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Poliovirus and enterovirus 71 (EV71) are both neurotropic enteroviruses that cause serious neurological diseases, such as poliomyelitis and encephalitis. The neurovirulence of EV71 in cynomolgus monkeys was demonstrated previously by intraspinal inoculation. In this study, an improved simian model of EV71 infection was established by using intravenous inoculation, which revealed clinical and neuropathological similarities between this model and human cases of encephalitis. Experimental EV71 infection induced direct neurological manifestations, such as tremor, ataxia and brain oedema, but not non-neurological complications, such as pulmonary oedema and cardiac failure. Using this model of EV71 infection, the neurotropic characteristics of the prototype strains of EV71 and poliovirus type 1 (PV1) were compared. Three monkeys were inoculated intravenously with 10(5.5) TCID50 EV71 and all developed neurological disease signs within 4-6 days of inoculation. However, after inoculation with 10(5.5) TCID50 PV1 strain OM1 (PV1-OM1), the major manifestation was flaccid paralysis, starting from the lower limbs 6-9 days post-inoculation. Histopathological and virological analyses of moribund monkeys revealed that disseminated EV71 infection was characterized by severe panencephalitis involving both the pyramidal and extrapyramidal systems. In contrast, the lesions induced by PV1-OM1 were mainly restricted to the pyramidal tract, particularly the spinal motor neurons, thalamus and motor cortex. In conclusion, neuropathological involvement in this model correlated well with the apparent differences in neurological disease induced by EV71 and PV1-OM1. Thus, intravenous inoculation with EV71 is an excellent model to study the neuropathology of EV71 and to evaluate candidate vaccines and potential antiviral agents.
J Gen Virol 2004 Oct
PMID:Differential localization of neurons susceptible to enterovirus 71 and poliovirus type 1 in the central nervous system of cynomolgus monkeys after intravenous inoculation. 1544 61

Biosurfactant production by Pseudomonas aeruginosa A41, a strain isolated from seawater in the gulf of Thailand, was examined when grown in defined medium containing 2% vegetable oil or fatty acid as a carbon source in the presence of vitamins, trace elements and 0.4% NH(4)NO(3), at pH 7 and 30 degrees C with 200 rpm-shaking for 7 days. The yield of biosurfactant steadily increased even after a stationary phase. Under such conditions the surface tension of the medium was lowered from 55-70 mN/m to 27.8-30 mN/m with every carbon source tested. However, types of carbon sources were found to affect biosurfactant yield. The yields of rhamnolipid biosurfactant were 6.58 g/L, 2.91 g/L and 2.93 g/L determined as rhamnose content when olive oil, palm oil and coconut oil, respectively, were used as a carbon source. Among them, biosurfactant obtained from palm oil was the best in lowering surface tension of the medium. Increase in biosurfactant activities in terms of oil displacement test and rhamnose content were observed to be higher with shorter chain fatty acids than that of the longer chains (C12>C14>C16). In addition, we found that C18:2, highly unsaturated fatty acid, showed higher oil displacement activity and rhamnose content than that of C18:1. The optimal oil displacement activity was found at pH 7-9 and in the presence of 0.5-3% NaCl. The oil displacement activity was stable to temperatures up to 100 degrees C for 15 h. Surface tension reduction activity was relatively stable at pH 2-12 and 0-5% of NaCl. Emusification activity tested with various types of hydrocarbons and vegetable oils showed similarity of up to 60% stability. The partially purified biosurfactant via TLC and silica gel column chromatography gave three main peaks on HPLC with mass spectra of 527, 272, and 661 m/z respectively, corresponding to sodium-monorhamnodecanoate, hydroxyhexadecanoic acid and an unknown compound, respectively.
J Gen Appl Microbiol 2006 Aug
PMID:Biosurfactant production by Pseudomonas aeruginosa A41 using palm oil as carbon source. 1711 70

Serotonin syndrome is a potentially life-threatening adverse drug reaction caused by excessive serotonergic agonism in central and peripheral nervous system serotonergic receptors (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Symptoms are characterized by a triad of neuron-excitatory features, which include (a) neuromuscular hyperactivity -- tremor, clonus, myoclonus, hyperreflexia and, in advanced stages, pyramidal rigidity; (b) autonomic hyperactivity -- diaphoresis, fever, tachycardia and tachypnea; (c) altered mental status -- agitation, excitement and, in advanced stages, confusion (Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth 2005;95:434-441). It arises when pharmacological agents increase serotonin neurotransmission at postsynaptic 5-hydroxytryptamine 1A and 5-hydroxytryptamine 2A receptors through increased serotonin synthesis, decreased serotonin metabolism, increased serotonin release, inhibition of serotonin reuptake or direct agonism of the serotonin receptors (Houlihan D. Serotonin syndrome resulting from coadministration of tramodol, venlafaxine, and mirtazapine. Ann Pharmacother 2004;38:411-413). The etiology is often the result of therapeutic drug use, intentional overdosing of serotonergic agents or complex interactions between drugs that directly or indirectly modulate the serotonin system (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Due to the increasing availability of agents with serotonergic activity, physicians need to more aware of serotonin syndrome. The following case highlights the complex nature in which serotonin syndrome can arise, as well as the proper recognition and treatment of a potentially life-threatening yet easily avoidable condition.
Gen Hosp Psychiatry
PMID:Serotonin syndrome: a complex but easily avoidable condition. 1843 63

1. The seven bacterial viruses of the T group active against E. coli, are rapidly inactivated at gas-liquid interfaces. 2. The kinetics of this inactivation whether brought about by shaking or by bubbling with nitrogen are those of a first order reaction. 3. This inactivation may be prevented by the addition of enough protein to maintain the gas-liquid interface in a saturated condition. 4. The analogy between this phenomenon and the surface denaturation of proteins is pointed out and discussed.
J Gen Physiol 1948 May 20
PMID:Surface inactivation of bacterial viruses and of proteins. 1891 25

Although neuromedin U (NMU) and neuromedin S (NMS) are reported to modulate stress responses mainly through corticotropin-releasing hormone system in rodents, the in vivo effects of centrally administered NMU or NMS on stress regulation have not been fully elucidated in cattle. We examined adrenocorticotropic hormone levels, body temperature, and behavioral responses to intracerebroventricularly (ICV) administered rat NMU or rat NMS in steers. ICV NMU and NMS (0.2, 2, and 20 nmol/200 microl) evoked a dose-related increase in plasma cortisol concentrations (CORT). There was a significant time-treatment interaction for the time course of CORT (p<0.001). ICV NMU evoked a dose-related increase in rectal temperature (RT). There was a significant time-treatment interaction for the change in RT from pre-injection value (p<0.05). There was a significant difference among treatments in the percentage of time spent lying (Friedman's test, chi(2)=15.6, p<0.01) and in the total number of head shaking (Friedman's test, chi(2)=14.49, p<0.01). A high dose of NMS tended to shorten the duration of lying and increase the number of head shaking. These findings indicate that both central NMU and NMS might participate in controlling the hypothalamo-pituitary-adrenal axis, that central NMU might participate in controlling body temperature, and that central NMS is likely to be involved in behavioral activation in cattle.
Gen Comp Endocrinol 2009 Sep 15
PMID:Effects of intracerebroventricular administration of neuromedin U or neuromedin S in steers. 1944 64

Irregularities in migration velocity of bacterial cells in the highly alkaline solutions are due to the buffering effect of the cells upon the immediately adjacent zone of menstruum. Consistent results can be obtained by shaking the suspension thoroughly before placing it in the electrophoretic cell. When observed in this way both Bacillus cereus and Bacterium coli show an isopotential point near pH 13.5, that for Bacillus cereus being slightly below, and that for Bacterium coli slightly above this point. At more alkaline reactions the cells acquire a positive charge which increases with further increase in pH to very high values.
J Gen Physiol 1924 Jul 20
PMID:THE ALKALINE ISOPOTENTIAL POINT OF THE BACTERIAL CELL. 1987 9

1. When solid blocks of isoelectric gelatin are placed in cold distilled water or dilute buffer of pH 4.7, only those of a gelatin content of more than 10 per cent swell, while those of a lower gelatin content not only do not swell but actually lose water. 2. The final quantity of water lost by blocks of dilute gelatin is the same whether the block is immersed in a large volume of water or whether syneresis has been initiated in the gel through mechanical forces such as shaking, pressure, etc., even in the absence of any outside liquid, thus showing that syneresis is identical with the process of negative swelling of dilute gels when placed in cold water, and may be used as a convenient term for it. 3. Acid- or alkali-containing gels give rise to greater syneresis than isoelectric gels, after the acid or alkali has been removed by dialysis. 4. Salt-containing gels show greater syneresis than salt-free gels of the same pH, after the salt has been washed away. 5. The acid and alkali and also the salt effect on syneresis of gels disappears at a gelatin concentration above 8 per cent. 6. The striking similarity in the behavior of gels with respect to syneresis and of gelatin solutions with respect to viscosity suggests the probability that both are due to the same mechanism, namely the mechanism of hydration of the micellae in gelatin by means of osmosis as brought about either by diffusible ions, as in the presence of acid or alkali, or by the soluble gelatin present in the micellae. The greater the pressures that caused swelling of the micellae while the gelatin was in the sol state, the greater is the loss of water from the gels when the pressures are removed. 7. A quantitative study of the loss of water by dilute gels of various gelatin content shows that the same laws which have been found by Northrop to hold for the swelling of gels of high concentrations apply also to the process of losing water by dilute gels, i.e. to the process of syneresis. The general behavior is well represented by the equations: See PDF for Equation and See PDF for Equation where P(1) = osmotic pressure of the soluble gelatin in the gel, P(2) = stress on the micellae in the gelatin solution before setting, K(e) = bulk modulus of elasticity, V(o) = volume of water per gram of dry gelatin at setting and V(e) = volume of water per gram of gelatin at equilibrium.
J Gen Physiol 1928 Nov 20
PMID:SYNERESIS AND SWELLING OF GELATIN. 1987 60

The rate of diffusion through the non-aqueous layer of the protoplasm depends largely on the partition coefficients mentioned above. Since these cannot be determined we have employed an artificial system in which chloroform is used in place of the non-aqueous layer of the protoplasm. The partition coefficients may be roughly determined by shaking up the aqueous solutions with chloroform and analyzing with the spectrophotometer (which is necessary with methylene blue because we are dealing with mixtures). This will show what dyes may be expected to pass through the protoplasm into the vacuole in case it behaves like the artificial system. From these results we may conclude that the artificial system and the living cell act almost alike toward methylene blue and azure B, which supports the notion of non-aqueous layers in the protoplasm. There is a close resemblance between Valonia and the artificial system in their behavior toward these dyes at pH 9.5. In the case of Nitella, on the other hand, with methylene blue solution at pH 9.2 the sap in the artificial system takes up relatively more azure B (absorption maximum at 650 mmicro) than the vacuole of the living cell (655 mmicro). But both take up azure B much more rapidly than methylene blue. A comparison cannot be made between the behavior of the artificial system and that of the living cell at pH 5.5 since in the latter case there arises a question of injury to cells before enough dye is collected in the sap for analysis.
J Gen Physiol 1929 Jan 20
PMID:SPECTROPHOTOMETRIC STUDIES OF PENETRATION : V. RESEMBLANCES BETWEEN THE LIVING CELL AND AN ARTIFICIAL SYSTEM IN ABSORBING METHYLENE BLUE AND TRIMETHYL THIONINE. 1987 69

The above data relating to the reaction between 16 hour cultures of S. aureus and antistaphylococcus bacteriophage in nutrient broth of pH 7.6 at 36 degrees C. and with mechanical shaking to maintain a uniform B suspension, bring out the following points: (a) B growth in P-B mixtures does not differ from growth in controls without P except in the case of a very high initial P/B ratio as noted below. There is no evidence that lytic destruction of B begins shortly after mixing P and B nor that B growth is stimulated by P, for the B growth curves in the presence of ordinary [P]'s and in controls are identical. Only at the sudden onset of the rapid lytic process does the B curve of a P-B mixture deviate from the control curve. (b) B growth is an essential conditioning factor for P formation. (c) Both B growth and P production exhibit short lags. During this time P diffuses into or becomes adsorbed to B so rapidly that by the end of the lag period only 10 to 30 per cent of the total P present is extracellular, the remainder being associated with the B. (d) During the logarithmic B growth phase, P formation is also logarithmic but proceeds at a much faster rate. That is, d P/d t is proportional to a power of d B/d t. Consequently the statement that each time a B divides a certain amount of P is formed is not correct. (e) As B growth enters the phase of positive acceleration equilibrium between the extracellular and intracellular P fractions becomes established and is maintained up to the onset of lysis, extracellular [P] representing a small constant percentage of total [P]. The distribution of P on a constant percentage basis suggests the manner in which a relatively simple chemical compound would be distributed and is not at all typical of the distribution one would expect if P were a complex organized parasite. (f) When the value of log P/B = 2.1 lysis begins. Obviously, this limiting value for any initial [B] is reached sooner the higher the initial [P]. When log P/B at the time of mixing P and B is already 2.1 or greater, there is no growth of B and lysis soon occurs. (g) While there is good evidence that lysis is brought about by the attainment of a particular [P] per B and not by a certain [P] per ml., it is not clear at this time which of the ratios intracellular P/B, extracellular P/B or total P/B is the major conditioning factor for B lysis. (h) Experimentally the maximal [P]'s of lysates made by mixing a constant initial [B] with widely varying Po's fall within a relatively narrow range. This fact is explained by the large value of d log P/d t as compared to d log B/d t. That is, the loci of points at which log P = 2.1 + log B (maxima-lysis begins) on the curves of log P against t originating in various [Po]'s will lie at a nearly constant level above the abscissa. Because of this same relationship the maximal [P]'s of such a series will be in the reverse order of magnitude of the Po's, i.e., the larger the Po the smaller will be the maximal [P] attained during the reaction (cf. Fig, 16). (i) The lytic destruction of B is logarithmic with time, in this respect being similar to most death rate processes. The value -d log B/d t for a particular initial [B] is constant for various initial values of [P]. There is good evidence that cells need not be growing in order to undergo lysis. (j) During B lysis a considerable percentage of the total maximal P formed is destroyed, the chief loss probably occurring in the intracellular fraction. The major portion (70 to 90 per cent) of the final P present after the completion of bacteriophagy is set free during the brief phase of bacterial dissolution. (k) When the entire process of bacteriophagy is completed the lysates are left with certain [P]'s determined by the foregone P-B reaction. The destruction of P during lysis is sufficiently regular to maintain the relationship established at the maximal [P]'s. Therefore the final [P]'s have the same points in common that were noted in "h" as applying to the maximal [P]'s. That is, they all are grouped within a narrow range of [P] values, those having been made with high Po's being of lower titre than those made with low initial [P]'s. (1) There is a significant difference in the temperature coefficients of P and B formation. Further, the temperature coefficients of P and B destruction during lysis differ in almost the same ratio. Consequently, while all experimental evidence postulates B growth as an essential conditioning factor for P formation, the temperature coefficient data suggest that the two processes are basically separate reactions. A similar interpretation holds in the case of B dissolution and P inactivation. (m) The major events in the complete process of "bacteriophagy" are mathematically predictable. The [B] at which lysis occurs under certain standard conditions for given values of Bo and Po may be calculated from the equation: See PDF for Equation Substitution of this value for log B in the equation: See PDF for Equation gives satisfactory agreement with observed values for t((lysis)). (n) The kinetic analysis of the P-B reaction predicts that the values of log Po plotted against t((lysis)) for a constant Bo will give a straight line. This plot is employed in a method for the quantitative estimation of P described in an earlier paper on the basis of experimental observation alone. Its use is made more rational by the facts given above.
J Gen Physiol 1930 Nov 20
PMID:THE KINETICS OF THE BACTERIUM-BACTERIOPHAGE REACTION. 1987 83

1. Unfertilized eggs of Chaetopterus consume about 2.4 mm.(3) O(2) per hour per 10 mm.(3) eggs at 21 degrees C. 2. In the 1st hour after fertilization, the fertilized eggs consume oxygen at about 53 or 54 per cent of this rate, which is about 1.3 mm.(3) O(2) per hour per 10 mm.(3) eggs at 21 degrees C. 3. For the first 6 hours after fertilization, at 21 degrees C., the curve of the rate of oxygen consumption is slightly asymmetrically sigmoid. The prefertilization rate is regained between 4(1/2) and 5 hours after fertilization. Soon after 6 hours, ciliary activity begins, and the rate of oxygen consumption rises rapidly. 4. The unfertilized eggs of Arbacia punctulata consume about 0.36-0.5 mm.(3) O(2) per hour per 10 mm.(3) eggs at 21 degrees C. The absolute determination is difficult as these eggs are highly sensitive to shaking in the manometer vessels, and these difficulties are discussed. 5. The fertilized eggs of Arbacia punctulata consume oxygen at the rate of about 2.0 mm.(3) O(2) per hour per 10 mm.(3) 21 degrees C. At 1 hour after fertilization the rate is already rising. 6. A comparison of the absolute rates of oxygen consumption, and the changes in rate at fertilization of these and a number of other eggs, together with a theoretical discussion, and a discussion of discrepancies in measurements on the eggs of Arbacia punctulata, is contained in the fifth paper of this series (21).
J Gen Physiol 1933 Jan 20
PMID:ON THE RATE OF OXYGEN CONSUMPTION BY FERTILIZED AND UNFERTILIZED EGGS : IV. CHAETOPTERHS AND ARBACIA PUNCTULATA. 1987 18


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