New treatment of a visible linear scar in the scalp: multiple hair-bearing flap technique.

Scars on the scalp have no hair, and can be conspicuous even when narrow. Alopecia, especially in the whorl of hair at the back of the parietal region, is very difficult to camouflage. We present a new technique using multiple hair-bearing flaps harvested from near the area of alopecia, each flap including 10-15 hairs. We treated 24 patients who were suffering from alopecia, with scar sizes ranging from 2 cm to 17 cm in length and from 0.5 cm to 2 cm in width. Between three and 12 flaps per patient were used to complete the treatment. All wounds healed without complications, and satisfactory results were achieved in 20 patients. Hair loss from the flap was rare. The scar could be hidden by the hair immediately after the operation. In four patients, a visible scar remained or was created at the donor site. These patients required a secondary repair. The major advantages of this technique are that the dense hair bundles in the flap are studded here and there in the scar, the scar can be reduced and the residual scar can be hidden by the flap hair. This technique is most useful for the parietal and occipital areas, especially near the whorl of hair.     

Nonfunctioning adrenocortical carcinoma revealed by metastasis to the base of the tongue

A 60-year-old man visited our clinic with the complaint of a tumor of the tongue base. Clinical and histological examination revealed that the tumor was metastasis from left adrenal carcinoma. Metastatic lesions were present in the tongue base, cervical lymph node and lung. There were no endocrinological abnormalities in the laboratory examination. The patient died about three months after admission. The autopsy disclosed nonfunctioning carcinoma of the adrenal cortex. Ninety-two cases of nonfunctioning adrenocortical carcinoma in Japan including the present patient are briefly reviewed.     

Induction of human glioma-specific cytotoxic T-lymphocyte lines by autologous tumor stimulation and interleukin 2

Summary Two human glioma-specific cytotoxic T-lymphocyte (G-S-CTL) lines were established by autologous tumor stimulation (ATS) with the aid of lectin free interleukin 2 (IL 2). Coculture of patient's peripheral blood lymphocytes and autologous irradiated glioma cells and subsequent addition of partially purified IL 2 enhanced the tumoricidal activity of the lymphocytes. These CTL lines possessed cross-cytotoxic activity against autologous and allogeneic glioma cells and exhibited low cytotoxic activity against non-glial tumor cells. They did not lyse autologous lymphoblasts. This phenomenon suggested the existence of a common gliomaspecific antigen recognized by the CTL lines.T-cell subset depletion test revealed that the major surface phenotype of G-S-CTL line, responsible for cytotoxic activity was OKT 3 positive, OKT 4 negative and OKT 8 positive.G-S-CTL lines were composed of a low proportion of OKT 8 positive subpopulation after primary ATS and successive propagation with IL 2. The proportion of OKT 8 positive subpopulation was increased by secondary ATS, which enhanced the cytotoxic activity to glioma cells more effectively.     

Possible role of glucocorticoids in a complement-activated state induced by cobra venom factor in rats

Activation of the complement system of adrenalectomized rats with an injection of cobra venom factor (CVF) caused death of the rats within 2.5 h. Morphologically, this activation provoked distinct congestion of the gastric glandular mucosa and pulmonary leukostasis. Pretreatment of the animals with dexamethasone abolished the undesirable responses completely. Injection of CVF to intact rats produced only slight responses, but caused a marked increase in the serum levels of corticosterone. Dexamethasone was found to be replaced by promethazine (H1-antihistamine) or dimethylsulphoxide (scavenger of hydroxyl radicals) but not by indomethacin, ibuprofen (cyclo-oxygenase inhibitors), deferoxamine mesylate (iron chelator) or imidazole (thromboxane synthetase inhibitor). These results suggest that glucocorticoids protect the animals from the adverse effects of excessive complement activation and that they act as an inhibitor of the production or action of histamine and toxic oxygen products induced by complement activation.     

Expression of ras oncogene p21 in relation to prognostic factors of human breast cancer]

For the purpose of demonstrating the relationship between the expression of ras oncogene p21 protein and clinico-pathological characteristics which reflected the prognosis, 253 women with breast cancer who underwent mastectomy were analyzed. Ras p21 was detected in 133 (52.6%). In histological types, scirrhous carcinomas were more often ras p21-positive, and papillo-tubular carcinoma were usually negative. And histological grade was significantly correlated with ras p21. The degrees of invasion to fat tissues and infiltration into lymphatic vessels were also significantly correlated with ras p21. Tumors with lymph node metastases expressed higher levels of ras p21 than nonmetastasizing tumors in smaller tumors, especially in papillo-tubular carcinomas. And patients with elevated ras expression tended to have a poor prognosis. These results suggested that an elevated ras expression may play an important role in the development of aggressive tumors.     

Dynamic MR imaging and radiotherapy.

Dynamic MRI has been used to improve the detection of tumors and to make differential diagnosis. Most malignant lesions show early enhancement and early washout of contrast media on dynamic MRI, but the characterization of the tumor remains unclear. Pharmacokinetic analysis of dynamic MRI can provide information about the permeability of contrast media in the tumor that may reflect the oxygen concentration of the tumor. This information may be useful in the prediction of a tumor's response to radiation therapy.     

Sporadic cerebral amyloid angiopathy presenting with dementia and prominent capillary beta-amyloid deposition: a case report]

We report a sporadic case of unusual cerebral amyloid angiopathy (CAA) with prominent capillary involvement. A 67-year-old doctor developed gait disturbance, resting tremor and rigidity. He was diagnosed to have Parkinson's disease, for which the treatment with levodopa was effective. Four years later he began to exhibit progressive cognitive decline and behavioral abnormalities consisting of hallucination and agitation. Subsequently, his condition steadily worsened and became bedridden with severe dementia, and he died eight years after the disease onset. During the clinical course, there had been no episode of stroke. Postmortem examinations revealed the typical pathology of Parkinson's disease with frequent cortical Lewy bodies in the amygdala. The most striking pathological feature of this patient was widespread CAA where prominent beta-amyloid (A beta) deposition was observed in the capillaries of the neocortex, most pronouncedly in the occipital lobe, as well as leptomeningeal and cerebral medium-sized and small vessels. Further, perivascular plaques were found in half of the amyloid-laden capillaries. Tau-positive dystrophic neurites were only sparsely detectable within a few perivascular plaques. Despite the severe A beta pathology, there was no microaneurysmal dilatation, fibrinoid necrosis or vascular occlusion. There was only one small ischemic lesion in the brain. The cerebral white matter was unremarkable. Senile plaques of neuritic type and neurofibrillary tangles were mostly limited to the hippocampal regions and, to a lesser degree, in the amygdaloid nucleus, which did not meet the neuropathological criteria of Alzheimer's disease. On the gene analyses, his apolipoprotein E (ApoE) genotyping was verified to be heterozygous epsilon 3/epsilon 4, and no mutation was seen in exons 16 and 17 of the amyloid precursor protein gene. Severe A beta capillary angiopathy as seen in our patient is exceptional in sporadic CAA. Further, A beta angiopathy of this patient was notable in the absence of an associated cerebrovascular disease despite prominent A beta deposition in the vessel walls. Regarding the development of his severe dementia, the limbic pathology of Lewy body disease might be one of the potential causes, but A beta angiopathy appears more likely because of its severity. We speculate that widespread A beta deposition disregulates the blood-brain barrier of the capillaries leading to a disturbance of the microcirculation throughout the cerebral cortex without obvious ischemic disintegration of the neuropil. We should take into consideration that A beta angiopathy can present as progressive dementia without cerebrovascular disease.     

Chronic hypoxia accelerates the progression of atherosclerosis in apolipoprotein E-knockout mice.

The aim of this study was to investigate the effect of chronic hypoxia on the development and progression of atherosclerosis in apolipoprotein E-knockout (apoE-KO) mice. Male and female apoE-KO mice (6 weeks old) and age- and sex-matched wild-type mice were kept under hypoxic conditions (10.0 +/- 0.5% O2) in a gas chamber or in room air for 3 weeks. Aortic atherosclerotic plaque was not observed in wild-type mice under normoxic or hypoxic conditions. In the apoE-KO mice, however, hypoxia induced proliferation of smooth muscle cells and plaque formation in the aorta, which were not observed under normoxic conditions. Although sexual dimorphism of the response to hypoxia was not observed, these hypoxia-induced atherogenic changes were accompanied by a significant increase of plasma low density lipoprotein (LDL) cholesterol and NADPH-dependent vascular superoxide (O2-) production. Furthermore, matrix metalloproteinase (MMP)-9 was activated in the aorta of apoE-KO mice. In conclusion, chronic hypoxia accelerated the development of atherosclerosis in apoE-KO mice, along with increased O2- production and activated MMP-9 in the aorta.