Low-dimensional organic−inorganic metal halide hybrids (OIMHs) with an ultrabroad-band emission are promising as downconversion phosphors for solid-state lighting. However, toxicity of Pb and low photoluminescence quantum efficiency (PLQE) hamper their application. Herein, two zero-dimensional (0D) lead-free organic antimony (Sb) chloride (Cl) hybrids with dual-band emissions and PLQEs: (TTA) 2 SbCl 5 (TTA = tetraethylammonium) and (TEBA) 2 SbCl 5 (TEBA = benzyltriethylammonium) are reported. Both compounds show a single broad-band orange emission with a near-unity PLQE upon low-energy photons (e.g., 360 nm) excitation. The dual-band emission with an additional blue emission band upon high-energy photons (e.g., 300 nm) excitation enable (TTA) 2 SbCl 5 to be a single-component phosphor for white light emission with a PLQE of 68%, correlated color temperature (CCT) of 2360 K and color rendering index (CRI) of 84. Based on photoluminescence spectra measurements and density functional theory calculations, the dual-band emission is assigned to the radiative recombination from both singlet and triplet self-trapped excitons in inorganic [SbCl 5 ] 2− pyramids. In addition, both luminescent compounds exhibit excellent stability against humidity and thermal attacks. Using (TEBA) 2 SbCl 5 as a yellow downconversion material, highly stable white-light-emitting diodes with a Commission Internationale de l'Eclairage (CIE) of (0.36, 0.33), CCT of 4282 K, and CRI of 82 were demonstrated. These results validate that the title 0D lead-free OIMHs with a dual-band emission and a near-unity PLQE are promising luminescent materials for solid-state lighting.

Much of the genetic predisposition to colorectal cancer (CRC) in humans is unexplained. Studying a Caucasian-dominated population in the United States, we showed that germline allele-specific expression (ASE) of the gene encoding transforming growth factor-β (TGF-β) type I receptor, TGFBR1, is a quantitative trait that occurs in 10 to 20% of CRC patients and 1 to 3% of controls. ASE results in reduced expression of the gene, is dominantly inherited, segregates in families, and occurs in sporadic CRC cases. Although subtle, the reduction in constitutive TGFBR1 expression alters SMAD-mediated TGF-β signaling. Two major TGFBR1 haplotypes are predominant among ASE cases, which suggests ancestral mutations, but causative germline changes have not been identified. Conservative estimates suggest that ASE confers a substantially increased risk of CRC (odds ratio, 8.7; 95% confidence interval, 2.6 to 29.1), but these estimates require confirmation and will probably show ethnic differences.The annual worldwide incidence of colorectal cancer (CRC) exceeds 1 million, being the second to fourth most common cancer in industrialized countries (1). Although diet and lifestyle are thought to have a strong impact on CRC risk, genes have a key role in the predisposition to this cancer. A positive family history of CRC occurs in 20 to 30% of all probands. Highly penetrant autosomal dominant and recessive hereditary forms of CRC account for at most 5% of all CRC cases (2). Although additional high-and low-penetrance alleles have been proposed, much of the remaining predisposition to CRC remains unexplained (3).Aberrations in the transforming growth factor-β (TGF-β) pathway are heavily involved in CRC carcinogenesis (4). Although mutations in the TGF-β type II receptor gene have been explicitly associated with CRC (5), the type I receptor gene (TGFBR1) has received less attention, although there is evidence that a common variant may be associated with cancer risk (6,7). We hypothesized that TGFBR1 is a notable candidate for a gene that, when mutated, causes predisposition to CRC or acts as a modifier of other genes, resulting in a predisposition. Our study was undertaken to test this assumption.

Selective intestinal malabsorption of vitamin B(12) causing juvenile megaloblastic anemia (MGA; MIM# 261100) is a recessively inherited disorder that is believed to be rare except for notable clusters of cases in Finland, Norway, and the Eastern Mediterranean region. The disease can be caused by mutations in either the cubilin (CUBN; MGA1; MIM# 602997) or the amnionless (AMN; MIM# 605799) gene. To explain the peculiar geographical distribution, we hypothesized that mutations in one of the genes would mainly be responsible for the disease in Scandinavia, and mutations in the other gene in the Mediterranean region. We studied 42 sibships and found all cases in Finland to be due to CUBN (three different mutations) and all cases in Norway to be due to AMN (two different mutations), while in Turkey, Israel, and Saudi Arabia, there were two different AMN mutations and three different CUBN mutations. Haplotype evidence excluded both CUBN and AMN conclusively in five families and tentatively in three families, suggesting the presence of at least one more gene locus that can cause MGA. We conclude that the Scandinavian cases are typical examples of enrichment by founder effects, while in the Mediterranean region high degrees of consanguinity expose rare mutations in both genes. We suggest that in both regions, physician awareness of this disease causes it to be more readily diagnosed than elsewhere; thus, it may well be more common worldwide than previously thought.

gastric intrinsic factor ͉ Imerslund-Grä sbeck syndrome ͉ intrinsic factor deficiency ͉ vitamin B 12 malabsorption ͉ megaloblastic anemia

Low-dimensional metal halide hybrids (OIMHs) have recently been explored as single-component white-light emitters for use in solid-state lighting. However, it still remains challenging to realize tunable white-light emission in lead-free zero-dimensional (0D) hybrid system. Here, a combination strategy has been proposed through doping Sb 3+ enabling and balancing multiple emission centers toward the multiband warm white light. We first synthesized a new lead-free 0D (C 8 NH 12 ) 6 InBr 9 •H 2 O single crystal, in which isolated [InBr 6 ] 3− octahedral units are separated by large organic cations [C 8 NH 12 ] + . (C 8 NH 12 ) 6 InBr 9 •H 2 O exhibits dual-band emissions with one intense cyan emission and a weak red emission tail. The low-energy ultrabroadband red emission tail can be greatly enhanced by the Sb 3+ doping. Experimental data and first-principles calculations reveal that the original dominant cyan emission is originated from the organic cations [C 8 NH 12 ] + and that the broadband red emission is ascribed to selftrapped excitons in [In(Sb)Br 6 ] 3− . When the Sb concentration is 0.1%, a single-component warm white-light emission with a photoluminescence quantum efficiency of 23.36%, correlated color temperature of 3347 K, and a color rendering index up to 84 can be achieved. This work represents a significant step toward the realization of single-component white-light emissions in environmental-friendly, high-performance 0D metal halide light-emitting materials.

Neuroblastoma (NB) is the most common malignant tumor in infancy and most common extracranial solid tumor in childhood. With the improvement of diagnosis and treatment, the survival rate of patients with low-risk and intermediate-risk NB can reach up to 90%. In contrast, for high-risk NBs, the long-term survival rate is still <40% because of heterogeneity of this tumor. The pathogenesis of NB is still not explicit, therefore it is of great significance to explore the mechanism of NB tumorigenesis and discover new therapeutic targets for NB. Polo-like kinase 4 (PLK4), one of the polo-like kinase family members, is an important regulator of centriole replication. The aberrant expression of PLK4 was found in several cancers and a recent study has unraveled a novel function of PLK4 as a mediator of invasion and metastasis in Hela and U2OS cells. However, the function of PLK4 in NB development and progression remains to be elucidated. The study showed the expression level of PLK4 in NB tissues was remarkably upregulated and high expression of PLK4 was negatively correlated with clinical features and survival, which suggested that PLK4 could be a potential tumor-promoting factor of NB. Functional studies indicated downregulation of PLK4 suppressed migration and invasion and promoted apoptosis in NB cells. Further experiments showed that downregulation of PLK4 in NB cells inhibited EMT through the PI3K/Akt signaling pathway. Animal experiments demonstrated that the downregulation of PLK4 in SK-N-BE(2) cells dramatically suppressed tumorigenesis and metastasis. PLK4 may be a promising therapeutic target for NB.

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