Boronyl Ligand as a Member of the Isoelectronic Series BO⁻ → CO → NO⁺: Viable Cobalt Carbonyl Boronyl Derivatives?

Recently the first boronyl (oxoboryl) complex [(c-C6H11)3P]2Pt(BO)Br was synthesized. The boronyl ligand in this complex is a member of the isoelectronic series BO− → CO → NO+. The cobalt carbonyl boronyls Co(BO)(CO)4 and Co2(BO)2(CO)7, with cobalt in the formal d8 +1 oxidation state, are thus isoelectronic with the familiar homoleptic iron carbonyls Fe(CO)5 and Fe2(CO)9. Density functional theory predicts Co(BO)(CO)4 to have a trigonal bipyramidal structure with the BO group in an axial position. The tricarbonyl Co(BO)(CO)3 is predicted to have a distorted square planar structure, similar to those of other 16-electron complexes of d8 transition metals. Higher energy Co(BO)(CO)n (n = 3, 2) structures may be derived by removal of one (for n = 3) or two (for n = 2) CO groups from a trigonal bipyramidal Co(BO)(CO)4 structure. Structures with a CO group bridging 17-electron Co(CO)4 and Co(BO)2(CO)3 units and no Co−Co bond are found for Co2(BO)2(CO)8. However, Co2(BO)2(CO)8 is not viable because of the predicted exothermic loss of CO to give Co2(BO)2(CO)7. The lowest lying Co2(BO)2(CO)7 structure is a triply bridged (2BO + CO) structure closely related to the experimental Fe2(CO)9 structure. However, other relatively low energy Co2(BO)2(CO)7 structures are found, either with a single CO bridge, similar to the experimental Os2(CO)8(μ-CO) structure; or with 17-electron Co(CO)4 and Co(BO)2(CO)3 units joined by a single Co−Co bond with or without semibridging carbonyl groups. Both triplet and singlet Co2(BO)2(CO)6 structures are found. The lowest lying triplet Co2(BO)2(CO)6 structures have a Co(CO)3(BO)2 unit coordinated to a Co(CO)3 unit through the oxygen atoms of the boronyl groups with a non-bonding ∼4.3 Å Co···Co distance. The lowest lying singlet Co2(BO)2(CO)6 structures have either two three-electron donor bridging η2-μ-BO groups and no Co···Co bond or one such three-electron donor BO group and a formal Co−Co single bond

Additional file 6 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 6: Table S1. Clinical characteristics of enrolled HNSCC patients

Additional file 3 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 3: Figure S3. Gene mutations in tissue samples of patients with advanced HNSCC receiving immunotherapy and efficacy evaluation. The patients were divided into the response group (n = 25) and non-response group (n = 8). SNV and indel mutations were detected in the patient’s tissues (A), and the identified mutations were summarized for the response group (B) and non-response group (C). Mutation diagram of the ten signaling pathways in tissue samples was illustrated (D)

Additional file 1 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 1: Figure S1. Diagram for the enrolled HNSC patients in the current study

Additional file 4 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 4: Figure S4. Statistical analysis of differences between the response and non-response groups. (A) TMB, (B) bTMB, (C) MATH values

Additional file 5 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 5: Figure S5. Boxplot analysis of percentages of immunomarker positive cells between the response and non-response groups. (A) tumor region, (B) stroma region, (C) total region

Additional file 2 of Identification of factors related to immunotherapy efficacy and prognosis in patients with advanced head and neck squamous cell carcinoma

Additional file 2: Figure S2. Multivariate survival analysis results for clinical characteristics and enriched tumor-associated inflammatory cells in the (A) stroma and (B) tumor and (C) total region

Additional file 1 of Genetic insights into the ‘sandwich fusion’ subtype of Klippel–Feil syndrome: novel FGFR2 mutations identified by 21 cases of whole-exome sequencing

Additional file 1: Fig. S1. Bioinformatics analysis workflow (the filtration strategy). Samples were initially mapped to the human reference genome GRCh37 (hg19) using BWA, followed by the removal of low-quality reads (< 80 bps) using CutAdapt and elimination of duplicate reads with Picard. Subsequently, SNP and INDEL variants were detected using GATK. In the third step, various software tools, including ANNOVAR, 1000Genome, ESP6500, dbSNP, ExAC, HGMD, ClinVar, were employed for sample annotation and further exclusion of deep intron variants. Comparative analysis with databases such as 1000Genome, ESP6500, and ExAC was performed to eliminate common SNPs. Pathogenicity prediction scores were determined using SIFT, Polyphen-2, MutationTaster, and Gerp++. GLUSTAL W and UGENE were utilized for cross-species comparison to ascertain sequence conservation, while ESE Finder 3.0 was employed to predict potential changes in protein structure. Finally, all suspicious variants underwent Sanger sequencing for further validation. Fig. S2. The animated diagram of FGFR2 (RCSB PDB number: 3B2T) and the arrowhead indicated the M584 site. A Ball-and-stick model of FGFR2; the sequence from 582 to 596 is shown in a dotted line. B Molecular surface model of FGFR2; the pink bulky region is P582. Mutation of M584V might result in a steric hindrance effect in the structural region of the protein and affect the folding of FGFR2 and reduce its catalytic capability. Table S1. Quality control of sequencing data

Enhanced Activation Energy Released by Coordination of Bifunctional Lewis Base d‑Tryptophan for Highly Efficient and Stable Perovskite Solar Cells

Perovskite defect passivation with molecule doping shows great potential in boosting the efficiency and stability of perovskite solar cells (PSCs). Herein, an efficient and low-cost bifunctional Lewis base additive d-tryptophan is introduced to control the crystallization and growth of perovskite grains and passivation defects. It is found that the additive doped in the solution precursors could retard crystal growth by increasing activation energy, resulting in improved crystallization of large grains with reduced grain boundaries, as well as inhibiting ion migration and PbI2 aggregation. As a result, the PSCs incorporated with d-tryptophan additives achieve an improved power conversion efficiency from 18.18 to 21.55%. Moreover, the d-tryptophan passivation agent improves the device stability, which retains 86.85% of its initial efficiency under ambient conditions at room temperature after 500 h. This work provides Lewis base small-molecule d-tryptophan for efficient defect passivation of the grain boundaries toward efficient and stable PSCs

sj-xls-4-tam-10.1177_17588359211070643 – Supplemental material for Mutational landscape of circulating tumor DNA identifies distinct molecular features associated with therapeutic response in patients with metastatic colorectal cancer

sj-xls-4-tam-10.1177_17588359211070643 for Mutational landscape of circulating tumor DNA identifies distinct molecular features associated with therapeutic response in patients with metastatic colorectal cancer by Min Shi, Hong Yuan, Jun Ji, Shouwei Zhang, Qingyuan Li, Yawei Chen, Xiaoli Gong, Zhenggang Zhu and Jun Zhang in Therapeutic Advances in Medical Oncology</p