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Biomedical subjects

H Kitajima

Publications and source records attributed to H Kitajima.

71 records · Page 4Linked to original sources
PubMed1987

Complement activation in fetuses: assessment by the levels of complement components and split products in cord blood.

The whole complement activity (CH50) and concentrations of components (C1q, C3, and C4) and C3 split product (C3d) were determined in the cord blood of 172 newborns between 16 and 42 weeks of gestation. Histological examination of their placentas revealed that the extent of complement activation was significantly higher in those with some degree of inflammation in the amnion than in those with normal amnion. The correlation between the complement levels and gestational age was higher in those with no amnionitis. In some cases the level of C3d at an early gestational age was as high as that in adults. The C3 activation system seems to be well developed even before week 25 of gestation. Among the complement components, C3d was the most sensitive indicator of placenta inflammation. As placenta inflammation may reflect intrauterine infection, the measurement of C3d levels may be of diagnostic value.

Adult↗
PubMed1985

Mouse skin melanoma induced in two stage chemical carcinogenesis with 7,12-dimethylbenz[a]anthracene and croton oil.

Mouse skin melanomas were induced in two stage skin carcinogenesis with 7,12-dimethylbenz[a]anthracene as initiator and croton oil as promoter. After approximately 25 weeks of promotion, small black macules of the skin were observed in C57BL, CDF1 and BDF1 mice, and progressively grew with time. Macules less than 2 mm in diameter were localized mostly in the lower portion of the dermis and, histologically, these lesions were consistent with the diagnosis of melanocytoma and were composed of polygonal to round cells loaded with large numbers of melanin granules. The cells were closely packed forming well-demarcated cell-nests with occasional columnar arrangement. In the macules over 2 mm in diameter, the cells were closely packed to form irregularly bordered cell-nests, showing invasive growth into the surrounding tissues. The lesions were diagnosed as malignant melanomas. The incidence of benign and/or malignant melanoma differed among strains: 80% in BDF1, 70% in CDF1, 30% in C57BL/6 and 0% in DBA/2 mice. One example of tumor induced in a CDF1 mouse was transplantable to homologous CDF1 mice.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

[Bilateral, symmetrical hemorrhagic infarction of the basal ganglia and thalamus following neonatal asphyxia].

With the advancement of perinatal intensive care, the occurrence of subependymal germinal matrix hemorrhage (= GMH) in low-birth-weight (premature) infants has became a major concern in perinatal medicine. The pathophysiology of the GMH has long been controversial. The introduction of computed tomographic (= CT) scanning to perinatal medicine has revealed various pathological events heretofore unknown in newborn infants having respiratory and circulatory distress. At our serving the entire Osaka Prefecture, infants suffering from birth asphyxia with severe perinatal brain damage were found to have CT findings distinguishable from those of GMH. We report three asphyxiated newborn infant who had hemorrhagic infarction in bilateral caudate nucleus, striatum and thalamus on the CT scan. Reports of similar findings are rare, and ours is the first serial observation of such CT scan image in newborn infants. The mechanism of development and pathology of this pathological condition have been variously argued as pathophysiology of GMH. The present study lacks postmortem examination, however, the findings in serial CT scans in three infants and review of the literatures related to the pathology of neonatal asphyxia indicate the following course. The thrombosis in the internal cerebral veins led to severe swelling of the brain, and hemorrhage occurred with the reduction in the swelling, eventually resulting in diffuse leukomalacia. Etat marbré (status marmoratus), mentioned earlier, is considered to represent a milder stage of this pathologic course.(ABSTRACT TRUNCATED AT 250 WORDS)

Asphyxia Neonatorum↗
PubMed1983

[Primary intracranial germ cell tumor in the right basal ganglia and its vicinity area--a report of the case with germinoma and choriocarcinoma histologically].

A case of intracranial germ cell tumor in the right basal ganglia and it's vicinity area was presented and previous reported cases were reviewed. The patient was a 11-year-old boy with precocious puberty. His illness started with left hemiparesis and mental disturbance, i.e. behavioral and emotional change one year prior to admission. Enhanced CT demonstrated a round lesion of high density, with relatively low density in the center portion. The tumor developed from the right putamen to thalamus, and involved toward hypothalamic region on coronary CT. Hormonal studies revealed abnormal levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), human chronic gonadotropin (HCG), and testosterone. In addition to excessively high levels of HCG in the urine, serum and CSF, high elevation of plasma LH and low of plasma FSH were revealed. On 3 June 1980, right temporal craniotomy was performed and a piece of the tumor was removed. Tumor's tissue was diagnosed as germinoma by pathohistological examination. As the effect of postoperative Co-60 radiation, high density area on CT disappeared and remained as well margined low density area. On repeated CTs and HCG-measurements on further, recurrent sign was not noted up to now. However, as a result of pathohistological studies in details, syncytiotrophoblast generally seen in the choriocarcinoma seem to be presented in it's tissue. Therefore, by means of peroxidase labeled antibody method, the authors proved HCG in syncytial cells of the tumor's tissue. There are very little reports on quantification of HCG in primary intracranial germ cell tumor with precocious puberty. Serial measurements of HCG are useful for following the diagnosis and therapy of primary intracranial germ cell tumors. In this report, the authors provide evidence that the syncytial cell mixed in intracranial germinoma secrets HCG.

Brain Neoplasms↗
PubMed1981

Further studies on complementation between mutants of Clostridium perfringens.

1. Mutants devoid of lambda- and kappa-toxin and hemagglutinin (HA), respectively, were isolated from Cl. perfringens PB6K. The lambda- and HA- mutants could be classified into a and b groups by complementation but the kappa- mutants were all of the a group. 2. All b group mutants isolated, irrespective of the marker used for isolation, were pleiotropically negative or leaky with respect to theta-, lambda- and kappa-toxin and HA production. 3. Lambda-toxin produced by complementation was proved to be a rennet-like protease. 4. The activities of 12 extracellular enzymes, including sialidase, of several b group strains and the parent PB6K were compared, but no definite differences were observed. From this finding, the productions of these enzymes were concluded not to be regulated by the same mechanism as theta-, lambda- and kappa-toxin and HA. 5. Cl. perfringens CN3870 was also studied. Findings were similar to those on PB6K except for very low activity of HA.

Bacterial Toxins↗
PubMed1981

Inhibitory effect of K-76 monocarboxylic acid, an anticomplementary agent, on the C3b inactivator system.

K-76COOH caused dose-dependent inhibition of the degradation, by C3b inactivator (C3bINA) and beta 1H, of membrane-bound C3b on EAC1-3b and of free C3b in the fluid phase, i.e., cleavage of the C3b alpha' peptide chain. K-76COOH primarily attacked C3bINA but not beta 1H or C3b. K-76COOH inhibited the suppression of immune adherence reactivity and the manifestation of conglutination reactivity of EAC1-3b cells by C3bINA and beta 1H. The drug also inhibited the reaction between conglutinin and EAC1-3b' cells derived from EAC1-3b by treatment with C3bINA and beta 1H. EAC1-3b cells did not form rosettes with either Daudi or Raji lymphoblastoid cells. Treatment with C3bINA and beta 1H rendered EAC1-3b cells reactive with Daudi cells, and this change was inhibited by K-76COOH. EAC1-3b cells became able to form rosettes with Raji cells after addition of beta 1H. This rosette formation was enhanced by further addition of C3bINA, and this enhancement was also suppressed by K-76COOH.

Animals↗
PubMed1978

Effect of age on C1q and C3 levels in human serum and their presence in colostrum.

The initiating complement component (C1q) in the classical pathway of 730 subjects and the first essential component (C3) in the alternative pathway of 461 subjects in Japan were examined. The study population consisted of normal healthy newborns, infants, children, adults and the old (from birth up to 75 years of age). In cord sera, both C1q and C3 were about 60% to the total mean level. At 3 days of age, C1q markedly increased to the mean level which remained relatively invariable up to 40 years of age. And above 40 years, the C1q level increased steadily with age up to about 75 years of age. C3 reached the mean level at about 1 month of age, and was highest during infancy. This level declined at about puberty and then continued to increase steadily with age up to around 55 years. In normal healthy subjects, a moderate positive rank correlation was found between C1q and C3 amounts. No significant differences of C1q and C3 levels were evident between male and female. No C1q was demonstrable in the colostrum from which lipids were previously removed, but after concentration by precipitation in a chelating agent with a low ionic strength, C1q, measured immunochemically, was detectable at concentrations of 300 ng/ml of colostrum. C3 was also detected at concentrations of about 200 microgram/ml of colostrum.

Adolescent↗
PubMedDate not supplied

Differences among acute, subacute, and chronic chorioamnionitis based on levels of inflammation-associated proteins in cord blood.

The serum concentration of inflammation-associated proteins and several complement components in the cord blood of 215 newborns with and without chorioamnionitis (CAM), who were delivered between 17 and 42 weeks of gestation, were measured. We investigated the relationship of levels of serum proteins to acute, subacute, and chronic CAM, and to subacute necrotizing funisitis (SNF). Complement components C3d, C3, and C4 levels increased in subacute CAM (P = 0. 0002, P = 0.0007, P = 0.0029, respectively), whereas factor B increased in each type of CAM (P = 0.0001, P = 0.0009, P = 0.0004, respectively). Among the immunoglobulins, IgG levels were unrelated to the presence or type of CAM, IgM levels increased in subacute CAM (P < 0.0001), and IgA levels increased in chronic CAM (P < 0.0001). Among the acute phase reactants (APR), haptoglobin and C-reactive protein (CRP) levels increased in acute (P < 0.0001, P = 0.0022, respectively) and chronic CAM (P = 0.0035, P = 0.0345, respectively), whereas orosomucoid levels increased in chronic CAM (P = 0.0003). IL-6 levels increased in acute (P = 0.0011) and subacute (P = 0. 0475) CAM. C3d (P = 0.0063), C3 (P = 0.0289), C4 (P = 0.0491), and IgM (P < 0.0001) levels were increased in SNF. These findings suggest that the histologic distinction of acute, subacute, and chronic CAM is a useful indicator of the inflammatory mediator status of the infants. The infants with SNF may have ended their initial active inflammatory states, but they still have subacute immune activation.

Acute Disease↗
PubMedDate not supplied

Significance of chorioamnionitis.

In preterm deliveries, we have reported a high incidence (30-50%) of histologic chorioamnionitis (CAM) in the placenta. There is little evidence about the effects of CAM on preterm infants. We investigated the levels of complements and cytokines in the cord blood, the pathological nature of the placenta, the L/S ratio of gastric and tracheal aspirate of each preterm infant at birth, and assessed the biological effects of CAM on them. CAM stimulates the immunological system by cytokine production (IL6 and IL8) and complement activation in the fetus. It has been suggested that CAM may be one of the factor accelerating fetal maturation of the immunological system such as complement activation and immunoglobulin production, and of surfactant synthesis in the lung. On the contrary, CAM may damage the structures along the lining cells in the airway by accumulating polymorphonuclear cells of the infants with Wilson-Mikity syndrome.

Chorioamnionitis↗