PURPOSE: Hyperhomocysteinemia has been identified as an independent risk factor in arterial and venous thrombosis. Mutations in genes encoding methylenetetrahydrofolate reductase (MTHFR), involved in the metabolism of homocysteine, may account for reduced enzyme activity and elevated plasma homocysteine levels. In this study, we investigated the interrelation of MTHFR C677T genotype and level of homocysteine in patients with arterial and venous thrombosis. MATERIALS AND METHODS: We retrospectively reviewed the medical records of 146 patients who were diagnosed as having arterial and venous thrombosis. We excluded patients diagnosed with atrial fibrillation. We examined routinely the plasma concentration of total homocysteine level and MTHFR C677T polymorphism for evaluation of thrombotic tendency in all patients. Screening processes of MTHFR C677T polymorphism were performed by real-time polymerase chain reaction. RESULTS: Investigated groups consisted of thrombotic arterial occlusion in 48 patients and venous occlusion in 63 patients. The distribution of the three genotypes was as follows: homozygous normal (CC) genotype in 29 (26.1%), heterozygous (CT) genotype in 57 (51.4%), and homozygous mutant (TT) genotype in 25 (22.5%) patients. There were no significant differences among individuals between each genotype group for baseline characteristics. Plasma concentration of homocysteine in patients with the TT genotype was significantly increased compared to the CC genotype (P<0.05). CONCLUSION: We observed a significant interaction between TT genotypes and homocysteine levels in our results. The results might reflect the complex interaction between candidate genes and external factors responsible for thrombosis.
Atrial Fibrillation ; Genotype ; Homocysteine* ; Humans ; Hyperhomocysteinemia ; Mass Screening ; Medical Records ; Metabolism ; Methylenetetrahydrofolate Reductase (NADPH2)* ; Plasma* ; Real-Time Polymerase Chain Reaction ; Retrospective Studies ; Risk Factors ; Thrombosis ; Venous Thrombosis

No abstract available.

Drowning is a leading cause of accidental deaths worldwide, but its pathological diagnosis remains a challenge for forensic pathologists owing to a lack of pathognomonic findings in drowning deaths and inconclusive autopsy findings caused by postmortem changes. The aim of the present study was to investigate the pathway taken by inhaled drowning medium through the airway after death in a variety of experimental conditions, including underwater pressurization. We used methylene blue dye to monitor the spread of drowning medium to the lungs. Results of theses experiments demonstrated that it is possible for a significant amount of downing medium to enter the airway during immersion after death. Our results suggest that autopsies of immersed bodies and interpretation of these findings should be performed with special care.
Animal Experimentation* ; Animals* ; Autopsy ; Diagnosis ; Drowning* ; Immersion ; Inhalation* ; Lung ; Methylene Blue* ; Postmortem Changes

PURPOSE: Lymph node analysis is essential for staging colorectal cancer. Intraoperative lymphatic mapping and sentinel lymphadenectomy remain to be investigated for most gastrointestinal neoplasms. Previous attempts to identify the sentinel node (SN) in solid tumors have used intraoperative techniques. This study describes a novel approach to identify the SN in colorectal cancer using ex vivo lymphatic mapping. METHODS: Eighty-two colorectal cancer patients underwent ex vivo lymphatic mapping and a sentinel lymph node biopsy using isosulfan blue dye following a standard surgical resection between March 2002 and September 2003. Within 5 minutes of resection, colorectal specimens were submucosally injected with isosulfan blue dye in four quadrants. Blue lymphatic channels were identified in the mesentery, and followed to the blue-stained SN(s), which were har vested. The specimens were fixed in formalin and subsequently analyzed in the usual fashion. In patients with T1 or T2 tumors, which were blue-stained nodes, but negative to hematoxylin and eosin staining, were further analyzed by serial section and immunohistochemical staining (IHC). RESULTS: At least one SN was identified in 79 patients of the 82 patients (96.3%). The average number of SNs identified per patient and nodes in each colorectal cancer specimen were 3 (range, 1~7) and 17.1 (range: 11~47). Thirty five patients had lymph nodes containing a metastatic disease. Thirteen patients had metastases in both sentinel and nonsentinel nodes. There were 7 sentinel lymph nodes as the only site of metastatic disease. In 15 patients the sentinel nodes were negative for disease, whereas the nonsentinel lymph nodes contained a metastatic disease (false negative rate = 42.9%). The false negative rates of SN(s) metastasis in the 26 patients with T1 or T2 tumors were 16.7 and 7.7% by H&E and by serial section and IHC. CONCLUSION: Ex vivo mapping of the colon is technically feasible, and may provide a useful approach to evaluate lymph node metastasis in patient with T1 or T2 colorectal cancers.
Colon ; Colorectal Neoplasms* ; Eosine Yellowish-(YS) ; Formaldehyde ; Gastrointestinal Neoplasms ; Hematoxylin ; Humans ; Lymph Node Excision ; Lymph Nodes ; Mesentery ; Neoplasm Metastasis ; Sentinel Lymph Node Biopsy

PURPOSE: The methylenetetrahydrofolate reductase (MTHFR) play a central role in converting folate to methyl donor for DNA methylation. Genetic variation in folate metabolism are believed to contribute to the risk of acute lymphoblastic leukemia, colon, esophageal and stomach cancer, as well as cardiovascular and cerebrovascular disease. Generally, low folate level is known that it is associated with gastrointestinal neoplasm. Three common single nucleotide polymorphisms (SNPs) resulting in amino-acid changes (C677T/Ala222Val, A1298C/Glu428Ala and G1793A/Arg594Glu) has been described in MTHFR. We studied the relation of MTHFR C677T, A1298C and G1793A polymorphisms derived from stomach cancers and a control group in Korean people. METHODS: We performed a case-control study to examine the relationship between MTHFR C677, A1298C and G1793A polymorphism and the risk of stomach cancer. 124 individuals with stomach cancer and 288 healthy persons were analyzed. Blood sampling of each groups were performed, PCR-RFLP analyzed, as a results, MTHFR polymorphism genotypes of 677C/C, 677C/T, 677T/T, 1298AA, 1298AC, 1298CC, 1793GG, 1793GA and 1793AA were obtained. RESULTS: The genotype frequency of MTHFR C677T polymorphisms were 23.4% (CC), 51.6% (CT), 25.0% (TT), 76.6% (CT+TT) in case patients and 39.2% (CC), 36.8% (CT), 24.0% (TT), 60.8% (CT+TT) in control groups. The genotype frequency of MTHFR A1298C polymorphisms were 38.7% (AA), 54.0% (AC), 7.3% (CC), 61.3% (AC+CC) in case patients and 55.6% (AA), 40.3% (AC), 4.2% (CC), 44.4% (AC+CC) in control groups. The genotype frequency of MTHFR G1793A polymorphisms were 82.3% (GG), 16.9% (GA), 0.8% (AA), 17.7% (GA+AA) in case patients and 85.8% (GG), 11.8% (GA), 2.4% (AA), 14.2% (GA+AA) in control groups. 677TT and 677CT genotype was associated with a significantly increased risk for gastric cancer (adjusted OR=2.15, 95% confidence interval 1.16~3.95 in TT, adjusted OR=2.49, 95% CI 1.47~4.20 in CT) than the 677CC genotype, and 1298CC and 1298 AC genotype also was associated with a significantly increased risk for stomach cancer (adjusted OR=2.87, 95% CI 1.10~|7.49 in CC, adjusted OR= 2.07, 95% CI 1.31~3.26 in AC). But 1793AA and 1793GA genotypes were not association with a significantly increased risk for stomach cancer (adjusted OR=0.29, 95% CI 0.03~|2.47 in AA, adjusted OR=1.55, 95% CI 0.84~2.86 in GA) CONCLUSION: MTHFR C677T and A1298C polymorphism may influence stomach cancer, but MTHFR G1793A polymorphism need careful interpretation and confirmation in larger studies.
Case-Control Studies* ; Colon ; DNA Methylation ; Folic Acid ; Gastrointestinal Neoplasms ; Genetic Variation ; Genotype ; Humans ; Metabolism ; Methylenetetrahydrofolate Reductase (NADPH2)* ; Polymorphism, Single Nucleotide ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Stomach Neoplasms* ; Stomach* ; Tissue Donors

Horizontal Mattress Suture Technique on Microvascular Anastomosis of rat (body weight: 200-250 gm) femoral artery was evaluated. The present study was conducted to compare the horizontal mattress suture with simple interrupted suture on the suture time, patency rate of the sutured vessels, and the histological changes of surgical site of the vessel wall during wound healing period. The mean suture time of the vessel wall with horizontal mattress suture technique was 15 min 49 sec ± 2.14, which is significantly shorter than that of simple interrupted suture technique. The patency rate of the sutured vessel in both groups was statistically not different each other till post-operative 3rd day but patency rate of horizontal mattress suture was higher than that of simple interrupted suture at post-operative 3rd week. The histological findings such as intimal noss, medial degeneration and intimal regeneration were similar in both groups.
Animals ; Femoral Artery ; Rats ; Regeneration ; Suture Techniques* ; Sutures* ; Wound Healing

No abstract available.
Dermatitis, Allergic Contact* ; Rosa*

Infantile acute hemorrhagic edema is a benign disease followed by a spontaneous eomplete recovery without sequelae, characterized by cockade purpura and inflamrntory edema on the face and extremities without any internal origin involvement in 4-month to 2-year-old infants. We report a case of infaniile acute hemorrhagic edema which occared in a 2-year-old female after an upper respiratory illness and compare the clinical and histologic features of this disorder with Henoch-Schonlein purpura.
Child, Preschool ; Edema* ; Extremities ; Female ; Humans ; Infant ; Purpura ; Purpura, Schoenlein-Henoch

PURPOSE: Recently, the role of vitamins, folate in particular, has been emphasized in the maintenance of health. Folate deficiency is known to give rise to developmental delay, pre-mature vascular disease, neural tube defects, acute leukemia, atherosclerotic vascular disease, delivery defects, breast cancers and gastrointestinal neoplasia. Methylenetetrahydrofolate reductase (MTHFR) is an essential enzyme in folate metabolism, and influences DNA synthesis and DNA methylation. Generally, a low folate level is known to be associated with gastrointestinal neoplasms. Also, the amino- acid-changing and enzyme-activity-reducing nucleotide polymorphism (677C-->T/Ala222Val) has been described in the MTHFR polymorphism and it brings about low enzyme activity, which may reduce DNA methylation and uracil misincorporation into DNA. These processes may be critical for the oncogenic transformation of human cells. Two common single nucleotide polymorphisms (SNPs) resulting in amino-acid changes (677C T/Ala222Val and 1298A C/Glu428Ala) have been described in MTHFR. We investigated the relation between the MTHFR C677T and A1298C polymorphisms derived from colorectal cancers and from controls in the Korean population. METHODS: One hundred forty-eight (148) individuals with colorectal cancer and 288 healthy persons were analyzed. Blood sampling of each group was performed by using a PCR- RFLP analysis, and MTHFR polymorphism genotypes of 677C/C, 677C/T, 677T/T, 1298AA, 1298AC, and 1298CC were obtained. RESULTS: The genotype frequencies of MTHFR C677T polymorphisms were 25.0% (CC), 48.0% (CT), 27.0% (TT), and 75.0% (CT+TT), respectively, in case patients and 39.2% (CC), 36.8% (CT), 24.0% (TT), and 60.8% (CT+TT) in controls. The genotype frequencies of MTHFR A1298C polymorphisms were 56.1% (AA), 372% (AC), 6.8% (CC), and 43.9% (AC+CC), respectively, in case patients and 55.6% (AA), 40.3% (AC), 4.2% (CC), and 44.4% (AC+CC) in controls. The 677TT and the 677CT genotypes were associated with significantly increased risks for colorectal cancer (adjusted OR=1.77 and 95% CI=1.02~3.04 in TT; adjusted OR=2.07 and 95% CI=1.28~3.35 in CT) than was the 677CC, genotype but the the 1298CC and 1298 AC genotypes were not associated with significantly increased risks for colorectal cancer (adjusted OR=1.75 and 95% CI= 0.71~4.26 in CC; adjusted OR=0.95 and 95% CI=0.62~1.45 in AC). CONCLUSIONS: The MTHFR C677T polymorphism may be influenced by colorectal cancer, but the role of the MTHFR A1298C polymorphism needs careful interpretation and confirmation in larger studies.
Breast ; Colorectal Neoplasms* ; DNA ; DNA Methylation ; Folic Acid ; Gastrointestinal Neoplasms ; Genotype ; Humans ; Leukemia ; Metabolism ; Methylenetetrahydrofolate Reductase (NADPH2)* ; Neural Tube Defects ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Uracil ; Vascular Diseases ; Vitamins

Prostate intraepithelial neoplasia (PIN) is a putative premalignant change in the human prostate, which is an intraluminal proliferation of the secretory cells of the prostatic duct-acinar system that is enveloped by a basal cell layer and displays a spectrum of dysplastic cytologic features ranging from minimal atypia (low grade PIN) to those which are ultimately indistinguishable from carcinoma cells (high grade PIN). To evaluate the clinical significance of the PIN in prostatic tumor and BPH, we reviewed the serum prostate specific antigen (PSA), prostate specific antigen density (PSAD), and pathologic findings in the specimen of 21 BPH and 11 Prostate cancers, which were pathologically confirmed. The distributions of PIN are 7/21 (33%) in BPH and 8/ 11 (73%) in prostatic ca (P<0.05). The mean value (+/-SD) of PSA and PSAD in BPH patient were 8.42+/-5.57 ng/ml, 0.16+/-0.09 for PIN(-), 10.13+/-5.97 ng/ml, 0.17+/-0.09 for PIN(+), and in prostatic cancer patient were 60.53+/-1.83 ng/ml, 1.42+/-0.25 for PIN(-), 54.15+/-34.61 ng/ml, 1.28+/-0.84 for PIN(+), respectively. The mean value (+/-SD) of PSA & PSAD according to histologic types of BPH were 9.04+/-3.88 ng/ml, 0.17+/-0.06 for glandular type, 5. 57+/-1.31 ng/ml, 0.10+/-0.03 for stromal type, and 11.18+/-8.93 ng/ml, 0.19+/-0.13 for mixed type. The distributions of PIN according to histologic types of BPH were 30% (3/10) for glandular type, 40% (2/5) for stromal type, and 33% (2/6) for mixed type. All 7 PIN(+) BPH were low grade, while, of the 8 PIN(+) prostatic Ca, 1 was low grade and 7 were high grade. From these results, the frequent of PIN was higher in prostatic cancer than BPH (P<0.05). PIN had no significant influence on PSA elevation in prostatic cancer and BPH. There was no correction between PSA, PSAD and histologic types of BPH (P>0.05). There was no significant difference in the distribution of PIN according to histologic types of BPH. And high grade PIN was observed only in prostatic cancer. Therefore, if high grade PIN is observed in pathologic specimens, undetected prostatic cancer should be found.
Humans ; Prostate* ; Prostate-Specific Antigen* ; Prostatic Hyperplasia* ; Prostatic Intraepithelial Neoplasia* ; Prostatic Neoplasms*