Plakların Sayısal Bir Yöntemle Elasto-plastik Dinamik Analizi

Konferans Bildirisi -- Teorik ve Uygulamalı Mekanik Türk Milli Komitesi, 2008Conference Paper -- Theoretical and Applied Mechanical Turkish National Committee, 2008Bu çalışmada amaç, dört kenarı ankastre dikdörtgen ince plakların elastik ve elasto-plastik dinamik deplasmanlarının, değişik yükler altında Newmark Doğrusal İvme Metodu ile hesaplamaktır. İlk olarak, dikdörtgen plakların genel hareket denklemi Kirchhoff Plak Teorisi uygulanarak elde edildi ve plakın özdeğerleri ve özvektörleri sonlu farklar metodu kullanılarak hesaplandı. Daha sonra, plakın rijitlik matrisi ve kütle matrisi direkt rijitlik metoduyla oluşturuldu. Sonuçta, plakın rijitlik matrisi, kütle matrisi ve yük vektöründen oluşan sistemin hareket denklemi Newmark doğrusal ivme metodu ile çözüldü.The aim of this study is to examine the elastic and elasto-plastic deflections of rectangular thin plates with clambed supported under various dynamic loads by Newmark’s linear acceleration method. Firstly, the general equation of motion of the rectangular plate has been derived by applying Kirchhoff’s Plate Theory and the eigenvalues and eigenvectors of the plate with clambed supported have been obtained using the finite difference method. Then the stiffness matrix and mass matrix of the plate was constructed by the direct stiffness method. Finally, the equation of motion of the system which consists of the stiffness matrix, the mass matrix, and the load vector has been solved using the Newmark’s linear acceleration method

STUB1 polyadenylation signal variant AACAAA does not affect polyadenylation but decreases STUB1 translation causing SCAR16

We present three siblings afflicted with a disease characterized by cerebellar ataxia, cerebellar atrophy, pyramidal tract damage with increased lower limb tendon reflexes, and onset of 31 to 57 years, which is not typical for a known disease. In a region of shared homozygosity in patients, exome sequencing revealed novel homozygous c.*240T>C variant in the 3'UTR of STUB1, the gene responsible for autosomal recessive spinocerebellar ataxia 16 (SCAR16). In other genes, such an alteration of the evolutionarily highly conserved polyadenylation signal from AATAAA to AACAAA is known to highly impair polyadenylation. In contrast, RNA sequencing and quantification revealed that neither polyadenylation nor stability of STUB1 mRNA is affected. In silico analysis predicted that the secondary structure of the mRNA is altered. We propose that this change underlies the extremely low amounts of the encoded protein in patient leukocytes

DYNAMIC ANALYSIS OF RECTANGULAR ELASTOPLASTIC COMPOSITE PLATES

Bu çalışmada dikdörtgen, ince ve tabakalı kompozit plakların, eşdeğer ızgara modeli kullanılarak elasto-plastik dinamik analizi yapılmıştır. Kirchhoff Plak Teorisine dayanarak kompozit plakların hareket denklemi elde edilmiş ve farklı sınır şartları dikkate alınarak sonlu farklar metoduyla çözüm yapılmıştır. Dikdörtgen tabakalı kompozit plakların doğal frekans parametrelerine her iki kenarın oranının (a/b), kenar-kalınlık oranının (a/h), fiber diziliş açısının ve tabaka diziliminin etkileri incelenmiştir. Eşdeğer kirişlerden oluşan bir plak eğilme modeli kullanılarak, plakın rijidlik matrisi ve kütle matrisi doğrudan rijidlik metoduyla elde edilmiştir. Kompozit plaklara farklı dinamik yükler uygulanmıştır. Modların ve frekansların hesaplanmasından sonra, ayrıştırılan sistemin çözümü Newmark Doğrusal İvme Metoduyla yapılmış ve her serbestlik derecesinde dinamik elasto-plastik deplasmanlar zaman adımlarına bağlı olarak hesaplanmıştır. Deplasmanlardan sonra, dinamik gerilme değerleri de zamana bağlı olarak hesaplanmıştır.Equation of motion of composite plates was derived making use of the Kirchhoff Plate Theory, and the solutions were obtained using the finite difference method by the cosideration of various boundary conditions. Certain factors that affect the natural frequency parameters of rectangular laminated composite plates, which are the aspect ratio (a/b), the span-to-depth ratio (a/h), the angle-ply and the lamination sequence were investigated. By making use of the direct stiffness method in the context of the equivalent gridwork model of plates, the stiffness and mass matrices were constructed. Various dynamic loading conditions on composite plates were investigated. After the determination of modes and frequencies of plates the uncoupled system was solved using the Newmark Linear Acceleration Method, hence, the dynamic displacements in each degree of freedom were computed at each time increment. Finally, the dynamic stresses were computed as a function of time

Novel NDE1 homozygous mutation resulting in microhydranencephaly and not microlyssencephaly

Lissencephaly is characterized by deficient cortical lamination. Recently homozygous NDE1 mutations were reported in three kindred afflicted with extreme microcephaly with lissencephaly or microlissencephaly. Another severe developmental defect that involves the brain is microhydranencephaly which manifests with microcephaly, motor and mental retardation and brain malformations that include gross dilation of the ventricles with complete absence of the cerebral hemispheres or severe delay in their development. In the three related patients with microhydranencephaly that we had reported previously, we identified a homozygous deletion that encompasses NDE1 exon 2 containing the initiation codon. The mutation is predicted to result in a null allele. Herein we compare the clinical phenotypes of our research patients to those reported as microlissencephaly. The clinical findings in our patients having the fourth NDE1 mutation reported so far widen the spectrum of brain malformations resulting from mutations in NDE1

Familial microhydranencephaly, a family that does not map to 16p13.13-p12.2: relationship with hereditary fetal brain degeneration and fetal brain disruption sequence

Microhydranencephaly (MHAC) is a serious developmental brain anomaly characterized by microcephaly with severe reduction of brain hemispheres and intracranial space filled with cerebrospinal fluid without signs of intracranial hypertension. Clinical findings are very similar to fetal brain disruption sequence - severe microcephaly, scalp rugae, and profound developmental delay; however, although fetal brain disruption sequence is a sporadic condition caused by an external disruptive event, familial cases of MHAC presumably result from a process of progressive brain damage also termed as 'hereditary fetal brain degeneration'. Familial occurrence of this phenotype is very rare - only three reports on four families have been published so far. Here we present two new patients affected brothers from Slovakia - and provide an update on a previously described case from a Turkish Anatolian family. We also present data excluding linkage to an MHAC locus 16p13.13-p12.2 in the Slovak family. We compare clinical and imaging findings in all five families and suggest genetic heterogenity for this condition. In genetic counseling for this phenotype, especially in the absence of any known teratogenic factors in pregnancy, we suggest that the possibility of recurrence should be considered. Clin Dysmorphol 19: 107-118 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins