Reinterpretation of the ultrastructure of cartilage matrix.

The epiphyseal cartilage from new-born mouse was treated with collagenase in two ways: either before fixation or after glutaraldehyde fixation. The electron dense granules of the matrix were not seen in the micrographs of cartilage treated with collagenase before fixation. It is concluded that collagen plays a definite role in the formation of the granules at the time of tissue fixation and that the granules are fixation artifacts.     

Action du succinate de soude sur la respiration

Summary Intravenous injection of sodium succinate in dogs anesthetized with chloralosane produces a prolonged stimulation of respiration and decreases the duration of the apnea following pulmonary hyperventilation.     

Observations expérimentales sur l'apnée acapnique chez le Chien

Summary Suppression of the chemo-receptors of the carotid sinus and aorta æreas prolongs the acapnic apnea markedly. Animals deprived of their chemo-receptors may even die in apnea.During hyperventilation, the expiratory position of the thorax increases. During the acapnic apnea the inspiratory position returns progressively to normal. During hyperventilation and acapnic apnea, rhythmic changes occur in the tonus of the respiratory muscles. These changes in tonus occur in normal animals as well as in animals deprived of their chemo-receptors and vagi nerves.In normal dogs, hyperventilation and acapnea do not induce a fall in arterial blood pressure. Arterial hypotension occurs, however, during hyperventilation in dogs deprived of their carotid sinus and aortic innervation. During acapnic apnea, the arterial blood pressure rises in animals deprived of their carotid sinus and aortic nerves. A secondary fall of arterial pressure occurs during prolonged acapnic apnea in these animals.     

Damage-associated molecular patterns and their receptors in upper airway pathologies

Inflammation of the nasal (rhinitis) and sinus mucosa (sinusitis) are prevalent medical conditions of the upper airways that are concurrent in many patients; hence the terminology “rhinosinusitis”. The disease status is further defined to be “chronic” in case symptoms persist for more than 12 weeks without resolution. A diverse spectrum of external factors including viral and bacterial insults together with epithelial barrier malfunctions could be implicated in the chronicity of the inflammatory responses in chronic rhinosinusitis (CRS). However, despite massive research efforts in an attempt to unveil the pathophysiology, the exact reason for a lack of resolution still remains poorly understood. A novel set of molecules that could be implicated in sustaining the inflammatory reaction may be found within the host itself. Indeed, besides mediators of inflammation originating from outside, some endogenous intracellular and/or extracellular matrix (ECM) components from the host can be released into the extracellular space upon damage induced during the initial inflammatory reaction where they gain functions distinct from those during normal physiology. These “host-self” molecules are known to modulate inflammatory responses under pathological conditions, potentially preventing resolution and contributing to the development of chronic inflammation. These molecules are collectively classified as damage-associated molecular patterns (DAMPs). This review summarizes the current knowledge regarding DAMPs in upper airway pathologies, also covering those that were previously investigated for their intracellular and/or ECM functions often acting as an antimicrobial agent or implicated in tissue/cell homeostasis, and for which their function as a danger signaling molecule was not assessed. It is, however, of importance to assess these molecules again from a point of view as a DAMP in order to further unravel the pathogenesis of CRS.     

Modelling T-cell memory by genetic marking of memory T cells in vivo.

Immunological memory is the ability of the immune system to respond with enhanced vigour to pathogens that have been encountered in the past. Following infection or immunization, most effector T cells undergo apoptotic cell death, but a small fraction of these cells, proportional to the early antigen load and initial clonal burst size, persist in the host as a stable pool of memory T cells. The existence of immunological memory has been recognized for over 2,000 years, but our understanding of this phenomenon is limited, primarily because memory lymphocytes cannot be unequivocally identified as they lack specific, permanent markers. Here we have developed a transgenic mouse model system whereby memory T cells and their precursors can be irreversibly marked with a reporter gene and thus can be unambiguously identified. Adoptive transfer of marked CD8+ T cells specific for lymphocytic choriomeningitis virus protected naive recipients following viral challenge, demonstrating that we have marked memory T cells. We also show that cytotoxic effector lymphocytes that develop into memory T cells can be identified in the primary response.     

The M-superfamily of conotoxins: a review

The focus of this review is the M-superfamily of Conus venom peptides. Disulfide rich peptides belonging to the M-superfamily have three loop regions and the cysteine arrangement: CC–C–C–CC, where the dashes represent loops one, two, and three, respectively. Characterization of M-superfamily peptides has demonstrated that diversity in cystine connectivity occurs between different branches of peptides even though the cysteine pattern remains consistent. This superfamily is subdivided into five branches, M-1 through M-5, based on the number of residues in the third loop region, between the fourth and fifth cysteine residues. M-superfamily peptides appear to be ubiquitous in Conus venom. They are largely unexplained in indigenous biological function, and they represent an active area of research within the scientific community.     

Effects of hexamethylenebisacetamide on the differentiation of embryonal carcinoma cells]

HMBA induces differentiation in the whole population of some multipotential embryonic carcinoma cells. Morphological, biochemical and immunological changes can be observed even after short treatment. The cells lose the embryonal F9 antigen without acquiring H-2 antigens.