This study tried to differentiate the consequences of chronic hypoxia on the electrophysiological and physiological properties and the histological characteristics of slow and fast muscles in rats. Animals inhaled a 10% O₂ concentration for a 1-month period. Then, slow [soleus (SOL)] and fast [extensor digitorum longus (EDL)] muscles were analyzed in vitro by physiological and electrophysiological measurements and histological analyses. The results were compared to those obtained in corresponding muscles of an age-matched normoxic group. After exposure to hypoxia: (1) in SOL, there was a tendency to elevated F_max, a significant increase in twitch force and tetanic frequency and a shortening of M-wave duration, and a reduced percentage of type I fibres, whereas the proportion of type IIa fibres doubled; (2) in EDL, F_max and tetanic frequency were lowered, the muscle became less resistant to fatigue, and the proportion of type IId/x fibres was halved. Then, after 1 month of hypoxia, in the SOL muscle, both the contractile and histological properties resemble those of a fast muscle. By contrast, the EDL became slower, despite its histology was modestly affected. Reduced muscle use in hypoxia could explain the tendency for deteriorating adaptations in EDL, and the faster properties of SOL could result from hypoxia-induced inhibition of the growth-related fast-to-slow shift in muscle fibre types.

The margination of a particle circulating in the blood stream has been analyzed. The contribution of buoyancy, hemodynamic forces, van der Waals, electrostatic and steric interactions between the circulating particle and the endothelium lining the vasculature has been considered. For practical applications, the contribution of buoyancy, hemodynamic forces and van der Waals interactions should be only taken into account, whilst the effect of electrostatic and steric repulsion becomes important only at very short distances from the endothelium (1–10 nm). The margination speed and the time for margination t_s have been estimated as a function of the density of the particle relative to blood Δ ρ, the Hamaker constant A and radius R of the particle. A critical radius R_c exists for which the margination time t_s has a maximum, which is influenced by both Δ ρ and A: the critical radius decreases as the relative density increases and the Hamaker constant decreases. Therefore, particles used for drug delivery should have a radius smaller than the critical value (in the range of 100 nm) to facilitate margination and interaction with the endothelium. While particles used as nanoharvesting agents in proteomics or genomics analysis should have a radius close to the critical value to minimize margination and increase their circulation time.

Brain cancer accounts for approx 1.4% of all cancers and 2.3% of all cancer-related deaths. The incidence of primary cerebral malignancies varies between 4 and 10/100,000 in the general population. This incidence tends to increase with age (4/100,000 up to the age of 12 yr; 6/100,000 up to the age of 35 yr; 18/100,000 up to the age of 55 yr; 70/100,000 up to the age of 75 yr).

Prevention of cross-species infection with porcine endogenous retroviruses (PERV) is crucial for xenotransplantation. Previous studies described the potential risk of infection for the PERV γ1 subfamilies A, B and C. Replication competent PERV γ1 proviruses designated to a particular subfamily and hybrid viruses originating from retroviral recombination events between the subfamilies were observed. Future pig genome sequencing projects will reveal multiple novel PERV proviruses from additional breeds and animals. Evaluation of these viral genomes has to be carried out to assess the potential risk of retroviral cross-species infection. In this study, we tested common sequence comparison methods for the classification of PERV sequences and the detection of hybrid clones. The examination of the polymorphic nucleotide positions was found to be the most suitable procedure. We describe a fast and simple method using bioinformatic software tools which can also be applied to analogous analyses of other viral genomes.

Most patients with depression report disturbed sleep.¹ Correspondingly sleep- EEG changes are frequent symptoms of depression. Furthermore a set of neuroendocrine aberrances, particularly overactivity of the hypothalamopituitary- adrenocortical (HPA) system and changes of the hypothalamo-pituitary- somatotrophic (HPS) system is characteristically in affective disorders. Since sleep is a time of considerable activity in endocrine systems it is an attractive approach to study sleep EEG and, by blood sampling during sleep via long catheter, nocturnal hormone secretion simultaneously. In young normal human subjects characteristical patterns of sleep-endocrine activity are found. During the first half of the night the major amounts of slow-wave sleep (SWS), slow-wave activity (SWA) and the growth hormone (GH) surge preponderate, whereas cortisol secretion reaches its nadir. During the second half of the night cortisol levels rise, the major portion of rapid-eyemovement sleep (REMS) occurs, and the amounts of SWS and GH are low^2,3 (see Figure 1). Already this pattern points to a reciprocal interaction between the HPS and the HPA systems with GH and cortisol, respectively, as their peripheral endpoints. Furthermore it is likely that common factors are links between the electrophysiological and the endocrine activity during sleep. This hypothesis is supported, since during depression (and similarly during normal aging) SWS and GH decrease, whereas HPA activity is enhanced. Clinical and preclinical studies showed that neuropeptides are these factors. Ehlers and Kupfer⁴ submitted first that a reciprocal interaction of the peptides corticotropin-releasing hormone (CRH) and GHreleasing hormone (GHRH) plays a key role in the pathophysiology of changes of sleep-endocrine activity in depression. Since then this view was corroborated and amplified. This chapter intends to present the state of the art in this field

This aim of this review is to describe the dynamics of learning-induced cellular modifications in the rat piriform (olfactory) cortex after olfactory discrimination learning and to describe their functional significance to long-term memory consolidation. The first change to occur is in the intrinsic properties of the neurons. One day after learning, pyramidal neurons show enhanced neuronal excitability. This enhancement results from reduction in calcium-dependent conductance that mediates the post burst after-hyperpolarization. Such enhanced excitability lasts for 3 days and is followed by a series of synaptic modifications. Several forms of long-term enhancement in synaptic connections between layer II pyramidal neurons in the piriform cortex accompany olfactory learning. Enhanced synaptic release is indicated by reduced paired-pulse facilitation. Post-synaptic enhancement of synaptic transmission is indicated by reduced rise time of post-synaptic potentials and formation of new synaptic connections is indicated by increased spine density along dendrites of these neurons. Such modifications last for up to 5 days. Thus, olfactory discrimination rule learning is accompanied by a series of cellular modifications which occur and then disappear at different times. These modifications overlap partially, allowing the maintenance of the cortical system in a ‘learning mode’ in which memories for specific odors can be acquired rapidly and efficiently.

Background

Growth characteristics of coliphage viruses indicate that they are adapted to live with their Eschericia coli hosts in the intestinal tract. However, coliphage experimentally introduced by ingestion persist only transiently if at all in the gut of humans and other animals. This study attempted to identify the barriers to long term establishment of exogenous coliphage in the gastrointestinal (GI) tracts of laboratory mice. Intestinal contents were screened for the presence of coliphage and host bacteria, and strains of E. coli bacteria from different segments of the GI tract were tested for susceptibility to six common laboratory coliphages.

Results

Contrary to expectations, coliphage were not evident in the GI tracts of laboratory mice, although they were occasionally detected in feces. Commensal flora showed extreme variability within groups of mice despite identical handling and diet. Less than 20% of 48 mice tested carried E. coli in their gut, and of 22 commensal E. coli strains isolated and tested, 59% were completely resistant to infection by lambda, M13, P1, T4, T7, and PhiX174 coliphage. Lysogeny could not be demonstrated in the commensal strains as mitomycin C failed to induce detectable phage. Pre-existing immunity to phages was not evident as sera and fecal washes did not contain significant antibody titers to six laboratory phage types.

Conclusion

Lack of sufficient susceptible host bacteria seems to be the most likely barrier to establishment of new coliphage infections in the mouse gut.