Winter forest soil respiration controlled by climate and microbial community composition

Most terrestrial carbon sequestration at mid-latitudes in the Northern Hemisphere occurs in seasonal, montane forest ecosystems. Winter respiratory carbon dioxide losses from these ecosystems are high, and over half of the carbon assimilated by photosynthesis in the summer can be lost the following winter. The amount of winter carbon dioxide loss is potentially susceptible to changes in the depth of the snowpack; a shallower snowpack has less insulation potential, causing colder soil temperatures and potentially lower soil respiration rates. Recent climate analyses have shown widespread declines in the winter snowpack of mountain ecosystems in the western USA and Europe that are coupled to positive temperature anomalies. Here we study the effect of changes in snow cover on soil carbon cycling within the context of natural climate variation. We use a six-year record of net ecosystem carbon dioxide exchange in a subalpine forest to show that years with a reduced winter snowpack are accompanied by significantly lower rates of soil respiration. Furthermore, we show that the cause of the high sensitivity of soil respiration rate to changes in snow depth is a unique soil microbial community that exhibits exponential growth and high rates of substrate utilization at the cold temperatures that exist beneath the snow. Our observations suggest that a warmer climate may change soil carbon sequestration rates in forest ecosystems owing to changes in the depth of the insulating snow cover.     

Melatonin,mitochondria, and the skin

The skin being a protective barrier between external and internal (body) environments has the sensory and adaptive capacity to maintain local and global body homeostasis in response to noxious factors. An important part of the skin response to stress is its ability for melatonin synthesis and subsequent metabolism through the indolic and kynuric pathways. Indeed, melatonin and its metabolites have emerged as indispensable for physiological skin functions and for effective protection of a cutaneous homeostasis from hostile environmental factors. Moreover, they attenuate the pathological processes including carcinogenesis and other hyperproliferative/inflammatory conditions. Interestingly, mitochondria appear to be a central hub of melatonin metabolism in the skin cells. Furthermore, substantial evidence has accumulated on the protective role of the melatonin against ultraviolet radiation and the attendant mitochondrial dysfunction. Melatonin and its metabolites appear to have a modulatory impact on mitochondrion redox and bioenergetic homeostasis, as well as the anti-apoptotic effects. Of note, some metabolites exhibit even greater impact than melatonin alone. Herein, we emphasize that melatonin–mitochondria axis would control integumental functions designed to protect local and perhaps global homeostasis. Given the phylogenetic origin and primordial actions of melatonin, we propose that the melatonin-related mitochondrial functions represent an evolutionary conserved mechanism involved in cellular adaptive response to skin injury and repair.     

Differential molecular regulation of processing and membrane expression of Type-I BMP receptors: implications for signaling

The Type-I bone morphogenetic protein receptors (BMPRs), BMPR1A and BMPR1B, present the highest sequence homology among BMPRs, suggestive of functional similitude. However, sequence elements within their extracellular domain, such as signal sequence or N-glycosylation motifs, may result in differential regulation of biosynthetic processing and trafficking and in alterations to receptor function. We show that (i) BMPR1A and the ubiquitous isoform of BMPR1B differed in mode of translocation into the endoplasmic reticulum; and (ii) BMPR1A was N-glycosylated while BMPR1B was not, resulting in greater efficiency of processing and plasma membrane expression of BMPR1A. We further demonstrated the importance of BMPR1A expression and glycosylation in ES-2 ovarian cancer cells, where (i) CRISPR/Cas9-mediated knockout of BMPR1A abrogated BMP2-induced Smad1/5/8 phosphorylation and reduced proliferation of ES-2 cells and (ii) inhibition of N-glycosylation by site-directed mutagenesis, or by tunicamycin or 2-deoxy-d-glucose treatments, reduced biosynthetic processing and plasma membrane expression of BMPR1A and BMP2-induced Smad1/5/8 phosphorylation.     

Micrometre-scale silicon electro-optic modulator

Metal interconnections are expected to become the limiting factor for the performance of electronic systems as transistors continue to shrink in size. Replacing them by optical interconnections, at different levels ranging from rack-to-rack down to chip-to-chip and intra-chip interconnections, could provide the low power dissipation, low latencies and high bandwidths that are needed. The implementation of optical interconnections relies on the development of micro-optical devices that are integrated with the microelectronics on chips. Recent demonstrations of silicon low-loss waveguides, light emitters, amplifiers and lasers approach this goal, but a small silicon electro-optic modulator with a size small enough for chip-scale integration has not yet been demonstrated. Here we experimentally demonstrate a high-speed electro-optical modulator in compact silicon structures. The modulator is based on a resonant light-confining structure that enhances the sensitivity of light to small changes in refractive index of the silicon and also enables high-speed operation. The modulator is 12 micrometres in diameter, three orders of magnitude smaller than previously demonstrated. Electro-optic modulators are one of the most critical components in optoelectronic integration, and decreasing their size may enable novel chip architectures.     

集成光子学

光通讯的优势在于纳米波导结构和新材料及结构的耦合，本书主要介绍集成光子学这一主题，侧重介绍了光波导和数值模拟技术，内容包括电磁理论的基本原理、波导、波导模式的模拟和光子结构。     

F#-Time, Functions and Processes: Towards Sustainable Investment Risk Benchmarks

‘I made a mistake’: Alan Greenspan (Financial Times: Alan Beattie and James Politi: Washington, 23rd October 2008). Such are the words of great men, for even in troubled times their self-effacing manner provides useful guidance. Whilst Mr Greenspan may feel this way, he is a product of his environment, one that has seen the cumulative development of financial instruments and strategies that have not been thought through as to their impact on a complex economy. Mainly this is because risk is thought to be discrete and the methods used to price it are flawed. To an engineer the control of a machine is built-in. Although the economy is not a machine, but an intensely connected complex of ever emerging businesses, the process of control needs to be structured in a similar manner. Pricing investment risk in this environment should never have been left to opaque institutions, or processes that do not recognise the co-dependencies of business and systemic functionality. To do so is to ignore the correlation of events in a highly connected world. These events are dynamic and conditional, whose outturns are unknowable. This does not mean unmanageable, but that the control process be built-in to businesses and government in a consistent manner, transparent yet using different parameters. Transparent means that data, assumptions and processes need to be monitored and published in timely manner. As far as accounting for results is concerned it should be recognised that budgeting and reporting to investors is founded on dynamic processes that are therefore changeable; usually out of date; and co-dependent upon others within a complex dynamic network that is both internal and external to the business. The works of Stafford Beer (Brain of the Firm, Heart of the Enterprise, Diagnosing the System) Fredrick Vestor (The Art of Interconnected Thinking) and others are examples of how to manage the internal dynamics of a business and point to a methodology that synthesises the approaches of investors such as Warren Buffett so that extreme outcomes such as the Credit-Crunch 2008 can be reduced in frequency but investors are free to ‘take their risks’. This research aims to compare two extreme events in the financial arena, the ‘Reinsurance Spiral of the late 1980s’ and the ‘2008 Credit-Crunch’, show their commonalities and propose methods that supply liquidity in all but gross systemic failure and allow investment risk to be more ably assessed and priced. It is not meant to be an exhaustive analysis but one focused on how ignoring the proper relationship of time, functions and processes brought about the current problem in both insurance and the capital markets and how a solution may be found. This research note offers an overview on the ongoing PhD research on the topic.