Inhibitory effect of regucalcin on protein phosphatase activity in the nuclei of rat kidney cortex.

The role of regucalcin, which is a regulatory protein of calcium signaling, in the regulation of protein phosphatase activity in the nuclei of rat kidney cortex was investigated. Protein phosphatase activity towards phosphotyrosine, phosphoserine, and phosphothreonine was found in the nuclei. The enzyme activity towards three phosphoamino acids was significantly increased by the addition of calcium chloride (10-50 microM) in the enzyme reaction mixture. This increase was significantly inhibited by trifluoperazine (25 or 50 microM), an antagonist of calmodulin. The presence of regucalcin (50 or 100 nM) in the enzyme reaction mixture caused a significant decrease in protein phosphatase activity towards three phosphoamino acids. This effect was also seen in the presence of calcium (25 microM) and/or calmodulin (5 microg/ml). Protein phosphatase activity towards three phosphoamino acids was significantly increased in the presence of anti-regucalcin monoclonal antibody (25 or 50 ng/ml) in the enzyme reaction mixture. This effect was completely blocked by the addition of regucalcin (100 nM). The effect of antibody (25 ng/ml) in increasing protein phosphatase activity towards phosphotyrosine was significantly inhibited by vanadate (10(-4) M). Also, the antibody's effect towards phosphoserine and phosphothreonine was significantly inhibited by cyclosporin A (10(-5) M). Endogenous regucalcin was found in the nuclei of rat kidney cortex using Western blot analysis. Nuclear regucalcin level was significantly reduced by the administration of saline (0.9% NaCl) for seven days in rats. Protein phosphatase activity towards three phosphoamino acids was significantly decreased by saline administration. The effect of anti-regucalcin monoclonal antibody (25 ng/ml) in increasing protein phosphatase activity towards three phosphoamino acids was weakened in the renal cortex nuclei of saline-administrated rats. The present study demonstrates that endogenous regucalcin plays a suppressive role in the regulation of protein phosphatase activity in the nuclei of rat kidney cortex cells.

Suppressive role of endogenous regucalcin in the regulation of protein phosphatase activity in rat renal cortex cytosol.

The role of endogenous regucalcin, which is a regulatory protein of calcium signaling, in the regulation of protein phosphatase activity in the cytosol of rat renal cortex was investigated. Protein phosphatase activity toward phosphotyrosine, phosphoserine, and phosphothreonine was found in the cytosol of kidney cortex. The addition of regucalcin (50-250 nM) in the enzyme reaction mixture caused a significant decrease in protein phosphatase activity toward three phosphoamino acids. The effect of calcium (25 microM) and calmodulin (2.5 microg/ml) in increasing protein phosphatase activity toward three phosphoamino acids was significantly decreased by the addition of regucalcin (100 nM). Protein phosphatase activity toward three phosphoamino acids was significantly increased in the presence of anti-regucalcin monoclonal antibody (10-50 ng/ml) in the enzyme reaction mixture. The effect of antibody (25 ng/ml) in increasing the enzyme activity was significantly inhibited by cyclosporin A (10(-5) M) or vanadate (10(-5) M). Regucalcin in the kidney cortex cytosol was clearly decreased by the administration of saline (0.9% NaCl) for seven days in rats. Protein phosphatase activity toward three phosphoamino acids was significantly decreased by saline administration. The effect of anti-regucalcin antibody (25 ng/ml) in increasing protein phosphatase activity toward three phosphoamino acids was not seen in the renal cortex cytocol of saline-administered rats. The present study demonstrates that endogenous regucalcin plays a suppressive role in the regulation of protein phosphatase activity in the cytoplasm of rat kidney cortex.

Dural arteriovenous malformation manifesting as dementia due to ischemia in bilateral thalami. A case report.

BACKGROUND: Although dementia is one of the curable manifestations of a dural arteriovenous malformation (AVM), the pathophysiology remains unclear. CASE DESCRIPTION: We describe an elderly patient who had an AVM in the tentorium and manifested signs of dementia from ischemia, predominantly in the bilateral thalami. Intravascular embolization of the dural AVM resulted in amelioration of signs of dementia, and this improvement was consistent with that of neuroradiological and hemodynamic conditions in the thalami. CONCLUSION: The coincidental improvement of CBF in the thalami and signs of dementia after embolization of the AV shunt supports the concept of primary participation of the thalami in the pathophysiology of dementia of vascular origin in our patient.

Clinicopathological features of superficial depressed-type colorectal neoplastic lesions.

OBJECTIVE: We performed this study to analyze the endoscopic findings, dissecting microscopic features, and p53 immunostaining in superficial depressed-type (depressed) colorectal neoplastic lesions. METHODS: Dissecting stereomicroscopy was used to ascertain the size and pit pattern of lesions removed by endoscopic snare polypectomy. Immunohistochemical staining of p53 was performed with an antigen retrieval system using a monoclonal antibody to p53. RESULTS: All depressed neoplastic lesions (submucosal carcinoma, n = 6; high-grade dysplasia, n = 14; and adenoma, n = 30) were small (< 1 cm in diameter) and were detected as a depression with or without a marginal elevation on colonoscopic examination. In the dissecting microscopic study, submucosal carcinomas and lesions of high-grade dysplasia almost exclusively showed irregular small pits, with the exception of four malignant lesions with moderate submucosal invasion in which the pit structure was absent. In contrast, adenomas had either regular small (29/30 lesions) or oval pits (1/30 lesions). Rates of p53 positivity were 100%, 64%, and 7% in depressed submucosal carcinomas, lesions of high-grade dysplasia, and adenomas, respectively, thus the prevalence of p53 positivity was significantly higher in the former two groups than in the adenoma group. CONCLUSIONS: The high frequency of invasive carcinoma and high-grade dysplasia found in depressed colorectal neoplastic tumors, despite their small size, indicates that these lesions may be a subtype of colorectal tumor with more aggressive malignant potential at an earlier stage.

Augmentation of Prolactin Release by alpha-Melanocyte Stimulating Hormone Is Possibly Mediated by Melanocortin 3-Receptors in the Mouse Anterior Pituitary Cells.

Suckling- and estrogen-induced prolactin release from the anterior pituitary is mediated by alpha-melanocyte stimulating hormone (alpha-MSH) secreted by the intermediate lobe of the pituitary in the rat. Melanocortin 5-receptors are expressed in the anterior pituitary and probably mediate the alpha-MSH function. In contrast, the mouse anterior pituitary does not express the receptor. To examine whether or not alpha-MSH regulates prolactin release in mice, we performed cell immunoblot assay using anterior pituitary cells from adult female mice. We found that alpha-MSH acted on mammotrophs (prolactin-secreting cells) and stimulated prolactin release in a dose dependent manner. A series of RT-PCR using oligonucleotide primer pairs specific for each subtypes of melanocortin receptors revealed that the melanocortin 3-receptor is the sole receptor expressed in the mouse anterior pituitary. These results suggest that alpha-MSH-induced prolactin release is mediated by melanocortin 3-receptors in female mice.

[Extracranial vertebral artery aneurysm complicating Klippel-Feil syndrome: case report].

The Klippel-Feil syndrome is one of the spinal malformations characterized by fusion of the cervical vertebrae. It is well known that the malformation can cause some neurologic disorders. However, an aneurysm in the vertebral artery associated with the Klippel-Feil syndrome is extremely rare, with only one case having been reported in the literature. We present a 39-year-old female with a sudden onset of disturbed consciousness. Lateral cervical x-ray films showed the Klippel-Feil syndrome and hypermobility between C1 and C2. MRI showed multiple infarctions in the posterior circulation, including bilateral thalami. Right vertebral angiogram identified the extracranial vertebral artery aneurysm as the source of the emboli. The patient gradually recovered with conservative therapy. The aneurysm was thought to be produced by chronic arterial trauma secondary to excessive movement between C1 and C2. We conclude that an extracranial vertebral artery aneurysm is a serious complication in a patient with the Klippel-Feil syndrome.

Combination chemotherapy with Tegafur. Uracil (UFT), etoposide, adriamycin and cisplatinum (UFT-EAP) for advanced gastric cancer.

Thirty-four patients with advanced gastric cancer were treated with combination chemotherapy employing Tegafur-Uracil (UFT), etoposide, Adriamycin, and Cisplatinum (CDDP) (UFT-EAP therapy). An objective partial response was obtained in 16 patients (47%) and the median duration of remission was 12.2 months. The 50% survival time for all 34 patients was 10 months. Patients with moderately or well differentiated adenocarcinoma responded well (13/19, 68%), while those with undifferentiated adenocarcinoma showed a poor response (3/15, 20%). Six responding patients were noted to have no evidence of viable cancer at the primary site by endoscopic biopsy, and underwent gastrectomies. The resected specimens showed complete disappearances of the primary tumors in four patients. The median survival time for the patients receiving gastrectomies was 24 months. The regimen was very well tolerated, apart from moderate bone marrow suppression. Our results suggest that patients with advanced gastric cancer can be effectively treated with UFT-EAP chemotherapy.

Cerebellar hemorrhage after supratentorial craniotomy--report of three cases.

We report on three cases of remote cerebellar hemorrhage after supratentorial craniotomy, which had much in common in their computed tomographic, operative, and clinical findings. We speculate that, when the patient is in the supine position, displacement of the cerebellum causes stretching of the superior vermian veins and their tributaries, resulting in tearing of these vessels. Postoperative cerebrospinal fluid overdrainage or massive air reflux into the cranial cavity through the drainage tube may accelerate this process. Meticulous management of the drainage system is necessary to prevent this postoperative complication.

[A case of moyamoya disease with repeated intraventricular hemorrhage due to a ruptured pseudoaneurysm].

A case of Moyamoya disease with ruptured aneurysm is reported. This is a rare case in that episodes of intraventricular bleedings were repeated. The size of the aneurysm was markedly increased after the second bleeding, and the ruptured aneurysm was histologically certified after operative resection to be a pseudo-aneurysm.

[Cerebral blood flow in subarachnoid hemorrhage: analysis in patients with poor outcomes].

Cerebral blood flow (CBF) of 6 patients with poor outcome after subarachnoid hemorrhage is analyzed. Neurological grades of these patients were grade III in 2 and grade IV in 4 patients, and subarachnoid hemorrhage on CT was diffuse and thick in all patients. Cerebral blood flow was continuously measured for 7 to 19 days by the thermal diffusion flow probe with a peltier stack which was left on the cerebral cortex at the surgery for ruptured aneurysm. Moreover, CBF studies by cold xenon CT and 133Xe inhalation methods were also performed in discussing cases. At the same time intracranial pressure was monitored. Cerebral angiography was carried out in all except for 2 patients who died due to severe cerebral vasospasm. The initial CBF value of all patients was 20 to 40 ml/100 g/min (mean value: 27 ml/100 g/min), and these were significantly low compared to normal value (50 ml/100 g/min). Moreover, these CBF was substantially decreased several days after surgery in all patients, and it was marked in 3 patients who died. From these results it was clear that the degree of vasospasm is important to determine the prognosis. One of 3 patients who died had ruptured left posterior cerebral artery aneurysm with occlusion of bilateral internal carotid arteries. In this case further decrease of CBF due to vasospasm was observed in addition to low initial CBF resulting diffuse low flow in both hemispheres although extracranial to intracranial bypass was performed. On the other hand, it was also shown that the intracranial pressure was an important factor to influence the outcomes.(ABSTRACT TRUNCATED AT 250 WORDS)

Familial intracranial aneurysms: report of four families.

The authors describe eight cases of familial intracranial aneurysms occurring in four families. In the literature reviewed, familial aneurysms have different characteristics in that the incidence of the anterior communicating aneurysms is lower and that of the middle cerebral aneurysms is somewhat higher, and the age of patients at diagnosis is often younger. Although the number of patients is few, our study does not support these characteristics. A family history of intracranial aneurysms should include such high-risk factors as polycystic kidneys, coarctation of the aorta, fibromuscular dysplasia, and other connective tissue disorders.

Aneurysm on a persistent hypoglossal artery.

The authors report a patient with saccular aneurysm on a left persistent hypoglossal artery who suffered subarachnoid haemorrhage from an aneurysm of the right distal anterior cerebral artery. A review of the literature emphasizes the rarity of the occurrence of an aneurysm on a persistent primitive hypoglossal artery itself.

Interhemispheric subdural empyema with enlarged meningeal arteries.

A successfully treated case of an interhemispheric subdural empyema is reported. In addition to the characteristic angiographic and computed tomographic findings, the present case was accompanied by enlarged middle meningeal and anterior falx arteries.

Dissecting aneurysm of the vertebral artery.

A patient presented with a subarachnoid hemorrhage associated with a vitreous hemorrhage. Angiography was first interpreted as revealed a saccular aneurysm at the junction of the vertebral and posterior inferior cerebellar arteries. At operation it was evident that the aneurysm was a dissecting one of the vertebral artery. The proximal portion of the intracranial vertebral artery was clipped. The patient survived without any attributable neurological deficit. A review of the relevant literature is presented.

Dural arteriovenous malformation in the anterior fossa.

A case of dural arteriovenous malformation in the anterior fossa is reported. It first caused a subarachnoid hemorrhage and subsequently an intracerebral hematoma. Pertinent literature is briefly reviewed. Such malformations may be divided into three groups; those involving primarily the basal dura mater of the anterior fossa, the anterior portion of the falx, or the dura mater of the frontal convexity. Principal blood supply comes from the ophthalmic artery with an additional supply from the external carotid system. The treatment of choice is surgical excision with or without artificial embolization of the feeding arteries from the external carotid artery.