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1.
RSC Adv ; 13(50): 35137-35144, 2023 Nov 30.
Article in English | MEDLINE | ID: mdl-38053689

ABSTRACT

Materials with a negative thermal expansion property are of great importance in the emerging family of two-dimensional materials. For example, mixing two materials with negative and positive coefficients of thermal expansion avoids volume changing with temperature. In this work, based on first-principles calculations and Grüneisen's theory, we investigated the thermal expansion properties of a silicon monolayer in biphenylene networks. Our results show that the thermal expansion is greatly negative and anisotropic, as the linear thermal expansion coefficient along the a-direction is significantly smaller than the one along the b-direction, even at high temperatures. At 300 K, the thermal expansion coefficients along the two lattice directions are -17.010 × 10-6 K-1 and -2.907 × 10-6 K-1, respectively. By analyzing the Grüneisen parameters and the elastic compliance, we obtained an understanding of the giant negative thermal expansion of the material. Rigid unit modes are also responsible for the negative thermal expansion behavior. Our work provides fundamental insights into the thermal expansion of silicon monolayer in biphenylene networks and should stimulate the further exploration of the possible thermoelectric and thermal management applications of the material.

2.
Phys Chem Chem Phys ; 24(46): 28295-28305, 2022 Nov 30.
Article in English | MEDLINE | ID: mdl-36382798

ABSTRACT

Janus α-STe2 and α-SeTe2 monolayers are investigated systematically using first-principles calculations combined with semiclassical Boltzmann transport theory. Janus α-STe2 and α-SeTe2 monolayers are indirect semiconductors with band gaps of 1.20 and 0.96 eV, respectively. It is found that they possess ultrahigh figure of merit (ZT) values of 3.9 and 4.4, respectively, at 500 K, much higher than that of the pristine α-Te monolayer (2.8). The higher ZT values originating from Janus structures reduce lattice thermal conductivities remarkably compared with the pristine α-Te monolayer. The much higher phonon anharmonicity in Janus monolayers leads to significantly lower lattice thermal conductivity. It is also found that electronic thermal conductivity can play an important role in thermoelectric efficiency of materials with quite low lattice thermal conductivity. This work suggests the potential applications of Janus α-STe2 and α-SeTe2 monolayers as thermoelectric materials and highlights that using a Janus structure is an effective way to enhance thermoelectric performance.

3.
Nucleic Acids Res ; 34(11): e76, 2006 Jun 21.
Article in English | MEDLINE | ID: mdl-16790564

ABSTRACT

We developed a conceptually new subtraction strategy for the detection and isolation of target DNA and/or RNA from complex nucleic acid mixtures, called Primer Extension Enrichment Reaction (PEER). PEER uses adapters and class IIS restriction enzymes to generate tagged oligonucleotides from dsDNA fragments derived from specimens containing an unknown target ('tester'). Subtraction is achieved by selectively disabling these oligonucleotides by extension reaction using ddNTPs and a double stranded DNA template generated from a pool of normal specimens ('driver'). Primers that do not acquire ddNTP are used to capture and amplify the unique target DNA from the original tester dsDNA. We successfully applied PEER to specimens containing known infectious agents (Hepatitis B Virus and Walrus Calicivirus) and demonstrated that it has higher efficiency than the best comparable technique. The strategy used for PEER is versatile and can be adapted for the identification of known and unknown pathogens and mutations, differential expression studies and other applications that allow the use of subtractive strategies.


Subject(s)
DNA/analysis , Nucleic Acid Hybridization/methods , Polymerase Chain Reaction , RNA/analysis , Caliciviridae/genetics , Caliciviridae/isolation & purification , DNA/isolation & purification , DNA Primers , Hepatitis B virus/genetics , Hepatitis B virus/isolation & purification , Oligonucleotide Probes , RNA/isolation & purification , Templates, Genetic
4.
Nat Genet ; 37(2): 198-204, 2005 Feb.
Article in English | MEDLINE | ID: mdl-15654337

ABSTRACT

Proteins with polyglutamine (polyQ) expansions accumulate in the nucleus and affect gene expression. The mechanism by which mutant huntingtin (htt) accumulates intranuclearly is not known; wild-type htt, a 350-kDa protein of unknown function, is normally found in the cytoplasm. N-terminal fragments of mutant htt, which contain a polyQ expansion (>37 glutamines), have no conserved nuclear localization sequences or nuclear export sequences but can accumulate in the nucleus and cause neurological problems in transgenic mice. Here we report that N-terminal htt shuttles between the cytoplasm and nucleus in a Ran GTPase-independent manner. Small N-terminal htt fragments interact with the nuclear pore protein translocated promoter region (Tpr), which is involved in nuclear export. PolyQ expansion and aggregation decrease this interaction and increase the nuclear accumulation of htt. Reducing the expression of Tpr by RNA interference or deletion of ten amino acids of N-terminal htt, which are essential for the interaction of htt with Tpr, increased the nuclear accumulation of htt. These results suggest that Tpr has a role in the nuclear export of N-terminal htt and that polyQ expansion reduces this nuclear export to cause the nuclear accumulation of htt.


Subject(s)
Huntington Disease/genetics , Peptides/metabolism , Proto-Oncogene Proteins/physiology , Amino Acid Sequence , Cell Nucleus/metabolism , Cells, Cultured , Humans , Molecular Sequence Data , Mutation , Nuclear Pore Complex Proteins/chemistry , Promoter Regions, Genetic , Proto-Oncogene Proteins/genetics , Transfection
5.
J Cell Biol ; 163(1): 109-18, 2003 Oct 13.
Article in English | MEDLINE | ID: mdl-14557250

ABSTRACT

Although NH2-terminal mutant huntingtin (htt) fragments cause neurological disorders in Huntington's disease (HD), it is unclear how toxic htt fragments are generated and contribute to the disease process. Here, we report that complex NH2-terminal mutant htt fragments smaller than the first 508 amino acids were generated in htt-transfected cells and HD knockin mouse brains. These fragments constituted neuronal nuclear inclusions and appeared before neurological symptoms. The accumulation and aggregation of these htt fragments were associated with an age-dependent decrease in proteasome activity and were promoted by inhibition of proteasome activity. These results suggest that decreased proteasome activity contributes to late onset htt toxicity and that restoring the ability to remove NH2-terminal fragments will provide a more effective therapy for HD than inhibiting their production.


Subject(s)
Cysteine Endopeptidases/metabolism , Multienzyme Complexes/metabolism , Nerve Tissue Proteins/metabolism , Nuclear Proteins/metabolism , Peptides/metabolism , Animals , Antibodies/immunology , Brain/metabolism , Humans , Huntingtin Protein , Huntington Disease/metabolism , Mice , Mutation , Nerve Tissue Proteins/genetics , Nerve Tissue Proteins/immunology , Nuclear Proteins/genetics , Nuclear Proteins/immunology , Proteasome Endopeptidase Complex
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