Hand, foot and mouth disease, a distinctive clinical syndrome caused by a coxsackie virus, is clinically characterized by vesicles appearing on the hands, feet and in the mouth. The infection begins with a fever and mouth lesions consisting of small vesicles surrounded by red areolae on the buccal mucosa, tongue, soft palate and gingiva. The disease usually lasts spontaneously between 7 to 10 days after onset. We observed 20 cases of hand, foot, and mouth disease from July, 12th to September, 4th, 1979 and examined histopathologically and virologically. We have isolated only one viral strain showing cytopathic effect on HeLa cell among the five cases of acute stage and also observed that viral particle in the electronmicroscope.
Fever ; Foot* ; Gingiva ; Hand* ; Hand, Foot and Mouth Disease ; HeLa Cells ; Humans ; Mouth Diseases* ; Mouth Mucosa ; Mouth* ; Palate, Soft ; Tongue ; Virion

We experienced a case of a 38 year old women in whom an alpha-fetoprotein producing carcinoma originated in the rectum. The patient had symptoms of hematochezia and bowel habit change, and a rectal examination revealed an ulcerative mass at the midrectum. The mass size was 6.5 cm 6 cm. The serum alpha-fetoprotein measured preoperatively was 9336 ng/ml, and the serum (carcinoembryonic antigen) was 6.4 ng/ml. The serum level of alpha-fetoprotein decreased to 830 ng/ml thirteen days after a low anterior resection. The tumor mass was a poorly differentiated adenocarcinoma. Using an immunohistochemical staining method, we detected alpha-fetoprotein producing cells in the tumor mass. During the follow up, the serum alpha-fetoprotein level began to increase continuously, and an abdomin opelvic CT scan showed a systemic, local tumor recurrence. Based on our experience with this patient and a review of the literature on the few cases previously reported, it seems that alpha-fetoprotein producing colorectal carcinamas have a tendency to produce frequent blood-borne metastasis and are associated with a poor prognosis.
Adenocarcinoma ; Adult ; alpha-Fetoproteins* ; Colorectal Neoplasms ; Female ; Follow-Up Studies ; Gastrointestinal Hemorrhage ; Humans ; Neoplasm Metastasis ; Prognosis ; Rectal Neoplasms* ; Rectum ; Recurrence ; Tomography, X-Ray Computed ; Ulcer

Cerebral venous thrombosis is commonly related to infectious processes, trauma, neoplasm, puerperium, and the use of oral contraceptives, etc., but this case was associated with a very rare condition, "polycythemia". This case was confirmed by hematologic study, brain C-T, conventional angiography, and digital subtraction angiography(DSA). The patient was treated by venesection, the use of urokinase and dicumarol, and lumbo-peritoneal shunt(L-P shunt), etc. Post-treatment DSA showed the complete recanalization of all dural sinuses except the left transverse sinus, suggesting normal variant.
Angiography ; Brain ; Contraceptives, Oral ; Dicumarol ; Humans ; Phlebotomy ; Polycythemia* ; Postpartum Period ; Sinus Thrombosis, Intracranial* ; Urokinase-Type Plasminogen Activator ; Venous Thrombosis

Since the discovery of CT scan for brain, the detection of hydrocephalus became easier than before. Of those hydrocephalus, non-parenchymatous in origin, in order words, normal pressure hydrocephalus can be differentiated by RISA cisternography. The etiology, symptomatology and surgical outcome of 16 cases of normal pressure hydrocephalus were presented. Followings are the results. 1) All of the cases revealed ventriculomegaly in brain CT scan and prolonged ventricular retention of dye in RISA cisternogram. 2) Ventriculoperitoneal shunt was done on all of the patients and outcome was excellent:3, good:6, fair:3 and poor:4. 3) It is thought that the prognosis is much related duration of clinical manifestation; the earlier surgery, the better outcome.
Brain ; Humans ; Hydrocephalus ; Hydrocephalus, Normal Pressure* ; Prognosis ; Tomography, X-Ray Computed ; Ventriculoperitoneal Shunt

BACKGROUND: Diverse injury to central nervous system results in proliferation and hypertrophy of astrocytes. The hallmark of this response is enhanced expression of the major intermediate filament protein of astrocyte, glial fibrillary acidic protein(GFAP). These obsevations suggested that GFAP may be a useful biochemical indicator of neurotoxicity. This study is designed for investigating the chronological effects of the thiamine deficiency on the astrogrial GFAP immunoreactivity in the rat forebrain, and for comparing the difference between time-sequenital morphological changes of luxol fast blue-cresyl violet stain reported in previous study and GFAP immunoreactivity. METHODS: A total of 40 healthy Sprague-Dawley strain rats, weighing about 200gm were used as experimental animals(10 control, 30 thiamine deficient rats). Pyrithiamine was injected intraperitonially for 9 days and thiamine deficient diet was continuously supplied until sacrifice. Thiamine deficient rats were subdivided into 3 groups according to thiamine deficient state. Immunohistochemical stains for GFAP in the regions of thalamus, medial mammillary nucleus and CA1 sector in hippocampus were performed by free floating method in cell culture plate. All preperations were observed with light microscope. RESULTS: GFAP immunoactivities at thalamus were tracely positive(+) in controls, strongly positive(+++) in group I, and moderately positive(++) in group II and III. But GFAP immunoactivities at medial mammillary nucleus were tracely positive( ) in controls, moderately positive(++) in group I and III , and strongly positive(+++) in group II. At the CA1 region of hippocampus, the immunoactivities were weakly positive in controls , strongly positive(+++) in group I and II, and moderately positive(++) in group III. The diverse patterns of GFAP immunoreactivities in each vulnerable site were different from the previous morphological study. In luxol-fast and cresyl violet staining, the neuronal damage and necrosis were marked in group III, group II, and group I, in that order, which findings are consistent in all regions. CONCLUSIONS: Different patterns of time-sequential GFAP immunoactivities at each vulnerable site suggest that there are regional differences in sensitivity and resistance to thiamine deficiency.
Animals ; Astrocytes ; Cell Culture Techniques ; Central Nervous System ; Coloring Agents ; Diet ; Glial Fibrillary Acidic Protein* ; Hippocampus ; Hypertrophy ; Intermediate Filaments ; Necrosis ; Neurons ; Prosencephalon* ; Pyrithiamine ; Rats* ; Rats, Sprague-Dawley ; Thalamus ; Thiamine Deficiency* ; Thiamine* ; Viola

PURPOSE: The authors studied the effect of the 3-AB, an inhibitor of poly(ADP-ribose)polymerase (PARP), on the changes of primary afferents and spinal cord after spinal nerve injury. METHOD: The L5 and L6 spinal nerve of the rats were cut, and 3-AB (10 mg/Kg) was injected intraperitoneally once per day. The animals were sacrificed 3 days, 7 days, 14 days and 28 days after nerve injury. Binding of isolectin B4 (IB4) and immunohistochemistry (IHC) of CGRP for the changes in primary afferents, IHC of NK1 for sensory neurons, and of cleaved caspase 3 and NeuN for the apoptotic changes in spinal neurons were performed. RESULT: Decreased binding of IB4 and immunoreactivity (IR) for CGRP, increase of IR for NK1, and cleaved caspase 3 in both neurons and glia in ipsilateral dorsal horn were observed after spinal nerve injury. These changes were attenuated, especially at between 3 days and 14 days, by administration of 3-AB. CONCLUSION: It is suggested that inhibition of PARP by 3-AB may attenuate alterations of primary afferents and spinal neurons, at least in early stage, after spinal nerve injury.
Animals ; Apoptosis ; Caspase 3 ; Horns ; Immunohistochemistry ; Lectins ; Neuroglia ; Neurons* ; Rats* ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerves*

PURPOSE: The authors studied the effect of the 3-AB, an inhibitor of poly(ADP-ribose)polymerase (PARP), on the changes of primary afferents and spinal cord after spinal nerve injury. METHOD: The L5 and L6 spinal nerve of the rats were cut, and 3-AB (10 mg/Kg) was injected intraperitoneally once per day. The animals were sacrificed 3 days, 7 days, 14 days and 28 days after nerve injury. Binding of isolectin B4 (IB4) and immunohistochemistry (IHC) of CGRP for the changes in primary afferents, IHC of NK1 for sensory neurons, and of cleaved caspase 3 and NeuN for the apoptotic changes in spinal neurons were performed. RESULT: Decreased binding of IB4 and immunoreactivity (IR) for CGRP, increase of IR for NK1, and cleaved caspase 3 in both neurons and glia in ipsilateral dorsal horn were observed after spinal nerve injury. These changes were attenuated, especially at between 3 days and 14 days, by administration of 3-AB. CONCLUSION: It is suggested that inhibition of PARP by 3-AB may attenuate alterations of primary afferents and spinal neurons, at least in early stage, after spinal nerve injury.
Animals ; Apoptosis ; Caspase 3 ; Horns ; Immunohistochemistry ; Lectins ; Neuroglia ; Neurons* ; Rats* ; Sensory Receptor Cells ; Spinal Cord ; Spinal Nerves*

PURPOSE: To determine the relationship between change in the expression of the p75 neurotrophin receptor (NTR) and transient receptor potential vanilloid 1 (TRPV1) after a spinal nerve injury with time. MATERIALS AND METHODS: The L5 and L6 spinal nerve of the rats were cut unilaterally. The spinal cord and dorsal root ganglion (DRG) were subjected to immunohistochemistry for p75 NTR and TRPV1. RESULTS: The immunoreaction (IR) for p75 NTR in the neuronal cytoplasm was persistently lower on the ipsilateral L5 and L6 DRG but higher in the satellite cells and fibers. The colocalization between p75 NTR and TRPV1 was increased temporarily in the L4 DRG in both sides. In the spinal cord, p75 NTR-IR decreased temporalily in the ipsilateral dorsal horn of the L4-L6 level and had recovered at 28 days after injury. CONCLUSION: These results show that a differential change in the expression of p75 NTR and TRPV1 is related to the different functional recovery of the sensory and motor system, and that increased colocalizations between p75 NTR and TRPV1 in a non-injured DRG might be related to the development of neuropathic pain after a peripheral nerve injury.
Animals ; Cytoplasm ; Diagnosis-Related Groups ; Ganglia, Spinal* ; Horns ; Immunohistochemistry ; Neuralgia ; Neurons ; Peripheral Nerve Injuries ; Rats* ; Receptor, Nerve Growth Factor* ; Spinal Cord* ; Spinal Nerve Roots* ; Spinal Nerves*

Although adriamycin is a potent chemotherapeutic agent, it elicits serious adverse effects, including cardiac toxicity. Evidence suggests that congestive heart failure induced by adriamycin is mediated by oxidative stress. We investigated whether regulators of adenosine A1 receptor and KATP channel, which have been demonstrated to mediate protective effects of ischemic -preconditioning in myocardium, are able to modulate adriamicin -induced impairment of cardiomyocyte. To study the effect of antioxidant, adenosine A1 receptor agonist & antagonist and KATP channel agonist & antagonist, ICR mice were pretreated with Cu,Zn -SOD, dimethyl thiourea, RPIA (R (-)N6 -(2 -Phenylisopropropyl)- adenosine, adenosine A1 receptor agonist), 8 -CPDPX (8 -Cyclopentyl -1, 3 -dipropylxanthine, adenosine A1 receptor antagonist), Pinacidil (KATP channel opener) and glibenclamide (KATP channel closer), followed by i.p injection with adriamycin. Mice were sacrificed day 1 or day 4 after adriamycin injection and cardiac toxicity was accessed by measurement of creatine phosphokinase (CK) levels in serum, immunohistochemistry using anti -Bcl -2 antibody and TUNEL histochemical assay. As expected, pretreatment of mice with Cu, Zn -SOD and DMTU reduced the frequency of TUNEL positive cells, indicating antioxidants protected cardiocytes from adriamycin -induced apoptosis. Interestingly, pretreatment with RPIA and pinacidil induced a significant decrease in adriamycin -induced cytotoxicity, whereas 8 -CPDPX and glibenclamide generated the opposite results. In Bcl -2 immunohistochemistry, an increased expression of Bcl -2 was found in all ADR treated groups, especially in glibenclamide pretreated group, and 8 -CPDPX pretreated groups, but Bcl -2 failed to protect myocytes from apoptosis. All ADR treated groups exhibited elevated levels of serum CK, compared with nomal controls, especially mice sacrificed at day 4 than those at day 1, and showed similar patterns of TUNNEL assay, reflecting heart tissue damages. This observation implicated cytoprotective roles of RPIA and pinacidil against adriamycin -induced cardiac toxicity. In conclusion, these results demonstrated that adriamycin -induced cardiotoxicity was associated with the generation of reactive oxygen species and that regulators including SOD, DMTU, RPIA and pinacidil elicited protective effects on this toxicity. In particular, pinacidil, the KATP channel opener, was more effective than RPIA, the adenosine A, receptor agonist, to attenate the adriamycin -induced cardiac toxicity.
Adenosine* ; Animals ; Antioxidants ; Apoptosis ; Creatine Kinase ; Doxorubicin* ; Glyburide ; Heart ; Heart Failure ; Immunohistochemistry ; In Situ Nick-End Labeling ; Mice ; Mice, Inbred ICR ; Muscle Cells ; Myocardium ; Myocytes, Cardiac ; Oxidative Stress ; Pinacidil ; Reactive Oxygen Species ; Receptor, Adenosine A1* ; Thiourea

Laminin, an extracellular matrix glycoprotein composed of three polypeptide chains such as alpha , beta, and gamma is distributed in basement membranes of epithelium, muscle, and nervous tissues. Laminin functions as an extracellular cytoskeleton and regulates the differentiation and polarization of cells adjacent to the basement membrane. Along with type IV collagen and heparan sulfate proteoglycan, laminin forms a spike -like structure in the renal glomerular basement membrane (GBM). It has been previously demonstrated that the distribution and immune reaction of laminin are changed in response to the conditions of glomerulonephritis and that laminin plays a role in the reformation of GBM as well as the regeneration of renal glomerular cells. In the present study, the profile of expression and distribution of laminin/laminin beta1 chain were examined in different developmental stages and upon adriamycin administration. Kidney obtained from fetuses (16, 18, and 20 days old) and infants (1 and 7 days old) of Sprague -Dawley rats were either cryosectioned for immunohistochemical assays or ultrathin -sectioned for electron microscopy using immunogold staining methods. The results were as follows: 1. Intensive expression of laminin was observed in the GBM and surrounding mesenchymal tissues obtained from 16, 18, and 20 days old fetuses and in the glomerulus from one day neonates, whereas the level of staining decreased in the glomerulus from 7 days old infants. 2. Immunogold particles were observed in the comma -shaped nephron, in particular in cisternae of rough endoplasmic reticulum, vesicles and nuclear membrane of endothelial cells and mesangial cells obtained from 18 days old fetuses. 3. The immune reactions of laminin beta1 chain were trace detected in the kidney from fetuses (16, 18, and 20 days old) and weakly in tissues surrounding blood capillary and mesangial tissues from one day old neonates. 4. After 24 hours following adriamycin treatment, the reactivity of laminin was slightly enhanced in the renal glomerulus, when compared with that of untreated controls. This enhancement persisted up to 1 week of adriamycin treatment. Laminin beta1 chain was weakly detectable, while further treatment with adriamycin for another 24 hours reduced the intensity of laminin beta1 chain. Taken together, these results suggest that laminin is localized in the GBM at the high level during early fetal stages but the expression levels decrease after birth. Moreover, administration with adriamycin may result in an increase in the immune reactivities of laminin and laminin beta1 chain by renal tissue damage followed by renal regeneration.
Animals ; Basement Membrane ; Capillaries ; Collagen Type IV ; Cytoskeleton ; Doxorubicin ; Endoplasmic Reticulum, Rough ; Endothelial Cells ; Epithelium ; Extracellular Matrix ; Fetus ; Glomerular Basement Membrane ; Glomerulonephritis ; Glycoproteins ; Heparan Sulfate Proteoglycans ; Humans ; Infant ; Infant, Newborn ; Kidney* ; Laminin* ; Mesangial Cells ; Microscopy, Electron ; Nephrons ; Nuclear Envelope ; Parturition ; Rats* ; Regeneration