Degradation-stage effect of self-etching primer on dentin bond durability.

It is well-known that self-etching primers can be altered. However, the effects from altered primers on the dentin bond durability have yet to be thoroughly identified. In this study, we examined the effects from 5 altered Liquid A primers in different stages of degradation-where 2-hydroxyethylmethacrylate (HEMA) and 10-methacryloyloxydecyl dihydrogen phosphate (MDP), used in Liquid A primers, were altered by the hydrolysis of the methacryloxy ester portion in the HEMA and MDP-on the hybrid layer's quality and dentin bond durability. The hypothesis was that degradation stages of altered Liquid A primers have no effect on the hybrid layer's quality and on dentin bond durability. Bond strengths, obtained after thermo-cycling, were strongly dependent on the degradation stage of the altered Liquid A primer. Alterations of self-etching primers reduced dentin bond durability and decreased the created hybrid layer's quality.

Embolization of the Middle Meningeal Artery for Refractory Chronic Subdural Haematoma. Usefulness for Patients under Anticoagulant Therapy.

SUMMARY: Endovascular embolization of the middle meningeal artery was performed in two cases of refractory chronic subdural haematoma (CSDH) after repeated burr hole and irrigation surgeries. The embolization prevented expansion of the CSDH in both cases, and the haematoma disappeared completely in one case. The expansion of CSDH is considered to result from repeated bleeding from the macrocapillaries on the haematoma capsule. Embolization of the middle meningeal artery appears to be useful to eliminate the blood supply to this structure.

Treatment of asymptomatic unruptured intracranial aneurysms. A clinical decision analysis.

SUMMARY: The indication of preventive surgery for patients who harbor asymptomatic un ruptured intracranial aneurysms remains controversial. To evaluate the benefit of this treatment, we investigated the management outcome in 128 patients with 157 unruptured aneurysms. Surgery was planned in patients 70 years old or younger without serious systemic complications. A total of 77 patients underwent surgery including four endovascular interventions, and conservative management was chosen in 51 patients. There was no mortality and 6.5% morbidity as postoperative results, and no complication was found after endovascular treatment. Among the patients in conservative management, four patients suffered from subsequent rupture during the total follow-up period of 148 person-years. The annual rupture rate was estimated at 2.7%. According to the clinical decision analysis based on our data, preventive surgery is beneficial for a Japanese 70 years old or younger. However, the expected utility decreases if the rupture rate is set at 0.5% or 0.05%, posing a doubt about the benefit of the surgery. Decision analysis provides an aid for logical and objective choice in the management of unruptured aneurysms. The actual risk of rupture has a major impact on decision making in therapeutic strategy.

Gamma knife treatment for multiple metastatic brain tumors compared with whole-brain radiation therapy.

OBJECT: The purpose of this retrospective study was to compare the effectiveness of gamma knife radiosurgery (GKS) for multiple cerebral metastases with that of whole-brain radiation therapy (WBRT). METHODS: Ninety-six consecutive patients with cerebral metastases from nonsmall cell lung cancer were treated between 1990 and 1999. The entry criteria were the presence of between one and 10 multiple brain lesions at initial diagnosis, no surgically inaccessible tumors with more than a 30-mm diameter, no carcinomatous meningitis, and more than 2 months of life expectancy. The patients were divided into two groups: the GKS group (62 patients) and the WBRT group (34 patients). In the GKS group, large lesions (> 30 mm) were removed surgically and all other small lesions (< or = 30 mm) were treated by GKS. New distant lesions were treated by repeated GKS without prophylactic WBRT. In the WBRT group, the patients were treated by the traditional combined therapy of WBRT and surgery. In both groups, chemotherapy was administered according to the primary physician's protocol. The two groups did not differ in terms of age, sex, initial Karnofsky Performance Scale (KPS) score, type, lesion number, and size of lesion, systemic control, and chemotherapy. Neurological survival and qualitative survival of the GKS group were longer than those of the WBRT group. In multivariate analysis, significant poor prognostic factors were systemically uncontrolled patients, WBRT group, and poor initial KPS score. CONCLUSIONS: Gamma knife radiosurgery without prophylactic WBRT could be a primary choice of treatment for patients with as many as 10 cerebral metastases from nonsmall cell cancer.

Cerebral vein disorders and postoperative brain damage associated with the pterional approach in aneurysm surgery.

The possible causes of postoperative brain damage were examined in 100 cases of cerebral aneurysms operated on by the pterional approach. Postoperative brain damage occurred in 15% of cases, located mostly in the inferior frontal lobe. Its incidence was higher in early than in delayed operation and increased with severity of preoperative clinical conditions but not correlated with patient age and aneurysm location. The venous perfusion patterns in the inferior frontal lobe were classified into three types based on preoperative venograms: Sylvian type drained mainly into the superficial Sylvian veins (SSVs), Frontal type drained mainly into the frontal bridging veins, and Intermediate type. Postoperative brain damage was most frequent in the Sylvian type with statistical significance (p < 0.01). The brain retraction procedure impairs regional cerebral blood flow (rCBF). Venous congestion in the retracted inferior frontal lobe, caused by stretching and narrowing of SSVs due to both brain retraction and dissection of the Sylvian fissure, also reduces rCBF. Thus, a marked reduction in rCBF in the retracted area causes postoperative brain damage. Postoperative venograms showed the SSVs to be obscured in 24% of patients, indicating that the pterional approach possibly influences the SSV perfusion. A venous perfusion disorder during the pterional approach is the most important factor in postoperative brain damage, and careful preoperative assessment of cerebral veins is indispensable.

Ruptured cerebral aneurysm associated with coarctation of the aorta--report of two cases.

Two cases of ruptured cerebral aneurysm associated with coarctation of the aorta are presented. The aneurysms were successfully clipped in the acute stage prior to correction of the coarctation. Ruptured aneurysm should be treated as early as possible, and unruptured aneurysm should also be treated before aortic repair, if the general condition of the patient allows.

[Three cases of non-traumatic acute subdural hematoma].

The authors present three cases of non-traumatic acute subdural hematoma showing interesting clinical features and operative findings. Case 1: A-50-year-old male was admitted because of sudden headache and epileptic seizure. Computed tomographic (CT) scan showed a right thin subdural hematoma, but cerebral angiography demonstrated no pathological findings, that might cause acute subdural hematoma on the follow-up CT scans. The hematoma changed to a chronic one within only 15 days, which was proved by the operation. Case 2: A 52-year-old male was hospitalized because of loss of consciousness. CT scan revealed a right subdural hematoma without subarachnoid hemorrhage and cerebral angiography demonstrated a right middle cerebral artery aneurysm. The hematoma was surgically proved to be due to rupture of the aneurysm. Case 3: A 52-year-old male was admitted because of headache, vomiting and left motor weakness. CT scan showed a thick right subdural hematoma and right carotid angiography revealed two internal carotid artery aneurysms. It was surgically certified that the subdural hematoma was caused by a tear in a cortical artery attached to the dura, not by the rupture of the aneurysms. Clinical cause and pathogenesis of so-called "non-traumatic" or "spontaneous" acute subdural hematomas were discussed, and the importance of emergency angiography for this condition is stressed.

[Intention tremor after head injury. Clinical features and computed tomographic findings].

Eight cases of intention tremor as a late complication of head injury were investigated. The patients ranged in age from 3 to 24 years. All received severe head injuries and lapsed into coma immediately afterward (Glasgow Coma Scale scores less than or equal to 8). Six patients exhibited decerebration or decortication. Hemiparesis was present in six cases and oculomotor nerve palsy in four. In the chronic stage, all patients displayed some degree of impairment of higher cortical function and five had dysarthria and/or ataxia. Initial computed tomography (CT) scans within 3 hours after the injury were obtained in five cases, of which four showed a hemorrhagic lesion in the midbrain or its surroundings. Other CT findings were diffuse cerebral swelling (four cases), intraventricular hemorrhage (three), and multiple hemorrhagic lesions (two). In the chronic stage, generalized cortical atrophy or ventricular enlargement was noted in five cases. These clinical features and CT findings indicate diffuse brain damage as well as midbrain damage and may reflect shearing injury.

Post-traumatic intention tremor--clinical features and CT findings.

Eight patients with post-traumatic intention tremor were reported. Intention tremor developed in the young as a late complication of severe head injury (Glasgow Coma Scale was below 8 in all cases) and impaired their functional outcome. This state was treatable with medication or by stereotactic thalamotomy. Neurologically, all the patients lapsed into coma immediately after the injury and many patients manifested clinical signs of a midbrain lesion in the chronic stage. The characteristic CT (computed tomography) findings in the acute stage were a high density area in the midbrain, accompanied by diffuse cerebral swelling or intraventricular hemorrhage, and in the chronic stage, brain atrophy or ventricular enlargement were the most prominent CT findings. These characteristics, indicating diffuse brain damage in addition to midbrain injury, may suggest the presence of shearing injury. The midbrain damage is consistent with the classical hypothesis that the damage to the Dentate-Rubro-thalamic system accounts for the occurrence of intention tremor. Furthermore, the presence of diffuse brain damage suggests that a more widespread brain injury may participate in its development.

[Partial oculomotor nerve palsy due to midbrain lesion--case report and discussion on its characteristics].

UNLABELLED: A case of partial oculomotor palsy due to midbrain infarction is reported. CASE PRESENTATION: Fifty-one-year old man noted a sudden onset of double vision. He transiently presented right hemiparesis, right hemihyposthenia and cerebellar ataxia. The main symptom was the left oculomotor palsy selectively involving extraocular muscles (levator and pupil sparing), lasting for more than 6 months. The CT scan showed localized and well demarcated low-density areas at the left tegmentum of midbrain and left anteromedial thalamus, diagnosed as lacunar infarction due to occlusion of paramedian perforators at the basilar bifurcation. This midbrain infarct was supposed to be responsible for the partial oculomotor palsy. Extramedullary compressive and ischemic lesions have been well-known main causes of partial oculomotor palsy. This case, however, has emphasized the importance of recognition of midbrain lesion as a causative location of the partial oculomotor palsy. While the anatomical elucidation of this infrequent palsy is not sufficient, a topography of oculomotor nuclear complex in rhesus monkey proposed by Warwick, is worthwhile to correlate with midbrain oculomotor palsy in human cases. The pupil and levator sparing oculomotor palsy is most frequently caused by the laterally localized lesion at the fascicular portion which extends transversely at the midbrain tegmentum. This is the most likely lesion in this reported case. It is reported, on the other hand, that the levator sparing type oculomotor palsy is caused by a paramedian lesion of rostral midbrain and pupil sparing type by caudal midbrain. These may be explainable by rostro-caudal extension of the nuclear complex.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-1. Toxicity of metabolites of miocamycin: acute toxicity of Mb1 in mice.

Miocamycin (MOM) is a derivative of midecamycin, a macrolide antibiotic isolated from a culture broth of Streptomyces mycarofaciens. MOM is metabolized into 4 main metabolites of Mb1, Mb2, Mb6 and Mb12. The object of this study was to evaluate acute toxicity in male and female mice after single oral administration of Mb1, a metabolite of MOM, at a dose level of 5,000 mg/kg as the maximum physically applicable dose. Observations were kept for 1 week after administration. In conclusion, Mb1 exhibited no acute toxicity in present study. The LD0 values were estimated as more than 5,000 mg/kg.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-2. Toxicity of metabolites of miocamycin: acute toxicity of Mb1 in rats.

Acute toxicity studies on miocamycin (MOM), non-crystalline solid, and its metabolite Mb1 were performed in mice in the previous studies. In the present studies, we evaluated acute toxicity of Mb1 in male and female rats after single oral administration at the maximum physically applicable dose of 5,000 mg/kg. Observations were continued for 1 week after treatment. It is concluded that LD0 values of Mb1 were estimated more than 5,000 mg/kg.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-3. Toxicity of metabolites of miocamycin: subacute toxicity of Mb1 in rats.

Miocamycin (MOM) is a derivative of midecamycin, a macrolide antibiotic and is metabolized into 4 main metabolites of Mb1, Mb2, Mb6 and Mb12. In the previous study, LD0 values of Mb1 were estimated more than 5,000 mg/kg in male and female rats as Mb1 did not exhibited any lethal toxicity even at the maximum physically applicable dose of 5,000 mg/kg. The object of this study was to examine subacute toxicity in male and female rats after repeated p.o. administration of Mb1 for 5 weeks at a daily dosage of 125, 250, 500 and 1,000 mg/kg. It is concluded that no manifest toxicity was observed in this subacute toxicity study on Mb1 in rats.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-4. Toxicity of metabolites of miocamycin: acute toxicity of Mb2 in mice.

Miocamycin (MOM) is a derivative of midecamycin and is metabolized into 4 main metabolites. At previous study, LD0 values of Mb1 were estimated more than 5,000 mg/kg in male and female mice. The object of this study was to evaluate acute toxicity in male and female mice after single oral administration of Mb2, a metabolite of MOM, at a dose level of 5,000 mg/kg as the maximum physically applicable dose. It is concluded that LD0 values of Mb2 were estimated more than 5,000 mg/kg.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-5. Toxicity of metabolites of miocamycin: acute toxicity of Mb2 in rats.

Miocamycin (MOM) is a derivative of midecamycin and is metabolized into 4 main metabolites. At previous study, LD0 values of Mb1 were estimated more than 5,000 mg/kg in male and female rats. The object of this study was to evaluate acute toxicity in male and female rats after single oral administration of Mb2, a metabolite of MOM. It is concluded that LD0 values of Mb2 were estimated more than 5,000 mg/kg.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-6. Toxicity of metabolites of miocamycin: subacute toxicity of Mb2 in rats.

Miocamycin (MOM) is a derivative of midecamycin, a macrolide antibiotic and is metabolized into 4 main metabolites of Mb1, Mb2, Mb6 and Mb12. At previous study, the acute and subacute toxicity of Mb1 and acute toxicity of Mb2 were performed that those metabolites did not exhibit any lethal toxicity even at the maximum physically applicable dose. The object of this study was to examine subacute toxicity in male and female rats after repeated p.o. administration of Mb2 for 5 weeks at a daily dosage of 125, 250, 500 and 1,000 mg/kg. It is, therefore, concluded that Mb2 exerted no toxic effects in this subacute toxicity.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-7. Toxicity of metabolites of miocamycin: acute toxicity of Mb6 in mice.

Miocamycin (MOM) is a derivative of midecamycin and is metabolized into 4 main metabolites. In the present studies, we evaluated acute toxicity and estimated LD50 values of Mb6, one of the main metabolites of MOM, in male and female mice after single oral administration. Observations were continued for 1 week after treatment. The LD50 values were calculated according to Litchfield-Wilcoxon's method. It is concluded that LD50 values of Mb6 were 4,150 mg/kg (3,577.6 approximately 4,814.0 mg/kg) in male mice and 4,000 mg/kg (3,389.8 approximately 4,720.0 mg/kg) in female mice, respectively.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-8. Toxicity of metabolites of miocamycin: acute toxicity of Mb6 in rats.

Miocamycin (MOM) is a derivative of midecamycin and is metabolized into 4 main metabolites of Mb1, Mb2, Mb6 and Mb12. In the previous studies, we estimated LD50 values of Mb6 in male and female mice after single oral administration. The LD50 values were 4,150 mg/kg in male mice and 4,000 mg/kg in female mice, respectively. In the present studies, we evaluated acute toxicity and estimated LD50 values of Mb6 in male and female rats after single oral administration. Observations were continued for 1 week after treatment. It is concluded that LD0 values of Mb6 in male and female rats, were estimated more than 5,000 mg/kg as Mb6 did not exhibit any manifest acute toxicity even at the maximum physically applicable dose of 5,000 mg/kg.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-9. Toxicity of metabolites of miocamycin: subacute toxicity of Mb6 in rats.

Miocamycin (MOM) is a derivative of midecamycin and is metabolized into 4 main metabolites of Mb1, Mb2, Mb6 and Mb12. It is also known that LD50 values of Mb6 were 4,150 mg/kg in male mice and 4,000 mg/kg in female mice but LD0 values in male and female rats were estimated more than 5,000 mg/kg. The object of this study was to examine subacute toxicological effects in male and female rats after repeated oral administration of Mb6 for 5 weeks at a daily dosage of 125, 250, 500 and 1,000 mg/kg. It is concluded that no manifest toxicity was observed in this study with Mb6 in male and female rats after oral administration at dosage levels of 125, 250, 500 and 1,000 mg/kg for 5 weeks.

Toxicological studies on a new macrolide antibiotic, midecamycin acetate (miocamycin). Part IV-10. Toxicity of metabolites of miocamycin: acute toxicity of Mb12 in mice.

We evaluated acute toxicity and estimated LD50 values of Mb12, one of the main metabolites of MOM, in male and female mice after single oral administration. Observations were continued for 1 week after treatment. The LD50 values were calculated according to Litchfield-Wilcoxon's method. It is concluded that LD50 values of Mb12 were 5,750 mg/kg (4,914.5-6,727.5 mg/kg) in male mice and 4,950 mg/kg (4,194.9-5,841.0 mg/kg) in female mice, respectively.