海南植物增补（三）

本文继续报道海南岛新记录的植物,计24个新记录种,4个新记录属。1个新记录科,其中指叶瓶蕨在我国是首次发现。本文引用的标本,全部收藏在中国科学院华南植物研究所标本室(SCBI)。     

成年去胸腺大鼠和老年大鼠肝微粒体混合功能氧化酶及血浆性激素水平的变化

成年去胸腺(ATx)大鼠和老年大鼠肝微粒体混合功能氧化酶(MFO,包括细胞色素P450、氨基比林-N-脱甲基酶)的活力比成年对照大鼠的低,且降低幅度雄性明显大于雌性。雄性ATx大鼠和老年大鼠血浆睾酮(T)水平降低,雌二醇(E_2)水平增高,E_2/T比值明显增高;雌性ATx大鼠和老年大鼠血浆E_2和T水平均降低,E_2/T比值无明显变化。给雄性ATx大鼠皮下注射丙酸睾丸素可使其肝微粒体MFO活力恢复。提示胸腺对肝脏MFO的影响可能是通过性激素介导的。     

Phosphorylation-dependent regulation of phospholipase A2 by G-proteins and Ca2+ in HL60 granulocytes.

We studied the regulation of arachidonic acid (AA) release by guanosine 5'-O-(3-thiotriphosphate (GTP gamma S) and Ca2+ in electropermeabilized HL60 granulocytes. Stimulation of AA release by GTP gamma S and Ca2+ was mediated by phospholipase A2 (PLA2) and required the presence of MgATP (EC50: 100-250 microM). The nucleotide effects were Ca(2+)-dependent (maximal effects detected at 1 microM free cation). UTP and ATP gamma S, which stimulate AA release in intact HL60 granulocytes with potencies and efficacies similar to those of ATP, were ineffective in supporting the effects of GTP gamma S in electropermeabilized cells. Pretreatment with pertussis toxin affected stimulation of AA release by ATP in intact cell, without altering the nucleotide effects in permeabilized cells. We observed the protein kinase C-dependent phosphorylation of PLA2 in permeabilized HL60 granulocytes, together with a correlation between the effects of phorbol esters and staurosporine on this reaction and on AA release. ATP-independent activation of PLA2 by GTP gamma S and/or Ca2+ was measured in subcellular fractions prepared from HL60 granulocytes. These data appear consistent with a model in which PLA2 activity in resting HL60 granulocytes is subjected to an inhibitory constraint that prevents its activation by Ca2+ and G-proteins. Removal of this constraint, either by the protein kinase C-dependent phosphorylation of the enzyme in vivo or physical disruption of the regulatory assembly (e.g. by N2 cavitation), allows its activation by Ca2+ and G-proteins.     

Monte Carlo studies of a model for lipid-gramicidin A bilayers.

This paper presents results of Monte Carlo simulations of a full bilayer of 200 lipid chains and one gramicidin A dimer. Simulations are described for systems with lipid chains of 14, 16, and 18 carbons, respectively. Using accepted potential functions to calculate interactions between all non-hydrogen atoms a Monte Carlo configuration sampling is generated from which order parameter profiles are calculated and specific configurations are displayed. Results are compared with experimental data for lipid-gramicidin bilayers.     

Production of MUC1 and MUC2 mucins by human tumor cell lines.

A mucus secreting, clonal derivative (HT29-SB) of the human colonic adenocarcinoma cell line HT29, and the LS174T colon cancer cell line, secrete mucin into the culture medium as a viscoelastic gel. Mab BC2, which defines a peptide epitope present in the variable number of tandem repeats (VNTR) of the MUC1 core protein, reacted with this material after deglycosylation. Two high molecular weight bands were detected in TFMSA treated gel-formed mucin from HT29-SB and LS174T by western blotting (Mr 580 kDa and 420 kDa). A similar pattern of reactivity was seen with the culture supernatants from HT29-SB, the ovarian tumor cell line COLO-316, and the breast cancer cell line MCF-7. Mab CCP58 (anti-MUC2 VNTR) reacted with a 580 kDa band in gel-formed mucin produced by LS174T, but was not reactive with mucin produced by the other cell lines. The findings indicate that human colonic cell lines, in addition to breast and ovarian cell lines, may both express and secrete the MUC1 protein core, and that the LS174T cell line expresses and secretes both the MUC1 and MUC2 core proteins.     

Circ_0008542 in osteoblast exosomes promotes osteoclast-induced bone resorption through m6A methylation

With an increasing aging society, China is the world’s fastest growing markets for oral implants. Compared with traditional oral implants, immediate implants cause marginal bone resorption and increase the failure rate of osseointegration, but the mechanism is still unknown. Therefore, it is important to further study mechanisms of tension stimulus on osteoblasts and osteoclasts at the early stage of osseointegration to promote rapid osseointegration around oral implants. The results showed that exosomes containing circ_0008542 from MC3T3-E1 cells with prolonged tensile stimulation promoted osteoclast differentiation and bone resorption. Circ_0008542 upregulated Tnfrsf11a (RANK) gene expression by acting as a miR-185-5p sponge. Meanwhile, the circ_0008542 1916-1992 bp segment exhibited increased m6A methylation levels. Inhibiting the RNA methyltransferase METTL3 or overexpressing the RNA demethylase ALKBH5 reversed osteoclast differentiation and bone resorption induced by circ_0008542. Injection of circ_0008542 + ALKBH5 into the tail vein of mice reversed the same effects in vivo. Site-directed mutagenesis study demonstrated that 1956 bp on circ_0008542 is the m6A functional site with the abovementioned biological functions. In conclusion, the RNA methylase METTL3 acts on the m6A functional site of 1956 bp in circ_0008542, promoting competitive binding of miRNA-185-5p by circ_0008542, and leading to an increase in the target gene RANK and the initiation of osteoclast bone absorption. In contrast, the RNA demethylase ALKBH5 inhibits the binding of circ_0008542 with miRNA-185-5p to correct the bone resorption process. The potential value of this study provides methods to enhance the resistance of immediate implants through use of exosomes releasing ALKBH5.Subject terms: Epigenetics, Predictive markers     

Chronic Exposure to Diquat Causes Reproductive Toxicity in Female Mice

Diquat is a bipyridyl herbicide that has been widely used as a model chemical for in vivo studies of oxidative stress due to its generation of superoxide anions, and cytotoxic effects. There is little information regarding the toxic effects of diquat on the female reproductive system, particularly ovarian function. Thus, we investigated the reproductive toxic effects of diquat on female mice. Chronic exposure to diquat reduced ovary weights, induced ovarian oxidative stress, resulted in granulosa cell apoptosis, and disrupted oocyte developmental competence, as shown by reactive oxygen species (ROS) accumulation, decreased polar body extrusion rates and increased apoptosis-related genes expression. Additionally, after diquat treatment, the numbers of fetal mice and litter sizes were significantly reduced compared to those of control mice. Thus, our results indicated that chronic exposure to diquat induced reproductive toxicity in female mice by promoting the ROS production of gruanousa cells and ooctyes, impairing follicle development, inducing apoptosis, and reducing oocyte quality. In conclusion, our findings indicate that diquat can be used as a potent and efficient chemical for in vivo studies of female reproductive toxicity induced by oxidative stress. Moreover, the findings from this study will further enlarge imitative research investigating the effect of ovarian damage induced by oxidative stress on reproductive performance and possible mechanisms of action in large domestic animals.