Porosity Reduction in the High-Speed Processing of Glass-Fiber Composites by Resin Transfer Molding (RTM)

High-speed processing is essential to achieve lower production cost in the fabrication of fiber-reinforced composites with the current liquid molding practices. A major consequence of increasing the resin injection velocity is the formation of defects such as voids and dry regions that decrease the load-bearing capability of the composite. Void formation mechanisms and analytical predictions of the detrimental effect of porosity on the structural integrity of molded parts have been studied extensively. In contrast, knowledge of void removal strategies is very limited. In this investigation, various postfill pressure levels were applied to disk-shaped random-mat glass/epoxy parts molded at high volumetric flow rates as a method to reduce their voidage content. Quantitative image analysis over cross-sections cut from these composites revealed that significant changes in porosity concentration take place with the postfill pressure. For instance, overall void content dropped more than 70% with the application of a postfill pressure as low as 300 kPa. Other important void morphometry characteristics such as void shape, size, and spatial distribution could also be manipulated by this method. As the packing pressure increases, large voids gradually disappear, and at the same time, the small circular voids are mobilized towards radial locations near the vents. In addition to this spatial voidage gradient in the radial direction, voidage gradient also exists through the specimen thickness. It seems that higher front velocities promote the appearance of secondary flow phenomena inside the mold cavity (e.g. microfountain flow), which may explain why more voids tend to concentrate at the surface of the specimen irrespective of the postfill pressure level reached inside the mold.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

MYC-containing double minutes in hematologic malignancies: evidence in favor of the episome model and exclusion of MYC as the target gene

Double minutes (dmin)-circular, extra-chromosomal amplifications of specific acentric DNA fragments-are relatively frequent in malignant disorders, particularly in solid tumors. In acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), dmin are observed in approximately 1% of the cases. Most of them consist of an amplified segment from chromosome band 8q24, always including the MYC gene. Besides this information, little is known about their internal structure. We have characterized in detail the genomic organization of 32 AML and two MDS cases with MYC-containing dmin. The minimally amplified region was shown to be 4.26 Mb in size, harboring five known genes, with the proximal and the distal amplicon breakpoints clustering in two regions of approximately 500 and 600 kb, respectively. Interestingly, in 23 (68%) of the studied cases, the amplified region was deleted in one of the chromosome 8 homologs at 8q24, suggesting excision of a DNA segment from the original chromosomal location according to the 'episome model'. In one case, sequencing of both the dmin and del(8q) junctions was achieved and provided definitive evidence in favor of the episome model for the formation of dmin. Expression status of the TRIB1 and MYC genes, encompassed by the minimally amplified region, was assessed by northern blot analysis. The TRIB1 gene was found over-expressed in only a subset of the AML/MDS cases, whereas MYC, contrary to expectations, was always silent. The present study, therefore, strongly suggests that MYC is not the target gene of the 8q24 amplifications

Clinical features of idiopathic inflammatory polymyopathy in the Hungarian Vizsla

Background A retrospective study of the clinicopathological features of presumed and confirmed cases of idiopathic inflammatory polymyopathy in the Hungarian Vizsla dog and guidelines for breeding. Results 369 medical records were reviewed (1992–2013) and 77 Hungarian Vizslas were identified with a case history consistent with idiopathic inflammatory polymyopathy. Inclusion criteria were: group 1 (confirmed diagnosis); histopathology and clinical findings compatible with an inflammatory polymyopathy and group 2 (probable diagnosis); clinical findings compatible with a polymyopathy including dysphagia, sialorrhea, temporal muscle atrophy, elevated serum creatine kinase (CK) activity, and sufficient clinical history to suggest that other neuromuscular disorders could be ruled out. Some group 2 dogs had muscle biopsy, which suggested muscle disease but did not reveal an inflammatory process. The mean age of onset was 2.4 years; male dogs were slightly overrepresented. Common presenting signs were dysphagia, sialorrhea, masticatory muscle atrophy, and regurgitation. Common muscle histopathological findings included degenerative and regenerative changes, with multifocal mononuclear cell infiltration with lymphoplasmacytic myositis of variable severity. A positive response to immunosuppressive treatment supported an immune-mediated aetiology. The mean age at death and survival time were 6.4 and 3.9 years, respectively. Recurrence of clinical signs and aspiration pneumonia were common reasons for euthanasia. Conclusions Diagnosis of Vizsla idiopathic inflammatory polymyopathy can be challenging due to lack of specific tests, however the presence of dysphagia, regurgitation and masticatory muscle atrophy in this breed with negative serological tests for masticatory muscle myositis and myasthenia gravis, along with muscle biopsies suggesting an inflammatory process, support the diagnosis. However, there is an urgent need for a more specific diagnostic test. The average of inbreeding coefficient (CoI) of 16.3% suggests an increased expression of a Dog Leukocyte Antigen Class II haplotype, leading to an increased disease risk. The prognosis remains guarded, as treatment can only manage the disease. Recurrence of clinical signs and perceived poor quality of life are the most common reasons for humane euthanasia.</p