What is Threatening Forests in Protected Areas? A Global Assessment of Deforestation in Protected Areas, 2001-2018.

The protection of forests is crucial to providing important ecosystem services, such as supplying clean air and water, safeguarding critical habitats for biodiversity, and reducing global greenhouse gas emissions. Despite this importance, global forest loss has steadily increased in recent decades. Protected Areas (PAs) currently account for almost 15% of Earth's terrestrial surface and protect 5% of global tree cover and were developed as a principal approach to limit the impact of anthropogenic activities on natural, intact ecosystems and habitats. We assess global trends in forest loss inside and outside of PAs, and land cover following this forest loss, using a global map of tree cover loss and global maps of land cover. While forests in PAs experience loss at lower rates than non-protected forests, we find that the temporal trend of forest loss in PAs is markedly similar to that of all forest loss globally. We find that forest loss in PAs is most commonly-and increasingly-followed by shrubland, a broad category that could represent re-growing forest, agricultural fallows, or pasture lands in some regional contexts. Anthropogenic forest loss for agriculture is common in some regions, particularly in the global tropics, while wildfires, pests, and storm blowdown are a significant and consistent cause of forest loss in more northern latitudes, such as the United States, Canada, and Russia. Our study describes a process for screening tree cover loss and agriculture expansion taking place within PAs, and identification of priority targets for further site-specific assessments of threats to PAs. We illustrate an approach for more detailed assessment of forest loss in four case study PAs in Brazil, Indonesia, Democratic Republic of Congo, and the United States.

Effect of premedication to provide analgesia as a supplement to inferior alveolar nerve block in patients with irreversible pulpitis.

BACKGROUND: The authors' objective was to determine whether scientific evidence supports the use of oral premedication to increase the efficacy of inferior alveolar nerve block (IANB) and to decrease endodontic treatment pain in patients with diagnosed irreversible pulpitis. TYPES OF STUDIES REVIEWED: The authors included randomized controlled trials that involved enteral premedication and 2% lidocaine IANB for adults with irreversible pulpitis compared with placebo. In particular, the authors reviewed studies comparing nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, acetaminophen, and corticosteroids with placebo. The authors searched the following electronic databases: the Cochrane Library, MEDLINE, and Web of Science. RESULTS: The authors analyzed 9 randomized controlled clinical trials. Patients who took the NSAIDs under study, including ibuprofen, ketorolac, diclofenac, indomethacin, and lornoxicam, 1 hour before endodontic treatment showed statistically significant improvement in the outcome of having "little or no pain" during endodontic treatment compared with patients who took a placebo 1 hour before endodontic treatment (risk ratio [RR], 1.989; 95% confidence interval [CI], 1.495-2.646; P < .001). Benzodiazepines were not as well represented in the literature, but the 2 included studies did not show a significant improvement in patients' having "little or no pain" during endodontic treatment over placebo (RR, 0.989; 95% CI, 0.677-1.444; P = .954). CONCLUSIONS AND PRACTICAL IMPLICATIONS: There is moderate evidence to support the use of oral NSAIDs-in particular, ibuprofen (600 milligrams)-1 hour before the administration of IANB local anesthetic (1.8-3.6 milliliters of 2% lidocaine) to provide additional analgesia to the patient.

Risk of Ischemic Stroke after Intracranial Hemorrhage in Patients with Atrial Fibrillation.

BACKGROUND: We aimed to estimate the risk of ischemic stroke after intracranial hemorrhage in patients with atrial fibrillation. MATERIALS AND METHODS: Using discharge data from all nonfederal acute care hospitals and emergency departments in California, Florida, and New York from 2005 to 2012, we identified patients at the time of a first-recorded encounter with a diagnosis of atrial fibrillation. Ischemic stroke and intracranial hemorrhage were identified using validated diagnosis codes. Kaplan-Meier survival statistics and Cox proportional hazard analyses were used to evaluate cumulative rates of ischemic stroke and the relationship between incident intracranial hemorrhage and subsequent stroke. RESULTS: Among 2,084,735 patients with atrial fibrillation, 50,468 (2.4%) developed intracranial hemorrhage and 89,594 (4.3%) developed ischemic stroke during a mean follow-up period of 3.2 years. The 1-year cumulative rate of stroke was 8.1% (95% CI, 7.5-8.7%) after intracerebral hemorrhage, 3.9% (95% CI, 3.5-4.3%) after subdural hemorrhage, and 2.0% (95% CI, 2.0-2.1%) in those without intracranial hemorrhage. After adjustment for the CHA2DS2-VASc score, stroke risk was elevated after both intracerebral hemorrhage (hazard ratio [HR], 2.8; 95% CI, 2.6-2.9) and subdural hemorrhage (HR, 1.6; 95% CI, 1.5-1.7). Cumulative 1-year rates of stroke ranged from 0.9% in those with subdural hemorrhage and a CHA2DS2-VASc score of 0, to 33.3% in those with intracerebral hemorrhage and a CHA2DS2-VASc score of 9. CONCLUSIONS: In a large, heterogeneous cohort, patients with atrial fibrillation faced a substantially heightened risk of ischemic stroke after intracranial hemorrhage. The risk was most marked in those with intracerebral hemorrhage and high CHA2DS2-VASc scores.