The Roadmap of 2D Materials and Devices Toward Chips.

Due to the constraints imposed by physical effects and performance degradation, silicon-based chip technology is facing certain limitations in sustaining the advancement of Moore's law. Two-dimensional (2D) materials have emerged as highly promising candidates for the post-Moore era, offering significant potential in domains such as integrated circuits and next-generation computing. Here, in this review, the progress of 2D semiconductors in process engineering and various electronic applications are summarized. A careful introduction of material synthesis, transistor engineering focused on device configuration, dielectric engineering, contact engineering, and material integration are given first. Then 2D transistors for certain electronic applications including digital and analog circuits, heterogeneous integration chips, and sensing circuits are discussed. Moreover, several promising applications (artificial intelligence chips and quantum chips) based on specific mechanism devices are introduced. Finally, the challenges for 2D materials encountered in achieving circuit-level or system-level applications are analyzed, and potential development pathways or roadmaps are further speculated and outlooked.

[Mutation and Clinical Feature of IL-7R in Adult Patients with Acute Lymphoblastic Leukemia].

OBJECTIVE: To investigate the IL-7R gene mutation and clinical features of adult patients with acute lymphoblastic leukemia (ALL). METHODS: One hundred sixty-four cases of newly treated adults with ALL from May 2016 to December 2018 were selected. Targeted and specific next-generation sequencing technology was used to detected a total of 16 types of Ph-like ALL mutations, which include IL-7R mutation, and the cilinical features, rate, types and sites of IL-7R were analyzed. RESULTS: IL-7R mutation was determined in 10 cases of 164 adult patients with ALL and the total mutation frequency was 13 times (6.1%). Out of 10 cases 5 cases were male (50%), 5 cases were female (50%). 6 cases of B-ALL ( 60% ) and 4 cases of T-ALL (40%). The mutation site of all cases was located at exon 6, among which 6 cases had replacement mutations, 3 cases had deletion mutations and 4 cases had insertion mutations. In addition, 1 triple and 1 double mutation of IL-7R were found. Besides, six mutation sites were newly identified, including: c.720_724del, c.723_726del, c.721_722insAGTG, c.727_728insTAACGGCCCCCTGCT, c.727_728insATGCAGGGAGCGAA and c.728_729insAAGTGTCA. CONCLUSION: Six novel mutation sites and a poor manifestation of IL-7R have been explored in this research. Thus more samples are required to study the effects of IL-7R mutation on ALL treatment.

TGF-beta driven lung fibrosis is macrophage dependent and blocked by Serum amyloid P.

The pleiotropic growth factor TGFß(1) promotes many of the pathogenic mechanisms observed in lung fibrosis and airway remodeling, such as aberrant extracellular matrix deposition due to both fibroblast activation and fibroblast to myofibroblast differentiation. Serum amyloid P (SAP), a member of the pentraxin family of proteins inhibits bleomycin-induced lung fibrosis through an inhibition of pulmonary fibrocyte and pro-fibrotic alternative (M2) macrophage accumulation. It is unknown if SAP has effects downstream of TGFß(1), a major mediator of pulmonary fibrosis. Using the lung specific TGFß(1) transgenic mouse model, we determined that SAP inhibits all of the pathologies driven by TGFß(1) including apoptosis, airway inflammation, pulmonary fibrocyte accumulation and collagen deposition, without affecting levels of TGFß(1). To explore the role of monocyte derived cells in this model we used liposomal clodronate to deplete pulmonary macrophages. This led to pronounced anti-fibrotic effects that were independent of fibrocyte accumulation. Administration of SAP mirrored these effects and reduced both pulmonary M2 macrophages and increased chemokine IP10/CXCL10 expression in a SMAD 3-independent manner. Interestingly, SAP concentrations were reduced in the circulation of IPF patients and correlated with disease severity. Last, SAP directly inhibited M2 macrophage differentiation of monocytes obtained from these patients. These data suggest that the beneficial anti-fibrotic effects of SAP in TGFß(1)-induced lung disease are via modulating monocyte responses.