ABSTRACT
We retrospectively evaluated the prognostic impact of the level of nodal involvement in patients with advanced oral squamous cell carcinoma (SCC). Between 2005 and 2010, 105 patients with clinical stage III or IV oral SCC had chemoradiotherapy preoperatively. Clinical (cN) and pathological nodal (pN) involvement was primarily at levels Ib and II. We defined nodal involvement at levels Ia and III-V as anterior and inferior extensions, respectively, and recorded such findings as extensive. With respect to pretreatment variables (age, clinical stage, clinical findings of the primary tumour, and nodal findings), univariate analysis showed that extensive cN was the only significant factor for overall survival (hazard ratio [HR], 3.27; 95% CI 1.50 to 7.13; p=0.001). Univariate analysis showed that all pN findings, including the nodal classification (invaded nodes, multiple, and contralateral) and extensive involvement were significant, and multivariate analysis confirmed that extensive pN (HR 4.71; 95% CI 1.85 to 11.97; p=0.001) and multiple pN (HR 2.59; 95% CI 1.10 to 6.09; p=0.029) were independent predictors of overall survival. Assessment based on the level of invaded neck nodes may be a better predictor of survival than the current nodal classification.
Subject(s)
Carcinoma, Squamous Cell/diagnosis , Mouth Neoplasms/diagnosis , Adult , Aged , Aged, 80 and over , Carcinoma, Squamous Cell/mortality , Carcinoma, Squamous Cell/pathology , Carcinoma, Squamous Cell/therapy , Combined Modality Therapy , Female , Humans , Lymphatic Metastasis/pathology , Male , Middle Aged , Mouth Neoplasms/mortality , Mouth Neoplasms/pathology , Mouth Neoplasms/therapy , Prognosis , Retrospective Studies , Survival AnalysisSubject(s)
Brain Neoplasms/therapy , Interferon Type I/therapeutic use , Medulloblastoma/therapy , Adolescent , Child , Child, Preschool , Combined Modality Therapy , Drug Evaluation , Female , Humans , Infant , MaleABSTRACT
In a companion paper (Ann Surg 1985; 201(3):391-398), clinical data which suggest that neurogenic hypertension may be caused by arterial compression of the left medulla oblongata was presented. A chronic pathophysiologic animal model of neurogenic hypertension using a substitute for arterial pulsation, the neurovascular compression simulator (NCS), was developed. This paper presents data that demonstrate how development of hypertension in a nonhuman primate baboon (5 subject animals, 5 control animals) can be caused by the NCS, and the blood pressure can subsequently return to normal following cessation of NCS activity. These experiments show that pulsatile compression of the left ventrolateral medulla oblongata results in cardiovascular changes consistent with the sequence found in human neurogenic hypertension. Arteriosclerosis and arterial ectasia in the human contribute to arterial elongation and looping at the base of the brain. An arterial loop, by causing pulsatile compression of neural structures, elicits an increase in blood pressure initiated by an increase in cardiac output. This may be due to interference with the autonomic control of the heart and/or by alteration of the relative capacitance of the vascular system.
Subject(s)
Cranial Nerves , Hypertension/etiology , Medulla Oblongata , Nerve Compression Syndromes/complications , Animals , Blood Pressure , Brain/pathology , Cardiac Output , Disease Models, Animal , Heart Rate , Hemodynamics , Hypertension/physiopathology , Male , Nerve Compression Syndromes/physiopathology , Nerve Compression Syndromes/surgery , Papio , Restraint, PhysicalABSTRACT
The genetic and immunologic abnormalities associated with the pathogenesis of moya-moya were assessed in 23, 13 children and 10 adults with angiographically diagnosed moya-moya. In HLA-A, -B, -C stereotyping, an association was found of AW24, BW46, and BW54 with relative risks of 3.83, 6.50, and 3.58 respectively. Natural T cell toxic autoantibody was detected by FACS analysis in sera from five out of 23 patients. Millipore filter assay for autoantibody against double-stranded DNA revealed higher than normal binding in sera from four out of 18 patients. Anti-vessel antibody which might be responsible for vascular change associated with moya-moya was not detected in any of the 23 patients studied. Significant association of the disease with certain HLA types, in addition to the presence of natural T cell toxic autoantibody and anti-double-stranded DNA antibody in patients' sera, supports the theory that genetic and immunologic disturbances may underly the pathogenesis of moya-moya.
Subject(s)
Arterial Occlusive Diseases/genetics , Moyamoya Disease/genetics , Adolescent , Adult , Autoantibodies/analysis , Child , Child, Preschool , DNA/immunology , Female , HLA Antigens/genetics , Humans , Male , Middle Aged , Moyamoya Disease/immunology , Muscle, Smooth, Vascular/immunology , T-Lymphocytes/immunologyABSTRACT
Findings in computed tomography (CT) with or without contrast infusion were analyzed in 8 patients with Sturge-Weber disease. From the extent of calcification in the CT, Sturge-Weber disease can be classified into two types, localized and diffuse. The extent of calcification or cortical atrophy is predictable, if it can be shown that enhanced areas in contrast infusion CT truly represent leptomeningeal angiomatosis. Thus, using enhanced CT, the capacity of prediciton as to whether the patient will have a localized or diffuse type of disease will be possible with further observations.
