There are rare reports of vascular complications in patients with cardiac myxoma, including both central and peripheral arterial thrombosis. We report on a patient with cerebral infarctions affecting multiple territories, which may have been related to cardiac myxoma. The patient also exhibited cyanosis of the hand. A diagnosis was made of peripheral artery occlusion with myxomatous emboli. A careful physical examination with suspicion of concomitant peripheral embolism is needed in patients with acute embolic stroke induced by cardiac myxoma.
Arteries ; Cerebral Infarction* ; Cyanosis ; Diagnosis ; Embolism* ; Hand ; Humans ; Myxoma* ; Physical Examination ; Stroke ; Thrombosis

No abstract available.
Cadaver

Epidural blood patch (EBP) is one of the treatments for spontaneous intracranial hypotension (SIH), and its complications have rarely been reported. We report a patient with SIH and developed intracranial hypertension after EBP. The mechanism of rebound intracranial hypertension was uncertain. If the patient presented with a different type of headache or newly developed neurological symptoms after treatment of SIH, rebound intracranial hypertension should be considered and the proper treatment needed quickly.
Blood Patch, Epidural* ; Headache ; Humans ; Intracranial Hypertension* ; Intracranial Hypotension*

BACKGROUND: The estrogen receptor (ER) in breast cancer specimens has traditionally been assessed using a biochemical ligand binding assay (LBA). Recently, the application of an immunohistochemical method (IHC) for formalin-fixed breast carcinoma tissue has greatly increased. Controversy exists over the accuracy of IHC compared with that of LBA in determining ER. METHODS: Breast-carcinoma tissues were obtained from 247 patients. ER was determined within 1 week or at 4 weeks after surgery by using the traditional LBA and by using IHC with monoclonal antibodies. The ER status was assessed with respect to age, size of tumor, and stage according to the two methods. RESULTS: The concordant rate of ER status was 75% between IHC and LBA. IHC-negative/LBA- positive results occurred in 31 cases (13%) and IHC-positive/LBA-negative were observed in 30 cases (12%). ER-positive cases were more common in older patients. The disconcordant rate was much higher in premenopausal females. There was a significantly lower ER positivity in tumors of larger than 5 cm. ER positivity was significantly lower at 4 weeks compared to within 1 week in both methods, but this did not change the concordance rate between the two methods. CONCLUSIONS: The ER-IHC method appears to be a reasonable substitute for a biochemical ligand binding assay. This is based on a 75% concordance of the method as well as on the findings in the disconcordant cases. The appropriate measured time for ER was within 1 week after the cancer tissues were obtained.
Antibodies, Monoclonal ; Biochemistry ; Breast Neoplasms* ; Breast* ; Estrogens* ; Female ; Humans ; Immunohistochemistry

BACKGROUND: Although abnormalities of p53 gene and their relation to clinicopathologic parameters have been identified in some human malignancies, there is little published data on their prevalence and clinical significance in ampullary adenocarcinoma (AAC). The aim of this study is to determine the prevalence of p53 abnormalities in AAC and to evaluate their relation to clinicopathologic features. METHOD:35 formaline-fixed paraffin-embedded tissues of AAC were examined for detection of p53 abnormalities by both single-strand conformation polymorphism (SSCP) analysis of polymerase chain reaction- amplified DNA fragments corresponding to exons 5-8 and immunohistochemistry (IHC) using monoclonal antibody to p53 protein (Novocastra, DO7), and the association between the p53 abnormalities and clinicopathologic parameters was analyzed. RESULT: In 22.9% of AAC, p53 gene muation was demonstrated by SSCP analysis, mainly at PCR-amplified exon 8 and exon 7. The p53 protein overexpression by IHC was 48.6% of AAC. Six SSCP and IHC-positive (17.2%) cases and 16 normal (45.7%) cases showed concordant results between the methods, although 13 cases (37.1%) showed discordance, including 11 IHC-positive (31.4%) and 2 SSCP-positive (5.7%) cases. Overall, the prevalence of p53 abnormalities was 54.3%. No significant associations between the p53 abnormalities and clinicopathological parameters such as clinical manifestations, histologic differentiation, and tumor stage were observed. CONCLUSION: The p53 abnormalities detected in 55% of AAC are not associated with prognostic factor, suggesting that abnormal p53 gene may play a role in the development of AAC, but not in its invasiveness.
Adenocarcinoma* ; DNA ; Exons ; Genes, p53* ; Humans ; Immunohistochemistry ; Polymorphism, Single-Stranded Conformational ; Prevalence*

Castleman's disease is uncommon lymphoproliferative disorder as giant lymph node hyperplasia and angiofollicular lymph node hyperplasia. Multicentric variant of Cagtleman's disease, plasma cell type has been, described that has mort generalized lymph node involvement as well as involvement of other organ systems than localized type. Multicentric plasma cell type is frequently accompanied by systemic manifestations, such as weight loss, lowgrade fever and weakness. But the reported cases of pulmonary parenchymal involvement are rare and have almost consisted of hyalinized ganuloma adjacent 13 a bronchus. We report a patient with Castleman's disease of the lung, pathologically proven interstitial pulmonary involvement.
Bronchi ; Fever ; Giant Lymph Node Hyperplasia* ; Humans ; Hyalin ; Lung* ; Lymph Nodes ; Lymphoproliferative Disorders ; Plasma Cells ; Weight Loss

Acute mercury inhalation poisoning is a rare cause of acute lung injury. It is usually fatal because of progressive pulmonary failure. We experienced a patient with acute respiratory distress syndrome (ARDS) after illicit use of mercury vapor for hemorrhoid treatment; he developed acute chemical pneumonitis following exposure to mercury vapor. Prompt treatment with corticosteroids and penicillamine for acute chemical pneumonitis was instituted; radiologic pulmonary infiltrates disappeared within a week, but late phase neurologic sequelae and pulmonary interstitial fibrosis progressed.
Adrenal Cortex Hormones/administration & dosage ; Aged ; Antidotes/administration & dosage ; Disease-Free Survival ; Human ; Inhalation Exposure/adverse effects* ; Male ; Mercury Poisoning/diagnosis ; Mercury Poisoning/complications* ; Penicillamine/administration & dosage ; Respiratory Distress Syndrome, Adult/drug therapy ; Respiratory Distress Syndrome, Adult/chemically induced* ; Substances:Penicillamine ; Substances: Antidotes ; Substances: Adrenal Cortex Hormones

BACKGROUND: Asthma is a chronic inflammatory disease of the airways characterized by a marked infiltration of ecsinophils in the bronchial mucosa. Asthmatic bronchial muosa produces many factors described as king chernotaetic for inflammatory cells. IL-5, RANTES, and MCP-1 alpha are the chemotactic factors for eosinophils, but their roles are controversiaL Recently eotaxin that is a potent eosinophil chernoattracttnt cytokine was detected in a guinea-pig model of allergic airway inflammation, and human eotaxin was cloned. Eotaxin is a specific chemoattractant for eosinophils, but its role in asthma is not confirmed. We examined the in vivo expression of a,taxin in bronchi of asthmatic patients. METHODS: 11 asthmatics and 2 normal controls were enrolled. All subjects were underwent brcnchcscopy with bronchial biopsies in 2nd or 3rd carina. RNA extraction from biopsy samples was done by acid-guanidium method. Semi-quantitaive RT-PCR was done for evaluation of eotaxin mRNA expression. The extent of eosinophil infiltrartion was evaluated by counting the eosinophils in submucosa in HPF of microscope. RESULTS: Eotaxin mRNA expressed in symptomatic, uncontrolled asthma. Steroid inhibited expression of eotaxin mRNA in asthma. Expression of eotaxin mRNA correlated with eosinohil infiltration in bronchial tissues. CONCLUISON: Expression of eotaxin mRNA increases in uncontrolled asthma and eotaxin is involved in the recruitment of eosinophils.
Asthma* ; Biopsy ; Bronchi ; Chemokine CCL5 ; Chemotactic Factors ; Clone Cells ; Eosinophils ; Humans ; Inflammation ; Interleukin-5 ; Mucous Membrane* ; RNA ; RNA, Messenger*

A 38-year-old woman presented with facial edema with neck vein engorgement for about 45 days. Chest roentgenography showed bulging soft tissue opacities in the right superoanterior mediastinum and a lobulated intraluminal mass was noted in the superior vena cava on the venacavogram. The superior vena cava was incised and the tumor located from the junction of the superior vena cava and internal jugular vein to the right atrial inlet was excised. Grossly, the tumor was myxoid or gelatinous in appearance. A combination of microscopic and immunohistochemical features showed myxoid leiomyosarcoma arising from the wall of the superior vena cava.
Adult ; Bays ; Edema ; Female ; Gelatin ; Humans ; Jugular Veins ; Leiomyosarcoma* ; Mediastinum ; Neck ; Radiography ; Superior Vena Cava Syndrome* ; Thorax ; Veins ; Vena Cava, Superior*

The tumor microenvironment (TME) is formed by several immune cells. Notably, tumorassociated macrophages (TAMs) are existed in the TME that induce angiogenesis, metastasis, and proliferation of cancer cells. Recently, a point-mutated variant of IL-32θ was discovered in breast cancer tissues, which suppressed migration and proliferation through intracellular pathways. Although the relationship between cancer and IL-32 has been previously studied, the effects of IL-32θ on TAMs remain elusive. Recombinant human IL-32θ (rhIL-32θ) was generated using an Escherichia coli expression system. To induce M0 macrophage polarization, THP-1 cells were stimulated with PMA. After PMA treatment, the cells were cultured with IL-4 and IL-13, or rhIL-32θ. The mRNA level of M1 macrophage markers (IL-1β, TNFα, inducible nitric oxide synthase) were increased by rhIL-32θ in M0 macrophages. On the other hand, the M2 macrophage markers (CCL17, CCL22, TGFβ, CD206) were decreased by rhIL-32θ in M2 macrophages. rhIL-32θ induced nuclear translocation of the NF-κB via regulation of the MAPK (p38) pathway. In conclusion, point-mutated rhIL-32θ induced the polarization to M1-like macrophages through the MAPK (p38) and NF-κB (p65/p50) pathways.