三种森林生物量估测模型的比较分析

森林生物量的定量估算为全球碳储量、碳循环研究提供了重要的参考依据。该研究采用黑龙江长白山地区的TM影像和133块森林资源一类清查样地的数据, 选取地学参数、遥感反演参数等71个自变量分别构建多元逐步回归模型、传统BP (back propagation)神经网络模型和基于高斯误差函数的BP神经网络改进模型(Gaussian error function, Erf-BP), 进而估算该地区的森林生物量, 并进行比较分析。结果表明, 多元逐步回归模型估测的森林生物量预测精度为75%, 均方根误差为26.87 t·m^-2; 传统BP神经网络模型估测森林生物量的预测精度为80.92%, 均方根误差为21.44 t·m^-2; Erf-BP估测森林生物量的预测精度为82.22%, 均方根误差为20.83 t·m^-2。可见, 改进后的Erf-BP能更好地模拟生物量与各个因子之间的关系, 估算精度更高。     

Identification and purification of NK cells with lysosomotropic vital stains: correlation of lysosome content with NK activity

The lysosome content of lymphocytes has been analyzed with lysosomotropic vital stains and the fluorescence-activated cell sorter (FACS). Large granular lymphocytes (LGL), which account for virtually all natural killing activity in peripheral blood, are quantitatively different from small lymphocytes (SL) in this respect. LGL obtained by Percoll gradient density centrifugation accumulate more of the lysosomotropic vital dyes than SL do, staining with either neutral red or mepacrine (quinacrine). Furthermore among the LGL-rich, low density lymphocyte population highly, granulated cells can be separated from less granulated ones by mepacrine staining and FACS. Thus, separated highly granulated LGL express very high natural killing, whereas the less granulated low density large lymphocytes do not kill.     

Suppression of lymphokine-activated killer induction by neutrophils

Peripheral blood polymorphonuclear neutrophils (PMN) suppressed the induction of PBL lymphokine-activated killer (LAK) function by rIL-2 in vitro. The suppression depended on the concentration of PMN in the IL-2 culture, and required intact PMN. However, PMN did not require treatment with immunoregulators such as IL-2, LPS, or TNF to express the suppressive activity, and no direct contact with PBL was needed for the suppression. Addition of anti-TNF antibodies had no effect on the suppression, suggesting that no endogenous TNF in the culture was involved in the suppression. PMN did not inhibit LAK function by preventing utilization of IL-2 by PBL or by selective depletion of NKH-1+ cells which constitute the majority of LAK precursors in PBL. The suppression was reversed by superoxide dismutase but not by catalase, suggesting that superoxide anion, not hydrogen peroxide, was involved in the suppression. No other suppressive factor was detectable in PMN culture supernates. Our results of PMN regulating LAK induction in vitro suggest that PMN may have a role in determining the outcome of immunotherapy with IL-2 in vivo.     

CTRP12 ameliorates atherosclerosis by promoting cholesterol efflux and inhibiting inflammatory response via the miR-155-5p/LXRα pathway

C1q tumor necrosis factor-related protein 12 (CTRP12), a conserved paralog of adiponectin, is closely associated with cardiovascular disease. However, little is known about its role in atherogenesis. The aim of this study was to examine the influence of CTRP12 on atherosclerosis and explore the underlying mechanisms. Our results showed that lentivirus-mediated CTRP12 overexpression inhibited lipid accumulation and inflammatory response in lipid-laden macrophages. Mechanistically, CTRP12 decreased miR-155-5p levels and then increased its target gene liver X receptor α (LXRα) expression, which increased ATP binding cassette transporter A1 (ABCA1)- and ABCG1-dependent cholesterol efflux and promoted macrophage polarization to the M2 phenotype. Injection of lentiviral vector expressing CTRP12 decreased atherosclerotic lesion area, elevated plasma high-density lipoprotein cholesterol levels, promoted reverse cholesterol transport (RCT), and alleviated inflammatory response in apolipoprotein E-deficient (apoE^−/−) mice fed a Western diet. Similar to the findings of in vitro experiments, CTRP12 overexpression diminished miR-155-5p levels but increased LXRα, ABCA1, and ABCG1 expression in the aortas of apoE^−/− mice. Taken together, these results suggest that CTRP12 protects against atherosclerosis by enhancing RCT efficiency and mitigating vascular inflammation via the miR-155-5p/LXRα pathway. Stimulating CTRP12 production could be a novel approach for reducing atherosclerosis.Subject terms: Non-coding RNAs, Cardiovascular diseases     

The mechanism of ageing of phosphonylated acetylcholinesterase

1. The extent of potential reactivation of organophosphate-inhibited acetylcholinesterase decreases with time, a phenomenon called ageing. Ageing is due to dealkylation of the alkoxyl group of the residue bound to the enzyme. The rate of ageing is proportional to the electron-donating capacity of the alkyl group. 2. The ageing of phosphophonylated cholinesterase cal also be demonstrated using a phrenic nerve-diaphragm preparation. The same relationship between the rate of ageing and the structure of the alkyl group was observed. 3. Ageing occurs much faster in electrically stimulated preparations than in resting preparations. This may be due to production of a more acidic environment for the enzyme at the active centre by the products of hydrolysis of the acetylcholine released by stimulation.