Assessing the accuracy of free automated plant identification applications

1. Widely available and inexpensive mobile phone applications offer users, whether professional ecologists or interested amateurs, the potential for simple and rapid automated identification of species, without the need to use field guides and identification keys. The increasing accuracy of machine learning is well established, but it is currently unclear if, and under what circumstances, free-to-use mobile phone applications are accurate for identifying plants to species level in real-world field conditions. 2. We test five popular and free identification applications for plants using 857 professionally identified images of 277 species from 204 genera. Across all applications, 85% of images were identified correctly in the top five suggestions, and 69% were correct with the first suggestion. Plant type (woody, forbs, grasses, rushes/sedges, ferns/horsetails) was a significant determinant of identification performance for each application. For some applications, image saliency was also important; exposure and focus were not significant. 3. Applications performed well, with at least one of the three best-performing applications identifying 96% of images correctly as their first suggestion. We conclude that, subject to some caveats, free phone-based plant identification applications are valid and useful tools for those wanting rapid identification and for anyone wanting to engage with the natural world

ATP Release from Vascular Endothelia Occurs Across Cx43 Hemichannels and Is Attenuated during Hypoxia

Background: Extracellular ATP is an important signaling molecule for vascular adaptation to limited oxygen availability (hypoxia). Here, we pursued the contribution of vascular endothelia to extracellular ATP release under hypoxic conditions. Methodology, Principal Findings: We gained first insight from studying ATP release from endothelia (HMEC-1) pre-exposed to hypoxia. Surprisingly, we found that ATP release was significantly attenuated following hypoxia exposure (2 % oxygen, 2263 % after 48 h). In contrast, intracellular ATP was unchanged. Similarly, lactate-dehydrogenase release into the supernatants was similar between normoxic or hypoxic endothelia, suggesting that differences in lytic ATP release between normoxia or hypoxia are minimal. Next, we used pharmacological strategies to study potential mechanisms for endothelialdependent ATP release (eg, verapamil, dipyridamole, 18-alpha-glycyrrhetinic acid, anandamide, connexin-mimetic peptides). These studies revealed that endothelial ATP release occurs – at least in part- through connexin 43 (Cx43) hemichannels. A real-time RT-PCR screen of endothelial connexin expression showed selective repression of Cx43 transcript and additional studies confirmed time-dependent Cx43 mRNA, total and surface protein repression during hypoxia. In addition, hypoxia resulted in Cx43-serine368 phosphorylation, which is known to switch Cx43 hemi-channels from an open to a closed state. Conclusions/Significance: Taken together, these studies implicate endothelial Cx43 in hypoxia-associated repression o

Partial Netrin-1 Deficiency Aggravates Acute Kidney Injury

The netrin family of secreted proteins provides migrational cues in the developing central nervous system. Recently, netrins have also been shown to regulate diverse processes beyond their functions in the brain, incluing the ochrestration of inflammatory events. Particularly netrin-1 has been implicated in dampening hypoxia-induced inflammation. Here, we hypothesized an anti-inflammatory role of endogenous netrin-1 in acute kidney injury (AKI). As homozygous deletion of netrin-1 is lethal, we studied mice with partial netrin-1 deletion (Ntn-1+/− mice) as a genetic model. In fact, Ntn-1+/− mice showed attenuated Ntn-1 levels at baseline and following ischemic AKI. Functional studies of AKI induced by 30 min of renal ischemia and reperfusion revealed enhanced kidney dysfunction in Ntn-1+/− mice as assessed by measurements of glomerular filtration, urine flow rate, urine electrolytes, serum creatinine and creatinine clearance. Consistent with these findings, histological studies indicated a more severe degree kidney injury. Similarly, elevations of renal and systemic inflammatory markers were enhanced in mice with partial netrin-1 deficiency. Finally, treatment of Ntn-1+/− mice with exogenous netrin-1 restored a normal phenotype during AKI. Taking together, these studies implicate endogenous netrin-1 in attenuating renal inflammation during AKI

Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease

BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. CONCLUSIONS: Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)

Muscular Contractions Facilitate Systemic Circulation of MicroRNA that Impact Cancer

Currently there is an evolving appreciation for exercise- combined therapies prescribed by clinicians for breast cancer patients; however there remains a of lack explanation of biological regulation of exercise on breast cancer, and the role that contracting skeletal muscle, the mechanistic machinery of exercise, has in the documented improved prognosis of exercising breast cancer patients. MicroRNAs (miRNA) are small non-coding RNAs found in abundance in skeletal muscle that have been proposed as possible myokines. Exogenous miRNA have post-transcriptional abilities allowing them to act as negative gene regulators of gene expression such as those in the mammalian target of rapamycin (mTOR) pathway. We have unique preliminary findings that myokines released during electrically-stimulated muscle contraction of hemicorpus-prepared rats affects the anabolic activity and capacity of breast cancer cells. When MCF-7 cancer cells were treated with perfusate collected during muscle contraction, a significant inhibition of proliferation was noted alongside diminished mTOR activity and global rates of protein synthesis. PURPOSE: The purpose of this study was to profile microRNA released into circulation during lower limb muscular contractions that may influence the anabolic signaling of breast cancer cells. METHODS: Female Wistar rats underwent a hemicorpus hindlimb perfusion preparation with and without electrically-stimulated muscular contractions. RT-PCR analysis of select microRNAs, known to impact cellular anabolism, was performed on both muscle and perfusate samples collected pre- and post-contraction (Non-Stim=4. E-Stim=4, respectively). RESULTS: A total of 52 microRNA were identified across all samples, with an average of 65 microRNAs detected per sample. We also noted a significant differential expression of 8 microRNA between E-Stim and Non-Stim samples within animals (p0.05), and was 147% higher in E-Stim perfusate samples compared to Non-Stim (pCONCLUSION: Our results suggest that skeletal muscle is a rich endogenous source of microRNA, including those associated with altered mTOR pathway gene expression. Muscular contraction comparable to resistance exercise facilitates the release of microRNA into systemic circulation which supports exercise facilitating cross-talk between muscle and other tissues, including cancer