In the present article, equilibrium and stability equations of rectangular functionally graded plates (FGPs) are determined using the variational approach. Derivation of equations are based on the classical plate theory. It is assumed that the material properties vary with the power product form of thickness coordinate variable z. Equilibrium and stability equations for FGPs are the same as the equations for homogeneous plates. The equilibrium and stability equations are employed to study the buckling behaviour of functionally graded plates with all edges simply supported and subjected to in-plane loading conditions. By equating power law index to zero, predicted relation is reduced to the buckling equation of homogeneous plates which is available in the literature.

Equilibrium and stability equations of a rectangular plate made of functionally graded material under thermal loads are derived, based on the classical plate theory. When it is assumed that the material properties vary as a power form of thickness coordinate variable z and when the variational method is used, the system of fundamental differential equations is established. The derived equilibrium and stability equations for functionally graded plates are identical with the equations for homogeneous plates. Buckling analysis of functionally graded plates under four types of thermal loads is carried out resulting in closed-form solutions. The buckling loads are reduced to the critical buckling temperature relations for functionally graded plates with linear composition of constituent materials and homogeneous plates. The results are validated with the reduction of the buckling relations for functionally graded plates to those of isotropic homogeneous plates given in the literature.

Biotinidase deficiency is an autosomal recessive defect in the recycling of biotin that can lead to a variety of neurologic and cutaneous symptoms. The disease can be prevented or effectively treated with exogenous biotin. The biotinidase locus (BTD) has been maped to 3p25 by in situ hybridization. The gene has been cloned, the coding region sequenced, the genomic organization determined, and a spectrum of mutations has been characterized in more than 90 individuals with profound or partial biotinidase deficiency. We have conducted haplotype analysis of 10 consanguineous and 39 nonconsanguineous probands from the United States and 8 consanguineous probands from Turkey to localize BTD with respect to polymorphic markers on 3p and to investigate the origins of five common mutations. The inbred probands were homozygous for overlapping regions of 3p ranging in size from 1.1 to 80 cM which were flanked most narrowly by D3S1259 and D3S1293. Radiation hybrids and haplotype analysis of markers within this region suggest that BTD is located within a 0.1-cM region flanked by D3S3510 and D3S1286. The radiation hybrid data suggest that the BTD gene is oriented 5′ to 3′ between the centromere and the 3p telomere. Association studies indicate that the gene is closer to a third locus D3S3613 than D3S3510, two markers which cannot be resolved by existing linkage data. The BTD locus and D3S3613 must therefore lie between D3S3510 and D3S1286. Comparison of haplotypes reveals evidence for possible founder effects for four of the five common mutations.

The three-dimensional theory of elasticity in curvilinear coordinates is employed to investigate the dynamic buckling of an imperfect orthotropic circular cylindrical shell under mechanical and thermal loads. Accurate form of the strain expressions of imperfect cylindrical shells is established through employing the general Green's strain tensor for large deformations and the equations of motion are derived in terms of the second Piola-Kirchhoff stress tensor. Then, the governing equations are properly formulated and solved by means of an efficient and relatively accurate solution procedure proposed to solve the highly nonlinear equations resulting from the above analysis. The proposed formulation is very general as it can include the influence of the initial imperfections, temperature distribution, and temperature dependency of the mechanical properties of materials, effect of various end conditions, possibility of large-deformation occurrence and application of any combination of mechanical and thermal loadings. No simplifications are done when solving the resulting equations. Furthermore, in contrast to the displacement-based layer-wise theories and the three-dimensional approaches proposed so far, the stress, force and moment boundary conditions as well as the displacement type ones, can be incorporated accurately in these formulations. Finally, a few examples of mechanical and thermal buckling of some orthotropic cylindrical shells are considered and results of the present three-dimensional elasticity approach are compared with the buckling loads predicated by the Donnell's equations, some single-layer theories, some available results of the layer-wise theory and the recently published three-dimensional approaches and the accuracy of the later methods are discussed based on the exact method presented in this paper.

Biotinidase deficiency is characterized by neurological and cutaneous abnormalities that can be prevented or ameliorated by oral biotin therapy. A child with biotinidase deficiency went undiagnosed for a long period and has irreversible neurological deficits despite biotin treatment. This child is homozygous for the most common mutation (G98:d7i3) found in symptomatic children with the disorder. The parents insisted on having prenatal diagnosis in a subsequent pregnancy to alleviate their anxiety about having another affected child. Mutation analysis of DNA obtained directly from amniotic fluid and from cultured amniocytes revealed that the fetus was heterozygous for the mutation. Maternal cell contamination of the amniocytes was excluded by genotype analysis. Biotinidase activity in extracts of cultured amniocytes revealed 40 per cent of mean normal activity. At birth, the infant was confirmed to be heterozygous by serum enzyme analysis. This is the first report of the use of molecular analysis for the prenatal diagnosis for biotinidase deficiency.

We report localization of the gene for autosomal dominant hereditary pancreatitis (HP) to a small region of the long arm of chromosome 7 in a large four-generation kindred. Affected family members may first become symptomatic in childhood or even infancy with progression to pancreatic calcification, pseudocyst formation, endocrine and exocrine insufficiency, and even pancreatic cancer in some cases. However, obligate gene carriers may remain virtually symptom free throughout life. HP is the most common cause of childhood pancreatitis in the United States. Gene mapping with microsatellite markers demonstrates that HP is tightly linked to the marker D7S684 (Zmax = 7.0, theta = 0.0). Three obligate recombinants place the HP locus within a 16-cM interval between markers D7S495 and D7S688. This confirms the localization of HP to 7q reported in a separate French kindred (2).