29 research outputs found
Mechanistic Investigation of RhI-Catalyzed Cycloisomerization of Benzylallene-Internal Alkynes via C-H Activation
Treatment of the benzylallene-internal alkynes with [RhCl(CO)2]2 effected a cycloisomerization via a Csp2-H bond activation to produce the tricyclo[9.4.0.03,8]pentadecapentaene skeleton. The reaction mechanism via formation of the rhodabicyclo[4.3.0] intermediates and σ-bond metathesis between the Csp2-H bond on the benzene ring and the Csp2-RhIII bond was proposed. In addition, a plausible alternative mechanism for the previously reported cycloisomerization of the benzylallene-terminal alkynes could also be proposed. © 2017 American Chemical Society.Embargo Period 12 month
Double-Network Hydrogels Strongly Bondable to Bones by Spontaneous Osteogenesis Penetration
Implanting hydroxyapatite-mineralized tough hydrogel into osteochondral defects of rabbits, osteogenesis spontaneously penetrates into the gel matrix owing to the semi-permeablility of the hydrogel. The gradient layer (around 40 μm thick) contributes quite strong bonding of the gel to bone. This is the first success in realizing the robust osteointegration of tough hydrogels, and the method is simple and feasible for practical use
Decreased Wave V Amplitude in Auditory Brainstem Responses of Children with Cerebellar Lesions
【Background】 This study aims to elucidate the effect of isolated cerebellar lesions sparing the brainstem on the auditory brainstem responses in children. 【Methods】 We enrolled 10 children (aged 1?16 years) with cerebellar lesions on neuroimaging but lacking clinical brainstem involvement signs and with normal brainstem volumes on magnetic resonance imaging. 【Results】 The interpeak latency of waves I and V was normal in 9 patients and was marginally prolonged in 1 patient. While amplitudes of waves I and III were normal, we noted a decreased amplitude of wave V and/or an increased I/V amplitude ratio in 6 patients; these included 5 of 8 patients with cerebellar hypoplasia/atrophy and 1 patient with acute cerebellar ataxia. 【Conclusion】 Our results support the hypothesis of an inhibitory input from the cerebellar fastigial nucleus on the inferior colliculus, which might be disinhibited because of Purkinje cells dysfunction due to cerebellar cortex lesions, especially within the cerebellar vermis
Relationship between mitochondrial DNA polymorphism and postnatal growth of Japanese beef cattle
Correlation coefficients (r) between mitochondrial DNA (mtDNA) haplotypes, maternal lineage (ML), birth weight (BWT), preweaning average daily gain (PREADG), weaning weight (WT6), post weaning average daily gain (POSTADG) and yearling weight (WT12) were computed in Japanese Black beef cattle within the same herd and management. The objective was to study the relationship between maternal and postnatal growth traits and to investigate if postnatal growth of calves to yearling age could be accurately predicted from mtDNA genotype at an early age. Blood samples and phenotypic records from 129 cattle which were part of a QTL mapping herd were utilized. mtDNA from the displacement-loop (D-loop) region (496 bp) was genotyped and classified into sub-groups 2 and 3 haplotypes and sequenced. General linear models procedure was utilized to adjust for genetic and non-genetic effects on postnatal growth traits. Simple and multiple linear regressions were fitted to predict postnatal growth traits from mtDNA haplotypes and the coefficients of determination (R2 ) were computed. Results revealed 19 maternal lineages and four mtDNA types (1, 11, 73 and a new hitherto unreported one). There were strong, positive and highly significant (P0.05) ranging from -0.05 to 0.1. Prediction of postnatal growth from mtDNA yielded very low R2 values ranging from 0.002 for BWT to 0.019 for WT6. The addition of ML, sub-group 2 and sub-group 3 haplotype information did not lead to any appreciable improvement in prediction accuracy. It was concluded that mtDNA polymorphism has no significant association with postnatal growth from birth to yearling age, and by implication, nuclear rather than cytoplasmic DNA, is most likely responsible for genetic variation observed in postnatal growth of Japanese Black cattle. Therefore, mtDNA genotyping at an early age has no bearing on future growth performance of calves
Mechanistic Investigation of Rh<sup>I</sup>–Catalyzed Cycloisomerization of Benzylallene-Internal Alkynes via C–H Activation
Treatment of the
benzylallene-internal alkynes with [RhCl(CO)<sub>2</sub>]<sub>2</sub> effected a cycloisomerization via a C<sub>sp2</sub>–H bond
activation to produce the tricyclo[9.4.0.0<sup>3,8</sup>]pentadecapentaene
skeleton. The reaction mechanism via formation
of the rhodabicyclo[4.3.0] intermediates and σ-bond metathesis
between the C<sub>sp2</sub>–H bond on the benzene ring and
the C<sub>sp2</sub>–Rh<sup>III</sup> bond was proposed. In
addition, a plausible alternative mechanism for the previously reported
cycloisomerization of the benzylallene-terminal alkynes could also
be proposed
Dynamic transition of molecular subtypes in relapsed small cell lung cancer treated with multimodal therapy: A case report
Abstract Several transcription factors in small cell lung cancer (SCLC), including achaete‐scute homolog 1 (ASCL1) and neurogenic differentiation factor 1 (NEUROD1), contribute to rapid tumor growth and early metastatic dissemination. Recent studies suggested that these molecular subtypes represent neuroendocrine differentiation in dynamic SCLC evolution. In the present case, a 62‐year‐old man was diagnosed with limited disease SCLC originating from the right upper lobe. Biopsy specimens were positive for ASCL1 but negative for NEUROD1. Six months after concurrent chemoradiotherapy and prophylactic cranial irradiation, the primary tumor had regrown and salvage surgery was performed. The pathological diagnosis was recurred SCLC, and postoperative histopathology was positive for both ASCL1 and NEUROD1. The patient was subsequently followed up; however, he had multiple bone metastases 9 months after surgery. It was speculated that the shift to NEUROD1‐high expression in tumor cells surviving concurrent chemoradiation therapy may be related to the poor outcome after combined modality treatment