Orbital Alignment for High Performance Thermoelectric YbCd₂Sb₂ Alloys

As a typical class of Zintl thermoelectrics, AB₂C₂ (A = Eu, Yb, Ba, Ca, Mg; B = Zn, Cd, Mg, and C = Sb, Bi) compounds have shown a superior thermoelectric performance, largely stemming from the existence of multiple transporting bands in both conduction types. Being similar to many III–V and elemental semiconductors, the transport of holes in AB₂C₂ Zintls usually involves multiple valence bands with extrema at the Brillouin zone center Γ. However, these valence bands, originating from different orbitals, are unnecessarily aligned in energy due to the crystal field splitting. Formation of solid solutions between constituent compounds having opposite arrangements in energy of band orbitals is believed to be particularly helpful for thermoelectric enhancements, because orbital alignment increases band degeneracy while alloy defects scatter phonons. These effects are simultaneously realized in this work, where the <i>p</i> orbitals of anions in YbCd_2–<i>x</i>Zn_<i>x</i>Sb₂ alloys are well-aligned for maximizing the electronic performance, and meanwhile high-concentration Cd/Zn substitutions are introduced for minimizing the lattice thermal conductivity. As a result, a significantly enhanced thermoelectric figure of merit, <i>zT</i> ∼ 1.3, is achieved, being a record among AB₂C₂ Zintls in <i>p</i>-type. This work demonstrates not only YbCd_2–<i>x</i>Zn_<i>x</i>Sb₂ alloys as efficient thermoelectrics but also orbital alignment as an effective strategy for advancing thermoelectrics

Exome Capture Sequencing of Adenoma Reveals Genetic Alterations in Multiple Cellular Pathways at the Early Stage of Colorectal Tumorigenesis

<div><p>Most of colorectal adenocarcinomas are believed to arise from adenomas, which are premalignant lesions. Sequencing the whole exome of the adenoma will help identifying molecular biomarkers that can predict the occurrence of adenocarcinoma more precisely and help understanding the molecular pathways underlying the initial stage of colorectal tumorigenesis. We performed the exome capture sequencing of the normal mucosa, adenoma and adenocarcinoma tissues from the same patient and sequenced the identified mutations in additional 73 adenomas and 288 adenocarcinomas. Somatic single nucleotide variations (SNVs) were identified in both the adenoma and adenocarcinoma by comparing with the normal control from the same patient. We identified 12 nonsynonymous somatic SNVs in the adenoma and 42 nonsynonymous somatic SNVs in the adenocarcinoma. Most of these mutations including OR6X1, SLC15A3, KRTHB4, RBFOX1, LAMA3, CDH20, BIRC6, NMBR, GLCCI1, EFR3A, and FTHL17 were newly reported in colorectal adenomas. Functional annotation of these mutated genes showed that multiple cellular pathways including Wnt, cell adhesion and ubiquitin mediated proteolysis pathways were altered genetically in the adenoma and that the genetic alterations in the same pathways persist in the adenocarcinoma. CDH20 and LAMA3 were mutated in the adenoma while NRXN3 and COL4A6 were mutated in the adenocarcinoma from the same patient, suggesting for the first time that genetic alterations in the cell adhesion pathway occur as early as in the adenoma. Thus, the comparison of genomic mutations between adenoma and adenocarcinoma provides us a new insight into the molecular events governing the early step of colorectal tumorigenesis.</p> </div

Validated somatic mutation in the colorectal adenoma.

<p>Validated somatic mutation in the colorectal adenoma.</p

Validated somatic mutation in the colorectal adenocarcinoma.

<p>Validated somatic mutation in the colorectal adenocarcinoma.</p

Summary of sequencing coverage of the normal mucosa, adenoma and adenocarcinoma from the same patient.

<p>Summary of sequencing coverage of the normal mucosa, adenoma and adenocarcinoma from the same patient.</p

Somatic SNVs pattern in the adenoma and the adenocarcinoma.

<p>(A) Somatic mutation spectrum in adenoma and adenocarcinoma, similar with 11 colorectal cancers previously reported <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053310#pone.0053310-Sjoblom1" target="_blank">[10]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053310#pone.0053310-Wood1" target="_blank">[11]</a>. (B) Fractions of guanine mutations at 5′-CpG-3′ dinucleotides in the exome of adenoma and adenocarcinoma. (C) Prevalence of somatic SNVs in the coding region and non-coding region of the exome of the adenoma and the adenocarcinoma.</p

Recurrent mutations in 288 additional cases of colorectal tumors.

<p>Recurrent mutations in 288 additional cases of colorectal tumors.</p

Mutated pathways in adenoma and adenocarcinoma.

<p>Mutated pathways in adenoma and adenocarcinoma.</p