Cost-reduction innovation under mixed economy

Industries with mixed oligopoly are exceedingly popular all over the world, especially in developing countries, such as China. This paper highlights the innovation strategies of mixed duopoly with a (semi-) public firm and another private firm, and the effects of mixed oligopoly on innovation are captured. Firstly, the (semi-) public firm innovates more and produces more than the private firm. Secondly, the degree of the public ownership stimulates the output and innovation. Finally, the price difference and the price dispersion all increase with the degree of the public ownership under independent goods

R&D subsidies under asymmetric Cournot competition

With a three-stage game model, this article theoretically assesses the effectiveness of different research and development subsidy strategies under asymmetric duopoly. The findings indicate that subsidising the small firm instead of the large is the optimum for the maximisation of social welfare in general. Meanwhile, if the initial marginal costs of the two firms are close to each other, providing subsidies to the small firm leads to more social R&D investment and higher aggregate production, but lower consumer surplus. Conversely, while the cost gap of the duopoly is large, subsidising the big firm becomes the preferable option for the authority to stimulate both R&D investment and total output of the industry, while sacrificing consumer surplus

Functionalized nido-C4B2, closo-C2B5 and -C2B10 Carboranes, and Reactivity Studies on Electron-Poor 2,3-Dihydro-1,3-diborolyl Complexes of Ruthenium

The dissertation describes work on organoborane/carborane compounds (Chapters 3.1, 3.2, 3.3, 3.5), on the reactivity of 2,3-dihydro-1,3-diborolyl complexes of ruthenium (3.4), and on aminoborane derivatives (3.6). In Chapter 3.1, a one-pot synthesis of 1,6-diiodo-2,3,4,5-tetracarba-nido-hexaborane(6) derivatives (nido-(RC)4(BI)2, R = Et, Me, Ph, 5a-c) is reported, involving disubstituted alkynes and BI3 (in 1:1 ratio) and NaK2.8 at low temperature. Whereas the reaction of 3-hexyne, BI3 (2 equiv.) and NaK2.8 at r.t. affords a mixture of 5a, nido-(EtC)4(BI)4 (4) and closo-(EtC)2(BI)5 (6). A possible mechanism of the formation of 5a is proposed and studied. The reactivity of 5a towards various nucleophiles has been investigated. In most cases, the substitution occurs regiospecifically at the basal boron atom. Replacement of the ‘inert’ apical iodine is realized by a Pd(0)-catalyzed Negishi-type cross-coupling, as demonstrated by the synthesis of apically alkynyl-substituted nido-(RC)4(BC2Ph)(BC2R) (R = SiMe3, Ph, 5q,r). A series of linked clusters with different types of linkages (via B–C bond, a C6H4C6H4 unit, a C2(CH2)4C2 unit, and an oxygen atom) are obtained. In Chapter 3.2, treatment of the nido-2,3-Et2C2B4H42- dianion with the reagents BX3 (X = Br, I) and PhC2Bcat lead to apically functionalized closo-1-R-2,3-Et2C2B5H4 derivatives (19a-c). A more efficient pathway is developed by the Pd-catalyzed cross-coupling reactions of 19b with R’C2ZnCl to give closo-1-C2R’-2,3-Et2C2B5H4 (R’ = SiMe3, Me, tBu, 19d-f). The reac- tions of the carboranyl-acetylenes with Co2(CO)8 and CpCo(C2H4)2, respectively, afford dicobaltatetrahedrane compounds 21c,d and CpCo(cyclobutadiene) complex 23. In Chapter 3.3, a series of C-boryl-o-carborane derivatives are reported by reacting dilithio-o-carborane and the corresponding aminochloroboranes, respectively. In Chapter 3.5, the unprecedented transformation of 1,3-diiodo-1,3-diborole 37d into the known 2,3,4,5,6-pentacarba-nido- hexaborane(6) cation (63+) is observed. A possible mechanism for its formation is proposed. In Chapter 3.4, the long-sought crystal structure of the (pentamethylcyclopentadienyl)(2,3-dihydro-1,3-diborolyl)-ruthenium derivative 35b is described. It finally confirms the folding along the B…B vector (40.7º) which is similar to the iron analog (41.3º). DFT calculations (by Dr. I. Hyla-Kryspin) on the electronic structures of the model sandwiches Ru (35) and Fe (36) indicate that the folding of the 1,3-diborolyl ligands is of electronic origin, and the parent compounds 35 and 36 with a folded 1,3-diborolyl ligand are more stable in energy (24.5 and 24.9 kcal/mol for Ru and Fe structures, respectively) than 35’ and 36’ with a planar ligand. The reactivity of 35 is studied with respect to insertion of terminal alkynes into its C3B2 heterocycle which results in novel 18 VE ruthenocene analogs Cp*Ru(C5B2) (38) with seven-membered 4-borataborepines as ligands. Additionally, boratabenzene complexes 39 and triarylbenzene species (in some cases) are identified as byproducts, the formation of 39 is a result of elimination of one boranediyl moiety [:BR2] from the intermediate 4-borataborepine complexes. The 4-borataborepine functions as 6e ligand and exhibits a reduced folding along the B…B vector (folding angle = 12.5º in 38a, 26º in 38b, and 15.2º in 38c) compared with 40.7º in 35b. The boratabenzene complexes 39f,g are formed as the main products in the reactions of 35a and disubstituted alkynes (3-hexyne and di-p-tolylacetylene, respectively). The comparative study on the reactivity of the [(1,3-diborole)RhCl]2 dimer 48 with PhCH2C2H is carried out, in which the cyclotrimerization occurs to give (1,3-diborolyl)Rh(arene) 49. The complex reaction of 35a with allylchloride in hexane affords a mixture of products, one is the novel complex 58 [Cp*Ru(C3B2Me5)(RuCp*)n] (n > = 2). Its identity and formation mechanism are not yet clear, however, the results from MS studies and two independent but only partially solved X-ray diffraction analyses indicate that it has a stack of ruthenium atoms with bridging Cp* and 1,3-diborolyl ligands. The stacks are along a threefold axis which would be consistent with either extensive disorder or a tripling of the crystals. In Chapter 3.6, the reactivity of (Me2N)2B4[B(NMe2)2]2 (70) with a rhombohedral B4 unit is studied, and some pyrrolidinoborane derivatives are prepared for new cyclo or polyhedral boranes

Surface Roughness Gradients Reveal Topography‐Specific Mechanosensitive Responses in Human Mesenchymal Stem Cells

The topographic features of an implant, which mechanically regulate cell behaviors and functions, are critical for the clinical success in tissue regeneration. How cells sense and respond to the topographical cues, e.g., interfacial roughness, is yet to be fully understood and even debatable. Here, the mechanotransduction and fate determination of human mesenchymal stem cells (MSCs) on surface roughness gradients are systematically studied. The broad range of topographical scales and high‐throughput imaging is achieved based on a catecholic polyglycerol coating fabricated by a one‐step‐tilted dip‐coating approach. It is revealed that the adhesion of MSCs is biphasically regulated by interfacial roughness. The cell mechanotransduction is investigated from focal adhesion to transcriptional activity, which explains that cellular response to interfacial roughness undergoes a direct force‐dependent mechanism. Moreover, the optimized roughness for promoting cell fate specification is explored

CyFormer: Accurate State-of-Health Prediction of Lithium-Ion Batteries via Cyclic Attention

Predicting the State-of-Health (SoH) of lithium-ion batteries is a fundamental task of battery management systems on electric vehicles. It aims at estimating future SoH based on historical aging data. Most existing deep learning methods rely on filter-based feature extractors (e.g., CNN or Kalman filters) and recurrent time sequence models. Though efficient, they generally ignore cyclic features and the domain gap between training and testing batteries. To address this problem, we present CyFormer, a transformer-based cyclic time sequence model for SoH prediction. Instead of the conventional CNN-RNN structure, we adopt an encoder-decoder architecture. In the encoder, row-wise and column-wise attention blocks effectively capture intra-cycle and inter-cycle connections and extract cyclic features. In the decoder, the SoH queries cross-attend to these features to form the final predictions. We further utilize a transfer learning strategy to narrow the domain gap between the training and testing set. To be specific, we use fine-tuning to shift the model to a target working condition. Finally, we made our model more efficient by pruning. The experiment shows that our method attains an MAE of 0.75\% with only 10\% data for fine-tuning on a testing battery, surpassing prior methods by a large margin. Effective and robust, our method provides a potential solution for all cyclic time sequence prediction tasks

Promotion of tumor development in prostate cancer by progerin

Progerin is a truncated form of lamin A. It is identified in patients with Hutchinson-Gilford progeria syndrome (HGPS), a disease characterized by accelerated aging. The contribution of progerin toward aging has been shown to be related to increased DNA damages. Since aging is one major risk factor for carcinogenesis, and genomic instability is a hallmark of malignant cancers, we investigated the expression of progerin in human cancer cells, and whether its expression contributes to carcinogenesis. Using RT-PCR and Western blotting, we detected the expression of progerin in prostate PC-3, DU145 and LNCaP cells at mRNA and protein levels. Ectopic progerin expression did not cause cellular senescence in PC-3 or MCF7 cells. PC-3 cells progerin transfectants were sensitized to DNA damage agent camptothecin (CPT); and persistent DNA damage responses were observed, which might be caused by progerin induced defective DNA damage repair. In addition, progerin transfectants were more tumorigenic in vivo than vector control cells. Our study for the first time describes the expression of progerin in a number of human cancer cell lines and its contributory role in tumorigenesis

CXCR4 is required for the quiescence of primitive hematopoietic cells

The quiescence of hematopoietic stem cells (HSCs) is critical for preserving a lifelong steady pool of HSCs to sustain the highly regenerative hematopoietic system. It is thought that specialized niches in which HSCs reside control the balance between HSC quiescence and self-renewal, yet little is known about the extrinsic signals provided by the niche and how these niche signals regulate such a balance. We report that CXCL12 produced by bone marrow (BM) stromal cells is not only the major chemoattractant for HSCs but also a regulatory factor that controls the quiescence of primitive hematopoietic cells. Addition of CXCL12 into the culture inhibits entry of primitive hematopoietic cells into the cell cycle, and inactivation of its receptor CXCR4 in HSCs causes excessive HSC proliferation. Notably, the hyperproliferative Cxcr4−/− HSCs are able to maintain a stable stem cell compartment and sustain hematopoiesis. Thus, we propose that CXCR4/CXCL12 signaling is essential to confine HSCs in the proper niche and controls their proliferation