Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)induces apoptosis in some cancer cells such as breast,prostate,lung,and colon cancer cells,but not normal cells.However,because the effects of TRAIL in gastric cancer cells is unclear,we undertook this study to clarify the effects of TRAIL and its mechanism. To assess the cytotoxicity of TRAIL,two human gastric cancer cell lines,SNU-484 and SNU601,were treated with TRAIL (0-200 ng/mL)in the presence or absence of cycloheximide (1 microgram/mL)for 24 h.Both SNU-484 and SNU-601 were sensitive to TRAIL-induced cell death in a dose-dependent manner.The combination of TRAIL (100 ng/mL)and cycloheximide (1 microgram/mL)for 24 h enhanced cell death and PARP cleavage by promoting activations of caspase-8, caspase-9,and caspase-3,relative to that of TRAIL alone.We further examined the expressions of death receptor 4 (DR4),death receptor 5 (DR5),and FLICE inhibitory protein (FLIP).Although DR4 and DR5 were expressed in both cell lines,the expression of long form (FLIPL )and short form (FLIPS )of FLIP were detected at the low levels. Overexpression of FLIPL or FLIPS in both cell lines rendered the cells resistant to TRAIL.Taken together,our results suggest that FLIP promotes human gastric cancer cell survival against TRAIL-induced apoptosis and is important modulator for TRAIL-induced cell death in human gastric cancer cells.
Apoptosis ; CASP8 and FADD-Like Apoptosis Regulating Protein ; Caspase 8 ; Cell Death ; Cell Line ; Cell Survival ; Colonic Neoplasms ; Cycloheximide ; Humans* ; Necrosis* ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Stomach Neoplasms*

The clinical syndrome of venoocclusive disease of the liver is one of several manifestations of regimen-related toxicity that can occur after high-dose cytoreductive therapy. Hepatic dysfunction after bone marrow transplantation may result from a number of causes such as pretransplant chemoradiation, graft-versus host disease, drugs for prophylaxis of graft-versus host disease, venoocclusive disease, various infections, and infiltration of recurrent malignancy. The clinical distinction of these causes may be difficult and the treatment of each cause is also quite different. Therefore the diagnosis of veno-occlusive disease is important. Veno-occlusive disease affects zone 3 of the liver acinus and produces a syndrome of jaundice, painful hepatomegaly, and fluid retention. Veno-occlusive disease occurs in up to 50% of the patients who undergo BMT and is usually associated with a high mortality rate. In Korea, there are a few case reports on venoocclusive disease after BMT which were only confirmed by clinical symptoms. This is a first report of two cases of hepatic veno-occlusive disease after allogenic BMT, which were proven by laparoscopic liver biopsy in our country.
Biopsy* ; Bone Marrow Transplantation* ; Bone Marrow* ; Diagnosis ; Hepatic Veno-Occlusive Disease* ; Hepatomegaly ; Humans ; Jaundice ; Korea ; Leukemia ; Liver* ; Mortality

The clinical syndrome of venoocclusive disease of the liver is one of several manifestations of regimen-related toxicity that can occur after high-dose cytoreductive therapy. Hepatic dysfunction after bone marrow transplantation may result from a number of causes such as pretransplant chemoradiation, graft-versus host disease, drugs for prophylaxis of graft-versus host disease, venoocclusive disease, various infections, and infiltration of recurrent malignancy. The clinical distinction of these causes may be difficult and the treatment of each cause is also quite different. Therefore the diagnosis of veno-occlusive disease is important. Veno-occlusive disease affects zone 3 of the liver acinus and produces a syndrome of jaundice, painful hepatomegaly, and fluid retention. Veno-occlusive disease occurs in up to 50% of the patients who undergo BMT and is usually associated with a high mortality rate. In Korea, there are a few case reports on venoocclusive disease after BMT which were only confirmed by clinical symptoms. This is a first report of two cases of hepatic veno-occlusive disease after allogenic BMT, which were proven by laparoscopic liver biopsy in our country.
Biopsy* ; Bone Marrow Transplantation* ; Bone Marrow* ; Diagnosis ; Hepatic Veno-Occlusive Disease* ; Hepatomegaly ; Humans ; Jaundice ; Korea ; Leukemia ; Liver* ; Mortality

BACKGROUND: Invasive Streptococcus agalactiae (group B streptococcus, GBS) infection most commonly occurs in infants; however, cases of GBS infection in adults, particularly in the elderly with significant underlying diseases, are being increasingly reported. We analyzed the serotype specific opsonophagocytic antibodies (the major mechanism of protection against GBS) in infants, adults, and the elderly. METHODS: The opsonization indices (OIs) of antibodies against serotype Ia, Ib, II, III, and V GBS were studied in 89 infants, 35 adults (age, 30–50 years), and 62 elderly individuals (age, 65–85 years) according to the University of Alabama at Birmingham GBS opsonophagocytic killing assay protocol (www.vaccine.uab.edu). RESULTS: In infants, adults, and elderly groups respectively, geometric mean of OI against GBS serotype Ia were 3, 7, and 32; against GBS serotype Ib were 7, 242, and 252; against serotype II were 93, 363, and 676; against serotype III were 8, 212, and 609; and against serotype V were 4, 639, and 610. The seropositive rate (% of subjects with OI ≥ 4) increased significantly in older age group for all five serotypes. CONCLUSION: During infancy, only a limited proportion of infants have functional immunity against serotype Ia, Ib, II, III, and V GBS. Furthermore, a lack of opsonic activities against GBS observed in some adults and the elderly might predispose such individuals to the risk of invasive GBS infection. Epidemiological monitoring and development of suitable vaccine for these populations are needed.
Adult ; Aged ; Alabama ; Antibodies* ; Epidemiological Monitoring ; Homicide ; Humans ; Infant ; Prevalence ; Seroepidemiologic Studies* ; Serogroup* ; Streptococcus agalactiae ; Streptococcus*

Non-sexually acquired genital ulceration, also known as Lipschutz ulcer, is a rare condition that typically occurs in prepubertal and pubertal girls. It can be misdiagnosed as a sexually transmitted disease or even a sign of child abuse, causing great anxiety for patients and their families. It is often accompanied by systemic symptoms such as fever, myalgia, or lymphadenopathy. Several viruses such as Epstein-Barr virus, cytomegalovirus, and mumps virus have been associated with this entity. Furthermore, Mycoplasma pneumonia has rarely been linked to such ulcers in the literature. We present a case of Lipschutz ulcer in a sexually inactive 11-year-old girl.

Non-sexually acquired genital ulceration, also known as Lipschutz ulcer, is a rare condition that typically occurs in prepubertal and pubertal girls. It can be misdiagnosed as a sexually transmitted disease or even a sign of child abuse, causing great anxiety for patients and their families. It is often accompanied by systemic symptoms such as fever, myalgia, or lymphadenopathy. Several viruses such as Epstein-Barr virus, cytomegalovirus, and mumps virus have been associated with this entity. Furthermore, Mycoplasma pneumonia has rarely been linked to such ulcers in the literature. We present a case of Lipschutz ulcer in a sexually inactive 11-year-old girl.

Typhoid fever can cause serious complications, such as enterobrosia, meningitis, pneumonia, myocarditis, hepatitis, osteomyelitis, and disseminated intravascular coagulation in 10-15% of the patients. Kidney complications are very rare, and a few cases have been reported in children. We are reporting a case of childhood typhoid fever complicated with acute nephritis present with albuminuria, hypertension, and renal failure.
Albuminuria ; Child ; Disseminated Intravascular Coagulation ; Hepatitis ; Humans ; Hypertension ; Kidney ; Meningitis ; Myocarditis ; Nephritis* ; Osteomyelitis ; Pneumonia ; Renal Insufficiency ; Typhoid Fever*

Loss of E-cadherin (E-cad) expression has been found in multiple cancers and is postulated to facilitate tumor cell dissociation and metastais. Promotor methylation may provides an alternative pathway for loss of gene function. This study evaluated the role of hypermethylation in the down-regulation of E-cad in oral squamous cell carcinoma (OSCC). We examined the E-cad expression by immunohistochemical staining and detected methylation status by methylation-specific polymerase chain reaction (MSP) in 20 OSCC tissues. Overally, 12 (60 %) cases of hypermethylation of E-cad were detected and we found there were no correlation between methylation and age, histologic grade, lympn node metastasis, tumor size and clinical stage. However, Eleven (73.3 %) of 15 samples which was negative for E-cad staining showed hypermethylation of E-cad promotor region. On the other hand, only one (20 %) of 5 E-cad positive sample was observed with methylated status. The underexpression of E-cad was found to be related to promotor hypermethylation (p=0.035). In conclusion, we suggest that hypermethylation play a role in inactivation of E-cad gene and may be a appreciable biomarker for diagnosis and treatment of OSCC.
Cadherins ; Carcinoma, Squamous Cell ; Dissociative Disorders ; Down-Regulation ; Hand ; Methylation ; Neoplasm Metastasis ; Polymerase Chain Reaction ; Promoter Regions, Genetic

Loss of E-cadherin (E-cad) expression has been found in multiple cancers and is postulated to facilitate tumor cell dissociation and metastais. Promotor methylation may provides an alternative pathway for loss of gene function. This study evaluated the role of hypermethylation in the down-regulation of E-cad in oral squamous cell carcinoma (OSCC). We examined the E-cad expression by immunohistochemical staining and detected methylation status by methylation-specific polymerase chain reaction (MSP) in 20 OSCC tissues. Overally, 12 (60 %) cases of hypermethylation of E-cad were detected and we found there were no correlation between methylation and age, histologic grade, lympn node metastasis, tumor size and clinical stage. However, Eleven (73.3 %) of 15 samples which was negative for E-cad staining showed hypermethylation of E-cad promotor region. On the other hand, only one (20 %) of 5 E-cad positive sample was observed with methylated status. The underexpression of E-cad was found to be related to promotor hypermethylation (p=0.035). In conclusion, we suggest that hypermethylation play a role in inactivation of E-cad gene and may be a appreciable biomarker for diagnosis and treatment of OSCC.
Cadherins ; Carcinoma, Squamous Cell ; Dissociative Disorders ; Down-Regulation ; Hand ; Methylation ; Neoplasm Metastasis ; Polymerase Chain Reaction ; Promoter Regions, Genetic

Pseudohypoparathyroidism type 1b (PHP 1b) is the result of end organ resistance to parathyroid hormone (PTH) in the absence of any features of Albright's hereditary osteodystrophy. There are two subtypes of PHP 1b with different genetic mechanisms. One subtype is related to a maternally derived 3kb microdeletion involving STX 16 gene, and is inherited in an autosomal dominant mode. Familial autosomal dominant inheritance of PHP 1b is relatively rare. The other subtype is associated with more extensive loss of imprinting at the GNAS locus that affects at least one additional differential methylated (hypermethylation at neuroendocrine secretory protein and hypomethylation at antisense transcript and or extra-large stimulatory G protein region) without microdeletion of the STX 16 or AS gene. It can be sporadic due to an imprinting defect in the GNAS gene. In our case, an 8-year-old girl was referred for suspected PHP with no feature of Albright hereditary osteodystrophy. Blood test results revealed hypocalcemia and hyperphosphatemia. Elevated PTH was also checked. There was no family history of endocrine or developmental problem. Her intelligence was normal, but she had inferior sociability at that time. Based on above, we diagnosed a rare case of paternal uniparental disomy of the long arm of chromosome 20 as the cause of PHP 1b by microsatellite marker test of chromosome 20.
Arm ; Child ; Chromosomes, Human, Pair 20 ; Female ; GTP-Binding Proteins ; Hematologic Tests ; Humans ; Hyperphosphatemia ; Hypocalcemia ; Intelligence ; Microsatellite Repeats ; Parathyroid Hormone ; Pseudohypoparathyroidism* ; Uniparental Disomy* ; Wills