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At least 343 records · Page 19Linked to original sources

The microscopic structure of fibrous articular surfaces: a review.

The present knowledge of the microscopic structure of fibrous articulating surface is reviewed. The influence of dissection, postmortem change, fixation, and dehydration on the microscopic appearances of these surfaces is considered. The results of those studies of surface morphology that investigate intact, supported specimens and that are controlled by surveys of fresh, unfixed, or frozen material are advantageous. New information on the effects of alterations in intermaxillary relationship on the morphology of fibrous articulating surfaces is presented. There is need for further work in this field of research.

Animals↗

Blood level of mitochondrial aspartate aminotransferase as an indicator of the extent of ischemic necrosis of the rat liver.

To assess the severity of ischemic liver injury, we examined release of mitochondrial aspartate aminotransferase (EC 2.6.1.1) and its cytoplasmic isozyme from the ischemic rat liver into the circulation. Their patterns of leakage were quite different: the level of cytoplasmic aspartate aminotransferase reached a peak soon after the circulation to the ischemic liver was restored, while that of mitochondrial aspartate aminotransferase increased slowly, reaching a maximum after more than 10 hr. On anoxic incubation of mitochondria isolated from the normal liver, oxidative phosphorylation capacity was lost within 2 hr, at which time no leakage of matrix enzymes was observed: more than 10 hr after-loss-of-oxidative phosphorylation were needed for the matrix enzymes to leak out of the mitochondrial membrane. Since the viability of cells is considered to depend on the capacity of oxidative phosphorylation, it is highly likely that the delayed appearance of mitochondrial aspartate aminotransferase in blood indicates the postmortem changes of injured cells. In fact, the cumulative activity of mitochondrial aspartate aminotransferase but not cytoplasmic aspartate aminotransferase in circulation after ischemic liver injury correlated fairly well with the decrease of total adenine nucleotides which were monitored to measure viable cells. The difference between mitochondrial aspartate aminotransferase and cytoplasmic aspartate aminotransferase as quantitative indices of hepatic necrosis may be due to the relative stability of the former and significant inactivation of the latter during hepatic ischemia. Therefore, the determination of mitochondrial aspartate aminotransferase in blood may be useful in the assessment of liver necrosis after ischemic injury.

Adenine Nucleotides↗

Environmental scanning electron microscopy observation of the ultrastructure of Demodex.

In this study, numbers of Demodex of hair follicles and sebaceous glands were prepared and the ultrastructure (especially the mouthparts) of Demodex was observed firstly with environmental scanning electron microscopy (ESEM). The most suitable treatment methods and optimal environmental condition for observing the genus samples were found. The samples were washed with detergent and rinsed with distilled water, and then were taken to the specimen stage, on which there was carbon adhesive tape, using special tools. When the temperature was at 5 degrees C and chamber pressure at 5 mbar respectively, the surface of the samples could be fully imaged without covering water or dehydration. The sample surfaces were plump and clear without postmortem changes and charging artifacts. Detailed information about each part of Demodex was observed by ESEM, and clear three-dimensional images were recorded. The mouthparts of D. folliculorum were composed of a complex set of structures, which included a round oral opening, a sharp oral needle, and a special hypostome that looked like a longitudinal spindle in the central position. On the end segment of palpus, there were seven strong palpal claws located on each side of the mouthparts. D. folliculorum had special piercing mouthparts, while the mouthparts of D. brevis were a simpler structure. We could not observe the oral needle of D. brevis, and there were only five pairs of palpal claws on the end segment of palpus. The offensive organs of Demodex resulted in its pathogenic effects. After studying hundreds of Demodex, we identified both female and male species of D. folliculorum, but only females of D. brevis in our sample.

Animals↗

Generation of 2-arachidonoylglycerol, an endogenous cannabinoid receptor ligand, in picrotoxinin-administered rat brain.

The levels of 2-arachidonoylglycerol, an endogenous cannabinoid receptor ligand, and other molecular species of monoacylglycerols in rat brain were examined. In this study, we sacrificed the animals in liquid nitrogen to minimize postmortem changes. We found that rat brain contains 0.23 nmol/g tissue of 2-arachidonoylglycerol, which accounts for 10.5% of the total monoacylglycerol present in this tissue. We next investigated the level of 2-arachidonoylglycerol after in vivo stimulation with picrotoxinin. We found that the level of 2-arachidonoylglycerol was elevated markedly in picrotoxinin-administered rat brain (4- to 6-fold over the control level). Changes in the levels of other molecular species were relatively small or negligible. Several cannabimimetic molecules as well as Delta(9)-tetrahydrocannabinol are known to depress neurotransmission and to exert anticonvulsant activities; endogenous 2-arachidonoylglycerol produced during neural excitation may play a regulatory role in calming the enhanced synaptic transmission.

Animals↗

Meat flavor: contribution of proteins and peptides to the flavor of beef.

While the majority of meat flavor is lipid in origin, the contribution of peptides and amino acids to overall meat flavor should not be overlooked. Amino acids and peptide levels have been shown to change with postmortem aging in muscle and with dry-curing, a process similar to PMA. Variation in protein, peptide, and amino acid composition have also been shown to occur with heating and with post-heating storage of meat. This makes a large pool of reactive components that may directly affect flavor or indirectly affect flavor by reacting with reducing sugars to form Maillard reaction products and Strecker degradation products that impact meat flavor. Further research in this area should continue with particular emphasis on natural peptide flavor enhancers, modulators, and potentiators.

Animals↗

[Malignant granular-cell tumor of the cerebral white matter: morphological, cytophotometrical and neurochemical studies (author's transl)].

This is a report of the second known case of a primary malignant granular-cell tumor of the cerebral hemispherical white matter. Two cell types may be distinguished apparently representing different developmental stages of otherwise identical tumor cells. Quantitative histochemical and biochemical studies have shown that tumor cells were containing markedly elevated levels of DNA and RNA. Only few ribosomes and polysomes could be detected, however, by electron microscopy. While cytophotometry disclosed only slightly elevated cytoplasmic proteins, there was a distinct increase in total protein concentration of tumor tissue per unit weight, as measured by conventional techniques. It is suggested that this increase is mainly attributable to structural proteins of cellular and subcellular elements of multiplicating malignant cells. A ratio of RNA to DNA in excess of 1 was found for white matter derived from the central tumor, while the ratios of control tissue were lowered to values far below one due to postmortem changes greatly reducing tissue concentrations of RNA. No detailed characterization of RNA was attempted. The nuclear DNA content of tumor cells reached values equivalent to chromosomal hexadekaploidy. This was in sharp contrast to control data from an Abrikossoff tumor of the oral cavity and from a neurohypophyseal tumorette ("choristoma"), respectively, displaying diploidy only associated with a much lesser increase of cytoplasmic RNA and proteins. Qualitative lipid studies were consistent with a marked active demyelination of the tumor centre as indicated by a severe reduction of cerebrosides and sulfatides and the presence of cholesterol esters. In addition there was a striking loss of phosphatidylethanolamine and a lesser one of sphingomyelin of white matter of both the tumor-stricken and the contralateral unaffected hemispherical regions, possibly suggesting a generally disturbed metabolism of myelin. It is not clear whether these general changes were resulting from the presence of the unilateral tumor or from precocious cerebral involution.

Brain Neoplasms↗

Microwave fixation: its potential for routine techniques, histochemistry, immunocytochemistry and electron microscopy.

Human tissues, both biopsy and postmortem, and tissues from rodents were fixed by microwaves at various temperatures and compared against formaldehyde-fixed material. Conventional stains, including trichromes, worked well. Red cells were lysed, but white cells were fixed, thus permitting diagnoses of various inflammatory states. Malignant cells were equally well-preserved by the two methods. Histochemical investigations of mucosubstances, lipids and various hydrolases showed no significant difference between the two techniques. Some neurological stains, however, were not as good following microwave treatment. Immunocytochemical localization of IgA, IgM and IgG showed no significant difference after microwave fixation compared to that in tissues fixed with formaldehyde. Microwave fixation did not lead to a greater tissue shrinkage than that obtained with formaldehyde fixation. Both were significantly less than that following treatment with phosphate-buffered saline alone. Electron microscopy gave results which were interpretable, but with damage resembling early postmortem change. Microwave fixation is complete in approximately 1-2 min. The mechanism of fixation appears to be due to denaturation associated with disulphide bond formation and a decrease in solubility of proteins.

Animals↗

Distribution of xanthine oxidoreductase activity in human tissues--a histochemical and biochemical study.

Localization of the activity of both the dehydrogenase and oxidase forms of xanthine oxidoreductase were studied in biopsy and postmortem specimens of various human tissues with a recently developed histochemical method using unfixed cryostat sections, poly-(vinyl alcohol) as tissue stabilizator, 1-methoxyphenazine methosulphate as intermediate electron acceptor and Tetranitro BT as final electron acceptor. High enzyme activity was found only in the liver and jejunum, whereas all the other organs studied showed no activity. In the liver, enzyme activity was found in sinusoidal cells and both in periportal and pericentral hepatocytes. In the jejunum, enterocytes and goblet cells, as well as the lamina propria beneath the basement membrane showed activity. The oxidase activity and total dehydrogenase and oxidase activity of xanthine oxidoreductase, as determined biochemically, were found in the liver and jejunum, but not in the kidney and spleen. This confirmed the histochemical results for these organs. Autolytic rat livers several hours after death were studied to exclude artefacts due to postmortem changes in the human material. These showed loss of activity both histochemically and biochemically. However, the percentage activity of xanthine oxidase did not change significantly in these livers compared with controls. The findings are discussed with respect to the possible function of the enzyme. Furthermore, the low conversion rate of xanthine dehydrogenase into xanthine oxidase during autolysis is discussed in relation to ischemia-reperfusion injury.

Animals↗

Fatality involving vinblastine overdose as a result of a complex medical error.

The purpose of the study is a presentation of a fatal case involving an 83-year-old woman, who died due to an overdose of vinblastine-a cytostatic agent of a vinca alkaloid employed in cancer chemotherapy. The postmortem investigation included an autopsy and histological examination, as well as a toxicological analysis of post-mortem specimens collected in the course of autopsy. The authors performed a toxicological assessment of vinblastine employing liquid chromatography-atmospheric pressure chemical ionization-tandem mass spectrometry (LC-MS-MS-APCI). The determined vinblastine concentration levels amounting to 29 ng/g in blood and 52.5 ng/g in liver were in a considerable excess of values encountered in patients on chemotherapy using the drug. The fatality was investigated in the context of medical error. In the described case, the erroneous and medically unjustified administration of vinblastine was identified by a series of unfortunate events involving as many as three acting consecutively individuals: a physician, a pharmacist and a nurse. The report may thus document the clinical course of vinblastine poisoning along with postmortem changes resulting from the drug action.

Accidents, Traffic↗

Intrauterine fetal death due to Farber disease: case report.

We report a case of Farber disease in a fetus who died in utero at a gestational age of 29 weeks. Macroscopic examination showed moderate postmortem changes in a microcephalic female fetus (46,XX) with mild internal hydrops, two vessels in the umbilical cord, and a moderately enlarged, relatively well-preserved spleen. Microscopic examination showed foamy cells in the spleen. Electron microscopic examination revealed the presence of Farber bodies within these foamy cells. Enzyme studies of the fetus were not possible because all tissues were formalin fixed. Lipids were extracted from formalin-fixed tissues and increased levels of ceramide and the presence of hydroxyceramide in tissue of the spleen, liver, and lung were found. Glucosylceramide was not increased excluding saposin-precursor-deficiency. Because of these findings, both parents were tested for acid ceramidase activity in their leukocytes. They both had markedly reduced enzyme activity consistent with heterozygosity for Farber disease. To the best of our knowledge, this is the first published case of Farber disease in Dutch nonconsanguineous parents.

Acid Ceramidase↗

Measurement of kynurenic acid in mammalian brain extracts and cerebrospinal fluid by high-performance liquid chromatography with fluorometric and coulometric electrode array detection.

Kynurenic acid is a broad-spectrum excitatory amino acid (EAA) receptor antagonist which is present in the mammalian central nervous system. We describe a method for the measurement of kynurenic acid using isocratic reverse-phase high-performance liquid chromatography (HPLC) with fluorometric detection enhanced by Zn2+ as a postcolumn reagent. The method requires no prior sample preparation procedures other than extraction with 0.1 M HClO4. The reliability of the primary fluorometric method was verified by comparing measurements of tissue concentrations of kynurenic acid in human cerebral cortex and putamen using three different methods of separation with fluorometric detection, as well as four methods utilizing HPLC with coulometric electrode array system (CEAS) detection. All seven methods produced comparable results. The concentration of kynurenic acid in human cerebral cortex was 2.07 +/- 0.61 pmol/mg protein, and in human putamen, 3.38 +/- 0.81 pmol/mg protein. Kynurenic acid was also found to be present in human cerebrospinal fluid (CSF) at a concentration of 5.09 +/- 1.04 nM. The regional distribution of kynurenic acid in the rat brain was examined. Kynurenic acid concentrations were highest in brainstem (149.6 fmol/mg protein) and olfactory bulb (103.9 fmol/mg protein) and lowest in thalamus (26.0 fmol/mg protein). There were no significant postmortem changes in kynurenic acid concentrations in cerebral cortex, hippocampus, and striatum at intervals ranging from 0 to 24 h. Perfusion of the cerebral vasculature with normal saline prior to sacrifice did not significantly alter kynurenic acid content in rat hippocampus, cerebral cortex, or striatum. The analytical methods described are the most sensitive (10-30 fmol injection-1) and specific (utilizing both excitation and emissions properties and electrochemical reaction potentials, respectively) methods for determining kynurenic acid in brain tissue extracts and CSF. These methods should prove useful in examining whether kynurenic acid modulates EAA-mediated neurotransmission under physiologic conditions, as well as in determining the role of kynurenic acid in excitotoxic neuronal death.

Animals↗

GABA concentrations in forebrain areas of suicide victims.

Concentrations of GABA and seven other amino acids, including the neurotransmitters or neuromodulators taurine, glycine, aspartate, and glutamate, were determined in postmortem brain samples from suicide victims and normal controls. The five brain areas (caudate nucleus, nucleus accumbens, frontal cortex, amygdala, and hypothalamus) contained very similar concentrations of the amino acids in both groups. The only significant difference between the groups was a low glutamine concentration in the hypothalamus of suicide victims. Even when the data were adjusted for differences in tryptophan concentration, a putative biochemical index for agonal and postmortem changes of brain tissue, no new differences emerged in the concentrations of neuroactive amino acids between suicide victims and control subjects.

Adolescent↗

Corticonigral degeneration with neuronal achromasia presenting with primary progressive aphasia: ultrastructural and immunocytochemical studies.

We describe a clinico-pathological variant of a degenerative disorder involving Broca's, Wernicke's, and supplementary motor areas, which presented as primary progressive aphasia, dysarthria, bucco-facial apraxia, and hearing loss as initial symptoms, followed by organic personality changes. Postmortem examination revealed severe focal atrophy of the cerebral convolutions in the frontal operculum, superior frontal gyrus, and superior and transverse temporal gyri in addition to diffuse atrophy of the frontal and temporal lobes in both hemispheres. Microscopical examination revealed argyrophilic neuronal inclusions (ANIs) in the neuronal perikarya and presynaptic terminal throughout the central nervous system, as well as neuronal loss and swollen chromatolytic neurons in the affected cortices. Neocortical ANIs showed a positive immunoreaction with an anti-tau antibody but only a weak reaction with an anti-ubiquitin antibody immunohistochemically. Ultrastructurally, neocortical ANIs consisted of 15-nm thick smooth-surfaced tubules and tubules with constrictions at 120-150-nm intervals; thus they were different from the typical paired helical filaments of the 80-nm interval constrictions observed in the subiculum. ANIs were also found in the basal ganglia, brain stem nuclei, and cervical cord. Accordingly, ANIs appear distinct from neurofibrillary tangles (NFTs) of progressive supranuclear palsy, NFTs of Alzheimer-type dementia, and Pick bodies. The authors consider that this case fits the histopathological criteria of corticonigral degeneration with neuronal achromasia except for the unusual extension to the temporal lobes.

Aphasia↗

Mesothelioma of spermatic cord: electron microscopic and histochemical characteristics of its mucopolysaccharides.

A mesothelioma of the spermatic cord occurred at the site of multiple hernial repairs. The aggressive biologic behavior of this tumor is exhibited by its early lymph node invasion and extensive metastases to the pleural cavities, lungs, and spleen. These tumor cells contained a large amount of stable of stable glycogen-like carbohydrate insoluble in formalin and tolerating postmortem changes. Electron microscopy revealed features similar to those mesotheliomas arising from body cavities.

Female↗

Determination of 9 alpha, 11 beta-prostaglandin F2 by stereospecific antibody in various rat tissues.

In view of the recent finding that prostaglandin D2 is stereospecifically converted to 9 alpha, 11 beta-prostaglandin F2, an isomer of prostaglandin F2 alpha, a highly specific and sensitive radioimmunoassay for 9 alpha, 11 beta-prostaglandin F2 was developed and applied to determine the content of this prostaglandin in various rat tissues. Antisera against 9 alpha, 11 beta-prostaglandin F2 were raised in rabbits immunized with the bovine serum albumin conjugate, and [3H]9 alpha, 11 beta-prostaglandin F2 was enzymatically prepared from [3H]prostaglandin D2. The assay detected 9 alpha, 11 beta-prostaglandin F2 over the range of 20 pg to 1 ng, and the antiserum showed less than 0.04% cross-reaction with prostaglandin F2 alpha, prostaglandin F2 beta and 9 beta, 11 beta-prostaglandin F2. To avoid postmortem changes, tissues were frozen in liquid nitrogen immediately after removal. The basal level of 9 alpha, 11 beta-prostaglandin F2 was hardly detectable in various tissues of the rat examined, including spleen, lung, liver and brain; although it was found to be 0.31 +/- 0.06 ng/g wet weight in the small intestine. During convulsion induced by pentylenetetrazole, enormous amounts of prostaglandin D2 (ca. 180 ng/g wet weight) and prostaglandin F2 alpha (ca. 70 ng/g) were produced in the brain; however, 9 alpha, 11 beta-prostaglandin F2 was detected neither there nor in the blood. This result demonstrates that the conversion to 9 alpha, 11 beta-prostaglandin F2 is a minor pathway, if one at all, of prostaglandin D2 metabolism in the rat brain.

Animals↗

Evaluation of microwave irradiation technique to quantitate acetylcholine in the diaphragm.

This report evaluates rapid enzyme inactivation prior to acetylcholine quantitation in the diaphragm. Methods of sacrifice were decapitation and microwave irradiation. Six-hundred millisecond exposure to microwave irradiation was sufficient to raise diaphragmatic temperature to 91 degrees C and inactivated 90% of the acetylcholinesterase enzyme. The acetylcholine content of the diaphragm was found to be 3.0 nmol/g, independent of the method of sacrifice. The postmortem changes observed in brain acetylcholine content following decapitation did not occur in the diaphragm.

Acetylcholine↗

Ninety-day toxicity study of sodium monochloroacetate in Sprague-Dawley rats.

Male and female Sprague-Dawley rats were administered the sodium salt of monochloroacetic acid (SMCA) by oral gavage for a period of 90 consecutive days. Dosage levels of 15, 30, 60 or 120 mg/kg per day were employed. SMCA clearly induced toxicity in both females and males, with the greatest severity in the male animals. Both the liver and kidneys were identified as target organs. At 120 mg/kg per day, 30% of females and 80% of the males died, most within the first 2 days of treatment. Hemorrhagic and congested lungs (possibly a postmortem change) were seen in the early deaths (1-3 days) whereas liver lesions were observed in later deaths. In addition, there was nephrotoxicity as evidenced by elevated creatinine, blood calcium (BCAL), and blood urea nitrogen (BUN) levels. Hepatotoxicity was indicated by increases in the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Both organs showed increased organ-to-body weight ratios. Microscopic examination revealed a significant (P less than or equal to 0.001) increase in chronic renal nephropathy and increased splenic pigmentation at 60 mg/kg per day in the males. Based on the observation of toxicity at all treatment levels in males, a lowest observed adverse effect level (LOAEL) of 15 mg/kg per day is proposed for a 90-day exposure to SMCA by oral gavage to the Sprague--Dawley rat.

Acetates↗

Establishment of camel isolates of Haemonchus longistipes and Trichostrongylus colubriformis in goats.

Two main nematode parasites, Haemonchus longistipes and Trichostrongylus colubriformis, have been reported to cause morbidity and mortality in camels. Although goats are usually reared with camels in the combined animal husbandry system prevailing in Northern India, these parasites have not been reported in goats. Therefore, it was planned to conduct an experimental cross-transmission study of H. longistipes and T. colubriformis isolated from camels and transferred to young goats. Twelve healthy kids (5-6 months) were divided into three groups of four each. Groups I and II were infected orally with third stage infective larvae of H. longistipes and T. colubriformis cultured in the laboratory from faecal isolates from camels, at the rate of 50,000 and 100,000 larvae, respectively; group III comprised uninfected healthy controls. Daily clinical and faecal examinations were made. Body weights and blood haematological indices were measured at weekly intervals. The infection became established in both infected groups, and the animals started passing ova 17 days postinfection. Egg counts varied from 275.00 +/- 248.74 to 6150 +/- 2830.63 eggs g-1. Animals were killed 28 days postinfection. On postmortem examination mature as well as immature worms were recovered from the abomasum and intestine with typical postmortem changes seen in both the groups. Clinical manifestations were weakness and loss of body weight but no diarrhoea. There was a marked fall in haemoglobin and packed cell volume, indicating anaemia in both infected groups.

Abomasum↗