Seminar khoa học của hai thực tập sinh Victoria Lan Friedl và Elise Y-Lan Tran

Vào 14h00, ngày 26/12/2024 Viện IAST tổ chức buổi trao đổi học thuật, báo cáo thực tập của 02 Thực tập sinh nước ngoài Phòng họp A101 với nội dung chi tiết như sau: 

Thực tập sinh Victoria Lan Friedl báo cáo về "Data driven dislocation-mediated plasticity and application to nickel"

Tóm tắt: 

Plastic deformation in materials arises from the intricate motion and interaction of dislocations. This study leverages Thermodynamic Dislocation Theory (TDT) to connect dislocation behavior with stress and configurational temperature, providing a thermodynamically consistent framework for investigating plastic flow. By employing MATLAB's optimization tools, we determined key material parameters for nickel by fitting TDT predictions to experimental stress-strain data. The resulting simulations accurately captured the stress-strain response of nickel across a range of strain rates and temperatures. Discrepanciesbetween simulated and experimental results highlight areas for potential model refinement and underscore the influence of uncertainties within the TDT framework.

Thực tập sinh Elise Y-Lan Tran báo cáo về  "A Comparative Analysis of Prevalent GJB2 Mutations Found in the Vietnamese Deaf Population"

Tóm tắt: 

Deafness and congenital hearing loss is one of the most prevalent genetic disorders in Vietnam, with over 1.2 million individuals affected. Although various sources of deafness exist, mutations in the gap junction beta-2 (GJB2) gene have arisen as a leading cause of deafness in Vietnam. In a comprehensive study of recessive diseases in the Vietnamese population, deafness was the most frequent disorder, with one in six participants having a single copy of a mutated GJB2 gene (1). With GBJ2 mutations accounting for the plurality of congenital hearing loss, gaining a more thorough understanding of the biophysical behavior of the protein associated with GJB2 is beneficial. Located on chromosome 13, GJB2 encodes for Connexin-26 (Cx26), a gap junction transmembrane protein responsible for communication between cells in the cochlea by regulating potassium ion flux. Mutations in GJB2 can disrupt this ion transport, leading to varying degrees of hearing impairment. Nonetheless, the structure and degree of potassium ion flow of these proteins can still differ depending on the specific mutation site and type. Past clinical studies have also found an association between different mutation types and the severity of hearing loss (2, 3). Despite this, most basic biomedical research regarding Cx26 focuses on the composition of a specific mutated protein compared to the wild-type, non-mutated protein rather than examining the variations across different mutation types (4-6). Thus, this project aims to elucidate the relationship between the mutations and the structural characteristics of the three most common Cx26 variants found in the Vietnamese population as identified by genetic screenings. The Cx26 protein model was constructed by Open-Source PyMOL 2.5.0 and AlphaFold 2.0 and solvated with ions using Visual Molecular Dynamics. In addition, the Cx26 protein comprises two hemichannels, each embedded in a cell membrane. Thus, double cell membranes were generated using the CHARMM-GUI Bilayer Membrane Builder and Multicomponent Assembler. The primary function of the Cx26 protein, potassium ion transport, will be simulated by employing steered molecular dynamics with GROMACS 2019. From these trajectories, the ion permeability will be quantified by computing the potential of mean force PMF and the average number of water molecules inside the pore during the simulation. Point mutations located in the transmembrane region of the protein are predicted to decrease the permeability of potassium ion transport.