[1] The existence of gas-phase ammonia (NH 3 ) in the atmosphere and its interaction with other trace chemical species could have a substantial impact on tropospheric chemistry and global climate change. China is a large agricultural country with an enormous animal population, tremendous nitrogen fertilizer consumption and, consequently, a large emission of NH 3 . Despite the importance of NH 3 in the global nitrogen (N) cycle, considerable inaccuracies and uncertainty exist regarding its emission in China. In this study, a comprehensive NH 3 emission inventory was compiled for China on a 1 km  1 km grid, which is suitable for input to atmospheric models. We attempted to estimate NH 3 emissions accurately by taking into consideration as many native experiment results as possible and parameterizing the emission factors (EFs) by the ambient temperature, soil acidity and other factors. The total NH 3 emission in China was approximately 9.8 Tg in 2006. The emission sources considered included livestock excreta (5.3 Tg), fertilizer application (3.2 Tg), agricultural soil (0.2 Tg), nitrogen-fixing plants (0.05 Tg), crop residue compost (0.3 Tg), biomass burning (0.1 Tg), urine from rural populations (0.2 Tg), chemical industry (0.2 Tg), waste disposal (0.1 Tg) and traffic (0.1 Tg). The regions with the highest emission rates are located in Central and Southwest China. Seasonally, the peak ammonia emissions occur in spring and summer.

Endoplasmic reticulum (ER) stress is a common cellular stress response that is triggered by a variety of conditions that disturb cellular homeostasis, and induces cell apoptosis. Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis induced by ER stress. There are common upstream signaling pathways between autophagy and apoptosis induced by ER stress, including PERK/ATF4, IRE1α, ATF6, and Ca . Autophagy can not only block the induction of apoptosis by inhibiting the activation of apoptosis-associated caspase which could reduce cellular injury, but also help to induce apoptosis. In addition, the activation of apoptosis-related proteins can also inhibit autophagy by degrading autophagy-related proteins, such as Beclin-1, Atg4D, Atg3, and Atg5. Although the interactions of different autophagy- and apoptosis-related proteins, and also common upstream signaling pathways have been found, the potential regulatory mechanisms have not been clearly understood. In this review, we summarize the dual role of autophagy, and the interplay and potential regulatory mechanisms between autophagy and apoptosis under ER stress condition.

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The new type of pneumonia caused by the SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) has been declared as a global public health concern by WHO. As of April 3, 2020, more than 1,000,000 human infections have been diagnosed around the world, which exhibited apparent person-to-person transmission characteristics of this virus. The capacity of vertical transmission in SARS-CoV-2 remains controversial recently. Angiotensin-converting enzyme 2 (ACE2) is now confirmed as the receptor of SARS-CoV-2 and plays essential roles in human infection and transmission. In present study, we collected the online available single-cell RNA sequencing (scRNA-seq) data to evaluate the cell specific expression of ACE2 in maternal-fetal interface as well as in multiple fetal organs. Our results revealed that ACE2 was highly expressed in maternal-fetal interface cells including stromal cells and perivascular cells of decidua, and cytotrophoblast and syncytiotrophoblast in placenta. Meanwhile, ACE2 was also expressed in specific cell types of human fetal heart, liver and lung, but not in kidney. And in a study containing series fetal and post-natal mouse lung, we observed ACE2 was dynamically changed over the time, and ACE2 was extremely high in neonatal mice at post-natal day 1~3. In summary, this study revealed that the SARS-CoV-2 receptor was widely spread in specific cell types of maternal-fetal interface and fetal organs. And thus, both the vertical transmission and the placenta dysfunction/abortion caused by SARS-CoV-2 need to be further carefully investigated in clinical practice.