structure predictions and previous in vitro studies that the p.Trp165Cys could result in decreased Aβ42/Aβ40 ratios. Conclusion We report a case of EOAD having a pathogenic PSEN1 (Trp165Cys) confirmed with in silico and in vitro predictions.This work was supported by a National Research Foundation of Korea (NRF) Grants, awarded by the Korean government (MEST, No. 2017R1A2B4012636 & 2017R1C1B5017807). Dr. An SS receives the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST, No. 2017R1A2B4012636). Dr. Eva Bagyinszky receives the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST, No. 2017R1C1B5017807). Dr. Giau VV reports no disclosure. Dr. Pyun JM reports no disclosure. Dr. Suh J reports no disclosure. Dr. Kim SY reports no disclosure

Novel PSEN1 G209A mutation in early-onset Alzheimer dementia supported by structural prediction

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Abstract Background Three main genes are described as causative genes for early-onset Alzheimer dementia (EOAD): APP, PSEN1 and PSEN2. We describe a woman with EOAD had a novel PSEN1 mutation. Case report A 54-year-old right-handed woman presented 12-year history of progressive memory decline. She was clinically diagnosed as familial Alzheimer's disease due to a PSEN1 mutation. One of two daughters also has the same mutation, G209A in the TM-IV of PS1 protein. Her mother had unspecified dementia that began at the age of 40s. PolyPhen2 and SIFT prediction suggested that G209A might be a damaging variant with high scores. 3D modeling revealed that G209A exchange could result significant changes in the PS1 protein. Conclusion We report a case of EOAD having probable novel PSEN1 (G209A) mutation verified with structural prediction

Whole brain white matter histogram analysis of diffusion tensor imaging data detects microstructural damage in mild cognitive impairment and Alzheimer’s disease patients

ABSTRACT Background: Amnestic mild cognitive impairment (MCI) is a transitional stage between normal aging and Alzheimer’s disease (AD). However, the clinical conversion from MCI to AD is unpredictable. Hence, identification of non-invasive biomarkers able to detect early changes induced by dementia is a pressing need. Purpose: To explore the added value of histogram analysis applied to measures derived from diffusion tensor imaging (DTI) for detecting brain tissue differences between AD, MCI and healthy subjects (HS). Study type: Retrospective. Population/subjects: Local cohort (57 AD, 28 MCI, 23 HS), Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort (41 AD, 58 MCI, 41 HS). Field Strength: 3T. Dual echo TSE; FLAIR; MDEFT; IR-SPGR; DTI. Assessment: Normal appearing white matter (NAWM) masks were obtained using the T1-weighted volumes for tissue segmentation and T2-weighted images for removal of hyperintensities/lesions. From DTI images, fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AXD) and radial diffusivity (RD) were obtained. NAWM histograms of FA, MD, AXD and RD were derived and characterized estimating: peak height, peak location, mean value (MV), and quartiles (C25, C50, C75), which were compared between groups. Receiver operating characteristic (ROC) and area under ROC curves (AUC) were calculated. To confirm our results, the same analysis was repeated on ADNI dataset. Statistical tests: One-way ANOVA, post-hoc Student’s t-test, multi-class ROC analysis. Results: For the local cohort, C25 of AXD had the maximum capability of group discrimination with AUC of 0.80 for “HS vs patients” comparison and 0.74 for “AD vs others” comparison. For ADNI cohort, MV of AXD revealed the maximum group discrimination capability with AUC of 0.75 for “HS vs patients” comparison and 0.75 for “AD vs others” comparison. Data conclusion: AXD of NAWM might be an early marker of microstructural brain tissue changes occurring during AD course and might be useful for assessing disease progression

Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

Alzheimer’s disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by systems biology approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework