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Biomedical subjects

Y Mizuno

Publications and source records attributed to Y Mizuno.

At least 271 records · Page 15Linked to original sources
PubMed1998

Influence of acute elevation of plasma AVP level on rat vasopressin V2 receptor and aquaporin-2 mRNA expression.

It is known that vasopressin V2 receptor (V2R) mRNA is downregulated by elevated plasma arginine vasopressin (AVP) following chronic osmotic stimulation. To elucidate the response in V2R mRNA expression to acute elevation of the plasma AVP level, we investigated the time-course change of rat V2R mRNA expression after subcutaneous injection of AVP (10 microg/body). Plasma AVP levels increased from 1.4+/-0.3 pg/ml to 56.8+/-10.7 pg/ml by an hour after injection,and returned to the control level at 6 h. By Northern blotanalysis, V2R mRNA expression decreased to 52.7+/-3.7% of the control level at 2 h, and then returned to the control level by 6 h. Furthermore we investigated the time-course change of aquaporin-2 (AQP2) mRNA expression. AQP2 mRNA expression increased gradually after injection and reached 240.3+/-7.5% of the control level at 6 h. Then it returned to the control level. This study showed that the downregulation of V2R mRNA occurred rapidly after acute elevation of the plasma AVP level, and AQP2 mRNA expression was upregulated despite the downregulation of V2R mRNA.

Animals↗
PubMed1998

[Irreversible airflow limitation in asthmatics].

To evaluate irreversible airflow limitation in asthmatics, we studied 168 patients admitted to our hospital with acute exacerbation of asthma. All patients were given intravenous methylprednisolone for at least 7 days to maximum 14 days and the best of PEF (% of predicted) was evaluated. In all subjects, the best of PEF showed significant correlations with both the patients' age (r = -0.411, p < 0.0001) and the duration of asthma (r = -0.494, p < 0.0001). A significant correlations between the best of PEF and the duration of asthma were also observed in both patients over 60 years old (r = -0.157, p < 0.0001) and non-smokers (r = -0.568, p < 0.0001). We conclude that asthma may develop irreversible airflow limitation in itself and the degree of impairment of lung function correlated with the duration of the disease.

Airway Obstruction↗
PubMed1998

The selective reduction in PTPdelta expression in hepatomas.

The mRNA levels for receptor-like protein tyrosine phosphatases (PTPases), PTPalpha, PTPdelta, PTPgamma and LAR, were evaluated by Northern blot analysis in two types of chemically-induced rat primary hepatomas. In the four PTPases the PTPdelta mRNA was selectively reduced in these hepatoma tissues. It was also diminished in HepG2 hepatoblastoma cell line and in all of the poorly differentiated ascites hepatoma cells examined. PTPalpha, PTPgamma and LAR did not show such a characteristic decrease. This selective reduction in PTPdelta expression strongly suggests PTPdelta plays an important role in hepatocarcinogenesis, possibly as a tumor suppressor gene.

Animals↗
PubMed1998

[A 49-year-old man with progressive bulbar palsy and respiratory failure].

We report a 49-year-old man with progressive bulbar palsy and respiratory failure. He was well until his 48 years of the age (December 1994) when he noted a difficulty in speaking in loud voice. In February, 1995, he noted regurgitation of foods to his nose and difficulty in his speech. He was admitted to our service in May 29, 1995. On admission, he was alert and oriented to all spheres and he was not demented. His higher cerebral functions were normal. In cranial nerves, he showed dysarthria and dysphagia; muscle atrophies were seen in the tongue, the bilateral sternocleidomastoid, supraspinatus, and infraspinatus muscles. Fasciculations were seen in these muscles. He showed no muscle weakness in his limbs except for the upper limb girdle muscles, no ataxia, no reflex abnormalities, nor sensory changes. EMG showed neurogenic changes in the affected muscles. MRI of the brain and the spinal cord was entirely normal. He was discharged for out patient follow-up, however, in October of 1995, he noted difficulty in swallowing solid foods. Gastrostomy was placed and he was discharged to his home. In February 11th of 1996, he was found unresponsive and brought into the ER of our hospital. On admission, he was comatose without spontaneous respiration. BP could not be obtained. He was immediately intubated and artificial ventilation was started. On the following morning, he became alert and he was not demented. He continued to show marked dysarthria and dysphagia; again no weakness was noted in the distal parts of the upper and lower extremities. Laboratory examination showed increase in serum CK to 2,173 IU/L and amylase to 2,032 IU/L. He was extubated on February 15th, however, his spontaneous respiration was not suffice to maintain his blood gas. According to his will, he was not placed on respirator and he died on February 24th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had ALS. Although no upper neuron signs were observed clinically, it is not uncommon to see degeneration in the corticospinal tract in post-mortem examination. The question was what might have been the cause of increase in CK and amylase. Many participants thought that they were secondary to multiple organ failure due to prolonged hypoxic state at his last admission; other possibilities raised included acute myocardial infarction and acute bowel necrosis. Post-mortem examination revealed muscle atrophy in the facial, lingual, cervical, intercostal, and the upper limb girdle areas. The lungs were unremarkable except for old organized pneumonic foci in the right middle and lower lobes. Marked to moderate congestion was seen in many internal organs, however, no other gross abnormality was found. It was thought that respiratory palsy itself was the direct cause of his agonal event. In the spinal cord, the anterior horns showed various degree of neuronal loss and gliosis. No clear evidence of pyramidal tract degeneration was seen at the light microscope level. Lower brain stem motor neurons were markedly reduced. But no Bunina body was found. The substantia nigra showed moderate degree of neuronal loss and extraneuronal neuromelanins. The locus coeruleus showed similar but milder changes. The degree of nigral degeneration appeared to be well beyond those which could be seen in usual ALS patients. The question was whether or not this patient might have been in an early stage of the extended form of ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1998

[An 81-year-old woman with progressive motor disturbance, extrapyramidal features, dementia, and oculomotor palsy].

We report an 81-year-old woman who presented with motor disturbance in her right hand which was followed by parkinsonism, dementia, and supranuclear gaze palsy. She was well until her age of 73 (1989) when she had an onset of difficulty in using her right hand; she did not have weakness. She also developed small step gait. These symptoms had progressively become worse. She was admitted to our hospital in July of 1992 when she was 75 years old. On admission, she was alert and oriented, but she showed some difficulty in recent memory. She did not have aphasia or ideomotor apraxia, but she showed limb-kinetic apraxia in her right hand, ideational apraxia, dressing apraxia, constructional apraxia, tactile agnosia, and left-right disorientation. Alien-hand syndrome was observed in her right hand. Ocular movement was within normal limit for her age. She had oro-lingual dyskinesia. Otherwise, cranial nerves were intact. She walked in small-steps. She had rigidity and fine myoclonic movements in her right upper extremity. Deep reflexes were within normal limits and symmetric. Superficial and deep sensations were intact. Laboratory findings were unremarkable. She was discharged on August 15, 1992 for outpatient follow-up. Her motor and mental symptoms were progressive. By October of 1992, she developed supranuclear vertical gaze palsy, marked rigidity in the neck, and astereognosis. By June 1993, she became unable to walk without support. MRI taken in May of 1994 revealed atrophy of insular cortices, temporal lobe tips and parietal lobes more on the left side; the third ventricle was slightly dilated. She was admitted to another hospital on June 30, 1994. She had become a bed-ridden state with marked dementia and dysphagia. She developed fever on November 5, 1996 and expired on December 16 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had corticobasal degeneration. Other diagnoses entertained included progressive supranuclear palsy, pallidonigroluysian atrophy, diffuse Lewy body disease, and Pick's disease. But the most of the participants agreed with the chief discussant's diagnosis. Post-mortem examination revealed aspiration pneumonia in the lungs and liver fibrosis apparently due to viral hepatitis. In the central nervous system, frontal and parietal lobes were atrophic more on the left side. Atrophy was accentuated in the superior frontal gyri, precentral and postcentral gyri, and superior and inferior parietal lobuli. Neuronal loss and astrocytosis were seen in these regions with scattered ballooned neurons. The substantia nigra showed marked neuronal loss and gliosis; neuronal loss was also seen in the pars reticulata. The outer and inner segments of globus pallidus and the periacqueductal gray matter showed gliosis, however, no apparent neuronal loss was seen. Putamen, subthalamic nucleus, and the dentate nucleus were preserved. Pathologic changes were consistent with the diagnosis of corticobasal degeneration. It was interesting to note that anti-tau immunostaining and Gallyas staining revealed neuropil threads and astrocytic plaques in the cortical areas, and intracytoplasmic inclusion bodies in the cortical neurons; these inclusions were not stained by Bodian stain. Tuft-shaped astrocytes which may be seen in progressive supranuclear palsy were not observed in this patient. Although corticobasal degeneration and progressive supranuclear palsy share some neurological features in common, this patient showed typical pathologic changes of corticobasal degeneration.

Aged↗
PubMed1998

[Spontaneous rupture of malignant fibrous histiocytoma arising from the renal capsule: a case report].

We report a case of spontaneous rupture of malignant fibrous histiocytoma. A 50-year-old male with right flank pain was referred to our hospital. Computed tomography (CT) showed a heterogeneous space-occupying lesion on the upper pole of the right kidney. Selective right renal arteriography revealed a hypovascular mass. Preoperative clinical diagnosis was spontaneous rupture of renal cell carcinoma. Radical nephrectomy was performed. Histopathological diagnosis was malignant fibrous histiocytoma arising from the renal capsule.

Histiocytoma, Benign Fibrous↗
PubMed1998

[Superficial siderosis of the central nervous system: an electrophysiological study].

Superficial siderosis of the central nervous system (SS) is a rare neurological disorder characterized by symptoms such as neurosensory hearing loss, ataxic gait, and spastic paraparesis. Recently, magnetic resonance imaging (MRI) enables us to make a clinical diagnosis. However, the exact pathophysiological mechanism underlying this disorder remains uncertain. Although iron chelation therapy has been attempted experimentally, it has not been successful and there is no effective medical treatment available. Towards the better understanding of the pathophysiological mechanism underlying SS, we performed electrophysiological studies, in which multiple evoked potential studies were included, in 3 patients with SS. Somatosensory evoked potentials (SEPs) evoked by median nerve stimulation were all normal, but those evoked by the posterior tibial nerve stimulation showed a significant delay of the latency of P40. In the auditory brainstem response (ABR) studies, there were no reproducible responses of the brainstem origin. In the blink reflex studies, R2 latency was delayed in one patient. In visual evoked potential (VEP) studies, the latency of P100 was delayed in two of three patients, unless all the patients clinically showed no visual symptom. The nerve conduction velocity studies performed in peripheral nerves of upper and lower extremities were all normal. The abnormal findings of ABR and SEP may suggest that the acoustic nerve and the posterior funiculus of the spinal cord are involved, respectively. These findings are also in a good agreement with pathological findings of SS reported in the literature. In SS, the hemosiderine accumulation is usually less severe in the visual tract; however, the delay of VEPs may suggest the latent dysfunctioning of the visual system in SS. It is suggested that multiple evoked potential study is useful for clinical evaluation of SS.

Aged↗
PubMed1998

[A 45-year-old man with peripheral monocytosis and right hemiparesis].

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.

Brain↗
PubMed1998

Activation of protein phosphatase 1alpha promoter in ascites hepatoma cells.

We have already reported the nucleotide sequence of 5'-flanking region of rat PP1alpha gene and identified the promoter region in NIH3T3 cells. Here we determined the promoter activity of PP1alpha gene in ascites hepatoma cells and compared with that of hepatocytes. Reporter analysis showed that the promoter activity was enhanced in an ascites hepatoma AH13 compared with normal hepatocytes at two regions, -37 to -198 bp and -492 to -848 bp upstream of the translation start site. At -37 to -198 bp region with high GC content, binding of Sp1 was markedly increased in all of five ascites hepatomas examined. At -492 to -848 bp region, two bands were clearly detected in two of the five ascites hepatomas, AH13 and AH7974F, by gel shift analysis. These results strongly suggest that the increase in PP1alpha mRNA expression in ascites hepatomas is at least in part due to the enhanced promoter activity of PP1alpha gene.

Animals↗
PubMed1998

[A patient with focal bi-parietal atrophy presenting motor clumsiness and cortical sensory loss].

We report a 73-year-old woman who presented progressive motor clumsiness, cortical sensory loss, and focal parietal lobe atrophy. She was well until one year prior to the present admission when she suffered from what appeared to be mild Fisher syndrome from which she showed excellent recovery. However, soon she noted a gradual onset of difficulty in hand movements and in the recognition of objects by hands. Neurologic examination revealed an alert and well oriented Japanese woman without dementia. Cranial nerves were unremarkable. Although, she did not have aphasia, apraxia, or agnosia, she showed marked clumsiness in skilled hand movements such as using chopsticks, hand writing, and buttoning. She had no motor weakness, ataxia, rigidity, or spasticity. Deep tendon reflexes were symmetrically diminished. Sensory examination revealed cortical sensory loss such as disturbances of two point discrimination, weight sensation, and stereotactic sensations. Her motor clumsiness appeared to be caused by her cortical sensory loss. MRI revealed marked focal atrophy in the bilateral parietal lobe, particularly in the postcentral gyrus and the adjacent association areas. Recently, neurodegenerative disorders with focal brain atrophy such as corticobasal degeneration, Pick's disease, and dementia of frontal lobe type have been reported, however, our patient does not fit to any of these known disorders nor clinical features are distinctly different from Alzheimer's disease. Our patient may be another example of progressive cerebral degeneration with emphasis on the parietal cortex.

Aged↗
PubMed1998

[A 74-year-old woman with parkinsonism and dementia who died four years after the onset].

We report a 74-year-old woman with parkinsonism and dementia, who died 4 years after the onset of the disease. She was well until 70 years of the age (1993) when she noted slowness in the movement in her left hand. She also developed gait disturbance and the similar symptoms spread to the right upper and lower extremities. Two years after the onset, she had difficulty in walk, and was admitted to our hospital on March 9, 1995. Her daughter had the onset of hand tremor at 50 years of the age and gait disturbance at 52. Her gait improved after levodopa treatment, but her MRI revealed a liner T2-high signal lesion along the outer surface of each putamen. On admission, the patient was alert but slighted demented. Higher cerebral functions were normal. She had a masked face and small voice. Her gait was of small step without arm swing. Retropulsion was present. Rigidity was noted in the neck but not in the limbs. She was bradykinetic but tremor was absent. She was treated with levodopa/carbidopa, dops, and bromocriptine with considerable improvement and was discharged on March 30, 1995. On January 19, 1996, she developed fever and hallucination; she became more akinetic and admitted again. She showed marked dementia and stage IV parkinsonism. She was treated by supportive measures with improvement in the general condition, but she was found to have a gastric cancer for which a subtotal gastrectomy was performed on March 11, 1996. Post-operative course was uneventful, but her parkinsonism progressed to stage V. She was transferred to another hospital on May 13, 1996. In July 21, 1996, she developed dyspnea and fever and was admitted to our hospital again. She was somnolent. Rigidity was moderate to marked and she was unable to stand or walk. By supportive cares, her general condition improved and was discharged to home on November 4, 1996. She developed fever on June 13, 1997 and admitted to our service again. Her BP was 150/90 mmHg. She was alert but markedly demented. Laboratory examination revealed increases in liver enzymes (GOT 75 IU/l, GPT 101 IU/l) and renal dysfunction (BUN 68 mg/dl, creatinine 3.27 mg/dl). Subsequent hospital course was complicated by renal failure and thrombocytopenia (33,000/ml). She expired on July 1, 1997. The patient was discussed in a neurologic CPC, and a chief discussant arrived at the conclusion that the patient had diffuse Lewy body disease and her daughter striatonigral degeneration. Some participants thought both the patient and her daughter had diffuse Lewy body disease. Post-mortem examination revealed marked degeneration of the substania nigra and the locus coeruleus. The medial part of the nigra also showed marked cell loss. Lewy bodies were found in the remaining nigral and coeruleus neurons. Cortical Lewy bodies were very few and the striatum was intact. Pathologic diagnosis was Parkinson's disease. Dementia was in part attributed to the marked degeneration of the medial part of the substantia nigra.

Aged↗
PubMed1998

[Thoracoscopic surgery for an aged patient with T1N0 non-small cell lung cancer: case report].

An 85-year-old woman was referred to our hospital because of an abnormal shadow in the right upper lung field in chest roentgenograms. CT scans revealed a tumor, 3 cm in diameter at the peripheral field of the upper lobe. The lesion was diagnosed adenocarcinoma of the lung by transbronchial lung biopsy (c-T1N0M0). She underwent a partial resection of he S3 in consideration of age and the clinical stage, by using thoracoscopic procedure. Her postoperative course was uneventful and she was discharged on the 14th postoperative day. Since then, she has been free from recurrence for the past 3 years. Thoracoscopic surgery appears to be useful for aged patients with peripheral early lung cancer because of low incidence of postoperative disability and complications.

Adenocarcinoma↗
PubMed1998

[A 64-year-old woman with progressive gait disturbance and dementia for one year].

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been

Brain Stem↗
PubMed1998

[A 61-year-old man with progressive gait disturbance, freezing, and vertical gaze paresis who developed esophagus cancer].

We report a 61-year-old Japanese man who died of complications of esophagus cancer surgery. He was well until his 55 years of the age, when he had an onset of speech disturbance and hand writing. He was seen by a neurologist who prescribed Menesit 600 mg/day. His symptoms improved with this medication. In 1993, three years after the onset, he started to show gait disturbance and easy to fall. In 1995, he noted difficulty in eye opening. He visited our clinic on October 26, 1996. On examination, he showed vertical gaze paresis, masked face, nuchal rigidity, small step gait, freezing phenomena, and festination. His mental status was normal. He was treated with 800 mg/day of Menesit, 800 mg/day of L-dops, and 10 mg/day of bromocriptine with little improvement in his symptoms. Cranial CT scan revealed some dilatation of the third ventricle. Subsequent clinical course was one of the slow progression of his parkinsonism. In September of 1997, he noted difficulty in swallowing. He was admitted to the gastrointestinal service of our hospital on October 14, 1997. On admission, neurologic status was essentially similar to the previous one, but he showed more advanced state of his parkinsonism. Upper gastrointestinal series revealed a mass lesion of about 11.5 cm in length protruding into the lower esophagus lumen. Subtotal esophagus resection including the mass was performed on December 2, 1997. The stomach was elevated for anastomosis with the upper esophagus. No metastases were found in the mediastinum except for two lymph nodes in the para-esophageal region. The subsequent course was complicated by marked elevation of GOT, GPT, LDH, total bilirubin as well as direct bilirubin, alkaliphosphatase, and amylase starting in the evening of the surgery. On December 7, leukocytosis and pneumonic shadow were seen involving his right lung. On December 10, he developed cardiopulmonary arrest. He was once resuscitated; however, he developed cardiac arrest again seven hours later and pronounced dead. He was discussed in a neurologic CPC. The chief discussant arrived at the conclusion that the patient had PSP and the cause of the death was ascribed to circulatory disturbance to the liver. The discussant also thought that the terminal course was complicated by cholangitis or cholecystitis, sepsis, and pulmonary embolism. Surgical specimen of the esophagus tumor revealed carcinosarcoma. Postmortem examination revealed yellowish discoloration of the peritoneum and mesenterium, and accumulation of clouded ascites indicating the presence of peritonitis. Inflammatory change extended to the mediastinum. On microscopic examination, various kinds of bacilli and candida spores were seen. The liver was enlarged and a perforation was noted in the gallbladder causing biliary necrosis in the adjacent liver. An extensive infarct was seen in the left lobe of the liver; this was found to be due to obstruction of the hepatic artery at the site of the duodenohepatic mesenterium and obstruction of intrahepatic portal vein secondary to retrograde intrahepatic cholangitis in the left lobe. A piece of surgical threads was seen adjacent to the hepatic artery; foreign body granulomatous reaction was seen surrounding the surgical thread. The rupture of the gallbladder appeared to be due to the obstruction of the left branch of the hepatic artery. Neuropathologic examination revealed extensive degeneration of the pallidum, the substantia nigra, and the subthalamic nucleus and presence of neurofibrillary tangles in the remaining neurons. The neuropathologic findings were consistent with progressive supranuclear palsy, although the pathologic changes in the midbrain tegmentum was only mild gliosis.

Carcinosarcoma↗
PubMed1998

Newly developed diabetic retinopathy and its preceding changes in biological markers.

To disclose the chronological changes prior to the manifestation of diabetic retinopathy (DR), we analyzed the time course of biological markers among apparently healthy diabetic subjects in a case-control study of 21,579 adults who had undergone comprehensive health examinations for > or = 10 years. We identified 54 cases who had newly developed DR, and selected 108 adults without fundus abnormalities, matching them for sex, age, and fasting plasma glucose (FPG) at the onset of the patient group's retinopathy as a referent group from the same population. In a multivariate analysis, a high average FPG (> 175 mg/dl) and a final-year FPG reduction (< -3%) were significantly associated with a 5.4 (95% CI, 1.8-15.7)- and 5.0 (95% CI, 1.0-24.7)-fold increased risk of DR, respectively. Thus, we surmised that sustained hyperglycemia and a subsequent drop in FPG might promote retinopathy in non-insulin dependent diabetes mellitus.

Biomarkers↗
PubMed1997

Dimethoxyphenylethylamine and tetrahydropapaverine are toxic to the nigrostriatal system.

We report the toxic effects of 3,4-dimethoxyphenylethylamine (DMPEA), and tetrahydropapaverine (THP) on the rat nigrostriatal system; THP is a tetrahydroisoquinoline compound which may be derived from DMPEA by conjugation of DMPEA and its oxidative metabolite, dimethoxyphenylacetaldehyde; both are potent inhibitors of mitochondrial complex I. These compounds were introduced to the unilateral caudate-putamen of male Sprague-Dawley rats over 7 days using a 200-microl mini-osmotic pump. Striatal dopamine on the injected side showed a significant decrease to 86% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA, and to 73% of the non-injected side after 7.90 micromol/7 days of THP infusion; as the non-injected side dopamine also reduced in the THP-injected rats, dopamine on the injected side was 55% of the saline control. Tyrosine hydroxylase (TH)-positive nigral neurons were decreased to 76% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA and to 77% after 7.90 micromol/7 days of THP infusion. Dimethoxyphenyl-tetrahydroisoquinoline compounds appear to be potent nigral neurotoxins.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

The characteristic gene expressions of MAPK phosphatases 1 and 2 in hepatocarcinogenesis, rat ascites hepatoma cells, and regenerating rat liver.

mRNA levels of mitogen-activated protein kinase phosphatases, MKP-1 and MKP-2, were determined during chemical hepatocarcinogenesis and during regeneration of rat liver. In chemical hepatocarcinogenesis, the mRNA levels of MKP-1 were increased in primary hepatomas but decreased in rat ascites hepatomas as compared with normal liver. MKP-2 was undetectable in normal liver but strongly expressed in hepatomas. The MKP-2 mRNA level was increased with expression of malignant phenotypes in hepatomas. In regenerating liver, the mRNA level of MKP-1 increased immediately but transiently after partial hepatectomy, and peaked again on day 10, the time when hepatocytes cease proliferation. The elevated expression of MKP-1 on day 10 suggests some roles of MKP-1 as a negative regulator in hepatocyte proliferation.

Animals↗