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Biomedical subjects

K Suda

Publications and source records attributed to K Suda.

At least 163 records · Page 9Linked to original sources
PubMed1994

A morphologic analysis of 'naked' islets of Langerhans in lobular atrophy of the pancreas.

The 'naked' islets of Langerhans (NIL) in randomly selected autopsy cases and in cases of chronic alcoholic pancreatitis, cystic fibrosis, and pancreatic carcinoma were studied histopathologically. The NIL were found in 55 of 164 randomly selected cases, with age-related frequency, in 21 of 30 cases of chronic alcoholic pancreatitis, in 2 of 2 cases of cystic fibrosis, and in 25 of 32 cases of pancreatic carcinoma. The NIL were frequently accompanied by ductal alterations: epithelial metaplasia and hyperplasia in randomly selected cases, protein plugs in chronic alcoholic pancreatitis, mucus plugs in cystic fibrosis, and obliterated ducts in pancreatic carcinoma. The NIL in randomly selected cases may have been formed by ductal alterations that caused stenosis of the lumen, those in chronic alcoholic pancreatitis and cystic fibrosis were the result of protein or mucus plugging, and those in pancreatic carcinoma were a result of neoplastic involvement of the distal pancreatic duct. Therefore, the common factor in the development of NIL is thought to be obstruction of the pancreatic duct system, and in cases of NIL that have a multilobular distribution and interinsular fibrosis, a diagnosis of chronic pancreatitis can usually be made.

Adolescent↗
PubMed1994

Increase in cytosolic free Ca2+ in corticotropin-stimulated white adipocytes.

The mechanism of the adrenal corticotropin hormone (ACTH)-stimulated increase in cytosolic free Ca2+ concentration ([Ca2+]i) was investigated in rat white adipocytes. ACTH at concentrations > 10 mU/ml caused a rapid and transient increase in [Ca2+]i followed by a small but sustained elevation of [Ca2+]i. A similar phenomenon was also induced by alpha-adrenergic or synthetic ACTH stimulation. The effect of norepinephrine (NE) plus ACTH on [Ca2+]i was nearly additive. Pertussis toxin completely blocked the ability of ACTH or NE to increase [Ca2+]i. NE but not ACTH caused a significant increase in inositol 1,4,5-trisphosphate levels. ACTH caused a rapid and transient accumulation of [3H]arachidonic acid (AA) and a marked loss of [3H]AA from phosphatidylinositol (PI) and phosphatidylcholine (PC) 10 s after stimulation. Neither a lipoxygenase inhibitor nor a dual inhibitor of cyclooxygenase and lipoxygenase blocked the increases in [Ca2+]i and the accumulation of [3H]AA in response to ACTH. On the other hand, either pertussis toxin or phospholipase A2 inhibitor drastically blocked both parameters in response to ACTH. These results indicate that ACTH stimulates AA release from PC and PI via the activation of phospholipase A2 coupled with pertussis toxin-sensitive GTP-binding protein(s), which leads to an increase in [Ca2+]i in rat white adipocytes.

Acetophenones↗
PubMed1994

Changes of synapse-related proteins (SVP-38 and drebrins) during development of brain in congenitally hydrocephalic HTX rats with and without early placement of ventriculoperitoneal shunt.

Hydrocephalic and nonhydrocephalic HTX rats served, respectively, as experimental and sham operation animals. They were treated by insertion of ventriculoperitoneal (V-P) shunts at 7 days after birth (early shunt). Monoclonal antibodies against synaptic vesicle proteins (SVP-38) and developmentally regulated brain proteins (drebrins) were used to assess these two synapse-related proteins by means of either a quantitative immunohistochemical method or a qualitative immunoblot analysis. The amount of SVP-38 progressively increased during a 3-week period after birth in both hydrocephalic and nonhydrocephalic HTX rats, but decayed suddenly at 4 weeks after birth in hydrocephalic HTX rats. When the hydrocephalic HTX rats were treated with V-P shunts, such perturbations in postnatal changes of SVP-38 were prevented completely. In nonhydrocephalic HTX rats, only the embryonic form of drebrins was detected at 1 day after birth, and this disappeared at the end of the 3rd week. The adult form of drebrin could be detected at 1 week after birth, and this completely replaced the embryonic form by 3 weeks of age. However, the postnatal decay of the embryonic form was considerably delayed in hydrocephalic HTX rats. These observations indicate that since synaptogenesis in the brain of hydrocephalic HTX rats has already been disturbed at the prenatal periods, which is the initial process of hydrocephalus, early shunt treatment of hydrocephalus would be beneficial not only for repairing but also for preventing impaired synaptogenesis.

Animals↗
PubMed1994

Health status comparison by urinalysis (dipstick test) among four populations in Papua New Guinea.

The health status of four populations depending on traditional subsistence in Papua New Guinea was compared by the dipstick test urinalysis. Conspicuous inter-population difference in the distribution of urinary pH was attributed to the levels of protein intake and the balances of sodium and potassium intake. The percentage of positive findings on protein differed by population along with the percentages of urobilinogen and bilirubin; the higher percentage of protein positives (12-16%) found in less urbanized populations suggests a high risk of hepatic and/or renal disorders in traditional societies. The very low percentage, 0.3 percent, of positive findings on glucose among 1,132 urine samples tested indicated that diabetes mellitus was not yet the major problem. Simultaneously, however, the fact that glucose positives were found only in the most urbanized villages indicates increasing risk of diabetes even in the traditional populations during future urbanization.

Adolescent↗
PubMed1994

Orbital reconstruction with hydroxyapatite ceramic implants.

Thirteen patients with fractures of the orbital floor (inferior wall), medial and lateral walls, or so-called "blowout" fractures with or without fractures of the zygoma were treated with artificially made hydroxyapatite ceramic implants made entirely from limestone, some of which were made with computer aided design and computer aided machinery (CAD-CAM) from data obtained from helical computed tomography. Orbital reconstruction with hydroxyapatite ceramic implants is a safe technique which is superior to previous ones in which autogenous or plastic materials were used.

Adult↗
PubMed1994

Evaluation of cytokines in donor site wound fluids.

The aim of the study was to measure concentrations of cytokines in wound fluid from donor sites. A film dressing was applied to the donor sites (mean size 10 x 15 cm) immediately after a split skin graft had been taken. Five days later the film was punctured with a needle and 2-3 ml of the fluid accumulated under the film dressing was withdrawn into a syringe. The fluid was snap frozen and stored immediately at -70 degrees C. The fluid was examined for epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), transforming growth factor (TGF) alpha, TGF beta, interleukin (IL)-1 alpha and IL-1 beta. The results showed that the fluid accumulated under the film dressing contained growth factors and cytokines that are thought to promote healing. The fluid was rich in TGF alpha but contained no EGF or bFGF, which indicates that TGF alpha plays a major part for promoting local wound healing.

Adult↗
PubMed1994

[Immunohistochemical study on keratin expression of uterine reserve cells].

An immunohistochemical expression in the reserve cells of the uterine cervix using monoclonal antibodies of cytokeratin which detected the different subtypes of keratin was studied. Although the reserve cells were positive for all the four cytokeratin antibodies (CAM5.2, M-20, M-888, M-630), different immunoreactivity was found as follows: CAM5.2 reacted uniformly and intensely in the cervical glands, but weak in the reserve cells. M-20 reacted similar to that of CAM5.2 in the cervical glands, but was weaker stained in the reserve cells than with CAM5.2. M-888 reacted uniformly and intensely in both the cervical glands and reserve cells. M-630 reacted only in the reserve cells, but seldom in the cervical glands. Hence, CAM5.2 and M-20, which detected No.8 and No.18 of antiserum for low-molecular weight cytokeratin, reacted more weakly in the reserve cells than in the cervical glands, and M-630, which detected No.5 and No.14 of antiserum for high-molecular weight cytokeratin, reacted uniformly and intensely in the reserve cells. That results suggested the reserve cells revealed the expression as the stratified squamous epithelium. As for cell proliferation on the cervical glands and reserve cells, the positive nuclear staining for proliferating cell nuclear antigen (PCNA) was found in both of them, especially in the cervical glands just above the reserve cells. Therefore, the reserve cells had characteristics of squamous cell epithelium and developed to metaplastic cells.

Antibodies, Monoclonal↗
PubMed1994

[A 85-year-old right-handed woman with aphasia and left hemiparesis].

We report a 85-year-old woman who developed speech disturbance and left hemiparesis. She had a gradual onset of gait disturbance 3 years prior to the present admission. Five days before admission, she started to pace up and down in her house; she did not want to take food on the following day, and she developed fever of 39 degrees C; it was also noted that she became mute. On the next day, she developed left hemiparesis; she was still mute but was able to communicate by hand writing to some extent. She was admitted to our service on February 24, 1992. On admission, she was alert but mute; her body temperature was 37.1 degrees C, and her BP 110/70 mmHg. The lungs were clear and general physical examination was unremarkable. Neurologic examination revealed that she did not utter even a word. She was unable to understand examiner's simple questions; communication by hand writing was also difficult, but she could draw her name and a circle; repetition was also impaired. Examination of other higher cerebral functions such as praxis and gnosis was impossible. Her optic fundi were unremarkable; no anisocoria was noted; extraocular muscles appeared intact, and the vestibulo-ocular reflex was normally elicited. The nasolabial fold was shallower on the left; the tongue showed a slight deviation to the left. She had near complete spastic left hemiplegia; deep tendon reflexes were increased bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy].

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1994

Pancreatic fibrosis in patients with chronic alcohol abuse: correlation with alcoholic pancreatitis.

OBJECTIVES: To investigate the incidence and histological features of pancreatic fibrosis, including chronic alcoholic pancreatitis, in patients with a history of chronic alcohol abuse. METHODS: Forty-six autopsy cases of alcoholic dependence syndrome, 53 cases of chronic alcoholism, and 30 cases of chronic alcoholic pancreatitis were studied histopathologically. RESULTS: Fibrosis was seen in 33 of 46 cases of alcoholic dependence syndrome, 20 of 53 cases of chronic alcoholism, and all 30 cases of chronic alcoholic pancreatitis. Fibrosis was categorized into three types: intralobular, perilobular, and mixed intralobular and perilobular sclerosis. In chronic alcoholic pancreatitis, fibrosis was found mainly in perilobular, or interlobular, areas, and in some advanced cases extended into intralobular areas, so that the pancreatic tissue was completely replaced by fibrosis. Hence, interlobular fibrosis was found in all cases of chronic alcoholic pancreatitis. In contrast, in cases that had predominantly intralobular fibrosis, which were usually cases of alcoholic dependence syndrome, the pancreatic tissue had not completely disappeared, even at an advanced stage, and some parenchymal regeneration similar to that seen in hemochromatosis was observed. CONCLUSION: Interlobular and intralobular pancreatic fibrosis associated with alcohol abuse appears in distinct pathological patterns with differing mechanisms.

Alcoholism↗
PubMed1994

[A 55-year-old man with prostate cancer, papilledema, and multiple cranial nerve palsies].

We report a 55-year-old man with papilledema and multiple cranial nerve palsies. He was well until 52 years of age when there was an onset of progressive difficulty in initiating urination; he visited the urology service of our hospital where a diagnosis of prostate cancer was made; the cancer was invading the bladder and was metastasizing to lymph nodes and bones. He was treated with oochiectomy and estrogen preparations with some improvement in his symptoms. Two years later, he developed difficulty in urination again, and transurethral resection of the tumor was performed in 1991. In December 1991, he noted tingling and numb sensation in his left face, which had become progressive worse within the next one month, and he developed blepharoptosis and deafness all on the left side. He was admitted to the urology service on February 4, 1992, and a neurological consultation was asked. On physical examination, general findings were unremarkable, except for lymph node enlargements of about 0.5 to 1.0 mm in size in cervical and inguinal regions. On neurologic examination, he was alert with normal mental activities; higher cerebral functions were intact. He had normal vision and visual fields, however, papilledema was present bilaterally; pupils and light reactions were normal. Extraocular muscles were intact on the right side, however, moderate restriction was noted in the left eye in that all the extraocular muscles except for the medial rectus were weak; blepharoptosis was noted on the left; no nystagmus was present. The sensation was diminished in the left face, and left facial paresis of the peripheral type was also noted; the taste sensation was also diminished in the left anterior two thirds of the tongue. He had sensorineural deafness on the left side. The other cranial nerves appeared intact. He walked normally; no weakness or muscle atrophy was noted; muscle tone was normal and no ataxia was observed. Deep reflexes were normally elicited and symmetric; the plantar response was flexor. No meningeal signs were present. Laboratory examination revealed following abnormalities: Hb 7.1 g/dl, platelet 47,000/cmm, WBC3,800/cmm, LDH 950IU/l, PAP232ng/ml (normal less than 1.6), PA2.631ng/ml (normal less than 7.4); a small amount of effusion was noted in the left pleural cavity; cytological examination of the fluid was class V. A cranial CT scan as well as MRI were entirely normal, as was the spinal tap. He was treated with glycerol, however, there was progressive increase in the pleural effusion, and he developed dyspnea; moist rale had become audible in the end of February.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗
PubMed1994

[A 54-year-old man with generalized muscle atrophy and oculomotor paresis].

We report a 54-year-old man with progressive generalized muscle atrophy and ophthalmoparesis in the terminal stage. He was well until 44 years of age (1982) when he noted weakness in his right hand and muscle atrophy; in May of 1985, he noted weakness in his left hand and in both legs. His weakness had become progressively worse, and he became unable to walk in November of 1985. He noted dysarthria one month later, and dysphagia in March of 1986. His difficulty in swallowing had also become worse; he regurgitated foods into the trachea in September of that year, and he developed a low grade fever on the same day. He was admitted to our service on September 24, 1987. On physical examination, general findings were unremarkable, except for low grade fever (37.3 degrees C). On neurologic examination, he was alert and mentally sound. He had normal vision and visual fields; ocular movements were normal. He had moderate weakness in facial muscles, dysarthria, dysphagia, and atrophy in his tongue. He had marked generalized muscle atrophy with fasciculation. He was unable to stand or walk. His muscle strength was not more than 1/6 in any part. The lower extremities were spastic. Deep reflexes were exaggerated in both lower extremities but were normal in upper extremities. Sensation was intact. Laboratory examination was unremarkable, and so was the cranial CT scan. He was treated with nasogastric feeding. He was able to communicate smoothly using his eyes, but a restriction in the vertical gaze was noted in February of 1989. The range of ocular movement was better in the oculocephalic reflex compared with his spontaneous vertical eye movements. In April of 1990, his horizontal gaze also had become slow, and he was complicated by bronchial asthma. He was treated with 20 mg/day of prednisolone; after the institution of prednisolone, his horizontal eye movement showed much improvement. In the terminal stage, he was able to move his eyes only very slowly; vertical gaze was impossible. His subsequent course was complicated by respiratory tract infection and septicemia, and he expired on July 15, 1992. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient had amyotrophic lateral sclerosis with oculomotor paresis. Post-mortem examination revealed spongy change involving the posterior column and the posterior spinocerebellar tract, in addition to severe degenerative change in the upper and the lower motoneurons, which were consistent with amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Amyotrophic Lateral Sclerosis↗
PubMed1994

[A 64-year-old man with recurrent blurred vision and an abdominal mass].

We report a 64-year-old man with recurrent bouts of blurred vision who died after developing an abdominal mass. He was well until June of 1985 when he was 59-years-old when he had an acute onset of loss of vision in his right eye. He was treated by prednisolone with a complete remission. In August of 1986, he had another bout of blurring of vision in his left eye. Once he lost his left vision completely, from which he showed slow recovery. In January of 1987, he developed blurring of his right eye and loss of pain and touch sensation in his right leg. Since then he repeated loss of vision in his right or left eye five times, and he was admitted to our hospital in May of 1990. On admission, he was alert and oriented. General physical examination was unremarkable. Neurologic examination revealed bilateral optic nerve atrophy. He could not discriminate light or dark by either eye. Other cranial nerves were unremarkable. He could walk in a wide-base only with support; spasticity was noted in his left leg. Muscle strength was preserved. Deep reflexes were exaggerated in both legs with extensor plantar reflex bilaterally. Pain and touch sensation was decreased in the left leg by 30%, and vibration was diminished in both feet. Position sense was preserved. Routine blood counts and chemistries were unremarkable. Cranial MRI scans revealed multiple high-signal intensity lesions in both pontine bases, basal ganglia, thalami, and in the deep cerebral white matters. He was treated with oral prednisolone, plasmapheresis, lymphocytapheresis, and then immuran. His vision showed only slight recovery to discriminate light and dark. In October of 1990, slight weakness appeared in his both legs. In December of that year, he developed nausea, and a fiber colonoscopic study revealed a stenosis in the transverse colon. In March of 1991, he developed anemia and liver dysfunction. In July of that year, jaundice appeared, and his serum bilirubin was increased. In October, his leg weakness became more prominent, and his cranial CT scans at that time revealed a low density change in the right cerebellum in the right superior cerebellar artery territory; in addition, multiple low density spots were scattered to be seen in both cerebral hemispheres including the basal ganglia and thalamic areas with ventricular dilatation and cortical atrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma, Mucinous↗
PubMed1994

[A 75-year-old man with parkinsonism and delirium].

We report a 75-year-old man with a ten-year history of parkinsonism, who developed acute delirium. He was well until 65 years of age, when there was an onset of tremor in his left hand. He had been treated with levodopa and trihexyphenidyl with marked improvement. He was doing well until July of 1991 at his age of 75-year-old, when he noted backache; he was found to have a compression fracture of the third lumbar spine. He had to use a wheel-chair most of the time since then. In December 1991, he started to have visual hallucinations and difficulty in swallowing. On December 25 of that year, he developed fever and delirium, and was admitted to our hospital on December 30. On admission, general physical examination was unremarkable except for low grade fever (37.3 degrees C). Neurologic examination revealed an alert but chronically ill patient. Apparently he had visual hallucinations. He was disoriented to all spheres; he could respond only to simple questions. Apparently he was demented. Cranial nerves were intact except for mumbling speech disturbance and masked face. He was unable to stand or walk. He had flexion contracture in his both knee joints. He had paratonic rigidity in all his limbs and marked bradykinesia. Once in a while, myoclonic jerks were seen in both upper and lower extremities. Deep reflexes were diminished bilaterally, and the plantar reflex was not elicited on either side. On laboratory examination, BUN was increased to 72 mg/dl, creatinine to 3.0 mg/dl, and WBC 16,000/microliter. Cranial CT scans were unremarkable.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

[A 78-year-old man with progressive gait disturbance, dysphagia, and dementia].

We report a 78-year-old man with progressive gait disturbance, dementia, and dysphagia. He was apparently well until 75 years of age in 1989 when he had an insidious onset of gait disturbance. In October of 1991, he was treated with levodopa and amantadine HCl in another hospital, but he developed visual hallucination right after these medications, and the drugs were discontinued. He also developed difficulty in swallowing with frequent aspiration pneumonia. He was admitted to our hospital on January 13, 1992. On admission, the patient was chronically ill Japanese man; his blood pressure was 118/70 mmHg, body temperature 35.4 degrees C, and heart rate 72 and regular. No anemia or jaundice was noted; lungs were clear and no heart murmur was audible. The abdomen was flat but rigid to palpation without tenderness; no organomegaly was noted. On neurologic examination, he was alert but disoriented to all spheres; he was apparently demented and the score of the mini-mental test was 11. He did not appear to have aphasia or apraxia. Cranial nerves appeared intact, but he had a mask-like face and a slight limitation in the upward gaze; his voice was small. He was unable to stand or walk; he showed marked akinesia and moderate rigidity in his neck and the trunk. Deep reflexes were generally elicited normally or slightly weakly. Plantar response was extensor on the left and flexor on the right. No grasp reflex was present. Sensory examination showed questionable loss of touch in the glove- and -stocking distribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Recovery of beta-receptors and adenylate cyclase from desensitization induced by short term heat exposure in rat parotid glands.

1. The recovery of rat parotid beta-adrenergic receptors (beta-AR) and adenylate cyclase (AC) from heat (33 degrees C)-induced desensitization was studied. 2. Down-regulated cell surface beta-AR and AC activity in response to isoprenaline (IPR) returned to the control level 120 hr after the termination of heat exposure. 3. However, beta-AR in parotid crude membranes increased over the control level for 48-120 hr. 4. Coupling between beta-AR and G protein(s) was attenuated at 120 hr. 5. These data suggest that beta-AR on the cell surface, but not those internalized, can transduce biological responses.

Adenylyl Cyclase Inhibitors↗
PubMed1993

In vivo adaptative regulation of muscarinic receptors and muscarinic stimulation-induced Ca2+ mobilization during short-term heat exposure in rat parotid glands.

1. Adaptation of muscarinic receptors (MR)--muscarinic stimulation--induced intracellular Ca2+ mobilization during short-heat exposure (33 degrees C). 2. Heat-exposure for 48 hr decreased the carbachol (CCh)-stimulated cytosolic Ca2+ concentration increase. 3. The number of MR on cell surface increased transiently at 24 hr with a subsequent decrease at 48 hr. 4. CCh-stimulated inositol triphosphate (IP3) formation decreased at 48 hr. 5. In saponin-permeabilized cells, 1,4,5-IP3-induced 45Ca2+ release decreased at 24 hr. 6. The data suggest that the adaptation for increased muscarinic stimulation occurs at IP3 generating sites as well as at intracellular IP3 receptor sites during heat exposure.

Acetylcholine↗