Effects of sex hormones on human PMN migration

It is believed that gingivitis at puberty is exaggerated by alterations of the hormonal balance. We have suggested that estradiol promotes the gingivitis at puberty while progesterone reduces it (J. Hiroshima Univ. Dent. Soc. 19: 1987). But the mechanisms of these hormones which influence gingival inflammation are not known yet. Therefore, we hypothesized that one of the possible mechanisms of sex hormones on gingival inflammation is through their action on polymorphonuclear leucocytes (PMNs) function because PMNs play an important role in periodontal disease. The purpose of this study was to investigate the effect of sex hormones on PMNs function, especially their migration in vitro. PMNs and plasma were obtained from heparinized peripheral blood of 23 healthy adults. PMNs were preincubated at 37 degrees C for 15 minutes with progesterone or 17 beta-estradiol at designated concentrations. After preincubation, PMNs migration was measured using 48-well chemotaxis micro-chamber with N-formyl-methionyl-leucyl-phenylalanine (FMLP) as chemoattractant. The levels of estradiol and progesterone in the plasma were determined using Direct Radioimmunoassay Kits and the correlation between sex hormone levels and PMNs migration was investigated. PMNs migration to 10(-6) M FMLP was enhanced significantly by progesterone at the concentrations of 200 ng/ml while it was reduced by estradiol at 0.4 ng/ml and 2.0 ng/ml. Random migration of PMNs was enhanced significantly by progesterone at 20 ng/ml while it was reduced by estradiol at 0.4 ng/ml. Significant positive correlation was found between progesterone level in plasma and the PMNs migration in vitro. Estradiol level in plasma did not have any correlation with the PMNs migration in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)     

Malignant Rhabdoid Tumor of the Breast: A Case Report

A 66-year-old woman time of 10 days. One month after radicalmastectomy, there was local recurrence, followed by multiplepulmonary metastases, and the patient died of respiratory failure5 months after surgery. The gray-white-colored tumor measured13x12x;10 cm, and its border was well defined. The tumor wascomposed of diffusely growing round or polygonal cells withvesicular nuclei, prominent nucleoli, and ample cytoplasm containingeosinophilic inclusions. Lymph node involvement was widespread.Both vimentin and keratin were clearly demonstrated by immunohistochemicalstaining. Ultrastructural studies revealed that the MRT cellscontained cytoplasmic whorls of intermediate filaments.     

Evaluation of myocardial disorders in patients with dilated cardiomyopathy and left ventricular eccentric hypertrophy--by 201Tl myocardial SPECT]

201Tl myocardial SPECT was performed in cases of dilated cardiomyopathy and valvular heart disease with left ventricular eccentric hypertrophy, and the two groups were compared from the standpoint of the mechanism of onset of myocardial disorders. Significant coefficients of correlation were seen between the Tl score and LVDd (r = 0.792, r = 0.785) and Tl score and LVEF (r = -0.634, r = -0.555) in both dilated cardiomyopathy and valvular heart disease. In cases of valvular heart disease, significant correlation coefficients (r = -0.756, r = -0.720) between LVDd and r-WR (relative-washout rate), and Tl score and r-WR were observed, but no such correlation was seen in dilated cardiomyopathy. In valvular heart disease, a decrease in myocardial perfusion associated with enlargement of the left ventricle appeared, while in dilated cardiomyopathy, there was a marked decrease in LVEF in proportion to the thallium defect. Therefore, it was assumed that left ventricular wall disorders occur due to myocardial metabolic disorders and coronary microcirculation disorders.     

Stroke in surgery of the arteriosclerotic descending thoracic aortic aneurysms: influence of cross-clamping technique of the aorta.

OBJECTIVE: The risk of stroke caused by dislodgment of loose atheromatous plaque or mural emboli is increased by cross-clamping of the aorta. Some patients undergo descending thoracic aortic aneurysm repair with proximal aortic cross-clamping between the left common carotid artery and the left subclavian artery. The objective of this study was to determine the influence of proximal aortic cross-clamping in arteriosclerotic aneurysm or dissecting aneurysm repair. METHODS: Between May 1984 and May 2003, 81 patients underwent elective surgery for distal arch or descending aortic aneurysm repair with proximal aortic cross-clamping between the left common carotid artery and the left subclavian artery. To evaluate the influence of the proximal aortic cross-clamping, patients were divided into two groups: patients who had undergone arteriosclerotic aneurysm repair (group I, n=25) and patients who had undergone dissecting aneurysm repair (group II, n=56). RESULTS: Eight (9.9%) of the 81 patients had a stroke. Six strokes occurred in operations for arteriosclerotic aneurysm repair group I and two strokes occurred in operations for dissecting aneurysm repair group II (24 vs 3.6%; p=0.009). In-hospital mortality rates were 12% in group I and 8.9% in group II (p=0.70). Major postoperative complications included renal failure requiring hemodialysis (in 4.2% of the patients in group I and in 8.3% of the patients in group II, p=0.99) and pulmonary complication (in 20% of the patients in group I and in 16% of the patients in group II, p=0.67). CONCLUSION: Cross-clamping between head vessels should be avoided if at all possible when operating on patients who have arteriosclerotic descending thoracic aneurysms.     

Studies on the metabolic fate of 14C-rokitamycin. III. Transmigration to fetus or milk

Transmigration of 14C-radioactivity to fetus or milk were studied in 17-18 day-pregnant rats and mother rats on the 14th day after parturition after a single oral administration of 14C-rokitamycin (TMS-19-Q) at a dose of 200 mg/kg. The blood concentration of the drug in the mother reached a maximum level of 22.8 micrograms/ml at 2 hours after administration. Maximum concentrations of TMS-19-Q in placenta, ovary and uterus were attained in 2 hours, and were 28.9, 26.0 and 26.2 micrograms/g, respectively. The distribution to these tissues were considered good. The maximum concentration of TMS-19-Q in the amniotic fluid was attained in 2 hours, at a level of 5.4 micrograms/ml. The transmigration to the amniotic fluid was considered poor. The maximum concentration of the drug in the fetus was achieved in 2 hours at a level of 13.7 micrograms/g. Maximum concentrations of the drug in fetal liver and brain were attained in 4 hours, and were 32.8 and 11.4 micrograms/g, respectively. Whole body autoradiography was done when the radioactivity in maternal blood reached peak concentration. It was found that radioactivities in placenta and fetal membrane were similar to the radioactivity in maternal blood, while the radioactivity in fetal brain was considerably lower than that in maternal blood. Maximum concentrations were found at 1 hour in the blood and at 4 hours in the milk, and were 14.8 and 21.5 micrograms/ml, respectively. Transmigration to the milk was good.     

Anti-bacterial defense mechanism of the urinary bladder. Role of mannose in urine

Bacterial adherence to mucosa is thought to be an initial and important stage to cause urinary tract infection. Among some mechanisms of bacterial adherence, the role of fimbriae and its receptor is worthy of notice. In particular, type 1 fimbriae, for which mannose is assumed as a receptor, is reported as the most common type and called "common fimbriae". Therefore if a certain amount of mannose is present in urine, it will cover the fimbriae of bacteria and competitively block the bacterial adherence to bladder mucosa. As the first step, we tried to detect mannose in urine by high performance liquid chromatography (HPLC). Sugar can be measured by detecting the fluorescence which is produced by a sugar separated by ion exchange, reacting with arginine at high temperature. The results using standard sugar samples should have highly stable retention time and concentration curve with the minimum detectable mannose concentration of 0.02 microgram. We investigated mannose in urine from 186 cases. Since the mannose peak was often masked by near unidentified peaks, the peak of mannose could be detected only in 80 cases and its concentration could be measured only in 24 cases. Mannose concentration in the urine of the 24 cases was between 2.6 and 108.7 micrograms/ml and in most of cases it was lower than 20 micrograms/ml. Secondary, we examined the possibility of a mannose in urine to prevent bacterial adherence to mucosa by the hemagglutination test using guinea pig erythrocytes and type 1 fimbriated E. coli.(ABSTRACT TRUNCATED AT 250 WORDS)     

Identification of breakpoint cluster regions at 1p36.3 and 3q21 in hematologic malignancies with t(1;3)(p36;q21)

The reciprocal translocation t(1;3)(p36;q21) is associated with myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML) characterized by trilineage dysplasia, in particular dysmegakaryocytopoiesis, and a poor prognosis. As yet no molecular genetic analyses of the t(1;3) have been reported. In four patients with t(1;3), all of whom had AML-M4, which evolved from MDS, the breakpoints at 3q21 clustered within a 60-kb region centromeric to the breakpoint of the inv(3)(q21q26), whereas the breakpoints at 1p36 clustered within a 90-kb region at 1p36.3. The presence of novel clusters in both the 3q21 and 1p36 breakpoints (BCRs) suggests a common, underlying molecular mechanism for the development of t(1;3)-positive MDS/AML. The Ribophorin I (RPN1) gene close to the BCR at 3q21 was highly expressed without gross structural changes, whereas the GR6 gene located within the BCR at 3q21 was not expressed. No other highly expressed genes were isolated in a 150-kb region at 3q21. Thus, it is likely that a gene at 1p36.3 is activated by the translocation of the 3q21 region or a gene important for transformation lies on 3q21, outside the 150-kb region. Further characterization of the BCRs at 1p36.3 and 3q21 should provide important insights into the molecular genetic mechanisms involved in the genesis of t(1;3)-positive MDS/AML. Genes Chromosomes Cancer 27:229-238, 2000.     

Specific Interaction of a 25-kilodalton Cellular Protein,a 40S Ribosomal Subunit Protein,with the Internal Ribosome Entry Site of Hepatitis C Virus Genome

Translation initiation of hepatitis C virus (HCV) RNA is controlled by an internal ribosome entry site (IRES) contained in 5 noncoding region (NCR) and in several nucleotides of the coding region. The ability of a 25-kilodalton cellular protein (p25) to bind the HCV 5 NCR is correlated with the efficiency of translation initiation of HCV RNA, indicating that this protein plays a critical role in HCV translation (S. Fukushi, C. Kurihara, N. Ishiyama, F. B. Hoshino, A. Oya, and K. Katayama, J Virol 71, 1662–1666, 1997). We have extended the study for identification of the IRES region required for p25 binding. For this purpose, we have performed UV cross-linking competition analyses using 5- or 3- deleted mutants of the HCV 5 NCR as competitor RNAs for binding of p25 to wild-type HCV 5 NCR. Competitor RNAs lacking nucleotides (nt) 47–74 or nt 279–331 did not inhibit p25 binding to the HCV IRES, indicating that these regions are necessary for interaction of the p25 and HCV IRES. Since p25 binding was not observed in the IRES elements of encephalomyocarditis virus and poliovirus in UV cross-linking competition analyses, the p25 binding may be specific for the HCV IRES. p25 bound to the HCV IRES was detected when a purified 40S ribosomal subunit was used for UV cross-linking experiment, indicating that p25 is one of 40S ribosomal subunit proteins. These results reveal an unique interaction between the 40S ribosomal subunit and HCV IRES to contribute to translation initiation of the HCV genome.