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I Furuta

Publications and source records attributed to I Furuta.

At least 19 recordsLinked to original sources

Erythropoietin, granulocyte-colony stimulating factor, interleukin-1 beta and interleukin-6 during the normal menstrual cycle.

OBJECTIVE: Menstruation and ovulation are the main events during the menstrual cycle. Menstruation may influence the complete blood count because of its blood loss. Since ovulation is an inflammatory-like phenomenon, white blood cell count may change during ovulation. For these reasons, we have investigated the complete blood count and peripheral serum concentrations of associated cytokines during the normal menstrual cycle. MATERIALS AND METHODS: Normal healthy female volunteers (N = 9; age, 21-33 years) with menstrual cycles of 25-33 days recorded basal body temperature every day and venous blood samples were collected three times per week. Complete blood count was performed and erythropoietin, granulocyte-colony, stimulating factor, interleukin-1 beta, interleukin-1 beta, interleukin-6 and hormones (FSH, LH, estradiol and progesterone) were measured. RESULTS: The red blood cell, total white blood cell, granulocyte and platelet counts showed no statistically significant changes during the menstrual cycle when using analysis of variance with the Scheffe F-test. No changes in erythropoietin, interleukin-1 beta and interleukin-6 were seen throughout the menstrual cycle. In contrast, serum granulocyte-colony stimulating factor concentrations increased significantly to 28.0 +/- 3.1 pg/ml (mean +/- S.E.M.) during the ovulatory phase, compared to 10.7 +/- 0.6 pg/ml in other phases. CONCLUSION: These results indicate that menstrual blood loss does not affect the complete blood count and suggest that granulocyte-colony stimulating factor plays and important role in the mechanism of ovulation.

Adult

Cytokines concentrations in the cervical mucus of pregnant women.

OBJECTIVE: Interleukin-1 alpha, interleukin-1 beta, interleukin-6 and interleukin-8 in specimens of cervical mucus were assayed to assess defense mechanisms against infection in the cervical canal during pregnancy. METHODS: Two hundred and thirty-nine pregnant women who attended the obstetrics outpatient clinic in our hospital were included as subjects. Cervical mucus was collected with a newly developed collection swab, and cytokines and granulocyte elastase in the samples of cervical mucus were quantified using enzyme immunoassay kits. The 1-factor ANOVA, the Kruskal-Wallis test, and scheffé's F were used for statistical analysis. RESULTS: Interleukin-1 alpha, interleukin-1 beta and interleukin-8 levels rose significantly as the concentrations of granulocyte elastase increased. High concentrations of interleukin-1 alpha (75.36 +/- 19.93 pg/ml), interleukin-1 beta (1005.29 +/- 238.75 pg/ml) and interleukin-8 (4822.4 +/- 633.2 pg/ml) were found in the specimens from the group of high granulocyte elastase levels. CONCLUSIONS: These cytokines might be involved in defense mechanisms against ascending infection from the vagina.

Adolescent

[A case of leiomyomatosis in pelvic lymph nodes].

We report a rare case of leiomyomatosis in iliac lymph nodes, which was found in a woman operated with a diagnosis as keratinizing epidermoid carcinoma of the cervix. A 39-year-old Japanese female, married, who had received hormonal therapy in her past history, visited the Department of Obstetrics and Gynecology at Kinki University Hospital, with a chief complaint of bloody discharge. Colposcopy and biopsy suggested a diagnosis of keratinizing epidermoid carcinoma of the cervix. A radical hysterectomy and bilateral salpingo-oophorectomy with pelvic lymph nodes dissection was performed. Histopathological examination showed a keratinizing epidermoid carcinoma of the cervix. An intramural leiomyoma nodule (0.5cm in diameter) was detected in the fundus of the uterus. Histopathologically, this was a typical benign leiomyoma. The lymph nodes were free of neoplasms. But bilateral iliac lymph nodes were enlarged up to soybean size. Microscopically, the iliac lymph nodes contained a large amount of well differentiated smooth muscle tissue (11/30). Immunohistochemical investigation showed a positive reaction for smooth muscle actin and desmins in the spindle cells proliferated in the lymph nodes; no cytokeratin positivity was detected. Leiomyomatosis of lymph node may rise through metaplasia of intranodal decidua or endometriosis by myofibroblasts or smooth muscle cells, reflecting the multipotentiality of the pelvic subcoelomic mesenchyme that can be found in the peripheral sinus of lymph nodes.

Adenocarcinoma, Papillary

[Future prospects of emergency laboratory tests--problems of immunoserologic tests].

Regarding problems in emergency and urgent immunoserologic tests, I mainly focused on infectious diseases and CPR and discussed the correspondence of dangerous needle stick injuries, and the significance of emergency CRP measurement in various body fluids using highly sensitive determination methods. The actual conditions and correspondence of infections due to dangerous needle stick injuries (accidental pricking with used needles) such as hepatitis, syphilis, acquired immunodeficiency syndrome (AIDS), adult T-cell leukemia (ATL), herpes simplex, falciparum malaria, tuberculosis, Rocky mountain spotted fever, and human colonic adenocarcinoma are discussed. With regard to emergency CRP measurement, application of highly sensitive determination methods and the significance of CRP measurement of various body fluids (healthy adult blood, cord blood, cerebrospinal fluid, urine and puncture fluid) are described. The reference values for CRP concentrations in various body fluids were established at 15 to 3,063 ng/ml for serum (male; 26 to 3.992 ng/ml, female; 11 to 1,672 ng/ml), 9 to 73 ng/ml for cord blood, 2 to 10 ng/ml for cerebrospinal fluid and less than 2 ng/ml for urine.

Accidents, Occupational

Serum concentration of endogenous G-CSF in women during the menstrual cycle and pregnancy.

Although granulocyte-colony stimulating factor (G-CSF) is commonly used in the field of supportive therapy for cancer treatment, the serum concentration of endogenous G-CSF in healthy women is still obscure due to the low sensitivity (30 pg mL-1) of the usual enzyme immunoassay. With the development of a highly sensitive (1.0 pg mL-1) chemiluminescent immunoassay by Kiriyama et al., we have clarified the changes of serum G-CSF levels in healthy women during the menstrual cycle and pregnancy. The G-CSF concentration showed a peak value of 27.3 +/- 2.5 pg mL-1 (mean +/- SEM) at the ovulatory phase during the menstrual cycle, which is significantly higher than in all other phases (P < 0.0001, unpaired t-test). A significantly higher value compared to the menstrual cycle, except during the ovulatory phase, was also revealed throughout pregnancy (P < 0.0001, unpaired t-test). These results suggest that G-CSF plays an important role in ovulation and the maintenance of pregnancy.

Adult

Apoptosis in testis germ cells: developmental changes in gonadotropin dependence and localization to selective tubule stages.

Recent studies have demonstrated apoptotic DNA fragmentation in the testis of immature rats deprived of gonadotropins. However, the exact cell type undergoing apoptosis during testis development and the age differences of gonadotropin dependence of testis cell apoptosis are unclear. The present study used gel fractionation and in situ methods to quantitate developmental changes of testis cell DNA fragmentation and to localize the specific cell type affected in developing rats with and without treatment with a GnRH antagonist. Apoptotic DNA fragmentation in whole testis was measured in rats between 8-70 days of age. A gradual increase (1.8- to 2.0-fold) in testis apoptotic DNA fragmentation was seen in rats between 16-28 days of age, compared with 8-day-old animals, followed by a decrease in adult animals. To study gonadotropin dependence of testicular apoptosis, serum FSH and, to a lesser extent, LH were suppressed by treatment with a long-acting GnRH antagonist (azaline-B, 250 micrograms/kg body wt, two injections at 2-day intervals). Pretreatment with the GnRH antagonist increased apoptotic DNA fragmentation in rats between 16-32 days of age but not in younger and adult animals demonstrating an age-related change in gonadotropin dependence. To identify the exact testis cell type undergoing apoptosis, in situ analysis of DNA fragmentation was performed. In rats at 16-24 days of age, spermatocytes in selected tubules were found to have increased DNA fragmentation. In contrast, neither Leydig cells nor Sertoli cells were affected. In 32-day-old and adult animals, increased DNA fragmentation was seen in early primary spermatocytes of some tubules. Treatment with GnRH antagonist increased the number of cells with DNA fragmentation as well as percentage of tubules affected. In animals between 16-32 days of age, meiotic spermatocytes were labeled, whereas early spermatids were also labeled in 24- and 32-day-old animals. In adult animals, the level of apoptotic DNA fragmentation was not affected by GnRH antagonist treatment. However, DNA isolated from specific stages of the seminiferous tubules of adult animals showed stage-specific changes of apoptotic DNA fragmentation with 2-fold higher levels found in stages I and XII-XIV compared with stage VIII. In situ analysis of adult testis demonstrated that spermatocytes were the major cell type affected. In conclusion, the present study demonstrated that at least three factors determine the onset of apoptosis of the male germ cells: 1) the developmental stage of the animal; 2) serum levels of gonadotropins, especially FSH; and 3) specific stage of the seminiferous epithelial cycle. The present approach provides the basis for future analysis of the role of gonadotropins and other factors in the regulation of testis cell degeneration in normal and pathological states.

Animals

[Vancomycin].

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Anti-Bacterial Agents

Photoperiod regulates testis cell apoptosis in Djungarian hamsters.

Reproductive activity in the Djungarian hamster is controlled by seasonal variations in day length. Exposure to long days stimulates testis development, while exposure to short days induces testis regression. We recently found that testis regression after gonadotropin deprivation in rats is associated with increases in apoptosis. Here we sought to determine whether or not apoptosis is associated with the testis regression and/or recrudescence that occurs naturally in seasonally breeding mammals. Newborn male hamsters were maintained on long days (16L:8D) until 3 wk of age before being transferred to short days (8L:16D). Following decreases in serum FSH within 3 days of exposure to short days, testis weight decreased by 52% at Day 10, reaching a 70% decrease after 21 days. Analysis of testis cell DNA fragmentation showed a 4.9-fold increase of low-molecular-weight DNA as early as 5 days after transfer to short days; this was followed by a time-dependent decrease. The observed increases in testis cell apoptosis were correlated with decreases in serum testosterone, but decreases in Leydig cell LH receptor content were delayed. In a second study, 6-wk-old hamsters with regressed testes due to a 3-wk exposure to short days were transferred back to long days. After increases in serum FSH within 3 days of photostimulation, a 2-fold elevation in testis weight was found at Day 5. The increase in testis weight was associated with a 65% decrease of testis apoptosis within 5 days of photostimulation. Also, increases in serum testosterone and LH receptor content were observed after 5 and 10 days of exposure to long days, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

[Retrospective analysis of deep-seated candidiasis among cases autopsied between 1982 to 1991].

Candida is present in the flora of the oral cavity, skin, intestinal tract and vagina, and is also known to be an opportunistic pathogen. Infection with this fungus has been increasing annually along with wide spread use of broad-spectrum antimicrobial agents. The subjects included 95 patients (48 males and 47 females) who had been diagnosed as having had deep-seated candidiasis, among patients autopsied between 1982 to 1991. In regard to annual changes in deep-seated candidiasis, the incidence reached a peak in the 1985 to 1988 period, and thereafter decreased. The number of cases with leukemia as the underlying disease was the largest, 36 (37.9%), followed by malignant lymphoma in 10, and aplastic anemia 5. The number of cases with infection of the stomach was largest, 42 (44.2%), followed by the esophagus in 33 (34.7%), the lung and kidney. The cases with deep-seated candidiasis showed low values of or level of lymphocyte, hemoglobin, CRP, total protein and cholesterol and high values or levels of LDH, urea N, creatinine and total bilirubin. Cases with marked decrease in neutrophils showed no regional infiltration of inflammatory cells in any of the organs infected with Candida. Cases with disseminated candidiasis showed vascular invasion by Candida. The laboratory findings also showed that most of the cases had been undernourished and had high values of CRP which supports the presence of inflammation. Common sites of infection are the esophagus, stomach, and intestinal tract. In the presence of granulocytopenia and immunodeficiency, tissue invasion become severe and associated with vascular invasion.

Aged

Gonadotropin-releasing hormone directly induces apoptotic cell death in the rat ovary: biochemical and in situ detection of deoxyribonucleic acid fragmentation in granulosa cells.

The majority of ovarian follicles undergo atresia through a mechanism involving apoptotic cell death. Although GnRH and its agonists have been shown to suppress ovarian growth and differentiation in hypophysectomized rats, studies on the induction of follicle atresia by GnRH are contradictory. In the present study, the direct effect of GnRH on the occurrence of apoptosis in the ovary was investigated in hypophysectomized estrogen-treated immature rats. Starting 2 days after operation and estrogen capsule implantation, rats were treated with a GnRH agonist (GnRHa; [desGly10,D-Phe6,Pro9-N-ethylamide] GnRH; 50 micrograms/injection, twice daily). Total ovarian DNA was isolated 48 h later, labeled at the 3'ends with [32P]dideoxy ATP, and size-fractionated. Compared to that in control animals, treatment with GnRHa increased DNA fragmentation in multiples of 180 basepairs, a hallmark of apoptosis, demonstrating that GnRH directly increases ovarian apoptotic cell demise. In contrast, FSH treatment (10 micrograms/injection, twice daily) decreased apoptotic DNA fragmentation, and the antiapoptotic effect of FSH was partially blocked by concomitant treatment with GnRHa. The apoptosis-inducing effect of GnRHa was time and dose dependent, with a significant increase seen after 24 h of treatment and a maximal 5.5-fold increase with 10 micrograms GnRHa/injection. Similar to studies using DNA isolated from whole ovaries, DNA obtained from isolated granulosa cells also showed a time- and dose-dependent increase in DNA fragmentation after GnRHa treatment. The effect on DNA fragmentation by GnRHa was mediated by ovarian GnRH receptors, because a potent GnRH receptor blocker, Azaline B, prevented GnRHa action. In addition, in situ end labeling of DNA using digoxigenin-dideoxy-UTP showed that DNA fragmentation was confined to the granulosa cells of preantral and antral follicles. No GnRHa-induced apoptosis was detected in granulosa cells of primary follicles or in thecal and interstitial cells. These data suggest that GnRH directly increases apoptotic cell death in the ovary, and the GnRH action is confined to the granulosa cells. These data provide a basis for future studies on the mechanism of follicular atresia and the regulation of ovarian endonuclease by GnRH.

Animals

Gonadotropin suppression of apoptosis in cultured preovulatory follicles: mediatory role of endogenous insulin-like growth factor I.

Although the majority of ovarian follicles undergo atresia through a mechanism involving apoptotic cell death, in vivo studies concerning the hormonal regulation of atresia have been difficult due to the presence of heterogeneous population of follicles in the ovary. In the present study, the regulation of follicle apoptosis by gonadotropins, insulin-like growth factor I (IGF-I), and IGF-binding protein 3 (IGFBP-3) was examined using a serum-free culture of preovulatory follicles. Immature rats at 26 days of age received a single dose of PMSG. Two days later, the largest preovulatory follicles were collected for in vitro culture with or without hormones. After 24 h of culture, follicular apoptotic DNA fragmentation was analyzed by autoradiography of size-fractionated DNA labeled at 3'-ends by [32P]dideoxy-ATP. A spontaneous increase in apoptotic DNA fragmentation occurred after 24 h of culture in the absence of hormones, whereas treatment with human CG (hCG) or FSH suppressed follicular apoptosis in a dose-dependent manner, with 0.1 microgram/ml causing maximal suppression by 60-62%. Cotreatment with hCG and FSH had no additional effect. Like gonadotropins, treatment with IGF-I and insulin also suppressed the spontaneous onset of apoptosis, with IGF-I being more effective than insulin. Cotreatment with IGFBP-3 and hCG dose-dependently reversed the suppressive effect of hCG on apoptosis by 42%, suggesting a mediatory role of endogenously produced IGF-I. The addition of IGFBP-3 also blocked the suppressive action of IGF-I by 49%, whereas it did not affect the suppressive action of an IGF-I agonist or insulin. Treatment with IGFBP-3 alone had no effect on apoptotic DNA fragmentation. Estrogen and progesterone production by the cultured follicles were also analyzed by RIA. Gonadotropin treatment resulted in a marked stimulation of the production of both steroid productions. In contrast, treatment with IGF-I caused a small increase in estrogen but decreased progesterone production. Although treatment with IGFBP-3 alone decreased both estrogen and progesterone production, cotreatment with IGFBP-3 and hCG resulted in a slight decrease in estrogen production but an increase in progesterone production. Furthermore, IGFBP-3 did not affect IGF-I action on steroid production. To further substantiate the hypothesis that IGFBP-3 blocks the suppressive effect of hCG on apoptosis by neutralizing endogenously produced IGF-I, solution hybridization analysis was performed, and hCG treatment was shown to increase IGF-I messenger RNA levels in cultured follicles by 1.9-fold.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals

Production of cytokines belonging to the interleukin-8 family by human gingival fibroblasts stimulated with interleukin-1 beta in culture.

Three major neutrophil chemotactic peptides belonging to the interleukin-8 (IL-8) family were purified to homogeneity from the conditioned medium of the IL-1 beta-stimulated human gingival fibroblasts culture. On the basis of their molecular masses and NH2-terminal amino acid sequences, these three neutrophil chemotactic factors were identical to melanoma growth stimulatory activity-alpha (MGSA/gro-alpha), MGSA/gro-gamma and Ala-Val-Leu-Pro-Arg-IL-8 (AVLPR-IL-8), each belonging to the IL-8 family. It has been shown by the chemotaxis studies in vitro that the chemotactic activity of MGSA/gro-gamma is similar to that of MGSA/gro-alpha for both human and rat neutrophils, while AVLPR-IL-8 is chemotactic for human neutrophils but not for rat neutrophils. The in vitro findings were supported by the histological studies in vivo on the intradermal injection of either MGSA/gro-alpha or AVLPR-IL-8 into the back of the rats. The results obtained in the present experiment suggest that human gingival fibroblasts play an important role in gingival inflammation through the production of neutrophil chemotactic factors newly characterized as the IL-8 family in response to inflammatory chemical mediators including IL-1 beta.

Amino Acid Sequence

Estrogens inhibit and androgens enhance ovarian granulosa cell apoptosis.

Apoptotic cell death has recently been suggested to be the underlying mechanism of ovarian follicle atresia. To study the regulation of follicle cell apoptosis by sex steroids, we have analyzed ovarian DNA fragmentation, the hallmark of apoptosis, in rats treated with estrogens and androgens. Immature rats were hypophysectomized and implanted with diethylstilbestrol (DES) capsules. Two days later, DES implants were removed in some animals, followed by treatment with estrogens with or without androgens. The extent of ovarian apoptotic DNA fragmentation was analyzed by autoradiography of size-fractionated DNA labeled at 3'-ends by [32P]dideoxy-ATP. After DES withdrawal, ovarian weight decreased and DNA fragmentation increased in a time-dependent manner. In granulosa cells, an increase in apoptotic DNA fragmentation was seen 12 h after withdrawal of DES implants, followed by a 25-fold increase at 48 h. In situ analysis of DNA fragmentation on histological sections of ovaries, using a nonisotopic labeling of DNA by digoxigenin-dideoxy-UTP, also demonstrated that apoptosis induced by DES withdrawal is confined to the granulosa cells in early antral and preantral follicles. No increase in DNA breakdown was detected in thecal cells and interstitial tissues or granulosa cells of primordial and primary follicles. In contrast, replacement with DES (0.5 mg twice daily) or estradiol benzoate (3 mg daily) completely prevented the observed ovarian weight loss and increases in granulosa cell apoptosis. Treatment with estradiol benzoate (0.003-3 mg/day) dose dependently suppressed the apoptosis seen 2 days after removal of DES implants. Furthermore, the antiatretogenic effect of estrogen was blocked by treatment with testosterone (0.5 mg twice daily), which increased ovarian apoptotic DNA fragmentation and decreased ovarian weight in DES-treated animals in a time-dependent manner. Also, in situ examination showed that androgen treatment increased apoptosis in the granulosa cells in a subpopulation of early antral and preantral follicles. The specificity of testosterone action was further demonstrated by the lack of effect of progesterone and cortisol on ovarian apoptosis. These data suggest that sex steroids play an important role in the regulation of ovarian apoptotic cell death, with estrogens preventing apoptosis and androgens antagonizing the effect of estrogens. These data provide the basis for future studies on the role of sex steroid hormones in follicular atresia and the regulation of endonuclease activity by steroid hormones.

Animals

[Intestinal flora of inpatients and isolation frequency of methicillin-resistant Staphylococcus aureus].

The authors compared intestinal flora from 30 healthy volunteers and 128 inpatients. E. coli, B. fragilis, and Bifidobacterium were each detected in the stools of healthy subjects at a frequency of more than 90%, while the incidences of such flora were low in the stools of inpatients: A significant difference was observed between the two groups. E. faecium, P. aeruginosa, Methicillin-resistant Staphylococcus aureus (MRSA), C. difficile, and Candida were detected at high frequencies in the stools of inpatients, as compared with healthy subjects. This finding is attributed to the administration of antimicrobial agents. It is also considered that microbial interaction in maintaining the balance among normal intestinal flora had been lost in patients from whom MRSA and/or C. difficile was isolated. The decrease or elimination of bacterial species antagonistic to such resistant strains must be guarded against, because this can lead to weakening of the defence mechanism against intestinal infection.

Enterococcus faecium

[An autopsy case of neoplastic angioendotheliosis mainly affecting the lung and presenting with atypical cells in peripheral blood].

Neoplastic angioendotheliosis (NAE) is a rare condition characterized by proliferation of atypical cells in small vessels of various organs. In the past, atypical cells seen in this condition were considered to originate from vascular endothelial cells. However, recent immunohistochemical studies have established that the tumor cells in this condition mainly originate from B-lymphocytes. NAE is likely to affect the central nervous system and skin. Cases of NAE with a primary lesion in the pulmonary vessels are rare. One such rare case of NAE was recently encountered by us. The patient was a 77-year-old woman who was admitted to our department because of fever and interstitial shadow in both lungs. After admission, fever did not subside, and the pulmonary shadow became more marked. Laboratory tests upon admission disclosed elevated LDH. Of isozymes, LDH2 and LDH3 were high. Anemia and thrombocytopenia gradually became aggravated, and atypical cells with large basophilic cell body and irregularly shaped nucleus subsequently appeared in peripheral blood. Thereafter, the patient's general condition worsened rapidly and she died about 5 months after admission. Post-mortem examination revealed pleomorphic atypical cells filling the lumen of small vessels in various regions of the body. This finding was particularly marked in pulmonary vessels. With various immunohistochemical stains, these cells were identified as cells of B-lymphocyte origin.

Aged

[Humoral immunity and lymphocyte subsets in patients with dilated cardiomyopathy].

We examined immunological abnormalities in patients with dilated cardiomyopathy (DCM) and reviewed their medical histories, NYHA classifications, electrocardiogram findings and chest X-Ray findings with regard to severity of DCM. Elevated CD4/CD8 ratio as well as decreased number of CD8 cells in lymphocyte subsets was recognized. These abnormalities were particularly noted in patients with past history of myocarditis. NYHA IV class increases in CTR and left ventricular dimension, and a reduced ejection fraction. These findings suggest that lasting of myocardial damage causes immunological abnormalities and the examination of DCM patients' immunological status is useful in anticipating disease process and determining medical treatment.

Autoantibodies