Biomedical subjects

Y Nagamine

Publications and source records attributed to Y Nagamine.

At least 37 records · Page 2Linked to original sources

PubMed1998

Rapamycin inhibition of the G1 to S transition is mediated by effects on cyclin D1 mRNA and protein stability.

The immunosuppressant rapamycin has been shown previously to inhibit the G1/S transition in several cell types by prolonging the G1 phase of the cell cycle. This process appears to be controlled, in part, by the rapamycin-sensitive FK506-binding protein-rapamycin-associated protein-p70 S6 kinase (p70(S6k)) pathway and the cyclin-dependent kinases (Cdk). We now show that in serum-stimulated NIH 3T3 cells, rapamycin treatment delays the accumulation of cyclin D1 mRNA during progression through G1. Rapamycin also appears to affect stability of the transcript. The combined transcriptional and post-transcriptional effects of the drug ultimately result in decreased levels of cyclin D1 protein. Moreover, degradation of newly synthesized cyclin D1 protein is accelerated by rapamycin, a process prevented by inclusion of the proteasome inhibitor, N-acetyl-Leu-Leu-norleucinal. The overall effect of rapamycin on cyclin D1 leads, in turn, to impaired formation of active complexes with Cdk4, a process which triggers retargeting of the p27(Kip1) inhibitor to cyclin E/Cdk2. In view of this novel experimental evidence, we discuss a possible mechanism for the rapamycin-induced cell cycle arrest at the G1/S transition.

3T3 Cells↗

PubMed1998

Two patients with premature labour associated with Mycoplasma hominis infection.

Because several reports have suggested that bacterial vaginosis causes premature labour and early rupture of the fetal membranes, the presence of a bacterial flora that causes bacterial vaginosis is thought to be a risk factor for premature labour. The present study investigated two patients with premature delivery and intra-uterine Mycoplasma hominis infection. In microbiological studies, Gram's staining of amniotic fluids revealed numerous neutrophils and epithelial cells but no micro-organisms. Culture of amniotic fluid before antibiotic therapy yielded only M. hominis under anaerobic conditions; aerobic culture was negative. Vaginal discharge taken on the day of delivery yielded no growth in case 1 and M. hominis and Enterococcus faecalis in case 2. Maternal sera showed specific antibodies to M. hominis by ELISA and immunoblotting. As no possible cause of premature labour other than M. hominis infection was detected, it is concluded that the intra-uterine M. hominis infection was associated with premature labour in these patients.

Adult↗

PubMed1998

UV irradiation induces the murine urokinase-type plasminogen activator gene via the c-Jun N-terminal kinase signaling pathway: requirement of an AP1 enhancer element.

UV irradiation leads to severe damage, such as cutaneous inflammation, immunosuppression, and cancer, but it also results in a gene induction protective response termed the UV response. The signal triggering the UV response was thought to originate from DNA damage; recent findings, however, have shown that it is initiated at or near the cell membrane and transmitted via cytoplasmic kinase cascades to induce gene transcription. Urokinase-type plasminogen activator (uPA) was the first protein shown to be UV inducible in xeroderma pigmentosum DNA repair-deficient human cells. However, the underlying molecular mechanisms responsible for the induction were not elucidated. We have found that the endogenous murine uPA gene product is transcriptionally upregulated by UV in NIH 3T3 fibroblast and F9 teratocarcinoma cells. This induction required an activator protein 1 (AP1) enhancer element located at -2.4 kb, since deletion of this site abrogated the induction. We analyzed the contribution of the three different types of UV-inducible mitogen-activated protein (MAP) kinases (ERK, JNK/SAPK, and p38) to the activation of the murine uPA promoter by UV. MEKK1, a specific JNK activator, induced transcription from the uPA promoter in the absence of UV treatment, whereas coexpression of catalytically inactive MEKK1(K432M) and of cytoplasmic JNK inhibitor JIP-1 inhibited UV-induced uPA transcriptional activity. In contrast, neither dominant negative MKK6 (or SB203580) nor PD98059, which specifically inhibit p38 and ERK MAP kinase pathways, respectively, could abrogate the UV-induced effect. Moreover, our results indicated that wild-type N-terminal c-Jun, but not mutated c-Jun (Ala-63/73), was able to mediate UV-induced uPA transcriptional activity. Taken together, we show for the first time that kinases of the JNK family can activate the uPA promoter. This activation links external UV stimulation and AP1-dependent uPA transcription, providing a transcription-coupled signal transduction pathway for the induction of the murine uPA gene by UV.

3T3 Cells↗

PubMed1998

Role of tissue-specific transcription factor LFB3 in a cyclic AMP-responsive enhancer of the urokinase-type plasminogen activator gene in LLC-PK1 cells.

A cyclic AMP (cAMP)-inducible enhancer in the pig urokinase-type plasminogen activator gene located 3.4 kb upstream of the transcription initiation site is composed of three protein-binding domains, A, B, and C. Domains A and B each contain a CRE (cAMP response element)-like sequence but require the adjoining C domain for full cAMP responsiveness. A tissue-specific transcription factor, LFB3/HNF1beta/vHNF1, binds to the C domain. Mutation analyses suggest that the imperfect CRE and LFB3-binding sequences are required for tight coupling of hormonal and tissue-specific regulation. CREB and ATF1 bind to domains A and B, and this binding is enhanced upon phosphorylation by cAMP-dependent protein kinase (protein kinase A [PKA]). Analysis in a mammalian two-hybrid system revealed that CREB/ATF1 and LFB3 interact and that transactivation potential is enhanced by PKA activation. Interestingly, however, phosphorylation of CREB at Ser-133 does not contribute to its interaction with LFB3. The region of LFB3 involved in its interaction with CREB/ATF1 lies, at least partly, between amino acids 400 and 450. Deletion of this region removed the ability of LFB3 to mediate cAMP induction of the ABC enhancer but did not impair its basal transactivation activity on the albumin promoter. Thus, the two activities are distinct functions of LFB3.

Activating Transcription Factor 1↗

PubMed1998

Persistent activation of mitogen-activated protein kinases p42 and p44 and ets-2 phosphorylation in response to colony-stimulating factor 1/c-fms signaling.

An antibody that specifically recognized phosphothreonine 72 in ets-2 was used to determine the phosphorylation status of endogenous ets-2 in response to colony-stimulating factor 1 (CSF-1)/c-fms signaling. Phosphorylation of ets-2 was detected in primary macrophages, cells that normally express c-fms, and in fibroblasts engineered to express human c-fms. In the former cells, ets-2 was a CSF-1 immediate-early response gene, and phosphorylated ets-2 was detected after 2 to 4 h, coincident with expression of ets-2 protein. In fibroblasts, ets-2 was constitutively expressed and rapidly became phosphorylated in response to CSF-1. In both cell systems, ets-2 phosphorylation was persistent, with maximal phosphorylation detected 8 to 24 h after CSF-1 stimulation, and was correlated with activation of the CSF-1 target urokinase plasminogen activator (uPA) gene. Kinase assays that used recombinant ets-2 protein as a substrate demonstrated that mitogen-activated protein (MAP) kinases p42 and p44 were constitutively activated in both cell types in response to CSF-1. Immune depletion experiments and the use of the MAP kinase kinase inhibitor PD98059 indicate that these two MAP kinases are the major ets-2 kinases activated in response to CSF-1/c-fms signaling. In the macrophage cell line RAW264, conditional expression of raf kinase induced ets-2 expression and phosphorylation, as well as uPA mRNA expression. Transient assays mapped ets/AP-1 response elements as critical for basal and CSF-1-stimulated uPA reporter gene activity. These results indicate that persistent activation of the raf/MAP kinase pathway by CSF-1 is necessary for both ets-2 expression and posttranslational activation in macrophages.

3T3 Cells↗

PubMed1998

Multimodality treatment for large and critically located arteriovenous malformations.

To define the current status of the multimodality treatment for large and critically located arteriovenous malformations (AVMs), we have made a retrospective review of 54 consecutive patients with Spetzler-Martin grade IV and V AVMs. The size of nidus is larger than 3 cm in diameter in all cases. Initially, all but one were treated by nidus embolization with the aim of size reduction. Only one patient had complete nidus occlusion by embolization alone. In 52 patients, the obliteration rate of nidus volume averaged 60% after embolization. Ten patients underwent complete surgical resection of AVMs following embolization with no postoperative neurological deterioration. Thirty-one patients underwent stereotactic radiosurgery following embolization. At the time of this analysis, 30 patients underwent follow-up angiography 2-3 years after radiosurgery. The results of radiosurgery correlated well with the preradiosurgical AVM volume. Of 16 patients with small residual AVMs (< 10 cm3, a mean volume of 4.7 cm3), nine (56%) had complete obliteration, and six (38%) had near-total or subtotal obliteration by 3 years after radiosurgery. In contrast, of 14 patients with large residual AVMs (> or = 10 cm3, a mean volume of 17.9 cm3), only two (14%) had complete obliteration, and eight (57%) had near-total or subtotal obliteration. Repeat radiosurgery was performed for the patients with remaining AVMs at 3-year follow-up review. This study indicates that a certain number of large and critically located AVMs can be safely treated by either microsurgery or radiosurgery following a significant volume reduction by nidus embolization. The present data also suggest the need and possible role of repeat radiosurgery in improving complete obliteration rate of large difficult AVMs, since many of those AVMs have significantly responded to initial radiosurgery.

Adolescent↗

PubMed1998

Dural arteriovenous shunts at the craniocervical junction.

OBJECT: A retrospective analysis was conducted of 10 patients (three women and seven men) who were treated for spinal dural arteriovenous shunts (AVSs) located at the craniocervical junction. This analysis was performed to evaluate the characteristics of this unusual location in contrast with those of the more common thoracic and lumbar AVSs. METHODS: Seven patients presented with subarachnoid hemorrhage (SAH) and one with slowly progressive quadriparesis and dyspnea due to myelopathy. The other two cases were detected incidentally and included a transverse-sigmoid dural AVS and a cerebellar arteriovenous malformation. Angiographic studies revealed that the spinal dural AVSs at the C-1 and/or C-2 levels were fed by the dural branches of the radicular arteries that coursed from the vertebral artery and drained into the medullary veins. Venous drainage was caudally directed in the patient with myelopathy. In contrast, the shunt flow drained mainly into the intracranial venous system in patients with SAH. Furthermore, in four of these patients a varix was found on the draining vein. In all patients, the draining vein was interrupted surgically at the point at which this vessel entered the intradural space, using intraoperative digital subtraction angiography to monitor flow. The postoperative course was uneventful in all patients and no recurrence was confirmed on follow-up angiographic studies obtained in seven patients at 6 months after discharge. CONCLUSIONS: If computerized tomography scanning shows SAH predominantly in the posterior fossa and no abnormalities are found on intracranial four-vessel angiographic study, proximal vertebral angiography should be performed to detect dural AVS at the craniocervical junction. The results of surgical intervention for this disease are quite satisfactory.

Adult↗

PubMed1998

[Differential diagnosis of hyponatremia following subarachnoid hemorrhage].

Hyponatremia is a common complication after subarachnoid hemorrhage (SAH). Although the mechanism of hyponatremia is still controversial, cerebral salt-wasting syndrome (CSNS) is currently regarded as being more responsible than the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The aim of our study was to assess the plasma volume status of a patient with hyponatremia following subarachnoid hemorrhage. In doing this it may be possible to indirectly differentiate its pathogenesis. Fifty patients with SAH were studied. Twenty patients demonstrated hyponatremia (serum sodium < 135 mEq/L) during day 7 to 13 after subarachnoid hemorrhage. Patients with hyponatremia were categorized on the basis of their daily body weight, and central venous pressure. Group A consisted of patients with hypovolemia (16 patients), with the onset time of hyponatremia being day 7 to 9. Group B included those with hypervolemia (4 patients); hyponatremia was observed during day 10 to 11 and was corrected in all patients within 72 hours after induction of fluid restriction. Our findings suggest that hyponatremia following subarachnoid hemorrhage usually occurs due to CSWS, although SIADH remains as a minor pathogenesis. We conclude that the combination of daily body weight and CVP measurements is a simple and practical method to distinguish promptly SIADH from CSWS.

Adult↗

PubMed1998

[Long lasting epidural anesthesia for a morbidly obese patient].

A forty-six year old woman (136 cm, 115 kg), with body mass index (BMI) of 62.2, was scheduled for osteotomy because of postoperative infection and pseudoarthrosis of the right lower leg. During the post two years, the patient had received several orthopedic surgeries under spina anesthesia, which repeatedly accompanied intraoperative respiratory difficulties. At the age of thirty one, she weighted more than 100 kg and needed cardiopulmonary resuscitation during cesarean section under general anesthesia. Considering the past history of anesthesic complications, we decided to perform epidural anesthesia with a written informed consent from the patient. Due to technical difficulties, the operative procedures took six hours and forty-five minutes without complications related to anesthesia. This case demonstrates the necessity of safe and comfortable anesthesia for morbidly obese patients.

Anesthesia, Epidural↗

PubMed1997

12-O-Tetradecanoylphorbol-13-acetate activates the Ras/extracellular signal-regulated kinase (ERK) signaling pathway upstream of SOS involving serine phosphorylation of Shc in NIH3T3 cells.

We investigated the activation of the Ras/ERK signaling pathway by 12-O-tetradecanoylphorbol-13-acetate (TPA) in NIH3T3 fibroblasts. Interestingly, the activation was suppressed not only by dominant negative Raf-1 but also by dominant negative Ras and SOS. Further analysis revealed that TPA treatment induced, dependently on protein kinase C, the mobility shift of p66(shc) in SDS-polyacrylamide gel electrophoresis, which could be prevented by treatment of the Shc immunoprecipitate with serine/threonine-specific protein phosphatase 1 (PP1) or 2A (PP2A). Phosphoamino acid analysis of Shc showed that unlike growth factor-induced Shc phosphorylation, where Shc is mainly phosphorylated at tyrosine residues, TPA-induced phosphorylation was only at serine residues. Like growth factor-induced Shc phosphorylation, which leads to the association of Shc with Grb2, TPA also induced this association, but, correspondingly to the above results, the TPA-induced association was disrupted by in vitro treatment of the Shc immunoprecipitate with PP1. Taken together, these results suggest that the TPA signal was fed at or upstream of Shc to activate the Ras/ERK signaling pathway involving serine phosphorylation of Shc.

3T3 Cells↗

PubMed1997

Cooperation of two PEA3/AP1 sites in uPA gene induction by TPA and FGF-2.

We have previously shown in NIH 3T3 fibroblasts that treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) or fibroblast growth factor-2 (FGF-2) activates the Ras/Erk signaling pathway in NIH 3T3 fibroblasts, leading to the induction of the urokinase-type plasminogen activator (uPA) gene. In this study, we characterize cis-acting elements involved in this induction. DNase I hypersensitive (HS) site analysis of the uPA promoter showed that two regions were enhanced after TPA and FGF-2 treatment. One was located 2.4kb upstream of the transcription start site (-2.4kb), where a known PEA3/AP1 (AGGAAATGAGGTCAT) element is located. The other was located in a previously undefined far upstream region. Sequencing of this region revealed a similar AP1/PEA3 (GTGATTCACTTCCT) element at -6.9 kb corresponding to the HS site. Deletion analysis of the uPA promoter in transient transfection assays showed that both PEA3/AP1 elements are required for full inducibility, suggesting a synergism between the two elements. When the two sites were inserted together upstream of a minimal promoter derived from the thymidine kinase gene, expression of the reporter gene was more strongly induced by TPA and FGF-2 than with either of the two elements alone. Alone, the -6.9 element was more potent than the -2.4 element. The involvement of AP1 as well as Ets transcription factors was confirmed by examining different promoter constructs containing deletions in either the AP-1 or the PEA3 element, and by using an expression plasmid for dominant negative Ets-2. Electromobility shift analyses using specific antibodies showed that c-Jun and, JunD bind to both elements with or without induction. In addition, ATF-2 binds to the -2.4-kb element even without induction and c-Fos to the -6.9-kb element only after induction. Accordingly, overexpression of c-Fos caused induction from the -6.9-kb element, but reduced induction from the -2.4-kb element. The involvement of the Ets-2 transcription factor was shown by using expression plasmids for wild-type and dominant negative Ets-2.

3T3 Cells↗

PubMed1997

Enhanced stability of urokinase-type plasminogen activator mRNA in metastatic breast cancer MDA-MB-231 cells and LLC-PK1 cells down-regulated for protein kinase C--correlation with cytoplasmic heterogeneous nuclear ribonucleoprotein C.

In LLC-PK1 cells, urokinase-type plasminogen activator (uPA) mRNA has a short half-life of 70 min. We have previously demonstrated that most of the regulatory regions responsible for the rapid turnover of uPA mRNA in LLC-PK1 cells reside in its 3' untranslated region (3' UTR), where there are at least three regulatory sites, one of which is A+U-rich. This A+U-rich sequence mediates uPA mRNA stabilization induced by protein kinase C (PKC) down-regulation. In this work, we found that uPA mRNA is rather stable in MDA-MB-231 cells with a half-life of 17 h. We compared the stability of hybrid globin mRNA containing different parts of uPA mRNA in its 3' UTR and found that the A+U-rich sequence of uPA mRNA renders otherwise stable globin mRNA unstable in LLC-PK1 cells but not in MDA-MB-231 cells. We identified a cytoplasmic protein of 40 kDa (p40) which specifically interacts with the A+U-rich sequence. Levels of p40 activity as detected by ultraviolet cross-linking were higher in MDA-MB-231 and PKC-down-regulated LLC-PK1 cells than in untreated LLC-PK1 cells. Prior treatment of the cytoplasm with a specific antibody against heterogeneous nuclear ribonucleoprotein C (hnRNP C) significantly reduced p40 activity. These results suggest a correlation between the A+U-rich sequence-dependent uPA mRNA stabilization in vivo and the binding of hnRNP C to the A+U-rich sequence in vitro.

Animals↗

PubMed1997

Regulation of the urokinase-type plasminogen activator gene by the oncogene Tpr-Met involves GRB2.

The oncogene Tpr-Met is a constitutively active form of the hepatocyte growth factor/scatter factor (HGF/SF) receptor Met. It comprises the intracellular moiety of Met linked to the dimerization domain of the nuclear envelope protein Tpr, thus functioning as a constitutively activated Met. HGF/SF is responsible for various biological processes including angiogenesis and wound healing, in which secreted serine protease urokinase-type plasminogen activator (uPA) is implicated. The action of HGF/SF on cells is mediated by the autophosphorylation of Met on two carboxyterminal tyrosine residues, Y1349VHVNATVY1356VNV. The two tyrosine residues provide docking sites for various effector molecules, suggesting that multiple signaling pathways are activated to exert biological effects of HGF/SF [Ponzetto et al., Cell (1994) 77: 261]. We found that Tpr-Met efficiently activates the uPA gene via a SOS/Ras/extracellular signal regulated kinase (ERK)-dependent signaling pathway. Mutation of Y1356, which abrogates GRB2 binding, reduced the induction to half of the control level, while mutation of Y1349 showed little effect on uPA induction, suggesting an important but partly replaceable role for GRB2 in Met-dependent uPA gene induction. Mutation of both Y1349VHV and Y1356VNV into optimal PI 3-kinase sites resulted in a residual induction of about one quarter of the control level, suggesting a potential role for PI 3-kinase. Dose-response analysis of the Tpr-Met showed a biphasic curve. These results suggest that the interplay among different signaling molecules on the receptor is important for full induction of the pathway leading to the activation of the uPA gene.

3T3 Cells↗

PubMed1997

Mode of transfection influences the stability of ectopically expressed mRNA.

In the study of mRNA metabolism, modified mRNAs are often analyzed after corresponding mRNA expression vectors have been transfected, either transiently or stably, into cells. Two differently transfected templates might be localized in distinct nuclear compartments: in transient transfection they remain in the nucleoplasm while in stable transfection they are integrated in the chromatin. Consequently, nascent transcripts may encounter different environments which may affect the physical state of mRNA and its fate. In this work, we addressed the question whether the two different modes of transfection affect the stability of expressed mRNA. We compared globin mRNA, which is characteristically stable, and globin-delta AU mRNA, which contains the 3' untranslated region of urokinase-type plasminogen activator mRNA and is unstable. In stably transfected cells, these mRNAs were degraded in a manner which mimicked the endogenous mRNA, whereas in transiently transfected cells, the regulated degradation of both mRNAs was impaired. However, when lower amounts of template DNA were used in transient transfection, mRNA was degraded in a manner similar to that of stably expressed mRNA, indicating that mRNA levels affect its stability. To monitor potential differences in the physical state of mRNAs in vivo, we developed a method based on a combination of chemical modification of cellular RNA and a modified RT-PCR. We found that patterns of chemical modification vary with the levels of mRNA expressed. Our results suggest that a proper interaction of mRNA with specific cellular proteins is important for regulated degradation and that overexpression of mRNA destroys such proper stoichiometry.

Animals↗

PubMed1997

Cytoskeleton reorganization induces the urokinase-type plasminogen activator gene via the Ras/extracellular signal-regulated kinase (ERK) signaling pathway.

Urokinase-type plasminogen activator (uPA) expression is induced upon cytoskeletal reorganization (CSR) by a mechanism independent of protein kinase C and cAMP protein kinase in nontransformed renal epithelial (LLC-PK1) cells. This CSR-dependent uPA gene activation is mediated by an AP-1-recognizing element located 2 kilobases upstream of the transcription initiation site. The phosphorylation of c-Jun, a component of AP-1, is induced by CSR, which seems to increase both the activity and stability of c-Jun (Lee, J. S., von der Ahe, D., Kiefer, B., and Nagamine, Y. (1993) Nucleic Acids Res. 21, 3365-3372). It has been shown that c-Jun is phosphorylated by members of the mitogen-activated protein kinase family, i.e. ERKs and JNKs. ERKs are activated through a growth factor-coupled Ras/Raf-dependent signaling pathway, while JNKs are activated through a stress-induced signaling pathway. Although CSR induces both ERK-2 and JNK activity, JNK does not seem to be involved in the uPA gene induction because UV irradiation, which activates JNK as efficiently as CSR, does not activate the uPA promoter. Further analysis showed the involvement of SOS, Ras, and Raf-1 in the pathway induced by CSR. Our results suggest that cells sense changes in cell morphology using the cytoskeleton as a sensor and respond by activating the ERK-involving signaling pathway from within the cell.

Animals↗

PubMed1997

[Reliability and factorial structure of a rating scale for persistent vegetative state].

We developed a new rating scale, Kohnan Vegetative Score, to measure severity and small clinical changes in vegetative state patients. It has 7 items corresponding to the conditions of vegetative state by Japanese Society of Neurosurgery: motor function, food ingestion, urination and defecation, eye movement, vocalization, communication, and facial expression. Each item is rated in 5 ordinal categories: slight (score = 1), mild(2), moderate(4), and extreme(5). The sum of the scores is used as the summary score, which ranges from 7 to 35, and high score means 'severe'. We examined the reliability and the factorial structure of the Kohnan Vegetative Score. The subjects were 10 patients who met the conditions of vegetative state. Four neurosurgeons rated the subjects, and then 2 of them repeated the rating after one week interval. As a measure of reliability, the (weighted) Kappa coefficient proposed Cohen (1960, 1968) was calculated for each item, and the intraclass correlation coefficient (ICC) was calculated for the summary score. To analyze the factorial structure, the factor analysis was carried out. The minimum and the maximum weighted Kappa values were 0.44 and 0.64 for intra-rater reliability, and 0.37 and 0.69 for inter-rater reliability, respectively. Concerning the factorial structure, the contribution of the first factor was 91.5% which indicated the unidimensionality of the scale. The ICC's estimate for the summary score were 0.90 (95% C.I.: 0.766-0.970). On the basis of these results, the Kohnan Vegetative Score has unidimensionality and high reliability enough for a practical use.

Aged↗

PubMed1996

Types of unruptured cerebral aneurysms reviewed from operation video-recordings.

To estimate the proportion of unruptured cerebral aneurysms with thin-walled sac, we have analyzed the operative findings of 78 incidental cerebral aneurysms found in 51 consecutive surgical cases by reviewing of intra-operative videotape recordings. Among 78 unruptured aneurysms, 23 (30%) were evaluated as thick-walled aneurysms (Type A), 39 (50%) with partially thin-walled sac (Type B) and 16 (20%) with entirely thin wall sacs (Type C). The mean size of Type A aneurysms was 10.4 mm (ranging from 3 to 22 mm), in Type B it was 9.8 mm (ranging 4 to 25 mm) and in Type C it was 4.4 mm (between 2-12 mm). Approximately two-thirds of Type C aneurysms were 4 mm in size or smaller, and Type C aneurysms were significantly smaller than Type A aneurysms. In summary, this preliminary study has provided two original data. 1) About 70% of incidental unruptured aneurysms have a partially or entirely thin-walled sac. 2) Many of the small aneurysms have an entirely thin sac. Assuming that thin-walled aneurysms are at a high risk of subsequent rupture, the surgical intervention for incidental unruptured aneurysms may be recommended irrespective of their size if the surgical risk is considered low.

Adult↗

PubMed1996

Indirect revascularization for moyamoya disease: is there a beneficial effect for adult patients?

BACKGROUND: It is generally accepted that excellent development of collateral circulation can be achieved through indirect nonanastomotic bypass procedures for pediatric patients with moyamoya disease. However, there are no definitive conclusions about the effect of indirect revascularization for adult patients. To clarify the value of indirect bypass surgery for adult moyamoya disease, we have analyzed their follow-up angiographic results in comparison with those of the pediatric patients. METHODS: Between 1989 and 1993, 23 patients underwent combined direct and indirect bypass surgery. They consisted of 16 adults (mean age, 35; range, 20-59) and seven children (mean age, 10; range, 3-16). The main symptoms were those due to cerebral ischemia in all but 1 of 23 patients. Preoperative cerebral blood flow studies showed all patients to have decreased vascular reserve (misery perfusion). Postoperative follow-up angiography was done in all patients at a median of 6 months after the surgery. RESULTS: All pediatric patients showed good or moderate development of collaterals through the indirect bypass. Among the adult group, seven patients aged 20 to 29 had angiographic results similar to those of the pediatric group . On the other hand, nine patients older than 30 had results contrary to those of pediatric patients: (1) the degree of indirect revascularization declined to moderate or poor grades (especially in patients older than 40) and (2) the degree of direct bypass filling improved to high or medium grades. CONCLUSIONS: The results suggest that advancing age apparently affects the development of collateral formation through the indirect bypass. Consequently, direct bypass is thought to be the main treatment option for patients older than 40.

Adolescent↗