MODIFIED GENETIC ALGORITHM APPLIED TO SOLVE PRODUCT FAMILY OPTIMIZATION PROBLEM

The product family design problem solved by evolutionary algorithms is discussed. A successful product family design method should achieve an optimal tradeoff among a set of competing objectives, which involves maximizing commonality across the family of products and optimizing the performances of each product in the family. A 2-level chromosome structured genetic algorithm （2LCGA） is proposed to solve this class of problems and its performance is analyzed in comparing its results with those obtained with other methods. By interpreting the chromosome as a 2-level linear structure, the variable commonality genetic algorithm （GA） is constructed to vary the amount of platform commonality and automatically searches across varying levels of commonality for the platform while trying to resolve the tradeoff between commonality and individual product performance within the product family during optimization process. By incorporating a commonality assessing index to the problem formulation, the 2LCGA optimize the product platform and its corresponding family of products in a single stage, which can yield improvements in the overall performance of the product family compared with two-stage approaches （the first stage involves determining the best settings for the platform variables and values of unique variables are found for each product in the second stage）. The scope of the algorithm is also expanded by introducing a classification mechanism to allow mul- tiple platforms to be considered during product family optimization, offering opportunities for superior overall design by more efficacious tradeoffs between commonality and performance. The effectiveness of 2LCGA is demonstrated through the design of a family of universal electric motors and comparison against previous results.

Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant rickets

Hereditary vitamin D-resistant rickets （HVDRR） is a rare autosomal recessive disorder characterized by severe rickets, hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and elevated alkaline phosphatase. This disorder is caused by homogeneous or heterogeneous mutations affecting the function of the vitamin D receptor （VDR）, which lead to complete or partial target organ resistance to the action of 1,25- dihydroxy vitamin D~ A non-consanguineous family of Chinese Han origin with one affected individual demonstrating HVDRR was recruited, with the proband evaluated clinically, biochemically and radiographically. To identify the presence of mutations in the VDR gene, all the exons and exon-intron junctions of the VDR gene from all family members were amplified using PCR and sequenced. The proband showed rickets, progressive alopecia, hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and elevated alkaline phosphatase. She also suffered from epilepsy, which is rarely seen in patients with HVDRR. Direct sequencing analysis revealed a homozygous missense mutation c.122G 〉 A （p.C41Y） in the VDR gene of the proband, which is located in the first zinc finger of the DNA-binding domain. Both parents had a normal phenotype and were found to be heterozygous for this mutation. We report a Chinese Han family with one individual affected with HVDRR. A homozygous missense mutation c.122G 〉 A （p.C41Y） in the VDR gene was found to be responsible for the patient＇s syndrome. In contrast to the results of treatment of HVDRR in other patients, our patient responded well to a supplement of oral calcium and a low dose of calcitriol.

The interaction of genetics and environmental toxicants in amyotrophic lateral sclerosis:results from animal models

Amyotrophic lateral sclerosis（ALS） is a devastating neurodegenerative disease that results in the progressive death of motor neurons, leading to paralysis and eventual death. There is presently no cure for ALS, and only two drugs are available, neither of which provide significant extension of life. The wide variation in onset and progression of the disease, both in sporadic and even in strongly penetrant monogenic familial forms of ALS, indicate that in addition to background genetic variation impacting the disease process, environmental exposures are likely contributors. Epidemiological evidence worldwide implicates exposures to bacterial toxins, heavy metals, pesticides, and trauma as probable environmental factors. Here, we review current advances in gene-environment interactions in ALS animal models. We report our recent discoveries in a zebrafish model of ALS in relation to exposure to the cyanobacterial toxin BMAA, and discuss several results from mouse models that show interactions with exposure to mercury and statin drugs, both leading to acceleration of the disease process. The increasing research into this combinatorial gene-environment process is just starting, but shows early promise to uncover the underlying biochemical pathways that instigate the initial motor neuron defects and lead to their rapidly progressive dysfunction.

Nitric Oxide:from a mysterious labile factor to the molecule of the Nobel Prize Recent progress in nitric oxide research

NO is now known to be an important messenger molecule in biology.It regulates a variety of functions within cells and tissues including vasodilation, neurotransmission and immunological process. This review will focus on the nitric oxide synthase gene family and recent progress on molecular genetic analysis of NOS1, NOS2 and N0S3 genes.

Effect of genetic sources on anatomical, morphological,and mechanical properties of 14-year-old genetically improved loblolly pine families from two sites in the southern United States

Tree improvement programs on loblolly pine(Pinus taeda) in the southeastern USA has focused primarily on improving growth, form, and disease tolerance.However, due to the recent reduction of design values for visually graded southern yellow pine lumber(including loblolly pine), attention has been drawn to the material quality of genetically improved loblolly pine. In this study,we used the time-of-flight(TOF) acoustic tool to assess the effect of genetic families on diameter, slenderness, fiber length, microfibril angle(MFA), velocity and dynamic stiffness estimated using green density(DMOEG) and basic density(DMOEB) of 14-year-old loblolly pine stands selected from two sites. All the 184 and 204 trees of the selected eight half-sib genetic families on sites 1 and 2 respectively were tested using TOF acoustic tool, and two 5 mm core samples taken at breast height level(1.3 m)used to for the anatomical and physical properties analysis.The results indicated a significant positive linear relationship between dynamic MOEs(DMOEGand DMOEB)versus tree diameter, slenderness, and fiber length while dynamic MOEs negatively but nonsignificant correlated with MFA. While there was no significant difference in DMOEBbetween sites; velocity 2 for site 1 was significantly higher than site 2 but DMOEGwas higher for site 2 than site 1. Again, the mean DMOEGand DMOEBreported in the present study presents a snapshot of the expected static MOE for green and 12% moisture conditions respectively for loblolly pine. Furthermore, there were significant differences between families for most of the traits measured and this suggests that forest managers have the opportunity to select families that exhibit the desired fiber morphology for final product performance. Lastly,since the dynamic MOE based on green density(DMOEG),basic density(DMOEB) and velocity 2 present difference conclusions, practitioners of this type of acoustic technique should take care when extrapolating results across the sites.