How long do nosocomial pathogens persist on inanimate surfaces? A systematic review

BACKGROUND: Inanimate surfaces have often been described as the source for outbreaks of nosocomial infections. The aim of this review is to summarize data on the persistence of different nosocomial pathogens on inanimate surfaces. METHODS: The literature was systematically reviewed in MedLine without language restrictions. In addition, cited articles in a report were assessed and standard textbooks on the topic were reviewed. All reports with experimental evidence on the duration of persistence of a nosocomial pathogen on any type of surface were included. RESULTS: Most gram-positive bacteria, such as Enterococcus spp. (including VRE), Staphylococcus aureus (including MRSA), or Streptococcus pyogenes, survive for months on dry surfaces. Many gram-negative species, such as Acinetobacter spp., Escherichia coli, Klebsiella spp., Pseudomonas aeruginosa, Serratia marcescens, or Shigella spp., can also survive for months. A few others, such as Bordetella pertussis, Haemophilus influenzae, Proteus vulgaris, or Vibrio cholerae, however, persist only for days. Mycobacteria, including Mycobacterium tuberculosis, and spore-forming bacteria, including Clostridium difficile, can also survive for months on surfaces. Candida albicans as the most important nosocomial fungal pathogen can survive up to 4 months on surfaces. Persistence of other yeasts, such as Torulopsis glabrata, was described to be similar (5 months) or shorter (Candida parapsilosis, 14 days). Most viruses from the respiratory tract, such as corona, coxsackie, influenza, SARS or rhino virus, can persist on surfaces for a few days. Viruses from the gastrointestinal tract, such as astrovirus, HAV, polio- or rota virus, persist for approximately 2 months. Blood-borne viruses, such as HBV or HIV, can persist for more than one week. Herpes viruses, such as CMV or HSV type 1 and 2, have been shown to persist from only a few hours up to 7 days. CONCLUSION: The most common nosocomial pathogens may well survive or persist on surfaces for months and can thereby be a continuous source of transmission if no regular preventive surface disinfection is performed

Cannibalism in spiderlings is not only about starvation

International audienceMany species show a transient group life, and dispersal often coincides with the onset of agonistic behaviors. Changes in the nature of interactions among conspecifics can rely on a variation in the production of communication cues and/or on a switch in the processing of social information. The relative contribution of each process on the initiation of aggression still remains to be investigated. Spiders constitute relevant models to address this issue since all solitary species undergo a transient gregarious phase prior dispersal. In this study, we developed a combination of behavioral and physiological assays to examine the mechanisms accompanying the onset of agonistic interactions in spiderlings of the solitary species Agelena labyrinthica. Juveniles of different developmental stages were supplied with diets differing in prey availability. We showed that unfed spiderlings never molted, retained their cuticular lipid signature, and did not behave aggressively. This contrasted with fed individuals that molted, changed their cuticular profiles, and displayed agonistic interactions and cannibalism. We demonstrated that depletion in lipid stores was not sufficient to elicit aggression or cannibalism. Our analysis also revealed that major shifts in cuticular profiles only occurred after the first molt outside the cocoon. The lack of agonistic interactions in unfed spiderlings suggests an absence of behavioral plasticity in response to food shortage at the earliest developmental stages. We propose that the initiation of aggression relies more on a shift in the production of cuticular cues accompanying molting rather than on changes in information processing depending on the physiological state of individuals

Intramuscular Anabolic Signaling and Endocrine Response Following Resistance Exercise: Implications for Muscle Hypertrophy

Maintaining skeletal muscle mass and function is critical for disease prevention, mobility and quality of life, and whole-body metabolism. Resistance exercise is known to be a major regulator for promoting muscle protein synthesis and muscle mass accretion. Manipulation of exercise intensity, volume, and rest elicit specific muscular adaptations that can maximize the magnitude of muscle growth. The stimulus of muscle contraction that occurs during differing intensities of resistance exercise results in varying biochemical responses regulating the rate of protein synthesis, known as mechanotransduction. At the cellular level, skeletal muscle adaptation appears to be the result of the cumulative effects of transient changes in gene expression following acute bouts of exercise. Thus, maximizing the resistance exercise-induced anabolic response produces the greatest potential for hypertrophic adaptation with training. The mechanisms involved in converting mechanical signals into the molecular events that control muscle growth are not completely understood; however, skeletal muscle protein synthesis appears to be regulated by the multi-protein phosphorylation cascade, mTORC1 (mammalian/mechanistic target of rapamycin complex 1). The purpose of this review is to examine the physiological response to resistance exercise, with particular emphasis on the endocrine response and intramuscular anabolic signaling through mTORC1. It appears that resistance exercise protocols that maximize muscle fiber recruitment, time-under-tension, and metabolic stress will contribute to maximizing intramuscular anabolic signaling; however, the resistance exercise parameters for maximizing the anabolic response remain unclear

Thermodynamics of freezing and melting

Although the freezing of liquids and melting of crystals are fundamental for many areas of the sciences, even simple properties like the temperature–pressure relation along the melting line cannot be predicted today. Here we present a theory in which properties of the coexisting crystal and liquid phases at a single thermodynamic state point provide the basis for calculating the pressure, density and entropy of fusion as functions of temperature along the melting line, as well as the variation along this line of the reduced crystalline vibrational mean-square displacement (the Lindemann ratio), and the liquid's diffusion constant and viscosity. The framework developed, which applies for the sizable class of systems characterized by hidden scale invariance, is validated by computer simulations of the standard 12-6 Lennard-Jones system