Anuran larvae transform their epidermis to the adult counterpart during metamorphosis. The major event of this process is the proliferation of larval epidermal basal cells and their differentiation into adult ones. The present study isolated novel type I keratin cDNA dubbed xak-c (Xenopus adult keratin-c) that was exclusively expressed in adult epidermal basal cells. The gene started its expression in the larval epidermis at the onset of metamorphosis. Thyroid hormone (TH) induced the precocious expression of the gene in the epidermis of premetamorphic tadpoles. To study the transcriptional regulation of this gene in relation to epidermal metamorphosis, a 2.8 kb 5 -flanking region of xak-c was cloned and its promoter activity was investigated. Gene constructs were made so as to contain the xak-c promoter region and gene of EGFP or luciferase as a reporter gene and were transfected into various types of cells, which revealed that the 5 -flanking region had an epidermal cellspecific transcriptional activity in both anurans and mammals. Larval skin tissues of Xenopus were transfected with the constructs and cultured in the presence and absence of TH, which showed that the promoter region is responsive to TH, although the region did not contain the consensus TH response element-like sequence. In sharp contrast, the promoter region did not respond to TH in the adult skin, clearly indicating that the cloned region contains specific sequences that respond to metamorphosis-dependent transcription factor(s).
The present study suggested that intracarotid administration of bFGF (100 ng) can reduce infarct size after MCA occlusion. It was speculated that the increased CBF in the penumbral areas of MCA may contribute to contraction of infarct size.
This study concerns 19 patients over 16 years of age with Moyamoya disease. Ten cases of intracranial haemorrhage, as the initial haemorrhagic event in patients aged from 21 to 55 (haemorrhagic group) and 9 cases of ischaemic events in 18- to 53-year-old patients (ischaemic group) were included. All haemorrhages were associated with intraventricular haemorrhages (IVH); and all but one case of thalamic haemorrhage were thought to be primary IVH (2 cases of small paraventricular haemorrhage; 2 of small haemorrhages in the splenium; 5 with no intracerebral haematoma). In the 9 patients of the ischaemic group, there were 2 cases of transient ischaemic attacks and 7 of cerebral infarction. Angiographic evaluations demonstrated that the abnormal basal vessel formation and the collateral supplies from the external carotid arteries were poorly developed in both groups. In contrast, the collateral circulation via the choroidal and posterior pericallosal arteries was well demonstrated. Furthermore, marked enlargement of the choroidal arteries and the medullary arteries derived from them was seen more frequently in the haemorrhagic group. These findings suggested that the haemodynamic load in the vessels supplying the walls of the posterior parts of the ventricles and the periventricular region was increased, especially in the haemorrhagic group. Those vessels were considered to be important sites of IVH in adult patients with Moyamoya disease.
IR and/or SRS provided results comparable with proton beam or heavy particle therapy in our series of cranial base chordomas probably because the radiation field must have covered the target of the tumour volume sufficiently, and reduction of gross tumour volume reduced the target size for radiotherapy. Pursuit of further effective combinations of IR and stereotactic radiotherapy (SRS, proton beam, heavy particle) after tangible resection, especially for residual and recurrent lesions, will be an acceptable framework to achieve a better therapeutic outcome for cranial base chordomas than at present.
Although the present study did not provide direct evidence that the occipital artery contributes to occipital neuralgia at the point of contact with the greater occipital nerve, the possibility still cannot be precluded, because the occipital artery may be palpable in areas corresponding to tenderness of the greater occipital nerve. Further studies, including clinical cases, are needed to clarify this issue.
Background-We report an unusual case of acquired dural-pial arteriovenous malformation (AVM) following sinus thrombosis. Case Description-Initial angiography performed in a 39-year-old man showed thrombosis of the superior sagittal sinus (SSS) and the right transverse sinus (TS) but no vascular malformations. Follow-up angiography 29 months later revealed recanalization of the SSS and the TS, retrograde cortical venous drainage which suggested that thrombosis of the sinuses probably propagated into the adjacent parietal cortical veins, and development of a dural-pial AVM at or near the site of thrombi in more than one cortical vein. Complete surgical excision of the lesion was accomplished without neurological deterioration. Conclusions-The present case suggests the possibility that the pial AVM is not only a congenital condition but also may develop as an acquired lesion. (Stroke. 1998;29:1721-1724.)Key Words: angiogenesis Ⅲ cerebral arteriovenous malformations Ⅲ sinus thrombosis D ural arteriovenous malformations (AVMs) appear to be acquired rather than congenital lesions, and it is well known that they often develop at the site of a sinus thrombosis. 1,2,3,4 On the other, hand, pial AVMs are generally considered to be congenital malformations. We report a case of acquired dural-pial AVM following superior sagittal and transverse sinus thrombosis and discuss the causes both of the unusual location of the dural AVM and of the development of the pial lesion in this case.
Case ReportThe patient was a 39-year-old man who, on July 27, 1994, experienced headache and vomiting, followed 2 days later by weakness in the upper part of his left arm. He was hospitalized 4 days later, and neurological examinations indicated left hemiparesis.CT scan revealed a low-density area with a mass effect in the right frontal lobe (Figure 1), and on enhanced CT an empty delta sign was observed in the superior sagittal sinus (SSS). MRI showed sinus thrombosis of the SSS and the right transverse sinus (TS). However, MRI revealed no abnormal findings suggestive of a vascular malformation. Because no image of the anterior half of the SSS or the right TS could be detected in angiograms of the right common carotid artery, a diagnosis of sinus thrombosis of the SSS and the right TS was made (Figure 2A and 2B). Nevertheless, no dural or pial AVMs were found ( Figure 2C and 2D).Immediately after admission, anticoagulant therapy was initiated. Both the headache and the left hemiparesis improved gradually and since, there were no clearly abnormal findings on neurological examination other than a slight exaggeration of the deep tendon reflex on the left side, the patient was discharged. Although MRI performed on September 27, 1996, revealed recanalization of the SSS and the right TS, at the same time a large number of flow void signals Figure 3A and 3B). It was also noted that the SSS was patent but there was a reflux of blood into the cortical veins, and the venous routes between the cortical veins and the SSS were occluded ( Figure 3C). Meanwh...
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