ABSTRACT
Proximal pulmonary artery aneurysms and dissection are rare and life-threatening conditions, which are usually detected only during autopsy examination in cases of sudden death. These pathological entities often occur as complications of chronic pulmonary hypertension and most commonly result from pulmonary arterial hypertension associated with various congenital cardiac lesions involving left-to-right shunting. This study describes an autopsy case of a 38-year-old man who was diagnosed with Eisenmenger syndrome 5 years prior to sudden death secondary to cardiac tamponade following a ruptured pulmonary trunk aneurysm.
ABSTRACT
Proximal pulmonary artery aneurysms and dissection are rare and life-threatening conditions, which are usually detected only during autopsy examination in cases of sudden death. These pathological entities often occur as complications of chronic pulmonary hypertension and most commonly result from pulmonary arterial hypertension associated with various congenital cardiac lesions involving left-to-right shunting. This study describes an autopsy case of a 38-year-old man who was diagnosed with Eisenmenger syndrome 5 years prior to sudden death secondary to cardiac tamponade following a ruptured pulmonary trunk aneurysm.
Subject(s)
Adult , Humans , Aneurysm , Autopsy , Cardiac Tamponade , Death, Sudden , Eisenmenger Complex , Hypertension , Hypertension, Pulmonary , Pulmonary Artery , RuptureABSTRACT
Extraskeletal chondromas are benign soft tissue tumor of hyaline cartilage. These tumors are rare and the pathogenesis is unclear. They are usually involves the hand or feet. We report the case of extraskeletal chondroma arising from subungual region of the finger with nail deformity and review of the literature.
Subject(s)
Chondroma , Congenital Abnormalities , Fingers , Foot , Hand , Hyaline CartilageABSTRACT
BACKGROUND: Mitotic arrest deficiency protein 2 (MAD2) is a key component of spindle assembly checkpoint function, which mediates cell apoptosis through microtubule kinetics. Aberrant expression of MAD2 is believed to be associated with the development of chromosome instability. MAD2 also has a signihicant role in cellular drug resistance to taxane chemotherapeutic agents. METHODS: Expression of MAD2 and p53 was investigated using immunohistochemistry in 85 cases of ovarian carcinomas. Clinicopathological data including progression-free survival were analyzed. RESULTS: A significant (p=.035) association was observed between the grade of serous carcinoma and the expression level of MAD2. While low-grade serous carcinoma showed a low-level expression of MAD2, high-grade serous carcinoma showed a high-level expression of MAD2. We also determined that low-level expression of MAD2 was associated with reduced progression-free survival (PFS) (p=.016) in high-grade serous carcinoma. CONCLUSIONS: MAD2 expression in ovarian carcinoma is related to the grade of serous carcinoma and PFS of high-grade serous carcinoma. Expression level of MAD2 detected by immunohistochemistry may serve as an indicator in predicting the response of microtubule-interfering chemotherapeutic agents.
Subject(s)
Apoptosis , Bridged-Ring Compounds , Calcium-Binding Proteins , Cell Cycle Checkpoints , Cell Cycle Proteins , Chromosomal Instability , Disease-Free Survival , Drug Resistance , Immunohistochemistry , Kinetics , M Phase Cell Cycle Checkpoints , Microtubules , Ovarian Neoplasms , Repressor Proteins , TaxoidsABSTRACT
The prognosis of an early gastric cancer (EGC) is generally excellent, with a 5-year survival rate of 90% in most reports; however, there have been few reports of EGC with distant metastases. Recently we encountered a rare case of EGC with synchronous multiple bone metastases. A 43-year-old woman visited a local clinic due to back pain. Lumbar spine metastases were suspected by MRI. She was transferred to our hospital and underwent bone marrow biopsy which revealed an adenocarinoma. After endoscopic evaluation for primary cancer work-up, we found a suspicious EGC lesion. The results of endoscopic biopsy was signet ring cell carcinoma. Our pathologist additionally reviewed the bone marrow biopsy slides and found signet ring cells in it. PET CT showed disseminated multiple bone metastases but, there wasn't any other malignant lesion. Here we report a rare case of EGC with synchronous multiple bone metastases.
Subject(s)
Adult , Female , Humans , Back Pain , Biopsy , Bone Marrow , Carcinoma, Signet Ring Cell , Magnetic Resonance Imaging , Neoplasm Metastasis , Prognosis , Spine , Stomach Neoplasms , Survival RateABSTRACT
The prognosis of an early gastric cancer (EGC) is generally excellent, with a 5-year survival rate of 90% in most reports; however, there have been few reports of EGC with distant metastases. Recently we encountered a rare case of EGC with synchronous multiple bone metastases. A 43-year-old woman visited a local clinic due to back pain. Lumbar spine metastases were suspected by MRI. She was transferred to our hospital and underwent bone marrow biopsy which revealed an adenocarinoma. After endoscopic evaluation for primary cancer work-up, we found a suspicious EGC lesion. The results of endoscopic biopsy was signet ring cell carcinoma. Our pathologist additionally reviewed the bone marrow biopsy slides and found signet ring cells in it. PET CT showed disseminated multiple bone metastases but, there wasn't any other malignant lesion. Here we report a rare case of EGC with synchronous multiple bone metastases.
Subject(s)
Adult , Female , Humans , Back Pain , Biopsy , Bone Marrow , Carcinoma, Signet Ring Cell , Magnetic Resonance Imaging , Neoplasm Metastasis , Prognosis , Spine , Stomach Neoplasms , Survival RateABSTRACT
BACKGROUND: Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production. METHODS: Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)-gamma , and tumor necrosis factor (TNF)-alpha on the culture medium to investigate the effects of ginsenoside Rb1. RESULTS: Compared with C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha, C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells. CONCLUSIONS: These results suggest that the induction of iNOS expression and subsequent
Subject(s)
Animals , Rats , Apoptosis , Ginsenosides , Glioma , Interferons , Nitric Oxide Synthase , Nitric Oxide , Panax , RNA, Messenger , Tumor Cells, Cultured , Tumor Necrosis Factor-alphaABSTRACT
Acute adrenal insufficiency may result from adrenal crisis, hemorrhagic destruction, or the rapid withdrawal of steroids from patient with chronic steroid medication, congenital adrenal hyperplasia or those on other drugs. Acute hemorrhagic destruction of both adrenal glands can occur due to infection, trauma, anticoagulant therapy, antiphospholipid syndrome or a coagulation disorder. However, there have been no reports on acute hemorrhagic adrenal insufficiency due to the Ebstein-Barr virus (EBV). Herein, a case of acute adrenal insufficiency, with bilateral adrenal hemorrhagic infarction, is reported in a patient with asymptomatic chronic adrenal insufficiency. A 42-year-old man presented with general weakness, weight loss and hyperpigmentation of several months duration. He suffered from a sore throat, general myalgia and a headache on admission. The laboratory findings were lymphocytosis, positive EBV IgM antibody, low cortisol level and a high level of adrenocorticotropic hormone (ACTH). Adrenocortical autoantibody and PCR for Mycobacterium tuberculosis showed negative findings. The serologic findings for CMV and HIV were negative. Fine needle aspiration of the adrenal gland revealed a hemorrhagic infarction and positive staining for the anti-EBV antibody. Acute adrenal insufficiency was then diagnosed with a bilateral adrenal hemorrhagic infarction due to the EBV infection in the patient, also with asymptomatic chronic adrenal insufficiency. This is the first case of acute adrenal insufficiency with bilateral hemorrhagic infarction, due to an EBV infection
Subject(s)
Adult , Humans , Adrenal Glands , Adrenal Hyperplasia, Congenital , Adrenal Insufficiency , Adrenocorticotropic Hormone , Antiphospholipid Syndrome , Biopsy, Fine-Needle , Epstein-Barr Virus Infections , Headache , Herpesvirus 4, Human , HIV , Hydrocortisone , Hyperpigmentation , Immunoglobulin M , Infarction , Lymphocytosis , Myalgia , Mycobacterium tuberculosis , Pharyngitis , Polymerase Chain Reaction , Steroids , Weight LossABSTRACT
We report here on a case of an epidermal cyst arising in the kidney. This cyst occurred in a 61-year-old woman with a past history of several attacks of ureteral stones and she received treatments of extracoporeal shock wave lithotripsy and open nephrolithostomy. On the intravenous pyelogram, a relatively well demarcated, 5x5 cm-sized lesion with calcification was detected in the renal pelvis and calices. The lesion was removed by percutaneous nephrolithotomy. Histologically, the lesion had the same morphologic feature as a typical epidermal cyst arising in the skin. It has been postulated that the intrarenal epidermal cyst arises either from epidermal remnants or it results from traumatic implantation of transformed epithelium. Considering the past history of the patient, it might well be suspected that the present case occurred as a result of traumatic implantation of metaplastic squamous epithelial cells. We report here on a very interesting case of an epidermal cyst in the renal pelvis with a review of the relevant literatures.
Subject(s)
Female , Humans , Middle Aged , Epidermal Cyst , Epithelial Cells , Epithelium , Kidney , Kidney Pelvis , Lithotripsy , Nephrostomy, Percutaneous , Shock , Skin , UreterABSTRACT
BCG(Bacillus Calmette-Guerin) is a vaccine from living attenuated Mycobacterium bovis which produces resistance to tuberculous infection. It induces specific and nonspecific dermatologic complications on the vaccination site or out of the site. The specific reactions include lymphadenitis, scrofuloderma-like, lupus vulgaris-like, lichen nitidus-like and tuberculid. On the contrary, nonspecific reactions such as toxicoderma hemorrhagica, urticaria, erythema multiforme, erythema nodosum and granuloma annulare have also been reported. Among them the term BCGitis is used to describe the skin reaction and enlargement of the regional lymph node, with or without suppuration. We present three cases of BCGitis developed around the vaccination site after BCG vaccination with spontaneous remission within 2~6 months. Histopathologic examination respectively showed foci of palisading granuloma with central caseation necrosis and surrounding lymphohistiocytic infiltration.
Subject(s)
Erythema Multiforme , Erythema Nodosum , Granuloma , Granuloma Annulare , Lichens , Lymph Nodes , Lymphadenitis , Mycobacterium bovis , Necrosis , Remission, Spontaneous , Skin , Suppuration , Tuberculosis, Cutaneous , Urticaria , VaccinationABSTRACT
Sarcoidosis is a systemic granulomatous inflammation with an unknown cause. The commonly involved sites are the lymph nodes, lungs, skin, eyes, and heart. Although cardiac involvement in sarcoidosis is rarely detected clinically, it is reported in 20-50% of autopsied sarcoidosis patients. Cardiac involvement is one of the most severe conditions of sarcoidosis and may cause sudden death. We report a case of a sudden death due to a massive cardiac sarcoidosis in a 43-year-old man. The microscopic examination revealed an extensive noncaseating granulomatous inflammation in the mediastinal lymph nodes and the heart with no evidence of myocyte necrosis. A special stain and molecular study excluded the possibility of other causes such as fungi or mycobacterium. The authors concluded that the cause of death was attributed to arrhythmia due to a cardiac sarcoidosis with massive involvement of the conduction system.
Subject(s)
Adult , Humans , Arrhythmias, Cardiac , Cause of Death , Death, Sudden , Death, Sudden, Cardiac , Fungi , Heart , Inflammation , Lung , Lymph Nodes , Muscle Cells , Mycobacterium , Necrosis , Sarcoidosis , SkinABSTRACT
BACKGROUND: Glial cell-derived nitric oxide (NO), and its regulation has significant implications for central nervous system pathophysiology. The aim of the present study was to see the production of NO in lipopolysaccharide (LPS)/interferon-gamma (IFN-)-treated C6 glioma cells and the effect of dexamethasone on NO production and apoptosis of LPS/IFN--treated C6 glioma cells. METHODS: The apoptosis of LPS/IFN- treated C6 glioma cell was examined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method and the production of NO in culture medium was measured. The expression of iNOS mRNA was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The effect of the N-monomethyl L-arginine (NMMA) and dexamethasone on the apoptosis and NO production was also examined. RESULTS: Inducible nitric oxide synthase (iNOS) mRNA and NO production were markedly increased in LPS/IFN--treated C6 glioma cells. The expression of iNOS mRNA arose at 3 hours, peaked at 12 hours, and declined 24 hours after LPS/IFN--treatment. Accumulation of NO derivatives in the culture media was increased at least upto 48 hours after LPS/IFN-. The induction of iNOS expression and NO production in LPS/IFN--treated C6 cells was correlated with apoptotic cell death judged by TUNEL staining. After treatment of NMMA, one of the NOS inhibitors, NO production and apoptosis were markedly decreased. Dexamehasone treatment suppressed the NO production by concentration depenedent manner. CONCLUSIONS: From the above results it is concluded that the LPS/IFN- induced apoptosis of C6 cells is mediated by iNOS-derived NO and NO production and apoptosis was suppressed by dexamethasone.
Subject(s)
Apoptosis , Arginine , Cell Death , Central Nervous System , Culture Media , Dexamethasone , Glioma , In Situ Nick-End Labeling , Lipopolysaccharides , Nitric Oxide Synthase Type II , Nitric Oxide , RNA, MessengerABSTRACT
BACKGROUND: A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation. METHODS: We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA. RESULTS: Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group. CONCLUSIONS: We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.