No abstract available.
Animals ; Embryonic Structures* ; Freezing* ; Mice* ; Sucrose*

No abstract available.
Fertility* ; Humans ; Infertility, Male* ; Male ; Male* ; Sperm Motility* ; Spermatozoa*

No abstract available.
Fertilization in Vitro* ; Gonadotropin-Releasing Hormone*

Bacterial infection has been implicated in premature labor in human. But it is impossible to undergo human study of bacteria-induced preterm delivery. If we carry out animal experiment which simulate human preterm delivery induced by bacteria, studies for mechanism, diagnosis, and treatment of preterm delivery will be progressed rapidly. To elucidate mechanisms and potential intervention strategies in preterm pregnancy loss, we observed bacteria-induced preterm labor and the protecting effect of administration of antibiotics with hysteroscopy-guided intracervical inoculation of Escherichia coli. Sterile saline solution(group I, n=5) or 2x10(7)cfu (colony-forming units) of E. coli bilaterally in the cervix of pregnant New Zealand White rabbits on day 20 or 21(70% of gestation) by hysteroscopy was inoculated and rabbits were assinged to ampicillin-sulbactam therapy beginning at 0hr(group II, n=4), 2 hr(group III, n=4), 4 hr(group IV, n=2), and 16 hr(group V, n=2) after inoculation with E. coli, or to no antibiotic therapy(group VI, n=3). Unasyn(ampicillin-sulbactam) was used and its daily dosage was 100 mg/kg/day. The occurrence of vaginal bleeding or preterm birth was observed every two hours. If one rabbit fetus was found to be delivered, exploratory laparotomy was done. Amniotic fluid culture on each sac, decidual culture on each uterine cavity, and pathologic examinations on each placenta were done. The results of experiments are as follows. In control group(0.2cc sterile saline inoculation only), there was no preterm labor and no bacterial growth in culture. In all three rabbits in group VI, preterm delivery occurred and the culture results were all positive in maternal blood, decidua, and amniotic sacs. Preterm delivery also occurred in group V, but results of maternal blood culture were all negative. Increased trend in the occurrence of preterm delivery was statistically significant in the order(p < 0.05) : group I(0/5), group II(0/4), group III(0/4), group IV(0/2), group V(2/2), and group VI(3/3). Pregnancy outcomes on the basis of the number of living fetus, dead fetus, and macerated fetus, have significant trend in the above order. Amniotic fluid culture results also had significant relationship(p < 0.05) : group I(0.20), group II(20/26), group III(18/30), group IV(10/11), and group VI(7/7). In group V, amniotic fluid fail to be obtained due to severe oligohydramnios. Decidual culture results also had an increased trend; group I(0/32), group II(21/29), group III(20/30), gorup IV(16/16), gorup V(11/11), and group VI(25/25). It is statistically significant(p < 0.05) Incidence of histologic chorioamnionitis was also significantly increased from group I to VI. These results indicate that E. coli inoculation has induced preterm delivery and antibiotic therapy has somewhat prevented preterm birth, amniotic fluid infection, decidual infection, and histologic chorioamnionits. Antibiotic effects were attenuated in cases of delayed antibiotic administration.
Amniotic Fluid ; Animal Experimentation ; Anti-Bacterial Agents* ; Bacteria ; Bacterial Infections ; Cervix Uteri ; Chorioamnionitis ; Decidua ; Diagnosis ; Escherichia coli ; Female ; Fetus ; Humans ; Hysteroscopy ; Incidence ; Laparotomy ; Models, Animal ; Obstetric Labor, Premature ; Oligohydramnios ; Placenta ; Pregnancy ; Pregnancy Outcome ; Premature Birth ; Prognosis* ; Rabbits ; Uterine Hemorrhage

No abstract available.
Splints* ; Sterilization, Tubal*

No abstract available.
Animals ; Embryonic Structures* ; Freezing* ; Mice*

Sepsis refers to the systemic response to serious infection. Patients with sepsis usually manifest fever, tachycardia, tachypnea, leukocytosis, and a localized site of infection. Methicillin-resistant Staphylococcus aureus(MRSA) is a gram-positive, nonmotile, aerobic, catalase- positive coccus, which is resistant to all the B -lactam antibiotics. Cutaneous manifestations in sepsis are maculopapules, nodules, petechiae, ecchymoses, purpurae, pustules, vesiculobullae, hemorrhagic bullae and ulcers. When MRSA is identified in blood cultures and skin tissue cultures, the skin lesions can be considered as cutaneous manifestations in sepsis caused by MRSA. We report two cases with erythematous pustules, petechiae, hemorrhagic bullae and maculopapules caused by MRSA sepsis. MRSA grew in blood cultures and skin tissue cultures.
Anti-Bacterial Agents ; Ecchymosis ; Fever ; Humans ; Leukocytosis ; Methicillin Resistance* ; Methicillin-Resistant Staphylococcus aureus* ; Purpura ; Sepsis* ; Skin ; Staphylococcus ; Tachycardia ; Tachypnea ; Ulcer

BACKGROUND: T cell mediated immune destruction is an important mechanism of liver injury in patients with chronic hepatitis C. Serum levels of soluble interleukin-2 receptor(sIL-2R) seem to serve as a marker for the T cell activation and progressive liver injury, This study examined serum levels of sIft-2R and hepatitis C virus (HCV) RNA in patients with chronic HCV infection to determine the correlation with the severity of chronic hepatocellular damage. METHODS: Serum levels of sIft-2R in 73 patients with HCV infection (chronic hepatitis 52, liver cirrhosis 9, hepatocellular carcinoma 12) and 40 healthy controls were measured by sandwich enzyme immunoassay (CELLFREE, T Cell Sciences, USA). HCV RNA was quantified by QUANTIPLEX(TM) HCV RNA 2.0 assay (Chiron, USA) with duplication. This assay is a sandwich nucleic acid hybridization procedure using branched DNA amplification for the quantitation of HCV RNA. RESULTS: The sIL-2R levels of 52 patients with chronic hepatitis (591.4+/-238.7U/mL), 9 with liver cirrhosis(949.4+/-721.9 U/mL), and 12 with hepatocellular carcinoma (1,167.4+/- 554.4 U/mL) were significantly higher than those of healthy controls(370.8+/-71.8 U/mL) (p<0.001). A progressive and significant increase occurred in sIL-2R levels with chronic hepatitis C, liver cirrhosis and hepatocellular carcinoma (HCC) in order (p(0.001). The HCV RNA was detected in all patients and the means of HCV viral load were 3.3 MEq/mL in chronic hepatitis, 2.8 MEq/mL in cirrhosis, and 3.7 MEq/mL in HCC. There was no significant correlation between HCV RNA and the severity of liver injury in chronic HCV infection. There were no correlations among sIL-2R, HCV RNA and serum ALT. CONCLUSIONS: These results suggest that chronic hepatocellular injury by HCV progress mainly by T cell mediated immune response, not by direct cytopathic injury. Also, sIL-2R can be useful as a marker in monitoring the patients with HCV infection at high risk of getting HCC.
Carcinoma, Hepatocellular ; DNA ; Fibrosis ; Hepacivirus* ; Hepatitis C* ; Hepatitis C, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Immunoenzyme Techniques ; Interleukin-2* ; Liver ; Liver Cirrhosis ; Nucleic Acid Hybridization ; RNA ; Viral Load

BACKGROUND: T cell mediated immune destruction is an important mechanism of liver injury in patients with chronic hepatitis C. Serum levels of soluble interleukin-2 receptor(sIL-2R) seem to serve as a marker for the T cell activation and progressive liver injury, This study examined serum levels of sIft-2R and hepatitis C virus (HCV) RNA in patients with chronic HCV infection to determine the correlation with the severity of chronic hepatocellular damage. METHODS: Serum levels of sIft-2R in 73 patients with HCV infection (chronic hepatitis 52, liver cirrhosis 9, hepatocellular carcinoma 12) and 40 healthy controls were measured by sandwich enzyme immunoassay (CELLFREE, T Cell Sciences, USA). HCV RNA was quantified by QUANTIPLEX(TM) HCV RNA 2.0 assay (Chiron, USA) with duplication. This assay is a sandwich nucleic acid hybridization procedure using branched DNA amplification for the quantitation of HCV RNA. RESULTS: The sIL-2R levels of 52 patients with chronic hepatitis (591.4+/-238.7U/mL), 9 with liver cirrhosis(949.4+/-721.9 U/mL), and 12 with hepatocellular carcinoma (1,167.4+/- 554.4 U/mL) were significantly higher than those of healthy controls(370.8+/-71.8 U/mL) (p<0.001). A progressive and significant increase occurred in sIL-2R levels with chronic hepatitis C, liver cirrhosis and hepatocellular carcinoma (HCC) in order (p(0.001). The HCV RNA was detected in all patients and the means of HCV viral load were 3.3 MEq/mL in chronic hepatitis, 2.8 MEq/mL in cirrhosis, and 3.7 MEq/mL in HCC. There was no significant correlation between HCV RNA and the severity of liver injury in chronic HCV infection. There were no correlations among sIL-2R, HCV RNA and serum ALT. CONCLUSIONS: These results suggest that chronic hepatocellular injury by HCV progress mainly by T cell mediated immune response, not by direct cytopathic injury. Also, sIL-2R can be useful as a marker in monitoring the patients with HCV infection at high risk of getting HCC.
Carcinoma, Hepatocellular ; DNA ; Fibrosis ; Hepacivirus* ; Hepatitis C* ; Hepatitis C, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Immunoenzyme Techniques ; Interleukin-2* ; Liver ; Liver Cirrhosis ; Nucleic Acid Hybridization ; RNA ; Viral Load

No abstract available.
Animals ; Embryonic Structures* ; Mice*