High Polarity Poly(vinylidene difluoride) Thin Coating for Dendrite‐Free and High‐Performance Lithium Metal Anodes

The high‐polarity β‐phase poly(vinylidene difluoride) (β‐PVDF), which has all trans conformation with F and H atoms located on the opposite sides of the polymer backbone, is demonstrated to be a promising artificial solid‐electrolyte interphase coating on both Cu and Li metal anodes for dendrite‐free Li deposition/stripping and enhanced cycling performance. A thin (≈4 µm) β‐PVDF coating on Cu enables uniform Li deposition/stripping at high current densities up to 5 mA cm^?2, Li‐plating capacity loadings of up to 4 mAh cm^?2, and excellent cycling stability over hundreds of cycles under practical conditions (1 mA cm^?2 with 2 mAh cm^?2). Full cells containing an LiFePO₄ cathode and an anode of either β‐PVDF coated Cu or Li also exhibit excellent cycling stability. The profound effects of the high‐polarity PVDF coating on dendrite suppression are attributed to the electronegative F‐rich interface that favors layer‐by‐layer Li deposition. This study offers a new strategy for the development of dendrite‐free metal anode technology.     

高陵土性狀的檢定

高陵土一名高嶺土,就是陶土,俗名白土子。主要成份为含水矽酸鋁(OH)_8Al_4 Si_4 O_(10)。由風化长石及石英二部分构成。盛产我国,瓷器原料。工业上用作填充剂的也很多。最近合成杀蟲剂应用方面又用牠来作稀释剂。本文的目的就在把高陵土主要的性状作一个檢定,以便明瞭牠的优点和缺点。     

用苏芸金杆菌孢子粉於防治玉米螟

在1953年用叶心灌药以防治玉米螟的春玉米小区试验中,作者等有意识地使用了细菌学家孟雨同志自法国带回的苏芸金杆菌孢子粉(内含孢子约1/10,余为大豆粉)。它们被稀释到1:2000,1:10000和1:20000三个等级(据孟同志谈:这个稀释量是过於低了)。     

Revision of Corallinaceae (Corallinales,Rhodophyta): recognizing Dawsoniolithon gen. nov., Parvicellularium gen. nov. and Chamberlainoideae subfam. nov. containing Chamberlainium gen. nov. and Pneophyllum

A multi‐gene (SSU, LSU, psbA, and COI) molecular phylogeny of the family Corallinaceae (excluding the subfamilies Lithophylloideae and Corallinoideae) showed a paraphyletic grouping of six monophyletic clades. Pneophyllum and Spongites were reassessed and recircumscribed using DNA sequence data integrated with morpho‐anatomical comparisons of type material and recently collected specimens. We propose Chamberlainoideae subfam. nov., including the type genus Chamberlainium gen. nov., with C. tumidum comb. nov. as the generitype, and Pneophyllum. Chamberlainium is established to include several taxa previously ascribed to Spongites, the generitype of which currently resides in Neogoniolithoideae. Additionally we propose two new genera, Dawsoniolithon gen. nov. (Metagoniolithoideae), with D. conicum comb. nov. as the generitype and Parvicellularium gen. nov. (subfamily incertae sedis), with P. leonardi sp. nov. as the generitype. Chamberlainoideae has no diagnostic morpho‐anatomical features that enable one to assign specimens to it without DNA sequence data, and it is the first subfamily to possess both Type 1 (Chamberlainium) and Type 2 (Pneophyllum) tetra/bisporangial conceptacle roof development. Two characters distinguish Chamberlainium from Spongites: tetra/biasporangial conceptacle chamber diameter (<300 μm in Chamberlainium vs. >300 μm in Spongites) and tetra/bisporangial conceptacle roof thickness (<8 cells in Chamberlainium vs. >8 cells in Spongites). Two characters also distinguish Pneophyllum from Dawsoniolithon: tetra/bisporangial conceptacle roof thickness (<8 cells in Pneophyllum vs. >8 cells in Dawsoniolithon) and thallus construction (dimerous in Pneophyllum vs. monomerous in Dawsoniolithon).     

Ca2+ Signaling and Cell Death Induced by Protriptyline in HepG2 Human Hepatoma Cells

The effect of protriptyline on Ca²⁺ physiology in human hepatoma is unclear. This study explored the effect of protriptyline on [Ca²⁺]_i and cytotoxicity in HepG2 human hepatoma cells. Protriptyline (50–150 μM) evoked [Ca²⁺]_i rises. The Ca²⁺ entry was inhibited by removal of Ca²⁺. Protriptyline‐induced Ca²⁺ entry was confirmed by Mn²⁺‐induced quench of fura‐2 fluorescence. Except nifedipine, econazole, SKF96365, GF109203X, and phorbol 12‐myristate 13 acetate did not inhibit Ca²⁺ entry. Treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5‐di‐tert‐butylhydroquinone (BHQ) inhibited 40% of protriptyline‐induced response. Treatment with protriptyline abolished BHQ‐induced response. Inhibition of phospholipase C (PLC) suppressed protriptyline‐evoked response by 70%. At 20–40 μM, protriptyline killed cells which was not reversed by the Ca²⁺ chelator 1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid‐acetoxymethyl ester (BAPTA/AM). Together, in HepG2 cells, protriptyline induced [Ca²⁺]_i rises that involved Ca²⁺ entry through nifedipine‐sensitive Ca²⁺ channels and PLC‐dependent Ca²⁺ release from endoplasmic reticulum. Protriptyline induced Ca²⁺‐independent cell death.