Soil nitrification, an important pathway of nitrogen transformation in ecosystems, produces soil nitrate that influences net primary productivity, while the by‐product of nitrification, nitrous oxide, is a significant greenhouse gas. Although there have been many studies addressing the microbiology, physiology, and impacting environment factors of soil nitrification at local scales, there are very few studies on soil nitrification rate over large scales. We conducted a global synthesis on the patterns and controlling factors of soil nitrification rate normalized at 25°C by compiling 3,140 observations from 186 published articles across terrestrial ecosystems. Soil nitrification rate tended to decrease with increasing latitude, especially in the Northern Hemisphere, and varied largely with ecosystem types. The soil nitrification rate significantly increased with mean annual temperature (MAT), soil nitrogen content, microbial biomass carbon and nitrogen, soil ammonium, and soil pH, but decreased with soil carbon:nitrogen and carbon:nitrogen of microbial biomass. The total soil nitrogen content contributed the most to the variations of global soil nitrification rate (total coefficient = 0.29) in structural equation models. The microbial biomass nitrogen (MBN; total coefficient = 0.19) was nearly of equivalent importance relative to MAT (total coefficient = 0.25) and soil pH (total coefficient = 0.24) in determining soil nitrification rate, while soil nitrogen and pH influenced soil nitrification via changing soil MBN. Moreover, the emission of soil nitrous oxide was positively related to soil nitrification rate at a global scale. This synthesis will advance our current understanding on the mechanisms underlying large‐scale variations of soil nitrification and benefit the biogeochemical models in simulating global nitrogen cycling.

Release of substance P (SP) from nociceptive nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transmission of pain signals. Nonetheless, the role of SP in muscle pain remains unknown. Here we show that a single i.m. acid injection in mice lacking SP signaling by deletion of the tachykinin precursor 1 (Tac1) gene or coadministration of NK1 receptor antagonists produces long-lasting hyperalgesia rather than the transient hyperalgesia seen in control animals. The inhibitory effect of SP was found exclusively in neurons expressing acid-sensing ion channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G protein-independent but tyrosine kinase-dependent manner. Furthermore, the SP signaling could alter action potential thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors. Thus, i.m. SP mediates an unconventional NK1 receptor signal pathway to inhibit acid activation in muscle nociceptors, resulting in an unexpected antinociceptive effect against chronic mechanical hyperalgesia, here induced by repeated i.m. acid injection.is an undecapeptide belonging to the tachykinin small-peptide family (1). SP is generated in primary nociceptive sensory neurons (nociceptors) and is released with noxious stimulation (2). The release from cutaneous peripheral terminals induces neurogenic inflammation and release from central terminals enhances the glutamate-dependent excitatory postsynaptic potential, thus leading to central sensitization (3-5). Although sensory neurons in muscle also contain SP, i.m. SP injection evokes a very low level of neurogenic inflammation and no pain (6, 7).Accumulating evidence has suggested that muscle pain might be closely related to acidosis and activation of proton-sensing ion channels (8-10). Lactate and ATP sensitize this acid activation (11,12). Human and animal studies have revealed that acidosis is an effective trigger of muscle pain. Thus, chronic muscle pain can be induced in rodents by repeated i.m. injection of acid (13,14), by i.m. injection of complete Freund's adjuvant (CFA), carrageenan, capsaicin, or proinflammatory cytokines (15-18), by arterial occlusion (19), and by eccentric muscle contraction (20). These stimuli might correspond to muscle pain related to acidosis, inflammatory and ischemic myalgia, or delayed-onset muscle soreness. Although these models might not reflect fully the complicated human pain conditions, and although repetitive acidosis is not known to produce chronic pain or central sensitization in humans, these rodent models are useful for probing the underlying mechanisms and analgesic modulation of chronic muscle pain. For instance, acid-sensing ion channel 3 (ASIC3) is essential for triggering acid-induced mechanical hyperalgesia in models of i.m. injection of acid, CFA, or carrageenan (13,17,(21)(22)(23). Coinjection of neurotrophin-3 reverses the acid-induced chronic hyperalgesia (24). Also, some muscle-derived pain can be attenu...

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