During the past few years, natural disasters, political or social unrest and institutional actions have imperiled herbaria. The question has been raised multiple times whether or not the data gathered about herbaria in Index Herbariorum could be used to predict which herbaria are at the greatest risk. Armed with such knowledge curators and the greater collections community might be in a better position to safeguard those herbaria. To explore the feasibility of using Index Herbariorum data in this way, we have identified a set of specific threats and then scored herbaria according to their susceptibility to those threats. These threats fall into two categories: Physical and Administrative. Physical threats are those that could lead to loss of collections through outright destruction due to catastrophic events (e.g., earthquake, flood) or loss of the protective controls (e.g., air conditioning, building security) that ensure a safe collections environment. Determination of these threats is based on location.Administrative threats involve decisions made by the governing body to remove staff support, appropriate space or climate control measures for the collection. Physical threats were determined using GIS to plot the location of all herbaria, and then overlaying these with map layers indicating current earthquakes, floods, cyclones and landslides and potential future threats (sea level rise and civil unrest). We deduced Administrative threats from Index Herbariorum data elements. These include the status of the herbarium (active or inactive), whether or not the Index Herbariorum entry for an institution has been updated ‡ ‡ ‡

Chronic intermittent hypoxia (CIH) is a hallmark of sleep apnoea, a condition associated with diverse clinical disorders. CIH and sleep apnoea are characterized by increased reactive oxygen species formation, peripheral and CNS inflammation, neuronal death and neurocognitive deficits. Few studies have examined the role of microglia, the resident CNS immune cells, in models of CIH. Thus, little is known concerning their direct contributions to neuropathology or the cellular mechanisms regulating their activities during or following pathological CIH. In this review, we identify gaps in knowledge regarding CIH-induced microglial activation, and propose mechanisms based on data from related models of hypoxia and/or hypoxia-reoxygenation. CIH Abstract figure legend Putative mechanisms whereby CIH may contribute to CNS inflammation. Schematic diagram depicting three independent, but interacting, mechanisms of CIH-induced inflammation and neuropathology, and potential interactions between them. CIH increases reactive oxygen species with subsequent peripheral inflammation (1), neuronal injury (2) and microglial activation (3). Peripheral inflammation can cause CNS inflammation via diffusion of inflammatory molecules across an intact or compromised blood-brain barrier (BBB), and/or via vagal afferent neuron activation leading to secondary inflammation in the CNS, and pro-inflammatory microglial activities (A). Peripheral inflammation can induce neuronal injury or cell death by similar mechanisms (B), and/or by microglial production of pro-inflammatory or neurotoxic molecules (C). Neuron-microglial communication propagates neuroinflammation with damaged neurons or glia releasing damage-associated molecular patterns (DAMPs) into the extracellular space where they elicit microglial inflammatory activities via activation of pattern recognition receptors (e.g. Toll-like receptors) or scavenger receptors (D).

Despite the absence of official guidelines, many physicians with a focus on pregnancy and rheumatic disease have developed similar patterns in the screening, prevention and treatment of CHB.

This new program, which serves a population known to be at very high risk for early pregnancy, appears to be effective at reducing rates of pregnancy and improving several pregnancy-related risk behaviors.