Endopectate lyase from Erwinia aroideae.
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Chromatography, Gel↗
Biomedical subjects
H Konno
Publications and source records attributed to H Konno.
Sequelae of the osmotic blood-brain barrier opening in rats.
Histopathological sequelae of the osmotic blood-brain barrier opening were studied in 69 adult Wistar rats sacrificed between 2 minutes and 6 days after infusion of 1.6 M mannitol into the unilateral internal carotid artery. The results were correlated with immunohistochemical localization of autologous albumin in the brain parenchyma on paraffin sections. Extravasation of serum albumin was evident in all rats, and the albumin immunoreactivity, commonly localized to the territories of the ipsilateral anterior, middle, and posterior cerebral arteries and contralateral anterior cerebral artery, showed maximum intensity in the rats sacrificed 30 minutes after infusion. The albumin immunoreactivity remained macroscopically visible in the brain parenchyma for 24 to 48 hours, and then gradually faded out. Serum extravasation was accompanied by widening of the perivascular space and focal edema, which largely subsided within 48 hours as the albumin immunoreactivity of the tissue diminished. Although no overt neurological sequelae were seen in the present experiment, minute but definite foci of infarction with focal accumulation of albumin were found in 23 (38%) of 61 rats surviving more than 30 minutes. In addition, ischemic neuronal death of delayed onset was encountered among neurons in the CA-1 region of the hippocampus, in the cerebellum, and in the thalamus in five (25%) of 20 rats sacrificed between Days 4 and 6. Thus, care should be exercised in the practice of this procedure.
Animals↗
Intraoperative imprint cytology of the thyroid gland with computer-assisted morphometric analysis of cell clusters.
Imprint preparations were used in addition to frozen sections in the intraoperative diagnosis of 37 cases of benign and malignant lesions of the thyroid gland, including adenomatous goiter, follicular adenoma, follicular carcinoma and papillary carcinoma. In the imprints, the cytologic features specific for carcinoma, as compared with benign lesions, were (1) the folding of the nuclear contour, (2) the increased density of the cytoplasmic matrix and (3) the frequent appearance of cell clusters of larger size. The size and frequency of cell clusters were morphometrically analyzed by a computer image analyzer. There was an increasing number of large clusters, plus the appearance of clusters of more than 300 micron in diameter, in both follicular and papillary carcinoma. In benign lesions, on the contrary, the majority of cells were isolated or in small clusters, the diameter of which never exceeded 300 micron in diameter. These results demonstrate that (1) the imprint cytology of the thyroid gland is useful in making a rapid intraoperative diagnosis and (2) the introduction of computer-assisted quantitative analysis is of practical value in the diagnosis of malignancy.
Adenocarcinoma↗
[On anterior horn cells of the spinal cord].
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Amyotrophic Lateral Sclerosis↗
[Repeated intra-abdominal administration of CDDP in carcinomatous peritonitis due to gastric cancer--a case report].
Two years and 10 months after gastrectomy, a 38-year-old man was diagnosed as having carcinomatous peritonitis due to gastric cancer. He was treated by intra-abdominal administration of 100 mg CDDP three times in addition to UFT. After each administration of CDDP, the amount of ascites and the serum value of CEA were decreased. Subjective symptoms, such as epigastric pain or sensation of fullness, were also improved. Although one year and 8 months has passed since the first administration of CDDP, the performance status of the patient remains 0. Nausea or vomiting was noted within 2 days after each administration. However, severe complications, like renal failure or intra-abdominal hemorrhage, were not observed. These findings suggest that repeated intra-abdominal administration of CDDP may be a useful therapy for carcinomatous peritonitis due to gastric cancer.
Adenocarcinoma↗
Antitumor effect of adriamycin entrapped in liposomes conjugated with anti-human alpha-fetoprotein monoclonal antibody.
The monoclonal antibody, 19-F-12 (IgG2b), against human alpha-fetoprotein was conjugated to liposomes containing Adriamycin, and the therapeutic effects of the conjugate were experimentally studied using the alpha-fetoprotein-producing human hepatoma strain, Li-7, maintained in BALB/c nu/nu male mice. Three i.v. injections of liposomes containing Adriamycin (7.5 mg/kg) into tumor-bearing mice significantly inhibited the tumor growth, and the therapeutic effect of the antibody-conjugated liposomes was greater than that of unconjugated liposomes, as judged from the tumor weights and histological findings. Furthermore, the experiments were repeated with Adriamycin (4-5 mg/kg) in free form, since administration of Adriamycin (7.5 mg/kg) in free form was highly toxic for the mice. The results still indicated that the therapeutic effect of Adriamycin in 19-F-12 conjugated liposomes was superior to that of free Adriamycin or Adriamycin in unconjugated liposomes. In contrast to the treatment for Li-7 in nude mice, the therapeutic effect of Adriamycin in 19-F-12 conjugated liposomes was not much different from that of Adriamycin in normal mouse IgG (IgG2b fraction) conjugated liposomes against alpha-fetoprotein-negative human breast cancer strain MX1. Tissue distribution studies after i.v. injection of Adriamycin in various forms into mice revealed that preferential delivery of Adriamycin to tumors occurred to some extent with antibody-conjugated liposomes as compared to the unconjugated liposomes. In addition, reduction of the distribution of Adriamycin to the heart was achieved by administering the drug in the liposome-entrapped form, and this enabled the use of a higher dose (7.5 mg/kg) of Adriamycin without toxic side effect.
Animals↗
Suppression of neurofilament degradation by protease inhibitors in experimental spinal cord injury.
Intraperitoneal administration of the neutral protease inhibitors leupeptin and E-64c substantially suppressed the degradation of neurofilament proteins (NFP) at the site of mechanical insult and secondary axonal degeneration, and facilitated the recovery of motor functions in acute spinal cord injury in rats. The drug effects were assessed by sodium dodecyl sulphate polyacrylamide gel electrophoresis of NFP fractions from the injured tissue and by morphometry of degenerating axons revealed by the Fink-Heimer method in distal spinal cord segments with the aid of an automated image analyzer. The role of calcium-activated neutral proteases in acute central nervous tissue damage and potential use of protease inhibitors as therapeutic modalities are discussed.
Animals↗
Nemaline bodies in spinal progressive muscular atrophy. An autopsy case.
Numerous nemaline bodies were demonstrated in the pectoralis major muscle of an autopsy case of a 52-year-old woman, who died of respiratory failure after having suffered from spinal progressive muscular atrophy for 1 year. Rod-like structures ultrastructurally indistinguishable from classical nemaline bodies were abundant in both normal-appearing and atrophic myofibers of the pectoralis major muscle but not in the appendicular skeletal muscles. Morphometric analysis of spinal anterior horn cells clearly showed severe depopulation of somatic motor neurons in the lower cervical cord segments. The present case may provide further support for the neurogenic nature of nemaline body formation.
Female↗
Gas chromatography-electron impact-mass spectrometry (GC-EI-MS) analysis of saturated fatty acid compositions in formalin-fixed human tissues.
Applicability of the gas chromatography-electron impact-mass spectrometry and data system (GC-EI-MS) for fatty acid analysis of formalin-fixed human tissues was evaluated by comparison of formalin-fixed and unfixed brain tissues, and the results of GC-EI-MS analyses of the formalin-fixed brain and adrenal cortex from cases with adrenoleukodystrophy (ALD) and the cerebro-hepato-renal syndrome of Zellweger (ZWS) were presented. When formalin-fixed and unfixed materials were compared, a reduction of polyunsaturated fatty acids was observed after formalin fixation, while saturated and monounsaturated fatty acids remained unchanged. The chromatographic patterns of brain tissues fixed in 10% formalin for 3 days or 17 months were basically the same. In ALD, increased C26:0/C22:0 ratios in the cerebral white matter (2.05 in ALD versus 0.74 in control) and in the adrenal gland (15.2 in ALD versus 0.1 in control), and the presence of unusual very long chain fatty acids (VLCFA), longer than C29:0, were demonstrated. In the ZWS brain, all of the VLCFAs were severely depleted. Thus, formalin-fixed tissue may be a reliable subject to fatty acid analysis.
Adrenal Cortex↗
Glutamine synthetase of the human brain: purification and characterization.
Glutamine synthetase (GS) isolated from human brain formed a single band on sodium dodecyl sulfate-polyacrylamide gel with a molecular weight of 44,000. The enzyme had a specific activity of 179.2 U/mg protein when assayed by measuring the rate of the formation of gamma-glutamylhydroxamate using hydroxylamine as a substrate. In the presence of manganese ions, the relative activity of human brain GS was much lower than that of the sheep brain enzyme. The suppression of activity by increasing the ADP concentration, however, was less marked in the human enzyme than that in the sheep enzyme. Antibodies were raised in rabbits against the purified enzyme. The double-immunodiffusion technique disclosed cross-reactivities among GSs isolated from human, sheep, and rat brains, but the enzymes were not immunologically identical. Immunohistochemically, GS was localized in the cytoplasm of astrocytes in the human and rat brains and in pericentral hepatocytes of the liver.
Adult↗
Retrograde transport and differential accumulation of serum proteins in motor neurons: implications for motor neuron diseases.
We found immunocytochemical evidence of serum albumin and immunoglobulin G in motor neurons of rats under physiologic conditions, but not when axoplasmic flow was abolished. The amount of serum proteins was highest in somatic motor neurons of the spinal anterior horn, nucleus ambiguous, and trigeminal motor nucleus; less in hypoglossal and facial neurons; and sparse in preganglionic autonomic, oculomotor, and hypothalamic neurons. Toxic or trophic substances, bound to serum proteins, could also be incorporated into motor neurons. Quantitative differences in accumulation paralleled the selective vulnerability of somatic motor neurons in motor neuron diseases.
Animals↗
Evolution of tissue damage in compressive spinal cord injury in rats.
The evolution of tissue damage in compressive spinal cord injuries in rats was studied using an immunohistochemical technique and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis. The rupture of small vessels accompanied by intense tissue permeation of serum components in and around the hemorrhagic foci appeared to be immediate consequences of the mechanical insult. The loss of cell membrane integrity in neural elements became evident within 1 hour after injury as shown by the diffuse albumin-immunoreactivity of the cytoplasm. At the site of mechanical insult, approximately 30% of the neurofilament proteins were degraded within 1 hour, and 70% of them were lost within 4 hours after injury. A large number of cells positive for glial fibrillary acidic protein were found to demarcate the injured tissue within 1 hour after injury. The progression of tissue damage largely subsided within 48 hours. One week after injury, severe degeneration of the ascending tracts in the posterior funiculus was shown clearly by axon staining and less convincingly by myelin staining. Secondary degeneration of the corticospinal tract in distal segments remained inconspicuous for up to 3 months.
Animals↗
Identification of cells undergoing physiological neuronal death in the neonatal rat brain by the Fink-Heimer method.
There are certain limitations in identifying cells undergoing physiological neuronal death (PND) by conventional histological methods. Here, the Fink-Heimer method for impregnation of degenerating axons and terminals was successfully employed in selectively visualizing PND in the neonatal rat brain. The cell bodies thus observed were in close correlation with the known distribution and time-course of PND. In addition, massive occurrences of PND were observed in the periaqueductal gray, inferior colliculus, hypothalamus, and the rostral portion of the hippocampus, findings hitherto undescribed. Thus, the Fink-Heimer method provides a useful adjunct to the study of PND in the neonatal period.
Animals↗
Glial bundle formation in spinal roots following experimental neuronopathy.
Spinal motor neurons and dorsal root ganglion cells were caused to degenerate by axoplasmic transport of toxic lectins via the sciatic nerve. Within a few months, loss of axons and glial bundle formation were seen in the proximal portions of the L4-6 ventral and dorsal roots. The glial bundles observed were structurally the same as those described in humans, but they were occasionally also invested with Schwann cell cytoplasmic processes, the cell membrane of which was directly apposed to that of astrocytes. Basal lamina surrounding the outer surface of the bundles was shared by these two as a continuous sheet. This unique complex of astroglial and Schwann cell processes, completely covered by basal lamina, may be a newly formed interface between the central and peripheral nervous systems and thus may severe as a guide and potential pathway for regenerating neurites.
Animals↗
Immunohistochemical demonstration of viral antigens in Japanese encephalitis.
Japanese encephalitis virus antigens were immunohistochemically demonstrated in formalin-fixed paraffin sections from an autopsied brain. Glial nodules were always associated with antigen-positive cell debris. Glia shrubs in the cerebellar cortex appeared to be formed along the apical dendrite of Purkinje cells. Most, but not all, of the neurons involved in neuronophagia were viral antigen positive. Antigenic masses were occasionally encountered in the center of so-called acellular plaques. Neurons with strong viral antigens were sporadically found in normal-appearing regions in the thalamus and cerebral cortex. Viral antigens were demonstrable only in neurons and not in glial or vascular endothelial cells.
Adult↗
Shy-Drager syndrome and amyotrophic lateral sclerosis. Cytoarchitectonic and morphometric studies of sacral autonomic neurons.
In order to elucidate the morphological correlates of bladder-rectal dysfunctions in Shy-Drager syndrome, the sacral spinal cord was cytoarchitectonically studied and 3 groups of sacral motor neurons, the posterolateral motor neuron column (PL), inferior intermediolateral nucleus (IML) and cell group X of Onuf (Onuf), were morphometrically quantitated at the S3 level (5 cases), after which the results were compared with those from amyotrophic lateral sclerosis (5 cases) and an age-matched control group (4 cases). The sacral autonomic preganglionic nucleus of IML was localized chiefly in the S3-4 segments and was maximally developed in the caudal one-third of S3. The cell group X of Onuf was localized between the middle of S2 and the rostral one-third of S3 as a longitudinal slender column in the ventral horn. Between these two nuclei at the rostral S3 level, a connecting cellular bridge of neurons of intermediolateral cell type was identified. Morphometry disclosed a marked deprivation of IML, Onuf and somatic motor neurons in Shy-Drager syndrome and a severe loss of somatic motor neurons and a modest deprivation of IML neurons in ALS. These results imply that these two disorders distinguished by different clinical manifestations share a common loss of somatic motor and parasympathetic motor neurons at least in the sacral cord. There are, however, certain gradients in the severity of involvement in these heterogeneous cell groups.
Amyotrophic Lateral Sclerosis↗
Eradication of herpes simplex virus persistence in rat trigeminal ganglia by retrograde axoplasmic transport.
Potential use of retrograde axoplasmic flow to eradicate virus persistence in ganglionic cells was studied in a new herpes simplex virus (HSV) persistence model in rat trigeminal ganglia. After injection of the F strain of HSV type 1 into the mental nerve, viral antigens were detectable in the ganglia by the immunofluorescence and peroxidase methods between postinoculation (p.i.) days 3 and 6 but not thereafter. None of 82 inoculated rats showed signs of acute illness, and some survived for more than 502 days without symptoms. By cocultivation of ganglion tissues with Vero cells, the virus was isolated from 42 of 49 ganglia (85.7%) between 15 and 386 days (p.i.). HSV DNA was solely localized in the nucleus of neurons by immunoperoxidase staining of paraffin sections with a biotinylated HSV DNA probe, and the presence of HSV DNA-positive cells was confirmed in four of four ganglia on p.i. day 6 and in five of six on p.i. day 502. The efficacy of axoplasmic flow in drug delivery to ganglionic cells was investigated by injection of doxorubicin (ADM) into the nerve once used for virus inoculation. As early as 19 h after injection, strong ADM-specific autofluorescence was seen in the nuclei of neurons parental to the mental nerve and in those of adjacent Schwann cells, and the death of ADM-positive cells subsequently ensued. A single injection of ADM reduced the virus isolation rate from 31/37 (84%) to 3/37 (8%).
Animals↗
Experimental spinal cord injury: quantitation of axonal damage by automated image analysis.
The severity of acute experimental spinal cord injury in rats was assessed quantitatively with the aid of an automated image analyzer by measuring the amount of degenerating axons that had developed distal to the site of mechanical insult. Spinal cord injury was produced in adult male rats by epidural compression at T-11 with a Biemer vascular clip. On the 7th postoperative day, the animals were graded according to the degree of hindlimb motor deficit, as follows: Grade 0: normal (three rats); Grade 1: crawling with difficulty (10 rats); Grade 2: some voluntary movement (nine rats); and Grade 3: no voluntary movement (nine rats). The rats were then sacrificed. The L-6 segment was chosen for selective silver impregnation of degenerating axons by the Fink-Heimer method. Silver grains, representing degenerating axons and their terminals, were accumulated in the descending tracts and in Rexed's laminae VII and VIII. The extent of axonal damage was expressed by the percentage of the area occupied by silver grains in Rexed's lamina VIII. The area occupied by silver grains was 17.0% (mean) in Grade 0 rats, 22.3% +/- 2.63% (mean +/- standard deviation) in Grade 1 rats, 28.7% +/- 3.35% in Grade 2 rats, and 35.9% +/- 2.76% in Grade 3 rats. The severity in Grade 3 rats was close to that of rats with transected cords (37.6% +/- 0.89%). The differences among the groups were statistically significant (p less than 0.001). This method may serve as a useful tool for the objective assessment of therapeutic modalities in large series of small experimental animals.
Animals↗