scholarly journals STUDIES ON EASTERN EQUINE ENCEPHALOMYELITIS

1939 ◽  
Vol 69 (5) ◽  
pp. 675-690 ◽  
Author(s):  
Lester S. King

After inoculation with equine encephalomyelitis virus by various routes, guinea pigs were sacrificed at early stages, before symptoms were apparent. The brains were studied histologically, with serial sections; all lesions were noted, and subjected to topographical analysis. Nine cases are presented in detail. With any given mode of inoculation the distribution of lesions varied very widely from one instance to another. In some cases, affected regions bore a striking and definite anatomical relationship to each other. These distributions can be explained only by the assumption that the anatomical pathways played some rôle in the spread of the virus. In other instances lesions were present in areas, the anatomical connections of which were entirely normal. Attention is called to the frequency of lesions in the neocortex, with intact subcortical centers. Such distribution is held to render nerve spread extremely improbable. The only satisfactory explanation of such random distributions is by direct passage of virus from the blood stream into the brain tissue. There is no histological difference between lesions which result from blood spread and those resulting from nerve spread.

2003 ◽  
Vol 23 (7) ◽  
pp. 838-844 ◽  
Author(s):  
Chie Seki ◽  
Jeff Kershaw ◽  
Paule-Joanne Toussaint ◽  
Kenichi Kashikura ◽  
Tetsuya Matsuura ◽  
...  

The authors tested the hypothesis that the oxygen content of brain tissue is negligible by injecting an intracarotid bolus of 15O-labeled tracer into rats. Under the hypothesis, the clearance rates of 15O radioactivity from the brain after injections of both 15O-labeled water (H215O) and 15O-labeled oxyhemoglobin (HbO15O) should be identical. However, the logarithmic slope of the 15O radioactivity curve after HbO15O injection (0.494 ± 0.071 min-1) was steeper than that after H215O injection (0.406 ± 0.038 min−1) ( P<0.001, n = 13), where the time range used in the comparison was between 60 and 120 seconds after the injection. A possible interpretation of this result is that nonmetabolized O15O may dwell in the brain tissue for a finite period of time before it is eventually metabolized or returned to the blood stream unaltered. These findings contradict assumptions made by models currently used to measure cerebral oxygen metabolism.


1923 ◽  
Vol 38 (2) ◽  
pp. 183-197 ◽  
Author(s):  
James B. Murphy ◽  
Ernest Sturm

In confirmation of Shirai's observation, we find that transplantable mouse tumors grow actively when inoculated into the brains of rats, guinea pigs, and pigeons, whereas subcutaneous or intramuscular grafts in the same animals fail. This growth of foreign tissue in the brain, however, takes place only when the grafted material lies entirely in the brain tissue; if it comes in contact with the ventricle a cellular reaction takes place with resultant destruction of the graft. The growth of foreign tissue in the brain may be completely inhibited by simultaneous inoculations of a small bit of autologous but not by a bit of homologous spleen tissue. Mice highly immune to subcutaneous transplants of mouse cancer show no resistance to such tumors when the inoculation is made into the brain. Although the brain is without obvious power of resistance to implants of transplantable heteroplastic mouse tumors, yet grafts of spontaneous tumors fail to grow there even, as a rule, when tumor implanted and animal host are of the same species.


1964 ◽  
Vol 206 (1) ◽  
pp. 1-7 ◽  
Author(s):  
W. Eugene Stern ◽  
R. V. Coxon

Changes in the osmolality of the blood plasma of guinea pigs were induced by peroral hydration, coupled with injections of Pitressin, by peritoneal dialysis, and by hypertonic intravenous infusions. Using freezing-point determinations on homogenates the effects of these changes upon the osmolality of the tissue fluids of the brain were investigated. The water content of the brain and its sodium and potassium content were also measured. It was found that a rise or fall in plasma tonicity exceeding about 45 mosmoles/kg water was accompanied by a change of osmolality of the tissue fluids of the brain in the same direction and by a corresponding loss or gain of water. The water movements were sufficient to produce variations in the bulk of the brain which might critically affect intracranial volume-pressure relationships. In untreated animals the osmolality of the brain fluids appeared to be somewhat greater than that of plasma.


1949 ◽  
Vol 95 (401) ◽  
pp. 930-944 ◽  
Author(s):  
H. Weil-Malherbe

The loss of consciousness in hypoglycaemia is generally regarded as a direct consequence of the fact that the brain cells are being increasingly deprived of glucose, their principal fuel. The prompt relief of symptoms by glucose administration led to a number of investigations on the effect of other substrates known to sustain the respiration of surviving brain slices in vitro. Amongst these are various mono- and disaccharides, and such acids as lactic, pyruvic, succinic or glutamic acid which may be formed from glucose in the course of its metabolism. It appeared, however, that, in contrast to their in vitro action, most of these substances, including glutamic acid, were unable to relieve the symptoms of hypoglycaemia in eviscerated or hepatectomized animals (Bollmann and Mann, 1931; Maddock, Hawkins and Holmes, 1939). Similarly, lactic and pyruvic acids were found to have no effect on the oxygen consumption of the brain or the comatose state of hypoglycaemic patients undergoing insulin shock therapy (Wortis and Goldfarb, 1940; Goldfarb and Wort is, 1941). It has been shown for several substrates, including glutamic acid, that their rate of diffusion from the blood stream into brain tissue was markedly slower than that of glucose, and that therefore the concentration necessary for the maintenance of nervous function was not reached (Klein, Hurwitz and Olsen, 1946; Klein and Olsen, 1947). In harmony with this are the observations of Fried berg and Greenberg (1947), and of Waelsch, Schwerin and Bessman (1949) that intravenously injected glutamic acid is not taken up by brain tissue. The differences between the in vitro and in vivo results seemed to be adequately explained by these experiments.


1936 ◽  
Vol 63 (3) ◽  
pp. 311-324 ◽  
Author(s):  
Peter K. Olitsky ◽  
Herald R. Cox

Active Eastern or Western equine encephalomyelitis virus in three forms,—chemically untreated but simply passaged through series of mice; adsorbed on alumina Gel C, and precipitated by tannin,—yielded practically the same results when employed for the immunization of guinea pigs. The virus is not inactivated by the process of adsorption or precipitation : guinea pigs and mice inoculated in the brain with these materials develop lethal encephalomyelitis in the same manner as when chemically untreated mouse passage virus has been used. Moreover, there is no difference in the rate of absorption in vivoof the chemically treated and untreated virus preparations. After storage of the three immunizing preparations—the longest periods thus far studied being 2 to 3 months for mouse passage and for precipitated suspensions, and 6 months for adsorbed material—each was found to contain an amount of virus sufficient to produce immunity in animals against the usual intracerebral test inoculation. Finally, the protection afforded by the three preparations is apparently durable, as is true of many active viruses utilized in preventive treatments. The amount of the virus necessary to confer protection may be defined as that which immunizes (a) with the least number of antigenic units and (b) with the minimum of febrile reaction and blood infection. In proportion as this amount is exceeded, the incidence of fever and of circulating virus increases and, on the other hand, as this amount is decreased, the degree of induced immunity is diminished. We have thus shown that for this particular virus and in the guinea pig, one or two subcutaneous doses of I cc. of any of the different virus preparations, each containing 3 x 103 to 3 x 104 mouse infective units, bring about protection regularly against experimental infection by way of the nose or subcutis. The results are irregular when the test is made by way of the brain. By three injections, resistance is invariably obtained against as many as 103 to 104 lethal doses, given intracerebrally. No matter in what form the virus is given, as mouse passage, or adsorbed, or precipitated material, in certain instances fever occurs and virus circulates. With the amount of virus adequate for immunization (3,000 to 30,000 m.i.u.) a mild or subclinical infection may occur in the guinea pig without other manifestation of disease. Lesser quantities of virus apparently fail to gain a foothold in the animal and thus fail to bring about resistance. To conclude, a quantitative basis has been established for the comparison of the immunizing capacities of preparations employed in experimental equine encephalomyelitis in guinea pigs.


2019 ◽  
Vol 15 (3) ◽  
pp. 251-257
Author(s):  
Bahareh Sadat Yousefsani ◽  
Seyed Ahmad Mohajeri ◽  
Mohammad Moshiri ◽  
Hossein Hosseinzadeh

Background:Molecularly imprinted polymers (MIPs) are synthetic polymers that have a selective site for a given analyte, or a group of structurally related compounds, that make them ideal polymers to be used in separation processes.Objective:An optimized molecularly imprinted polymer was selected and applied for selective extraction and analysis of clozapine in rat brain tissue.Methods:A molecularly imprinted solid-phase extraction (MISPE) method was developed for preconcentration and cleanup of clozapine in rat brain samples before HPLC-UV analysis. The extraction and analytical process was calibrated in the range of 0.025-100 ppm. Clozapine recovery in this MISPE process was calculated between 99.40 and 102.96%. The limit of detection (LOD) and the limit of quantification (LOQ) of the assay were 0.003 and 0.025 ppm, respectively. Intra-day precision values for clozapine concentrations of 0.125 and 0.025 ppm were 5.30 and 3.55%, whereas inter-day precision values of these concentrations were 9.23 and 6.15%, respectively. In this study, the effect of lipid emulsion infusion in reducing the brain concentration of drug was also evaluated.Results:The data indicated that calibrated method was successfully applied for the analysis of clozapine in the real rat brain samples after administration of a toxic dose to animal. Finally, the efficacy of lipid emulsion therapy in reducing the brain tissue concentration of clozapine after toxic administration of drug was determined.Conclusion:The proposed MISPE method could be applied in the extraction and preconcentration before HPLC-UV analysis of clozapine in rat brain tissue.


2020 ◽  
Vol 11 (1) ◽  
pp. 241-250
Author(s):  
Zhenyu Li ◽  
Guangqian Ding ◽  
Yudi Wang ◽  
Zelong Zheng ◽  
Jianping Lv

AbstractTranscription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotype 8 (AAV8) vectors overexpressing mouse TFEB (pAAV8-CMV-mTFEB), or AAV8 vectors expressing green fluorescent proteins (GFPs) in the barrel cortex. The brain tissue samples were collected at 2 months after injection. Western blotting and immunofluorescence staining showed that mTFEB protein levels were significantly increased in the brain tissue samples of mice injected with mTFEB-overexpressing vectors compared with those injected with PBS or GFP-overexpressing vectors. pAAV8-CMV-mTFEB injection resulted in significant elevations in the mRNA and protein levels of lysosomal biogenesis indicators in the brain tissue samples. No significant changes were observed in the expressions of GFAP, Iba1, and proinflammation mediators in the pAAV8-CMV-mTFEB-injected brain compared with those in the control groups. Collectively, our results suggest that AAV8 successfully mediates mTFEB overexpression in the mouse brain without inducing apparent local inflammation, supporting the safety of TFEB-based gene therapy in treating neurodegenerative diseases.


2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.


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