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If a long period has passed after plastic wheel speed sensors were assembled into an automobile, the sensing error may occur when the outer holes of speed sensor crack and water enter through the crack. This not only may put the automobile into the danger of malfunctioning, but the driver may at the psychologically very anxious situation. To resolve this problem, an injection molding method that can remove the outer holes of the plastic wheel speed sensor was developed, and the developed injection molding process was numerically simulated. In the newly developed forming methodology, the pins for securing the wheel speed sensor within the cavity are forced to be removed while the forming process is completed so that the outer pin holes disappear. But, in the conventional methodology, the pins for securing the wheel speed sensor are kept without being removed until the forming process is completed so that the outer pin holes remain. Besides, a real injection mold was manufactured and the comparative study of injection molding process between real conduction and numerical simulation was performed. The filling length in actual molding was about 1.5 mm longer than the length of the simulation. This was a relatively good match since it corresponds to 5% of the major reference length. And, for the real molded wheel speed sensors, the performance tests such as the dimension precision, insulation resistance, X-ray scan and thermal shock test were made. In particular, any damage did not occur at the interior and exterior of the sensor during the 600 cycle thermal shock test. Furthermore, all the performance test results satisfied the regulated standards. Thus, the validity of the developed new injection molding method was justified.

The tumor suppressor protein p53 is an essential molecule in cell proliferation and programmed cell death (apoptosis), and has been postulated to play a principal part in the development of atherosclerosis. We have examined the effect of p53 inactivation on atherogenesis in apoE-knockout mice, an animal model for atherosclerosis. We found that, compared with p53+/+/apoE-/- mice, p53-/-/apoE-/- mice developed considerably accelerated aortic atherosclerosis in the presence of a similar serum cholesterol in response to a high-fat diet. Furthermore, the atherosclerotic lesions in p53-/-/apoE-/- mice had a significant (approximately 280%) increase in cell proliferation rate and an insignificant (approximately 180%) increase in apoptosis compared with those in p53+/+/apoE-/- mice. Our observations indicate that the role of p53 in atherosclerotic lesion development might be associated with its function in cell replication control, and that p53-independent mechanisms can mediate the apoptotic response in atherosclerosis.

Patients with severe nonthyroidal illnesses (NTIs) frequently have decreased serum concentrations of triiodothyronine (T3) and less often of thyroxine (T4) without clear evidence of hypothyroidism. To determine whether T3 and T4 levels are also reduced in the tissues, we analyzed autopsy samples from 12 patients dying of NTI and 10 previously healthy individuals dying suddenly from trauma. Mean serum T3, T4, and free T4 index values were lower by 79%, 71%, and 49%, respectively, in the NTI group than in controls, but serum thyrotropin (TSH) values did not differ significantly. Mean T3 concentrations in cerebral cortex, hypothalamus, pituitary, liver, kidney, and lung were lower in the NTI group than in controls by 43% to 76%, but mean values in heart and skeletal muscle did not differ significantly between the groups. The mean liver T4 concentration was 66% lower in the NTI group, but mean T4 concentrations in the cerebral cortex were similar in the two groups. These results indicate that many tissues may be deficient in thyroid hormones in patients with fatal NTI, although the severity of the reduction in thyroid hormone concentrations may vary from one organ to another.

Background Cushing's Syndrome (CS) which is caused by isolated Corticotropin-releasing hormone (CRH) production, rather than adrenocorticotropin (ACTH) production, is extremely rare. Methods We describe the clinical presentation, course, laboratory values and pathologic findings of a patient with isolated ectopic CRH causing CS. We review the literature of the types of tumors associated with this unusual syndrome and the behavior of these tumors by endocrine testing. Results A 56 year old woman presented with clinical and laboratory features consistent with ACTH-dependent CS. Pituitary imaging was normal and cortisol did not suppress with a high dose dexamethasone test, consistent with a diagnosis of ectopic ACTH. CT imaging did not reveal any discrete lung lesions but there were mediastinal and abdominal lymphadenopathy and multiple liver lesions suspicious for metastatic disease. Laboratory testing was positive for elevated serum carcinoembryonic antigen and the neuroendocrine marker chromogranin A. Serum markers of carcinoid, medullary thyroid carcinoma, and pheochromocytoma were in the normal range. Because the primary tumor could not be identified by imaging, biopsy of the presumed metastatic liver lesions was performed. Immunohistochemistry was consistent with a neuroendocrine tumor, specifically small cell carcinoma. Immunostaining for ACTH was negative but was strongly positive for CRH and laboratory testing revealed a plasma CRH of 10 pg/ml (normal 0 to 10 pg/ml) which should have been suppressed in the presence of high cortisol. Conclusions This case illustrates the importance of considering the ectopic production of CRH in the differential diagnosis for presentations of ACTH-dependent Cushing's Syndrome.

A 49-year-old man with the acquired immune deficiency syndrome (AIDS) developed epigastric pain, nausea, vomiting, and gastrointestinal bleeding secondary to a cytomegalovirus (CMV)-induced ulceration in the distal esophagus and proximal stomach. All symptoms improved on treatment with ganciclovir. However, 1 month later severe dysphagia led to discovery of a fibrous stricture in the area of the healed ulcer. The dysphagia was controlled by esophageal dilation. Ulcerative lesions caused by CMV can heal with ganciclovir treatment but, as with other esophageal ulcers, healing may be associated with fibrosis and stricture.

We attempted to reassess the significance of cervicovaginal Papanicolaou smear(s) in identifying adenocarcinoma (AC) by comparing Papanicolaou smears with histopathology in a pool of 188 patients. The first part of study dealt with 95 patients, seen over a 12-yr period (1975-1986), who had tissue diagnosis of cervical or endometrial AC, all with prior papanicolaou smears available. Of the 95 patients, Papanicolaou smears were positive and/or inconclusive for uterine AC in 37 (38.9%) and falsely negative in 58 (61.1%) patients. Of the latter, six were either positive and/or inconclusive for squamous carcinoma and moderate to severe dysplasia; thus, the effective detection rate (sensitivity) for malignancy and related condition of Papanicolaou smears was 45.3% (43 of 95). The second part of the study concerned the analysis of 130 patients with 148 Papanicolaou smear in whom cytologic diagnosis positive and/or inconclusive for AC was made during the same study period. Tissue diagnoses were available in 107 of these as follows: AC and glandular hyperplasia in 66 patients (61.7% predictive value), with 11 (10.3%) from extrauterine sources; squamous carcinoma in 12 and moderate to severe dysplasia in 5, totalling 17 patients (15.9%); miscellaneous conditions (polyps, radiation change, and glandular atrophy) in 11 patients (10.3%); and no pathologic change in 13 patients (12.1%). The effective predictive value of positive and/or inconclusive Papanicolaou smears for all malignancy and related states is 77.6%.

An unusual case of adenomyomatous hamartoma of ileum leading to ileo-ileal intussusception in a 22-month-old child is reported.

Few studies of human cardiac myocyte proliferation in the perinatal period have been conducted. We measured the proliferative activity of left ventricular myocytes in tissue obtained at autopsy in three surgically induced abortuses, 20 preterm infants with gestational ages ranging from 12 to 35 weeks, eight term infants with ages ranging from 1 day to 11 months, and five adults. The preterm infants lived less than 24 h, thus simulating the in utero condition of developing hearts. To assess the proliferative activity of the myocytes, we measured immunoreactivity using the monoclonal antibody MIB-1 against the recombinant Ki-67 nuclear antigen. Immunostained sections were examined by light microscopy, and the results expressed as a staining index (SI) of 0–3, according to the percentage of positively stained myocyte nuclei. Myocyte proliferative activity remained constant during the early preterm period and decreased in the late preterm and early postterm periods. Adult myocytes, regardless of cardiac weight, did not reveal proliferative activity as assessed by immunostaining. This proliferation pattern is consistent with findings in most earlier studies in animal models.

Oxidative modification of LDL increases its atherogenicity, and 15-lipoxygenase (15-LO) has been implicated in the process. To address this issue, we generated transgenic rabbits that expressed 15-LO in a macrophage-specific manner and studied their susceptibility to atherosclerosis development when they were fed a high-fat, high-cholesterol (HFHC) diet (Teklad 0533 rabbit diet 7009 with 10% corn oil and 0.25% cholesterol) for 13.5 wk. Transgenic and nontransgenic rabbits developed similar degrees of hypercholesterolemia and had similar levels of triglyceride, VLDL, LDL, and HDL. Quantitative morphometric analysis of the aortic atherosclerosis indicated that the transgenic animals (n = 19) had significantly smaller lesion areas (9.8+/-6.5%, mean+/-SD) than their littermate controls (n = 14, 17.8+/-15.0%) (P < 0.05). In a subgroup (n = 9) of transgenic rabbits that received the HFHC diet plus the antioxidant N',N '-diphenyl-phenylenediamine (1%), the extent of lesion involvement (9.8+/-7.5%) did not differ from the subgroup (n = 10) that received the regular HFHC diet (9.7+/-5.9%). Since the results were unexpected, we repeated the experiments. Again, we found that the nontransgenic littermates (n = 12) had more extensive lesions (11.6+/-10.6%) than the transgenic rabbits (n = 13; 9.5+/-7.8%), although the difference was not significant. In a third set of experiments, we crossed 15-LO transgenic rabbits with Watanabe heritable hyperlipidemic (WHHL) rabbits and found that the lesion area in the 15-LO transgenic/heterozygous WHHL rabbits (n = 14) was only about one third (7.7+/-5.7%) that found in nontransgenic heterozygous WHHL littermate controls (n = 11, 20.7+/-19.4%) (P < 0.05). These data suggest that overexpression of 15-LO in monocytes/macrophages protects against lipid deposition in the vessel wall during early atherogenesis in these rabbit models of atherosclerosis.

Carcinoid tumor metastatic to the breast is very uncommon. The rarity of this finding may be the reason for its common misinterpretation as primary breast carcinoma. A patient with primary ovarian carcinoid that presented initially with a solitary breast mass is reported. A review of the literature discloses only 12 reported cases of carcinoid tumor metastatic to the breast, with none of the primaries found to be the ovary.

Chest pain is not an uncommon symptom in patients who abuse cocaine. A small number also develop acute myocardial infarction. 1,2 Most, however, show electrocardiographic ST-segment or T-wave abnormalities as the only objective evidence of myocardial ischemia. Coronary artery spasm has been popularly invoked as the possible cause for chest pain. 3,4 However, evidence for spasm is largely circumstantial at present. An alternative source of pain may be myocarditis, 5 which has been demonstrated in some patients dying of cocaine abuse. 6,7

To test the hypothesis that genetic susceptibility or resistance to diet-induced atherosclerosis is correlated with serum levels of specific lipids, lipoproteins, or apoproteins, male mice of a genetically susceptible and a genetically resistant strain were fed either a normal or an atherogenic diet. After 20 weeks on a normal diet, neither the resistant nor the susceptible strain mice had atherosclerosis; resistant strain mice had serum cholesterol of 66 +/- 11 while the susceptible strain mice had 90 +/- 1 mg/dl serum cholesterol, and lipoproteins were dominated by a single alpha-migrating HDL. After 20 weeks on an atherogenic diet, resistant strain mice had 185 +/- 55 mg/dl cholesterol, their lipoproteins remained dominated by alpha-migrating HDL, and two of eight mice had mild atherosclerotic lesions; susceptible strain mice had 510 +/- 94 mg/dl cholesterol, multiple alpha- and pre-beta-migrating lipoprotein species, and all 13 had advanced aortic atherosclerosis. The resistant strain mice had an apolipoprotein E/total lipoprotein protein ratio of 0.42 on the normal diet and 0.53 on the atherogenic diet, while the susceptible strain mice had the significantly lower ratios of 0.07 and 0.31, respectively. These data indicate that genetic resistance to diet-induced aortic atherosclerosis in mice is correlated with capacity to prevent large increases in serum cholesterol, to suppress abnormal alpha- and pre-beta-migrating lipoproteins, and to maintain elevated serum apolipoprotein E/total lipoprotein protein ratios. Our data do not preclude the possibility of additional gene control at the level of arterial end organ response.

A case of congenital generalized fibromatosis in a black male infant with involvement of lungs, subcutaneous tissue, pancreas, adrenal, lymph nodes, and bone is described. Fifteen prior cases with pulmonary involvement are reviewed, emphasizing the poor prognosis associated with pulmonary lesions. This case demonstrated, in addition to previously described histologic features, broad bands of fibroblastic proliferation in the interlobular septa producing retraction of the visceral pleura. Possible etiologic factors are discussed, with suggestions for additional studies in future cases.

This study reports a case of type VII mucopolysaccharidosis (beta-glucuronidase deficiency) presenting as lethal hydrops fetalis. Skin fibroblast cultures established postmortem revealed deficient beta-glucuronidase activity. Mucopolysaccharides were stored in various cells of the brain, heart, kidney, liver, and spleen. The stages of maturation of the bones, kidneys, and brain were discrepant, the brain being the least mature organ. A delay in central nervous system maturation may account for psychomotor retardation in some patients with this enzyme deficiency.

The role of lipoxygenase activation in the genesis of postischaemic myocardial dysfunction was investigated in open chest dogs undergoing a 15 min occlusion of the left anterior descending artery followed by 4 h of reperfusion. Treated animals (n = 9) received nafazatrom, a potent lipoxygenase inhibitor, 10 mg.kg-1 orally 4 h before occlusion followed by intravenous boluses of 1.5 mg.kg-1 and 0.5 mg.kg-1 5 min before occlusion and 1 min before reperfusion respectively. Control animals (n = 10) received saline. No discernible haemodynamic effects were produced by the drug. Collateral flow to the ischaemic zone (radioactive microspheres) was 0.14(0.02) ml.min-1.g-1 in the control group and 0.16(0.05) ml.min-1.g-1 in the treated group. The size of the occluded bed as determined by postmortem perfusion was 25.5(0.8)% of the left ventricle in the control and 24.3(1.3)% in the treated group. Histological examination showed a decrease in neutrophil infiltration of the non-ischaemic myocardium and, to a lesser extent, of the reperfused myocardium in nafazatrom treated animals, suggesting lipoxygenase inhibition. Systolic wall thickening (an index of regional function) was assessed using an epicardial pulsed Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions. Though treated animals showed less dyskinesis during coronary occlusion (p less than 0.05), recovery of function was not enhanced over controls and in both groups the reperfused myocardium was still dyskinetic at 4 h. Thus nafazatrom failed to improve postischaemic ventricular dysfunction, suggesting that leukotrienes do not contribute importantly to this phenomenon.

An unusual, uniformly stenotic arteriopathy involving the aorta and its major branches, the pulmonary trunk, and the left and right pulmonary arteries was found in association with a persistent common atrioventricular canal in an otherwise normal stillborn female infant. The uniform arterial thickening was due to hyperplastic medial elastic laminae, which were in an orderly arrangement in the inner two thirds but dysplastic in the outer third of the media of the arteries.

Clinical reports support acetylcysteine as an effective agent in the prevention of severe hepatic necrosis and mortality in acetaminophen toxicity [2, 8, 13]. The agent is safe and easily administered to the patient. Further studies are needed before acetylcysteine is considered the agent of choice in the management of acetaminophen overdosage in this country.

In a review of 768 consecutive autopsies, 21 (2.7%) clinically unsuspected cases of disseminated intravascular coagulation (DIC) syndrome were diagnosed by histologic examination. DIC was diagnosed by the presence of fibrin thrombi in arterioles, capillaries, venules, and medium-sized veins. Fibrin thrombi were found, in the descending order of frequency, in the brain, heart, lungs, kidneys, adrenals, spleen and liver. Most patients had multiple visceral involvement, with three showing fibrin thrombi in as many as ten organs. The density of fibrin thrombi was greatest in the spleen, followed by kidneys, liver, lungs, adrenals, brain, and heart. A review of clinical data showed that infections were the most common underlying conditions in 13 cases, including nine with positive bacterial cultures from blood or cerebrospinal fluid, or both. The results suggest that, despite increasing clinical recognition of DIC, a great number of patients remain unsuspected of having the DIC syndrome prior to postmortem examination.

Fibromuscular dysplasia of the systemic artery and cerebral "berry" (sac cular) aneurysm are nonatheromatous lesions of uncertain etiology. The coexistence of these vascular disorders in the individual reported here is unusual and may provide a possible explanation of their pathogenesis.

A review of postmortem materials from two teaching hospitals, accumulated in a 14-year period (1962--1975), disclosed 63 patients with myocardial abscesses among 12,359 autopsies, an incidence of 0.5%. All 63 patients had multi-focal myocardial abscesses; the lesions were grossly discernible in six patients. Coexisting infective endocarditis was present in approximately 20% (12) of the 63 patients with myocardial abscesses. Candida and Staphylococcus aureus were most common organisms responsible for the abscesses. Candida was identified in 23 patients (37%) by histologic examination of the heart sections, and 11 of these also had antemortem blood cultures positive for Candida. Staphylococcus aureus was cultured from the antemortem blood of 22 patients, two of whom also showed candidal organisms in the heart at necropsy. Eighty-one per cent (51) of 63 patients had abscesses in one or more extracardiac organs. It appeared that most of the myocardial abscesses had resulted from disseminated sepsis. Surgical conditions, malignancy and alcoholic hepatic disease were the most frequent primary conditions in patients with myocardial abscesses.

In contrast to the abundance of reports on chemical analyses of plasma or serum lipids, studies concerning lipids of leukocytes have been few. The purpose of the present study is to establish a method for quantification of various lipid fractions of human blood leukocytes and to define the concentration of the cellular lipids, for reference in future studies on the role of leukocytes in lipid transport. The importance of such studies lies in the possibility that lipid-laden leukocytes in the circulation enter the arterial intima and become tissue foam cells, as has been postulated in the pathogenesis of human and experimental atherosclerosis.