Brain structure morphology after being fixated with ethanol on electron microscope / Morfología de la estructura cerebral después de la fijación con etanol en microscopio electrónico

Fixation is one of the processes in preparing histology and pathology. The common material for fixation is buffered formalin including paraformaldehyde. However, the effect of the damaged cells, which is fixed for a long time, causes the research for other fixation materials to become necessary. In addition, paraformaldehyde is also harmful to human body and natural environment. Ethanol is one of the alternative fixation materials, which has been used for two hundred years. It has been used for many purposes, both in routine staining and immunohistochemistry. Nonetheless, no research confirms its effect on the electron microscope. The authors studied the effect of 50 % of ethanol on the cell membrane, organelles, and nucleus of Purkinje cells (Neuron purkinjense) observed on a light microscope and Transmitted Electron Microscope (TEM). Then it was compared to buffered formalin. In the light microscope, it shows that both of fixations have no different effects of the morphology of the cell membrane, cytoplasm, the nucleus of Purkinje cells and the neutrophils. We assume that our 50 % of ethanol concentration is almost the same as BF 10 % in the ability of hardening tissue and color absorption based on the previous study. In TEM, the structure of the cell membrane, organelles, and cytoplasm of Purkinje cell look broken in the cerebellum of 50 % of ethanol except for the nucleus. There was no significant difference diameter of the nucleus. It happened in general because of the shrinkage effect of ethanol. However, the authors recommend using 50 % of ethanol for routine staining.

La fijación es uno de los procesos en la preparación de muestras para histología y patología. El material más común para la fijación es la formalina tamponada. Sin embargo, el daño a las células que se mantienen en formalina durante mucho tiempo, hace necesario buscar otros materiales de fijación. Además, el paraformaldehido también es perjudicial para el cuerpo humano y el medio ambiente natural. El etanol es uno de los materiales de fijación alternativos que se ha utilizado durante muchos años, con diversos objetivos, tanto en la tinción de rutina como en la inmunohistoquímica. Sin embargo no se ha confirmdo su efecto con microscopio electrónico. Los autores estudiaron el efecto del 50 % de etanol sobre la membrana celular, los orgánulos y el núcleo de las células de Purkinje observados en un microscopio óptico y un microscopio de transmisión electrónico (TEM). Luego se comparó con la formalina tamponada. En el microscopio óptico se observó que ambas fijaciones no tienen efectos diferentes a la morfología de la membrana celular, el citoplasma, el núcleo de las células de Purkinje y los neutrófilos. Suponemos que nuestra concentración de 50 % de etanol es casi la misma que BF 10 % en la capacidad de endurecer el tejido y la absorción de color según el estudio anterior. En TEM, la estructura de la membrana celular, los orgánulos y el citoplasma de la célula de Purkinje presentaban daño en el cerebelo con un 50 % de etanol, a excepción del núcleo. No hubo diferencia significativa en el diámetro del núcleo. En general lo anterior se debió al efecto de contracción del etanol. En conclusión los autores recomiendan usar 50% de etanol para la tinción de rutina.

Ultrastructural effects of the propineb on brain of fetuses during rat pregnancy / Efectos ultraestructurales de propineb en el cerebro de fetos durante el embarazo de ratón

Propineb is a fungicide with a propylene-bis-dithiocarbamate structure. Pregnant Wistar rats were exposed to 400 ppm propineb concentrations in 5 ml distilled water, 5 days per week until the end of pregnancy. The rats were treated with propineb for 16 days and the brains of litter rats were sacrificed at first day of birth after which their brains were collected. Ultrastructural examination of the brains of the fetuses and propineb-treated pregnant females revealed a variety of histopathological effects. We suggest that mitochondrial damage may be an effective factor for neuron necrosis. These results supported the proposal that the exposure to fungicides such as propineb and to other naturally occurring compounds which inhibit mitochondrial function, may contribute to Parkinson's disease development.

El Propineb es un fungicida con una estructura de propileno-bis-ditiocarbamato. Ratas Wistar preñadas fueron expuestas a concentraciones de depropineb (400 ppm) en 5 ml de agua destilada, 5 días por semana hasta el final de la preñez. Las ratas fueron tratadas por 16 días y las crías fueron sacrificados el primer día de nacimiento para recolectar sus cerebros. El examen ultraestructural de los cerebros de los fetos y las hembras preñadas tratadas con propineb reveló una variedad de efectos histopatológicos. Sugerimos que el daño mitocondrial puede ser un factor eficaz para la necrosis neuronal. Estos resultados apoyaron la propuesta de que la exposición a los fungicidas tales como propineb y de otros compuestos de origen natural que inhiben la función mitocondrial, puede contribuir al desarrollo de la enfermedad de Parkinson.

Elevated ferric, calcium and magnesium ions in the brain induce protein aggregation in brain mitochondria / El aumento de iones férricos, calcio y magnesio en el cerebro induce la agregación de proteínas en las mitocondrias del cerebro

OBJECTIVE: Alzheimer s disease and Parkinson s disease are two of several neurodegenerative disorders that affect the elderly. Although their aetiology remains uncertain, studies suggest that elevated aluminium or other metal ions in the brain directly influence the development of the histological abnormalities normally associated with these diseases; other investigations suggest that metal-ion-induced-dysfunction of mitochondria might be a critical factor. METHODS: In this study, the impact of elevated aluminum (Al3+), ferric (Fe3+), calcium (Ca2+) and magnesium (Mg2+) ions on brain histology and on the protein composition of brain mitochondria were evaluated. Rabbits were injected intra-cerebrally with 1.4% solutions of either aluminium chloride (AlCl3), ferric chloride (FeCl2), calcium chloride (CaCl2) or magnesium chloride (MgCl2) and sacrificed 10 days later. RESULTS: Histological analysis revealed that Al3+ but not the other ions induced neurofibrillary degeneration within the midbrain and medulla. Alternatively, SDS-PAGE revealed that Fe3+, Ca2+ and Mg2+ but not Al3+ induced alterations to the distribution of brain mitochondrial proteins. Both Fe3+ and Ca2+ triggered decreased concentration of three low molecular weight proteins (~7-14 kd) but Ca precipitated their total absence. Both ions led to increased concentration of a high molecular weight protein (~ 110 kd). In contrast, Mg2+ led to the total absence of the protein of lowest molecular weight (~7 kd) and increased concentration of a ~36 kd protein. CONCLUSION: These results suggest that elevation of some metal ions in the brain induces protein aggregation with the nature of the aggregation being highly ion dependent. The results also point toward major differences between the histopathological effect of Al3+ and other ions.

OBJETIVO: La enfermedad de Alzheimer y la enfermedad de Parkinson son dos de los varios trastornos neurodegenerativos que afectan al anciano. Aunque su etiologia sigue siendo incierta, los estudios sugieren que el aumento de los iones de aluminio, influyen directamente sobre el desarrollo de las anormalidades histológicas asociadas normalmente con estas enfermedades. Otras investigaciones sugieren que la disfunción de las mitocondrias, inducida por iones metálicos, pudiera ser un factor critico. MÉTODOS: Este estudio evalúa el impacto del aumento de los iones de aluminio (Al3+), los iones férricos (Fe3+), y los iones de calcio (Ca2+) y magnesio (Mg2+) sobre la histologia del cerebro y la composición proteica de las mitocondrias del cerebro. Un número de conejos recibieron inyecciones intracerebrales de soluciones al 1.4% de soluciones de cloruro de aluminio (AlCl3), cloruro ferroso (FeCl3), cloruro de calcio (CaCl2), o cloruro de magnesio (MgCl2), y fueron sacrificados después de 10 días. RESULTADOS: El análisis histológico reveló que el Al3+ indujo una degeneración neurofibrilar dentro del mesencéfalo y la médula, Sin embargo, esto no ocurrió con los otros iones. Alternativamente, la técnica de electroforesis SDS-PAGE reveló que los iones Fe3+, Ca2+ y Mg2+, a diferencia del ión Al3+, inducían alteraciones de la distribución de las proteínas mitocondriales cerebrales. Tanto el Fe3+ como el Ca2+ desencadenaron una disminución de la concentración de tres proteínas de bajo peso molecular (~7-14 kd) pero Ca2+ precipitó su ausencia total. Ambos iones condujeron a un aumento de una proteína de peso molecular alto (~ 110 kd). En cambio, Mg2+ llevó a la ausencia total de la proteína de más bajo peso molecular (~7 kd) y al aumento de la concentración de una proteína de ~36 kd. CONCLUSIÓN: Estos resultados parecen sugerir que la elevación de algunos iones de metal en el cerebro induce la agregación de la proteína, siendo la naturaleza de la agregación altamente dependiente de los iones. Los resultados también apuntan a grandes diferencias entre el efecto histopatológico del Al3+ y otros iones.

GM1 improves neurofascin155 association with lipid rafts and prevents rat brain myelin injury after hypoxia-ischemia

White matter injury characterized by damage to myelin is an important process in hypoxic-ischemic brain damage (HIBD). Because the oligodendrocyte-specific isoform of neurofascin, neurofascin 155 (NF155), and its association with lipid rafts are essential for the establishment and stabilization of the paranodal junction, which is required for tight interaction between myelin and axons, we analyzed the effect of monosialotetrahexosyl ganglioside (GM1) on NF155 expression and its association with lipid rafts after HIBD in Sprague-Dawley rats, weighing 12-15 g, on day 7 post-partum (P7; N = 20 per group). HIBD was induced on P7 and the rats were divided into two groups: one group received an intraperitoneal injection of 50 mg/kg GM1 three times and the other group an injection of saline. There was also a group of 20 sham-operated rats. After sacrifice, the brains of the rats were removed on P30 and studied by immunochemistry, SDS-PAGE, Western blot analysis, and electron microscopy. Staining showed that the saline group had definite rarefaction and fragmentation of brain myelin sheaths, whereas the GM1 group had no obvious structural changes. The GM1 group had 1.9-2.9-fold more GM1 in lipid rafts than the saline group (fraction 3-6; all P < 0.05) and 0.5-2.4-fold higher expression of NF155 in lipid rafts (fraction 3-5; all P < 0.05). Injection of GM1 increased the content of GM1 in lipid rafts as well as NF155 expression and its lipid raft association in HIBD rat brains. GM1 may repair the structure of lipid rafts, promote the association of NF155 (or other important proteins) with lipid rafts, stabilize the structure of paranodes, and eventually prevent myelin sheath damage, suggesting a novel mechanism for its neuroprotective properties.

Morphological changes induced in the brain of rats exposed prenatally to iron and the possible protective role of folic acid

Iron supplementation is recommended during pregnancy to meet the demands of both the mother and rapidly growing fetus. However, newborns and particularly preterm infants are highly susceptible to free radical oxidative damage resulting from iron. Folic acid supplementation is needed during pregnancy and it has been shown to reduce the tissue damage resulting from iron induced oxidative stress. Thirty pregnant female albino rats were used in this experiment and divided into three groups [A, B, C]. Group [A]: Was kept as control. Group [B]: Treated with iron gluconate orally in a dose of 50 mg/kg for eleven days [from day 6-16] of gestation. Group [C]: Treated with the same dose of iron glunonate concomitantly with folic acid in a dose of 5mg/kg for the same previous duration. Samples from the brain striatum of newborns were taken and processed for light and electron microscopic investigation. The light microscopic examination of striatal area of group [B] showed necrotic changes appeared in some neurons in the form of shrinkage and condensation in their nuclei, others appeared degenerated with irregular nuclear outline and multiple vacuoles in their cytoplasm. Aggregated glial cells were observed around the blood capillary and mitotic division could be detected in some of them. Enhanced level of glial fibrillary acidic protein [GFAP] was observed in comparison to control group. Multiple iron deposits in the cytoplasm of neurons and glial cells were observed in group [B] animals. Marked improvement was observed in both neurons and glial cells of group [C]. Electron microscopy revealed apoptotic changes affecting mainly glial cells and some neurons in group [B] associated with swelling of Golgi cisternae and vacuolated mitochondria. Marked improvement was observed in both neurons and glial cells of group [C]. These results indicate that folic acid appears to reduce the iron induced neuronal damage in the brain of newly born rats exposed prenatally to iron

Histological study on the effect of aluminium chloride on frontal cortex of adult male albino rats

Several studies implicated aluminium in the pathogenesis of many neurodegenerative disorders especially Alzheimer disease, although the underlying histopathological changes in the brain were not clear with many controversies. So we aimed to elucidate these histological, immunohistochemical and ultrastructural changes that might occur in the rat brain after aluminium exposure. In this study we used 18 adult male albino rats divided into 2 groups; a control group and an experimental group taking 600 mg/ kg aluminium chloride orally daily for 4 weeks. At the end of the fourth week, samples from the frontal cortex were obtained and stained with H and E, and glial fibrillary acidic protein [GFAP]. Other samples were processed for electron microscopic examination. Morphometric study was done for GFAP immunostaining. The group taking 600 mg/ kg aluminium chloride showed decreased body weight and had developed some neurological symptoms. Routine H and E revealed presence of some shrunken pyramidal cells with pyknotic nuclei; immunoreactivity for glial fibrillary acidic protein [GFAP] was decreased compared to control group. Ultrastructurally; some neurons showed shrunken nuclei, swelling and damage of the mitochondria and dilated saccules of Golgi apparatus and endoplasmic reticulum with the appearance of vacuolated areas in the cytoplasm with splitting of myelin sheath and degeneration of some nerve fibres. Aluminium in high doses can cause alterations in neurons and nerve fibers with decreased immunoreactivity for GFAP in astrocytes in the brain, so further studies would be needed to evaluate the effects of chronic exposure in apparently healthy individuals

Evaluation of the structural changes of extremely low frequency electromagnetic fields on brain and testes of adult male mice

The increasing number of devices emitting magnetic fields raised valid questions concerning their safety and potential risk for human exposure and its limits. For this purpose fifteen adult mice were exposed to extremely low frequency electromagnetic field [ELMF] at a frequency of 60 Hertz [Hz] and intensity of 20 millitesla [mT] for 2 hours for 2 consecutive days. Other 10 animals served as a control. After their sacrifice, serum testosterone was determined. In addition, electron microscopic study of mice brains and testes was done. The present study revealed that exposure to EMF caused significant increase in serum testosterone. Electron microscopic examination of brain cells showed marked demyelination of nerve fibres with degeneration of nerve cells. There was also degeneration of some spermatogenic cells with abnormal sperm morphology. In conclusion, the present study showed evident biochemical and histopathological changes of ELMF on the brain and testis. Further studies would be useful to assess the effect of other doses of exposure and to follow the degree of reversibility of these changes. Other investigations are also advisable to minimize the above biological effects and protect against ELMF

Sildenafil citrate abuse [II]: an ultrastructural study of the long-term administration of sildenafil citrate in male albino rats

It has been reported that the most affected organs on abusing sildenafil citrate were the testis, retina, brain and heart; and that these changes were dose-and frequency-dependent. This study was set up to elucidate the ultra-structural alterations and hence the mechanism of toxicity in the retinal, cerebral, myocardial and testicular tissues which could result from administration of sildenafil citrate at a dose equivalent to the 100 mg tablet in humans administered at different frequencies. In addition, the study aimed at the assessment of the suitable dose and frequency of administration of the drug. Forty-eight male Wistar albino rats were used; and they were divided into: [n=12] negative control group. [n=36] rats received sildenafil citrate by gavage in a dose of 0.008 mg/g rat. This group was subdivided into 3 subgroups: [n=12] rats received the dose daily. [n= 12] rats received the dose day after day. [n= 12] rats received the dose once per week. The study extended for 18 weeks. Small portions from the brain, retina, heart and testes were excised and processed for electron microscopic examination. Sildenafil citrate causes histopathological alterations in the brain, retina, heart and testis in a dose-and time-dependent manner. It exerts its pathologic effects partly through persistent dilatation and thickening of t he blood vessel walls of the a forementioned tissues; and partly via direct action on the tissue cells and in particular on the mitochondria and rough endoplasmic reticulum

Changes of tumor necrosis factor-alpha and the effects of ulinastatin injection during cardiopulmonary cerebral resuscitation / 华中科技大学学报（医学）（英德文版）

The changes of tumor necrosis factor-alpha (TNF-alpha) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-alpha were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-alpha among different time points (P>0.05). In resuscitation group, the level of TNF-alpha was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-alpha showed in UTI group. There were no differences in TNF-alpha among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-alpha was expressed rapidly and kept increasing. It indicated that TNF-alpha might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-alpha and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.

Histological study of age-related alterations in the memory system of male albino rats

Fifteen male albino rats were utilized in this research aiming to study the histological alterations in the memory system [hippocampal formations] during aging, They were divided into three age groups [5 animals each]. The first group was the young one [2weeks] and the second one was the adult group [5 months]. Whereas, the third one was the aged group [15 months]. All the animals were anaesthetized with ether inhalation and their brains were dissected out carefully. Specimens from the hippocampal formations were obtained and processed for light and electron microscope examinations. Light microscope examination of the different age groups revealed that the hippocampus in coronal sections had three areas, CA1, CA2 and CA3.Each area was formed of three layers. The first and third ones contained few cells. Whereas, the second layer was formed of numerous pyramidal cells. Pyramidal cells in area CA1 in the young age group were impacted and their nerve processes were not defined. Whereas, pyramidal cells in the same area in the adult group were slightly dispersed and their nerve processes were apparent. Few glial cells were observeved. However, pyramidal cells in the aged group showed an observable decrease in their number with many glial cells in between. Also, their nerve processes were not prominent. Electron microscope examination of the same groups revealed that pyramidal cells in the young group appeared with large rounded euchromatic nuclei and their cytoplasm contained many free ribosomes. The surrounding neuropil showed astrocytes with small rounded euchromatic nuclei and electron lucent cytoplasm. Also, pyramidal cells in the adult group had large euchromatic nuclei and the cytoplasm contained many free ribosomes and rough endoplasmic reticulum. The surrounding neuropil was packed with nerve processes and glial cells. Astrocytes appeared as that demonstrated in the young group.Whereas, oligodendrocytes showed electron dense cytoplasm with few processes. In the aged group, some pyramidal neurons showed apoptosis. These affected neurons were in close contact with large oligodendrocytes with their characteristic electron dense cytoplasm and euchromatic indented nuclei with prominent nucleoli. The surrounding neuropil showed astrocytes with an increase in their nuclear heterochromatin contents and many electron lucent spaces. In conclusion, the hippocapmus showed an observable loss in its pyramidal cells during aging especially that in area CA1 with glial cell alterations which may contribute to this neuronal loss. These histological changes may clarify why amnesia is a wide spread age- related memory disorder

Inhibition of rat microsomal lipid peroxidation by the oral administration of D002

The effect of D002, a defined mixture of higher primary alcohols purified from bee wax, on in vivo and in vitro lipid peroxidation was studied. The extent of lipid peroxidation was measured on the basis of the levels of thiobarbituric acid reactive substances (TBARS). When D002 (5-100 mg/kg body weight) was administered orally to rats for two weeks, a partial inhibition of the in vitro enzymatic and non-enzymatic lipid peroxidation was observed in liver and brain microsomes. Maximal protection (46 percent) occurred at a dose of 25 mg/kg. D002 behaved differently depending on both the presence of NADPH and the integrity of liver microsomes, which suggests that under conditions where microsomal metabolism was favored the protective effect of D002 was increased. D002 (25 mg/kg) also completely inhibited carbon tetrachloride- and toluene-induced in vivo lipid peroxidation in liver and brain. Also, D002 significantly lowered in a dose-dependent manner the basal level of TBARS in liver (19-40 percent) and brain (28-44 percent) microsomes. We conclude that the oral administration of D002 (5, 25 and 100 mg/kg) for two weeks protected rat liver and brain microsomes against microsomal lipid peroxidation in vitro and in vivo. Thus, D002 could be useful as a dietary natural antioxidant supplement. More studies are required before these data can be extrapolated to the recommendation for the use of D002 as a dietary antioxidant supplement for humans

The central projection of cephalic mechanosensory axons in the haematophagous bug Triatoma infestans

The projections of mechanosensory hairs located on the dorsal and lateral head of the adult haematophagous bug Triatoma infestans were analyzed by means of cobalt filling. Axons run into the anterior and posterior tegumentary nerve and project through the brain to the ventral nerve cord. The fibres are small in diameter and run as a fascicle. Some branches run into suboesophageal and prothoracic centres; others run as far as to the mesothoracic ganglion. These sensory projections resemble that of wind-sensitive head hairs of the locust. The functional role of this sensory system in this species is discussed.

Esclerose tuberosa: relato de caso com estudo histopatológico e ultraestrutural / Tuberous sclerosis: case report with histopathological and ultrastructural study

O complexo esclerose tuberosa constitui grupo de desordens autossômicas dominantes caracterizadas por hamartomas e lesoes neoplásicas benignas que invariavelmente acometem o sistema nervoso central. Relatamos um caso de esclerose tuberosa que é o primeiro com descriçao dos achados ultraestruturais na literatura latino-americana. A paciente era feminina, tinha 2 anos de idade e apresentava síndrome de West nao responsiva ao tratamento clínico com vigabatrina, trileptal e clonazepan, sendo submetida a lobectomia frontal esquerda. Os achados histopatológicos e ultraestruturais foram condizentes com esclerose tuberosa. Estes resultados aproximam-se daqueles discutidos na literatura e auxiliam na eventual compreensao desta controversa facomatose, bem como alertam para a apresentaçao clínica como síndrome de West.

Achados anatomo-patológicos e ultraestruturais na mucopolissacaridose: relato de caso / Anatomo-pathological and ultrastructural features in mucopolysaccharidosis: case report

As mucopolissacaridoses (MPS) sao doencas de acumulo lisossomal em que ocorre defeito enzimatico especifico com consequente acumulo de glicosaminoglicanos nos tecidos. Os autores relatam o caso de necropsia de paciente do sexo masculino, com 10 anos de idade, com diagnostico clinico e laboratorial de MPS. O exame de necropsia revelou espessamento acentuado de meninges e das valvas cardiacas e hepatomegalia. O exame microscopico do encefalo evidenciou acumulo de histiocitos espumosos ao redor dos vasos e nas meninges, assim como neuronios contendo material citoplasmatico condizente com gangliosideo. Alteracoes sistemicas como acumulo de histiocitos espumosos em valvas cardiacas e figado foram evidenciados. O exame ultra-estrutural do encefalo, figado e baco demonstrouacumulo de material grumoso no interior de vacuolos em histiocitos e hepatocitos, alem de acumulo de gangliosideo nos neuronios.

Effect of noise stress on rat brain histopathology, ultrastructure and neurotransmitter activity

Exposure to noise can elicit generalized stress disturbances in the body by way of neuroendocrine mediation. The effect of exposure of a group of albino rats to noise produced by a full range loud speaker installed 50 cm directly above the animal cage producing a sine wave noise of 135 dB at 500 HZ for 3 hours daily for 7 days, was studied. Histopathological and electron microscopic [EM] examination of rat's cerebral cortex [temporal lobe], medulla oblongata and cerebellum and monoamineoxidase [MAO] and a cetyicholinesterase [AChE] enzyme activity changes in the same brain parts were recorded. The results revealed non specific degenerative reactions to stress caused by noise in exposed rats and decreased enzyme activity of AChE and MAO in the medulla oblongata and temporal lobe respectively. These changes may explain the mental, neurobehavioural changes caused by noise stress

Immunohistochemical, ultrastructural & immunoelectron microscopic study of glial fibrillary acidic protein in corpora amylacea.

Brain tissues from 10 patients (of non-neurological disease) were studied for the presence of corpora amylacea (CA) using light microscopy (LM), immunohistochemistry (IH) for localisation of glial fibrillary acidic protein (GFAP) and transmission electron microscopy (TEM). Immunoelectron microscopy (IEM) by post-embedding technique using colloidal gold was also performed in two of these patients for more precise localisation of GFAP. Three types of immunoreactivity were noted by IH under LM; some CA were completely negative for GFAP (type III), while others showed positivity, which was either diffuse (type I) or confined to the periphery (rim positivity-type II). TEM showed variable sizes in electron dense material in the centre associated with different amounts of glial filaments (GFs) at the periphery. Thus the different types of IH staining appeared to corroborate with the presence and amount of GFs in CA. The sensitive technique of IEM confirmed the presence of GFAP in all CA irrespective of their IH typing at LM. It is suggested that CA formation in astrocytes is associated with progressive fragmentation and disintegration of GFs with resulting increase in the accumulation of electron dense GFAP-negative material. As more and more of GFs get incorporated and disintegrated, it results in increase in the size of the CA. Thus, the present study clearly demonstrates that GFAP in the GFs contributes to the composition of CA.

Biochemical alterations in the levels of DNA, RNA and protein in discrete areas of rat brain following nuvacron toxicity

The levels of DNA, RNA and Protein were estimated in cerebral hemisphere, cerebellum and brain stem of male albino rats with Nuvacron [0, 0, dimethyl - 0 -1 methyl 3 - methylamino - 3 - oxe -1 - propenyl phosphate] 4 mg/kg body weight intraperitoneally [i.p.] daily for 10 days. The daily i.p. dose of Nuvacron depleted the level of DNA and protein in all brain regions. Increased level of RNA was observed in cerebral hemisphere, cerebellum and brain stem

Electron microscopy of the human brain in cerebral malaria.

Ultrastructure of erythrocytes infected with Plasmodium falciparum in human brain, obtained 3 hours post mortem revealed gross distortion of host red cells with abnormality of the red cell surface. The superficial alterations of the parasitized cells as knob-like protrusion appear to be the sites of attachment to vascular endothelium. There was evidence of platelets sticking to the injured endothelium. The endothelial vesicular membrane is in close adhesion to the parasitized red cell, and also to the platelets involved in this mechanism. Thus, explaining the sequestration of parasitized red cell and obstruction in cerebral microcirculation, cerebral oedema and low peripheral platelet count. The was no evidence of inflammation, fibrin or thrombus formation observed in our studies.

Reaction of some neuronal . to morphine administration [a histochemical study]

The Available Findings showed that morphia induce dysfunction of the ultrastructure of the nerve cells by direct injury to the mitochondria which are intimately linked with the energy and oxidation metabolism. Serious disorders of the respiratory function in nerve cells cause accumulation of incompletely oxidised products, impairment of intracellular homeostasis and reaction of other cell organelles which are not directly related to energy prodution. So, great increase of lysosmal enzymes activity occur that taking upon themselves the function of removal of semide-composition products and fatal cases cell autolysis. The features of cellular reaction to morphine showed unequal vulnerability of different types of neurones and selective sensitivity of various C.N.S. Formations