Germ-line mutations in WDR77 predispose to familial papillary thyroid cancer.

The inheritance of predisposition to nonsyndromic familial nonmedullary thyroid cancer (FNMTC) remains unclear. Here, we report six individuals with papillary thyroid cancer (PTC) in two unrelated nonsyndromic FNMTC families. Whole-exome sequencing revealed two germ-line loss-of-function variants occurring within a 28-bp fragment of WDR77, which encodes a core member of a transmethylase complex formed with the protein arginine methyltransferase PRMT5 that is responsible for histone H4 arginine 3 dimethylation (H4R3me2) in frogs and mammals. To date, the association of WDR77 with susceptibility to cancer in humans is unknown. A very rare heterozygous missense mutation (R198H) in WDR77 exon 6 was identified in one family of three affected siblings. A heterozygous splice-site mutation (c.619+1G > C) at the 5' end of intron 6 is present in three affected members from another family. The R198H variant impairs the interaction of WDR77 with PRMT5, and the splice-site mutation causes exon 6 skipping and results in a marked decrease in mutant messenger RNA, accompanied by obviously reduced H4R3me2 levels in mutation carriers. Knockdown of WDR77 results in increased growth of thyroid cancer cells. Whole-transcriptome analysis of WDR77 mutant patient-derived thyroid tissue showed changes in pathways enriched in the processes of cell cycle promotion and apoptosis inhibition. In summary, we report WDR77 mutations predisposing patients to nonsyndromic familial PTC and link germ-line WDR77 variants to human malignant disease.

Coexistence of Three Different Spin States in a Cyanido-Bridged Trinuclear Iron(III) Complex with an Unusual FeIII to Ligand Charge Transfer.

We report a trinuclear iron(III) cyanido-bridged complex trans-[CpMe3 FeIII (dppe)(CN)]2 [FeIII (LN4 )][PF6 ]4 (2[PF6 ]4 ) as the oxidation product of binuclear complex [CpMe3 (dppe)FeII CN-FeIII (LN4 )][PF6 ] (1[PF6 ]) (CpMe3 =1, 2, 4-trimethyl-1,3-cyclo-pentadienyl, dppe=1,2-bis(diphenylphosphino)ethane, LN4 =pentane-2,4-dione-bis(S-methylisothiosemicarbazonato). Complex 1[PF6 ] possesses an intermediate-spin five-coordinated FeIII (S=3/2) which couples antiferromagnetically to the π-radical ligand (L⋅N4 )2- and shows a LMCT (ligand to metal charge transfer) transition from (L⋅N4 )2- to FeIII and the FeII →FeIII MMCT transition. Upon oxidation of 1[PF6 ], (L⋅N4 )2- loses one electron to be the strong electron-attracting ligand (LOx N4 )- and the intermediate-spin five-coordinated FeIII (S=3/2) becomes a low-spin six-coordinated FeIII (S=1/2) in 2[PF6 ]4 . Also interestingly, 2[PF6 ]4 presents the coexistence of three different spin states (one S=3/2 and two S=1/2) and an uncommon FeIII →(LOx N4 )- MLCT transition, confirmed by the experimental results and supported by the TDDFT calculations.

Electronic Transition and Magnetic Coupling Regulation in Trimetallic Complexes Featuring a New Bridging Ligand Obtained by Oxidative Addition.

A series of trimetallic complexes [FeIII(µ-L)(py)]2MII(py)n (n = 2, MII = MnII, 1; FeII, 2; CoII, 3; ZnII, 4; n = 3, MII = CdII, 5) with a new bridging ligand L4- (deprotonated 1,2-N1,N2-bis(2-mercaptoanil) oxalimidic acid) were synthesized and fully characterized by elemental analysis, single-crystal X-ray crystallography, IR, and Mössbauer spectra. Interestingly, the bridging ligand was obtained by oxidative addition of the (gma•)3- ligand from the mononuclear precursor Fe(gma)py (gma = glyoxal-bis(2-mercaptoanil)). In the obtained complexes, the bridging ligand L4- coordinates to the terminal FeIII ions (intermediate-spin with SFe = 3/2) by the N, S atoms, and coordinate to the central metal MII ion by the four O atoms. The resonance structure of the bridging ligand can be described as the two 4π-electron delocalized systems connected by one single-bond (C1-C2), which is different from the electronic structure of the precursor Fe(gma)py. Remarkably, the magnetic coupling interaction can be regulated through the central metal. The ferromagnetic coupling constant J gradually decreases as MII changes from FeII to CoII and MnII, while the paramagnetic behaviors are presented when MII = ZnII and CdII, confirmed by the magnetic susceptibility measurements and further supported by using the PHI program. Furthermore, the bridging ligand to the terminal FeIII charge transfer (LMCT) transitions emerged in all complexes but the central FeII to terminal FeIII charge transfer (MMCT) only presented in complex 2, strongly supported by the UV/vis-NIR electronic spectra and TDDFT calculations.

Preparation of copper-based catalysts from electroplating sludge by ultrasound treatment and their antibiotic degradation performance.

The recovery of heavy metals from electroplating sludge is important for alleviating heavy metal pollution and recycling metal resources. However, the selective recovery of metal resources is limited by the complexity of electroplating sludge. Herein, CuFe bimetallic Fenton-like catalysts were successfully prepared from electroplating sludge by a facile room-temperature ultrasonic-assisted co-precipitation method. The prepared CuFe-S mainly consisted of nanorods with diameters of 20-30 nm and lengths of 100-200 nm and a small number of irregular particles. Subsequently, we performed tetracycline (TC) degradation experiments, and the results showed that the product CuFe-S had very good performance over a wide pH range (2-11). At an initial pH = 2, CuFe-S could degrade 91.9% of 50 mg L-1 TC aqueous solution within 30 min, which is better than that of a single metal catalyst. Free radical scavenging experiments and electron paramagnetic resonance (EPR) tests revealed that ·OH was the main active species for the degradation of TC by CuFe-S. In conclusion, a CuFe bimetallic Fenton-like catalyst was developed for the catalytic degradation of antibiotics, which provides a novel technical route for the resource utilization of electroplating sludge and shows an important practical application prospect.

Cognitive Activities, Lifestyle Factors, and Risk of Cognitive Impairment, with an Analysis of the Apolipoprotein Epsilon 4 Genotype.

INTRODUCTION: Cognitive stimulating activities and a healthy lifestyle are associated with less cognitive impairment. However, whether the association is varied by Apolipoprotein epsilon 4 (APOE ε4) allele carrier status remains inconclusive. We aimed to investigate whether the association of cognitively stimulating activities and a healthy lifestyle with the risk of cognitive impairment varied by APOE ε4 allele carrier status. METHODS: A case-control study was conducted for adults aged 60 years and above. Six province administrative units (Beijing, Shanghai, Hubei, Sichuan, Guangxi, and Yunnan) were included using stratified multistage cluster sampling. A total of 1,300 individuals were identified with cognitive impairment (cases) at enrollment and were matched 1:2 on sex, age (±2 years), and residential district with controls who were cognitively normal at the time of the evaluation. We used a standardized questionnaire to collect information on cognitive stimulating activities, lifestyle factors, demographics, and comorbidity. Cognitive stimulating activities included reading books or newspapers, playing cards or mahjong, using the Internet, socializing with neighbors, and community activities. Lifestyle factors included smoking, alcohol drinking, daily tea drinking, and regular exercise. We used logistic regression to assess the interaction between cognitive stimulating activities, lifestyle factors, and APOE ε4 allele carrier status (yes/no) on the risk of cognitive impairment. We tested for additive interaction by estimating relative excess risk (RERI) due to interaction and multiplicative interaction employing the p value of the interaction term of each lifestyle factor and APOE ε4 into the model. RESULTS: Four cognitive stimulating activities were associated with less cognitive impairment regardless of APOE ε4 status. Using the Internet (odds ratio [OR]: 0.53, 95% confidence interval [CI]: 0.30-0.95), daily tea drinking (OR: 0.79; 95% CI: 0.63-0.98), and regular exercise (OR: 0.78; 95% CI: 0.65-0.94) were associated with less cognitive impairment only in noncarriers. Multiplicative and additive interactions were found between community activities and APOE ε4 carrier status (multiplicative p value = 0.03; RERI 0.738, 95% CI: 0.201-1.275). CONCLUSION: The associations between cognitive activities and cognitive impairment were robust regardless of the APOE ε4 carrier status, while the associations between lifestyle factors and cognitive impairment varied by APOE ε4 carrier status.

Acute myeloid leukemia with cup-like blasts and FLT3-ITD and NPM1 mutations mimics features of acute promyelocytic leukemia: a case of durable remission after sorafenib and low-dose cytarabine.

Some previous researches raised the possibility of a novel acute myeloid leukemia (AML) entity presenting cup-like cytomorphology with mutations of both FLT3 and NPM1 or one of them. However, the clinical implications of this subtype remain unknown. We describe a 63-year-old patient belonging to this distinct AML subtype, who presented similar features of acute promyelocytic leukemia (APL) including nuclear morphology, negative for CD34 and HLA-DR, and abnormal coagulation. He had no response to both arsenic trioxide and CAG regimen (cytarabine, aclarubicin, and G-CSF). Given that the patient carried the FLT3-ITD mutation, we switched to a pilot treatment of FLT3 inhibitor sorafenib combined with low-dose cytarabine (LDAC). To date, the patient achieved durable complete remission over 58 months. These findings suggest that AML with cup-like blasts and FLT3-ITD and NPM1 mutations mimic APL, and the prognosis of this subtype may be improved by sorafenib combined with LDAC.

A description of the relationship in healthy longevity and aging-related disease: from gene to protein.

Human longevity is a complex phenotype influenced by both genetic and environmental factors. It is also known to be associated with various types of age-related diseases, such as Alzheimer's disease (AD) and cardiovascular disease (CVD). The central dogma of molecular biology demonstrates the conversion of DNA to RNA to the encoded protein. These proteins interact to form complex cell signaling pathways, which perform various biological functions. With prolonged exposure to the environment, the in vivo homeostasis adapts to the changes, and finally, humans adopt the phenotype of longevity or aging-related diseases. In this review, we focus on two different states: longevity and aging-related diseases, including CVD and AD, to discuss the relationship between genetic characteristics, including gene variation, the level of gene expression, regulation of gene expression, the level of protein expression, both genetic and environmental influences and homeostasis based on these phenotypes shown in organisms.

Copper exposure association with prevalence of non-alcoholic fatty liver disease and insulin resistance among US adults (NHANES 2011-2014).

BACKGROUND: Excessive copper (Cu) has risky effect on insulin resistance (IR), oxidative stress and inflammation. Instead, some studies reported serum Cu to be protective for non-alcoholic fatty liver disease (NAFLD). The aim of this study was to reevaluate the evidence for a potential risky correlation of serum Cu to NAFLD in large-scale and non-institutionalized American subjects. METHODS: A cross-sectional study of 3211 subjects was from the National Health and Nutrition Examination Survey (NHANES). Logistic regression and cubic spline-based curve-fitting analyses were used to estimate the independent risky effect of Cu to hepatic steatosis index (HSI), US fatty liver index (USFLI) and NAFLD and their dose-effect relationship. Moreover, this association was analyzed in stratification of HOMA-IR, Metabolic syndrome (MetS) and severity of NAFLD, besides age and gender. RESULTS: The average level of serum Cu was 18.67 µmol/L and the prevalence of NAFLD was 54.53% and 32.60%, respectively defined by HSI and USFLI. Generally, the level of Cu was higher in females than males. Serum Cu was positively associated with higher HSI, USFLI index and risk of NAFLD. In fully adjusted models, compared with the lowest quartile, the risk of NAFLD increased 97% in the highest quartile of Cu. Interestingly, stratified analysis showed that the risky effect of Cu to NAFLD was more prominent in the middle-aged, females and subjects with improved status of IR (lower HOMA-IR and non-Mets) compared with their counterparts. Moreover, we further found that circulating copper was correlated to severity of NAFLD only in males. CONCLUSION: Excess serum Cu is significantly associated with risk of NAFLD, which is prominent in females, middle-aged and subjects with improved status of IR, and seems to be related to the severity of NAFLD, additionally. It is necessary to be cautious of the toxic effect of Cu and prospective cohort and mechanism studies are needed to verify the causal effect of Cu to NAFLD.

The Electron Transfer Process in Mixed Valence Compounds with a Low-lying Energy Bridge in Different Oxidation States.

Mixed-valence compounds with the iso-cyanidometal-ligand bridge in different oxidation states are used as models for the investigation of the electron-transfer process. We synthesized a series of trimetallic isocyanidometal-bridged compounds with [Fe-CN-Ru-NC-Fe]n+ (n=2-4), in which the one-electron oxidation product (N3+ ) and two-electron oxidation product (N4+ ) compounds possess an isocyanidometal bridge whose energy is, respectively lower and slightly higher than the terminal metal centers energies. For the N3+ compounds, the bridge state (FeII -RuIII -FeII ) and mixed-valence states (FeIII -RuII -FeII or FeII -RuII -FeIII ) could be simultaneously observed on the IR timescale. For the N4+ compounds, as the donor becomes stronger the electron transfer bridge excited state (FeIII -RuII -FeIII ) becomes more and more stable, and even becomes ground state due to the strong electronic coupling between Fe and Ru.

Identification of potential molecular targets associated with proliferative diabetic retinopathy.

BACKGROUND: This study aimed to identify and evaluate potential molecular targets associated with the development of proliferative diabetic retinopathy (DR). METHODS: The microarray dataset "GSE60436" generated from fibrovascular membranes (FVMs) associated with proliferative DR was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) from the active FVMs and control or inactive FVMs and control were evaluated and co-DEGs were identified using VEEN analysis. Functional enrichment analysis, and protein-protein interactions (PPI) network and module analyses were performed on the upregulated and downregulated coDEGs. Finally, several predictions regarding microRNAs (miRNAs) and transcription factors (TFs) were made to construct a putative TF-miRNA-target network. RESULTS: A total of 1475 co-DEGs were screened in active/inactive FVM samples, including 461 upregulated and 1014 downregulated genes, which were enriched for angiogenesis [Hypoxia Inducible Factor 1 Subunit Alpha (HIF1A) and Placental Growth Factor (PGF)] and visual perception, respectively. In the case of the upregulated co-DEGs, Kinesin Family Member 11 (KIF11), and BUB1 Mitotic Checkpoint Serine/Threonine Kinase (BUB1) exhibited the highest values in both the PPI network and module analyses, as well as the genes related to mitosis. In the case of downregulated co-DEGs, several G protein subunits, including G Protein Subunit Beta 3 (GNB3), exhibited the highest values in both the PPI network and module analyses. The genes identified in the module analysis were found to be from the signal transduction-related pathways. In addition, we were able to identify four miRNAs and five TFs, including miR-136 and miR-374. CONCLUSIONS: In brief, HIF1A, PGF, KIF11, G protein subunits, and miR-136, miR-374 may all be involved in angiogenesis, retinal endothelial cell proliferation, and visual signal transduction in proliferative DR. This study provides a number of novel insights that may aid the development of future studies dedicated to discovering novel therapeutic targets in proliferative DR.

TWIST2: A new candidate tumor suppressor in prostate cancer.

BACKGROUND: Prostate cancer (PCa) is a leading cause of cancer morbidity and mortality in men worldwide; however, PCa incidence and mortality rates vary widely across geographic regions and ethnic groups. The current study was designed to elucidate the pivotal factors involved in PCa occurrence and development. METHODS: We performed RNA sequencing on the prostate tumor and adjacent normal tissues from Chinese PCa patients. Genes identified via genome-wide expression profile analysis were validated by quantitative reverse-transcription polymerase chain reaction and immunohistochemistry. Hypermethylation of CpG islands was assessed by nested methylation-specific PCR. Whole genome microarray analysis was performed using an Affymetrix GeneChip. RESULTS: We identified nine possible abnormally expressed genes (P < .05) and then revealed TWIST2 as having strikingly lower expression in tumors than in control tissues (P < .01). Low messenger RNA expression levels of TWIST2 were associated with hypermethylation of CpG islands in its promoter region. In accordance with these findings, PCa tumor tissues showed markedly decreased TWIST2 protein expression compared to that in both normal and prostatic intraepithelial neoplasia tissues by immunohistochemical staining. Ectopic expression of TWIST2 in LNCap cells not only inhibited cell proliferation and colony formation in vitro and tumor growth in vivo but also induced transcriptional repression of a cell proliferation-related gene cohort, including androgen receptor signaling mediators, cyclins, homeobox genes, forkhead box genes, and SOX2. CONCLUSIONS: Our results suggest that TWIST2 could function as a tumor suppressor involved in the pathogenesis of PCa by influencing the expression of target genes and that hypermethylation of the TWIST2 promoter in prostate tumors may be an underlying mechanism for TWIST2 transcriptional silencing.

A Diruthenium-Based Mixed Spin Complex Ru2 5+ (S=1/2)-CN-Ru2 5+ (S=3/2).

An unusual tetra-nuclear linear cyanido-bridged complex [Ru2 (µ-ap)4 -CN-Ru2 (µ-ap)4 ](BPh4 ) (1) (ap=2-anilinopyridinate) has been synthesized and well characterized. The crystallographic data, magnetic measurement, IR, EPR and theoretical calculation results demonstrate that complex 1 is the first example of mixed spin Ru2 5+ -based complex with uncommon electronic configurations of S=1/2 for the cyanido-C bound Ru2 5+ and S=3/2 for the cyanido-N bound Ru2 5+ . This phenomenon can be understood by the theoretical calculation results that from the precursor Ru2 (µ-ap)4 (CN) (S=3/2) to complex 1 the energy gap between π* and δ* orbitals of the cyanido-C bound Ru2 5+ core increases from 0.57 to 1.61 eV due to the enhancement of asymmetrical π back-bonding effect, but that of the cyanido-N bound Ru2 5+ core is essential identical (0.56 eV). Besides, the analysis of UV/Vis-NIR spectra suggests that there exists metal to metal charge transfer (MMCT) from the cyanido-N bound Ru2 5+ (S=3/2) to the cyanido-C bound Ru2 5+ (S=1/2), supported by the TDDFT calculations.

Different Degrees of Electron Delocalization in Mixed Valence Ru-Ru-Ru Compounds by Cyanido-/Isocyanido-Bridge Isomerism.

The two stable pairs of trimetallic compounds trans-[Cp*(dppe)Ru(µ-NC)Ru(dmap)4 (µ-CN)Ru(dppe)Cp*][PF6 ]n (1[PF6 ]n , n=2, 3; Cp*=1,2,3,4,5-pentamethylcyclopentadiene; dppe=1,2-bis-(diphenylphosphino)ethane; dmap= 4-dimethylaminopyridine) and trans-[Cp*(dppe)Ru(µ-CN)Ru(dmap)4 (µ-NC)Ru(dppe)Cp*][PF6 ]n (2[PF6 ]n , n=2, 3), which demonstrate cyanide/isocyanide isomerism, have been synthesized and fully characterized. 13+ [PF6 ]3 and 23+ [PF6 ]3 are the one-electron oxidation products of 12+ [PF6 ]2 and 22+ [PF6 ]2 , respectively. The results suggest that 1[PF6 ]3 is a class III mixed valence compound, whereas 2[PF6 ]3 might be an unusually symmetrical class II-III mixed valence compound composed of the two asymmetrical delocalized RuIII -NC-RuII mixed valence subunits.

A gain-of-function mutation in Tnni2 impeded bone development through increasing Hif3a expression in DA2B mice.

Distal arthrogryposis type 2B (DA2B) is an important genetic disorder in humans. However, the mechanisms governing this disease are not clearly understood. In this study, we generated knock-in mice carrying a DA2B mutation (K175del) in troponin I type 2 (skeletal, fast) (TNNI2), which encodes a fast-twitch skeletal muscle protein. Tnni2K175del mice (referred to as DA2B mice) showed typical DA2B phenotypes, including limb abnormality and small body size. However, the current knowledge concerning TNNI2 could not explain the small body phenotype of DA2B mice. We found that Tnni2 was expressed in the osteoblasts and chondrocytes of long bone growth plates. Expression profile analysis using radii and ulnae demonstrated that Hif3a expression was significantly increased in the Tnni2K175del mice. Chromatin immunoprecipitation assays indicated that both wild-type and mutant tnni2 protein can bind to the Hif3a promoter using mouse primary osteoblasts. Moreover, we showed that the mutant tnni2 protein had a higher capacity to transactivate Hif3a than the wild-type protein. The increased amount of hif3a resulted in impairment of angiogenesis, delay in endochondral ossification, and decrease in chondrocyte differentiation and osteoblast proliferation, suggesting that hif3a counteracted hif1a-induced Vegf expression in DA2B mice. Together, our data indicated that Tnni2K175del mutation led to abnormally increased hif3a and decreased vegf in bone, which explain, at least in part, the small body size of Tnni2K175del mice. Furthermore, our findings revealed a new function of tnni2 in the regulation of bone development, and the study of gain-of-function mutation in Tnni2 in transgenic mice opens a new avenue to understand the pathological mechanism of human DA2B disorder.

An Unusually Delocalized Mixed-Valence State of a Cyanidometal-Bridged Compound Induced by Thermal Electron Transfer.

The heterometallic complexes trans-[Cp(dppe)FeNCRu(o-bpy)CNFe(dppe)Cp][PF6 ]n (1[PF6 ]n , n=2, 3, 4; o-bpy=1,2-bis(2,2'-bipyridyl-6-yl)ethane, dppe=1,2-bis(diphenylphosphino)ethane, Cp=1,3-cyclopentadiene) in three distinct states have been synthesized and fully characterized. 13+ [PF6 ]3 and 14+ [PF6 ]4 are the one- and two-electron oxidation products of 12+ [PF6 ]2 , respectively. The investigated results suggest that 1[PF6 ]3 is a Class II mixed valence compound. 1[PF6 ]4 after a thermal treatment at 400 K shows an unusually delocalized mixed valence state of [FeIII -NC-RuIII -CN-FeII ], which is induced by electron transfer from the central RuII to the terminal FeIII in 1[PF6 ]4 , which was confirmed by IR spectroscopy, magnetic data, and EPR and Mössbauer spectroscopy.

Transforming growth factor (TGF) ß1 acted through miR-130b to increase integrin α5 to promote migration of colorectal cancer cells.

Transforming growth factor (TGF)-ß1 is a significant stimulator of tumor invasion and metastasis. More recently, it has been found that TGF-ß1 acts through microRNAs to regulate their target genes to promote cancer progresses. However, such similar regulation is rarely reported in colorectal cancer (CRC). Here, we observed a decrease in TGF-ß1 expression in CRC specimens, compared with matched adjacent normal tissues. In parallel, there was an increase in miR-130b characterized in the same samples by microarray assay. Further, treatment of CRC cells with TGF-ß1 caused a significant decrease in the expression of miR-130b and an increased CRC cell migration. Luciferase reporter assay revealed that miR-130b directly targeted the 3' untranslated region (3'UTR) region of integrin α5 gene, which encodes a key molecule involved in cell motility. Subsequently, in the overexpression of miR-130b CRC cells, we observed a decreased level of integrin α5 protein. The regulation of integrin α5 by miR-130b was further shown using the miR-130b mimics and inhibitor of miR-130b. And, knockdown miR-130b with inhibitor in the overexpression of miR-130b CRC cells recovered integrin α5 expression and integrin α5-mediated cell motility. Moreover, the inverse relevance between miR-130b and integrin α5 was also observed in CRC specimens. At last, the enhancement of integrin α5 in TGF-ß1-treated cells can be reversed partly when rescuing miR-130b expression. Together, our findings suggested that TGF-ß1 acted through miR-130b to promote integrin α5 expression, resulting in the enhanced migration of CRC cells.

Intercalation of Varied Sulfonates into a Layered MOC: Confinement-Caused Tunable Luminescence and Novel Properties.

The pores/channels of porous 3D metal-organic frameworks (MOFs) have been widely applied to incorporate gas, solvent, or organic molecules. On the contrary, the utilization of the interlamellar void of layered metal-organic complexes (MOCs) remains underappreciated, although it is more flexible and available to accommodate molecules with different sizes. In this work, diverse sulfonates have been intercalated purposely into an identical layered MOC, which constructed various novel intercalation compounds possessing fluorescent, white-light emitting, photochromic, homochiral, or nonlinear optical (NLO) properties. With the help of single-crystal X-ray diffraction, their structures and the mutual interactions between the MOC host and the sulfonate guests were characterized. The properties of the guest molecules were tuned and meanwhile some new performances were generated after confining them into the interlayer region. Such a hybrid approach provides an efficient strategy to design and prepare multifunctional materials.

1D to 3D and Chiral to Noncentrosymmetric Metal-Organic Complexes Controlled by the Amount of DEF Solvent: Photoluminescent and NLO Properties.

A mixture of 2D and 1D metal-organic complexes, [ZnL(H2O)2·G1·DEF·2H2O]n (1a: G1 = naphthalene-2,7-disulfonate; DEF = N,N-diethylformamide) and [ZnL(H2O)3·G1·DEF·2H2O]n (2), has been prepared from a hydrogenated Schiff base L and Zn(II) in a DEF-contained solvent system under mild conditions. The yields of 1a and 2 are equivalent; however, they can be tuned by varying the amount of DEF solvent. Increasing the use of DEF tends to form pure 1a, while decreasing it generates 2. Without DEF, another novel 3D four-connected CdSO4 (cds) framework [ZnL(H2O)2·G1·2H2O]n (3) composed of alternated right-handed and left-handed helical chains has been constructed. The amount of DEF solvent has a significant impact on the diverse coordination architectures of 1-3, which is rare in the preparation of metal-organic complexes. The photoluminescence of complexes 1-3 along with naphthalene-2,7-disulfonate has been investigated in the solid state. The luminescent emission of G1 was enhanced greatly after being confined into metal-organic networks. In addition, complexes 1-3 display second-harmonic generation efficiencies, which are approximately 0.58, 0.42, 0.32, and 0.52 times as much as that of potassium dihydrogen phosphate.

The inferior cochlear vein: surgical aspects in cochlear implantation.

The patency of the inferior cochlear vein (ICV) may be challenged in cochlear implantation (CI) due to its location near the round window (RW). This may be essential to consider during selection of different trajectories for electrode insertion aiming at preserving residual hearing. Venous blood from the human cochlea is drained through the ICV. The vein also drains blood from the modiolus containing the spiral ganglion neurons. Surgical interference with this vein could cause neural damage influencing CI outcome. We analyzed the topographical relationship between the RW and ICV bony channel and cochlear aqueduct (CA) from a surgical standpoint. Archival human temporal bones were further microdissected to visualize the CA and its accessory canals (AC1 and AC2). This was combined with examinations of plastic and silicone molds of the human labyrinth. Metric analyses were made using photo stereomicroscopy documenting the proximal portion of the AC1, the internal aperture of the CA and the RW. The mean distance between the AC1 and the anterior rim of the RW was 0.81 mm in bone specimens and 0.67 mm assessed in corrosion casts. The AC1 runs from the floor of the scala tympani through the otic capsule passing parallel to the CA to the posterior cranial fossa. The mean distance between the CA and AC1 canal was 0.31 and 0.25 mm, respectively.

From pair quadruple- to single-stranded helices to lines in a mixed ligand system via adjusting the N-substituent of L-Glu.

Utilizing the mixed-ligand strategy, a novel fourfold-interpenetrated 3D homochiral metal-organic framework (1) with rare pair quadruple-stranded helices was assembled from bpee (1,2-bis(4-pyridyl)ethylene) and NCG (N-carbamyl-l-glutamate). Changing the carbamyl substituent of NCG with benzoyl group (NBzG: N-benzoyl-l-glutamate), a non-interpenetrated 3D homochiral coordination polymer (2) composed of alternate right-handed and left-handed single helix was obtained. When p-tolylsulfonyl substituent was used instead, an interesting homochiral linear structure (3) was formed from mixed-ligand bpee and NTsG (N-p-tolylsulfonyl-l-glutamate), with all individual NTsG being lined up orderly. The steric hindrance of N-substituent of l-glu has a tremendous impact on the construction of these diverse frameworks. Complexes 1-3 display second harmonic generation (SHG) efficiencies, which are approximately 0.32, 0.45, and 0.55 times as much as that of KDP powder.