A Face-like Structure Detection on Planet and Satellite Surfaces using Image Processing

This paper demonstrates that face-like structures are everywhere, and can be de-tected automatically even with computers. Huge amount of satellite images of the Earth, the Moon, the Mars are explored and many interesting face-like structure are detected. Throughout this fact, we believe that science and technologies can alert people not to easily become an occultist.Comment: 4 page

NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria

Nuclear factor κB (NF-κB), a key activator of inflammation, primes the NLRP3-inflammasome for activation by inducing pro-IL-1β and NLRP3 expression. NF-κB, however, also prevents excessive inflammation and restrains NLRP3-inflammasome activation through a poorly defined mechanism. We now show that NF-κB exerts its anti-inflammatory activity by inducing delayed accumulation of the autophagy receptor p62/SQSTM1. External NLRP3-activating stimuli trigger a form of mitochondrial (mt) damage that is caspase-1- and NLRP3-independent and causes release of direct NLRP3-inflammasome activators, including mtDNA and mtROS. Damaged mitochondria undergo Parkin-dependent ubiquitin conjugation and are specifically recognized by p62, which induces their mitophagic clearance. Macrophage-specific p62 ablation causes pronounced accumulation of damaged mitochondria and excessive IL-1β-dependent inflammation, enhancing macrophage death. Therefore, the "NF-κB-p62-mitophagy" pathway is a macrophage-intrinsic regulatory loop through which NF-κB restrains its own inflammation-promoting activity and orchestrates a self-limiting host response that maintains homeostasis and favors tissue repair

NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria

NF-κB, a key activator of inflammation primes the NLRP3-inflammasome for activation by inducing pro-IL-1β and NLRP3 expression. NF-κB, however, also prevents excessive inflammation and restrains NLRP3-inflammasome activation through a poorly defined mechanism. We now show that NF-κB exerts its anti-inflammatory activity by inducing delayed accumulation of the autophagy receptor p62/SQSTM1. External NLRP3-activating stimuli trigger a form of mitochondrial (mt) damage that is caspase-1- and NLRP3-independent and causes release of direct NLRP3-inflammasome activators, including mtDNA and mtROS. Damaged mitochondria undergo Parkin-dependent ubiquitin conjugation and are specifically recognized by p62, which induces their mitophagic clearance. Macrophage-specific p62 ablation causes pronounced accumulation of damaged mitochondria and excessive IL-1β-dependent inflammation, enhancing macrophage death. Therefore, the “NF-κB-p62-mitophagy” pathway is a macrophage-intrinsic regulatory loop through which NF-κB restrains its own inflammation-promoting activity and orchestrates a self-limiting host response that maintains homeostasis and favors tissue repair

Miscellaneous antibacterial drugs

The Side Effects of Drugs Annuals is a series of volumes in which the adverse effects of drugs and adverse reactions to them are surveyed. The series supplements the contents of Meyler's Side Effects of Drugs: the International Encyclopedia of Adverse Drug Reactions and Interactions. This review of the January 2012 to June 2013 publications on miscellaneous antibacterial drugs covers aminoglycosides (amikacin, gentamicin and tobramycin), fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin and ofloxacin), glycopeptides (oritavancin, teicoplanin, telavancin and vancomycin), ketolides (solithromycin and telithromycin), the lincosamide clindamycin, macrolides (azithromycin, clarithromycin, erythromycin and spiramycin), nitrofurantoin, oxazolidinones (linezolid and torezolid), the polymyxin colistin, the streptogramin pristinamycin, sulphonamides, trimethoprim and co-trimoxazole, daptomycin, fosfomycin and fusidic acid