Response of the receptive fields of the lateral geniculate body to temporal changes in the area of a light stimulus

Neuronal responses of the cat LGB to light spots the area of which was changing in time with different speed, were studied. All the neurons responding to switching on and off of the test spot respond to changing in time of the spot area too. The on-neurons respond to enlargening of the area while the off-neurons - to its reducing. The on- and off-responses of these fields occurred at the moment of passing of the margin of reducing (growing) spot across a certain point of neuron's receptive field. This point changed when the speed of reducing (growing) of the test spot changed.     

Aldehyde disinfectants and health in endoscopy units. British Society of Gastroenterology Endoscopy Committee

Summary of main recommendations(1) Glutaraldehyde, used in most endoscopy units in the United Kingdom for the disinfection of flexible gastrointestinal endoscopes, is a toxic substance being an irritant and a sensitiser; symptoms associated with glutaraldehyde exposure are common among staff working in endoscopy units.(2) The Control of Substances Hazardous to Health Regulations 1988 (COSHH) obliges the employer to make a systematic assessment of risk to staff of exposure to glutaraldehyde and institute measures to deal effectively with exposure.(3) At present glutaraldehyde remains the first line agent for the disinfection of flexible gastrointestinal endoscopes. Other agents are being developed; a standard means of assessment for flexible endoscope disinfectants should be devised.(4) Equipment and accessories that are heat stable should be sterilised by autoclaving; disposable accessories should be used wherever possible.(5) Flexible gastrointestinal endoscopes should be disinfected within automated washer/disinfectors; trays, bowls or buckets for this purpose are unacceptable.(6) Local exhaust ventilation must be used to control glutaraldehyde vapour. Extracted air may be discharged direct to the atmosphere or passed over special absorbent filters and recirculated. Such control measures must be regularly tested and records retained.(7) Endoscope cleaning and disinfection should be carried out in a room dedicated to the purpose, equipped with control measures to maintain the concentration of glutaraldehyde vapour at a level certainly below the current occupational exposure standard of 0.2 ppm and preferably below the commonly used working limit of 0.1 ppm. Sites other than the endoscopy unit where endoscopy is regularly performed, such as the radiology department, should have their own fully equipped cleaning and disinfection room.(8) COSHH limits the use of personal protective equipment to those situations where other measures cannot adequately control exposure. Such equipment includes nitrile rubber gloves, apron, chemical grade eye protection, and respiratory protective equipment for organic vapours.(9) Monitoring of atmospheric levels of glutaraldehyde should be performed by a competent person such as an occupational hygienist; the currently preferred method of sampling uses a filtration technique, the commercially available meters being less reliable.(10) Health surveillance of staff is mandatory; occupational health records must be retained for 30 years.(11) Endoscopy staff must be informed of the risks of exposure to glutaraldehyde and trained in safe methods of its control. Only staff who have completed such an education and training programme should be allowed to disinfect endoscopes.(12) The unsafe use of glutaraldehyde has significant health and legal consequences; the safe use of glutaraldehyde may have revenue consequences that contribute significantly to the cost of gastrointestinal endoscopy.     

The gp200-MR6 molecule which is functionally associated with the IL-4 receptor modulates B cell phenotype and is a novel member of the human macrophage mannose receptor family

The human gp200-MR6 molecule has previously been shown to have either an antagonistic or agonistic effect on IL-4 function, demonstrated by inhibition of IL-4-induced proliferation of T cells or mimicking of IL-4-induced maturation of epithelium, respectively. We now show that gp200-MR6 ligation can also mimic IL-4 and have an anti-proliferative pro-maturational influence within the immune system, causing up-regulation of co-stimulatory molecules on B lymphocytes. Biochemical analysis and cDNA cloning reveal that gp200-MR6 belongs to the human macrophage mannose receptor family of multidomain molecules. It comprises 1722 amino acids in toto (mature protein, 1695 amino acids; signal sequence, 27 amino acids) organized into 12 external domains (an N-terminal cysteine-rich domain, a fibronectin type II domain and 10 C-type carbohydrate recognition domains), a transmembrane region and a small cytoplasmic C terminus (31 amino acids) containing a single tyrosine residue (Y1679), but no obvious kinase domain. Strong amino acid sequence identity (77%) suggests that gp200-MR6 is the human homologue of the murine DEC-205, indicating that this molecule has much wider functional activity than its classical endocytic role. We also show that the gp200-MR6 molecule is closely associated with tyrosine kinase activity; the link between gp200-MR6 and the IL-4 receptor may therefore be via intracellular signaling pathways, with multifunctionality residing in its extracellular multidomain structure.     

Clinical assessment of spasticity in spinal cord injury: a multidimensional problem

OBJECTIVE: To determine the relation between various components of spasticity evaluated clinically in persons with spinal cord injury (SCI). DESIGN: Case series evaluating spasticity using clinical scales commonly referenced in contemporary literature, including the Penn Spasm Frequency Scale, the Ashworth Scale, and standard scales of tendon taps, clonus, and plantar stimulation. SETTING. A Veterans Affairs Medical Center Spinal Cord Injury Center. PATIENTS. Eighty-five spinal cord injured individuals with varying degrees of spasticity. RESULTS: Correlations demonstrated weak relationships between Spasm Frequency Scale and self-report scales of interference with function (.407) and painful spasms (.312). No clinical examination score correlated with self-report scores greater than 0.4. Three clinical examination scores correlated modestly (> 0.5)-Ashworth score with patellar tendon taps (.553), ankle clonus with Achilles tendon tap (.663), and patellar tendon tap with adductor tendon tap (.512). Two other clinical scales correlated weakly (> 0.4)-Achilles tendon tap with patellar tendon tap (.417) and plantar reflex with adductor tendon taps (.423). CONCLUSIONS: Clinical scales currently used to evaluate spasticity in SCI correlate poorly with each other, suggesting that they each assess different aspects of spasticity. The use of any single scale is likely to underrepresent the magnitude and severity of spasticity in the SCI population. In the absence of agreement among these various scales and with the absence of an appropriate criterion standard for evaluation of spasticity, assessments of spasticity, whether clinical or neurophysiological in nature, should be comprehensive in scope.     

Particle deposition onto a human head: influence of electrostatic and wind fields

Steatosis--accumulation of triacylglycerol in hepatocytes--is a common finding in liver biopsy specimens. The commonest form is macrovesicular change, which occurs in response to a wide range of insults. In the absence of other features, the pathologist cannot ascertain the likely cause on morphological features alone but can give an indication of the severity of steatosis. Close clinicopathological correlation is required to establish the cause. In most instances, macrovesicular steatosis is at least potentially reversible. Although it may be thought of as a benign condition, it may be associated with the development of necroinflammation and fibrosis--so-called steatohepatitis. The classic example of this is alcoholic hepatitis, but there is increasing awareness of steatohepatitis occurring in nonalcoholics: NASH. Distinction between alcoholic hepatitis and NASH on purely histological grounds may be impossible; careful clinicopathological discussion is mandatory. Microvesicular steatosis is generally a more severe disease than the macrovesicular form and is seen in a variety of conditions in which there is either an inherited or an acquired defect in beta-oxidation of fatty acids; the former includes mitochondrial cytopathies and disorders of ureagenesis, and the latter includes acute fatty liver of pregnancy and Reye's syndrome. This review describes the morphological features of steatosis and steatohepatitis, considers their pathogenesis, and outlines the clinical significance of the different patterns of injury.