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J Manuel

Publications and source records attributed to J Manuel.

At least 19 recordsLinked to original sources
PubMed1997

Influence of soft tissue (fat and fat-free mass) on ultrasound bone velocity: an in vivo study.

RATIONALE AND OBJECTIVES: The authors determine the relative effect of soft-tissue compartments, body fat (percent [%Bfat] and weight [Bfat kg]) and fat-free mass (FFM kg), on measurements of ultrasound bone velocity (UBV m/second). METHODS: The authors measured UBV in proximal phalanxes and body fat and fat-free mass by near infrared interactance in 40 healthy premenopausal women (mean age +/- standard deviation 28.2 +/- 3.8 years). RESULTS: Correlation study (Fisher's r to z) showed that UBV correlated negatively with %Bfat (r = -0.61, P < 0.0001), Bfat kg (r = -0.56, P = 0.0001) and marginally with body weight (r = -0.33, P = 0.0403), but did not correlate with FFM kg or H2O L (both r = -0.08, P not significant). When the correlation test was adjusted for weight and age (partial correlation), the negative correlation between UBV and %Bfat persisted (r = -0.54, P < 0.0005; and r = -0.63, P < 0.0001, respectively) and the correlation with FFM kg, adjusted for weight, became positive and significant (r = 0.55, P < 0.0005). CONCLUSIONS: These results, to our knowledge, are the first to be obtained by in vivo evaluation of UBV in relation to body fat and fat-free mass. Body fat, but not fat-free mass, was the main factor affecting UBV. This confirms the deficiency of UBV measurements, considering that obesity is a protective factor for bone mass.

Adipose Tissue↗
PubMed1997

Stress triggered abortions are associated with alterations of granulated cells into the decidua.

PROBLEM: Stress is known to be abortogenic in animals and humans. An increased decidual release of cytokines such as TNF-alpha and reduction in TGF-beta 2-related immunosuppressive activity has been proposed as the triggering mechanism. Substance P release by nerves in endometrium/decidua has been found to be the key neurotransmitter in this pathway. It is still unclear which cells are stimulated by substance P to produce the increased TNF-alpha level. METHOD: As a measure of local activation, the granulation of granulated material gland (GMG) cells was measured by flow cytometry after sonic plus immobilization stress of mice or substance P treatment of GMG cells (both isolated GMG cells and GMG-cell containing decidua). TNF-alpha release from decidua and isolated GMG cells was investigated using a TNF-alpha bioassay. The degranulation of uterine mast cell, another potential source of TNF-alpha, was examined in situ by Toluidine blue staining. RESULTS: We observed a striking increase in percentage of degranulated mast cells (8% -->24%) in the uteri of stressed animals, whereas the granularity of GMG cells was decreased by stress but increased with treatment with substance P in vitro. Isolated GMG cells appeared to release in vitro cytotoxins active in the TNF-alpha bioassay, but the magnitude of this activity was not increase by stress or by substance P treatment. In contrast, disaggregated decidual tissue which is known to release increased amounts of TNF-alpha after stress, did increase activity in response to substance P in vitro. CONCLUSIONS: Uterine mast cells show activation as reflected by degranulation after stress exposure of pregnant mice and mast cells might be the cellular link between the neurotransmitter substance P and increase in decidual TNF-alpha release that leads to abortion.

Abortion, Spontaneous↗
PubMed1997

Prime suspect.

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Animals↗
PubMed1996

Psycho-neuro-cytokine/endocrine pathways in immunoregulation during pregnancy.

PROBLEM: Some mammalian pregnancy failure is thought to occur by immunological or immunologically modifiable mechanisms. The original model wherein spontaneous abortion was proposed to represent rejection of the conceptus as an allograft has been supplanted by a model of maternal paraimmunological natural effector cell toxicity to fetal trophoblast more closely related to tumor rejection. The problem is to integrate current information concerning the role of immunological, paraimmunological, endocrinological, and stress-triggered neural factors that determine whether or not abortion will occur. METHODS: Review of existing data. RESULTS: An integrated model is proposed. CONCLUSION: Immunological factors play an important role in abortion processes and prevention of abortions. The existence of abortogenic mechanisms and their regulation appears to be based upon optimizing survival of the species. Two new conceptual models provide a useful framework for further investigation of human pregnancy failure and its treatment.

Abortion, Spontaneous↗
PubMed1996

Sentinel school.

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Animals↗
PubMed1995

Stress-induced murine abortion associated with substance P-dependent alteration in cytokines in maternal uterine decidua.

Stress is known to induce abortions, but underlying mechanisms are unknown. Both alloimmunization and injection of antibody to the asialoGM1 determinant of natural killer cells have been shown to prevent stress-triggered abortion in mice. DBA/2J-mated CBA/J female mice were used to investigate the influence of stress during early gestation on systemic hormone levels and on cytokines in the decidua that are thought to be relevant to abortion in nonstress-related murine abortion. Lowered levels of progesterone did not occur as a result of stress. In stressed mice, increased levels of the abortogenic cytokine tumor necrosis factor alpha (TNF alpha) were associated with decreased levels of pregnancy-protective transforming growth factor beta 2-related suppressive activity in uterine decidua. In the alloimmunized animals where stress failed to boost the abortion rate, these effects were abrogated. Production of TNF alpha may be stimulated by the neurotransmitter substance P (SP); after injection of an SP receptor antagonist or SP-antibody, stress failed to increase the abortion rate above the background level. The increased levels of TNF alpha we observed in the stressed animals were completely abrogated in the animals that had received the SP receptor antagonist; stress also failed to decrease the pregnancy-protective suppressive activity in the decidua of these animals. The data indicate that stress may inhibit protective suppressor mechanisms and promote secretion of abortogenic cytokines such as TNF alpha via neurotransmitter SP.

Abortion, Spontaneous↗
PubMed1995

Stress-triggered abortion: inhibition of protective suppression and promotion of tumor necrosis factor-alpha (TNF-alpha) release as a mechanism triggering resorptions in mice.

PROBLEM: Stress adversely affects pregnancy outcome and has been implicated as an abortogen in both animals and humans. However, the mechanisms whereby stress aborts are largely unknown. Alloimmunization can prevent stress-triggered abortion, and immunization is known to increase transforming growth factor-beta 2 (TGF-beta 2)-related suppressive activity. METHOD: To investigate these mechanisms, DBA/2J males were mated to CBA/J or C3H/HeJ females, and the pregnant females were exposed to ultrasonic sound stress for a period of 24 h between day 4.5 to 8.5 of pregnancy. RESULTS: Ultrasonic stress significantly elevated the resorption rate with a peak effect on day 5.5 in the CBA/J females and on day 4.5 in the LPS-resistant C3H/HeJ females. The tumor necrosis factor-alpha (TNF-alpha) release from the decidua was also elevated and the TGF-beta 2-mediated suppressive activity was significantly decreased. The resorption rate only increased when the TNF-alpha/TGF-beta 2 ratio was increased compared to the control. CONCLUSION: These data suggest that stress may inhibit protective suppressor mechanisms and promote secretion of abortogenic cytokines such as TNF-alpha. Possible mechanisms are discussed.

Abortion, Spontaneous↗
PubMed1994

Evaluations of children who have disclosed sexual abuse via facilitated communication.

OBJECTIVE: To review the findings of interdisciplinary team evaluations of children who disclosed sexual abuse via facilitated communication. DESIGN: Case series. SETTING: Tertiary care hospital outpatient child sexual abuse program in central New York. PATIENTS: Between January 1990 and March 1993, 13 children who disclosed sexual abuse via facilitated communication and were referred to a university hospital child abuse referral and evaluation center. The range of previously determined developmental diagnosis included mental retardation, speech delay, and autism. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Medical records were reviewed for (1) disclosure, (2) physical evidence, (3) child's behavioral and medical history, (4) disclosures by siblings, (5) perpetrator's confession, (6) child protective services determinations, and (7) court findings. RESULTS: Four children had evidence of sexual abuse: two had physical findings consistent with sexual abuse, one also disclosed the allegation verbally, and one perpetrator confessed. CONCLUSIONS: These results neither support nor refute validation of facilitated communication. However, many children had other evidence of sexual abuse, suggesting that each child's case should be evaluated without bias.

Adolescent↗
PubMed1994

Spontaneous abortion in immunodeficient SCID mice.

PROBLEM: Immunodeficient SCID mice on the CB-17 have been used to test the role of "rejection" in a xenogeneic blastocyst transfer model of recurrent miscarriage, but interpretation of the data requires knowing syngeneic within-species matings have a high success rate and do not require immunotrophic factors expected only in immunocompetent non-T-cell deficient mice. METHOD: Resorption rates were studied in a SCID CB-17 barrier facility that provided the mice used to test the role of immunology in the resorption model. RESULTS: Spontaneous resorption in syngeneically mated immunodeficient SCID mice on the CB-17 background occurred at an unexpectedly high rate and could not be prevented by treatment with anti-asialo GM1 antibody or GM-CSF, both of which are effective in ameliorating abortion in DBA/2J-mated CBA/J mice. Immunocompetent CB-17 +/+ mice showed an even higher rate of loss. The latter was also not affected by treatment with antiasialo GM1 antibody or by GM-CSF and was not prevented by tetracycline (which is effective in the DBA/2-CBA/J system) or progesterone treatment. Mating experiments showed a scid/+ x scid@+ cross gave the highest rate of loss, and it appeared that the presence of +/(+)-type embryos in the uterus could be augmenting abortion with selective discrimination against scid/scid embryos. High abortion rates were associated both with appearance of a coagulase-negative Staphylococcus sp. in feces and with loss of one component of the SPF flora. Decidual tissue from mated CB-17 +/+ mice showed premature release of TNF-alpha in absence of TGF-beta 2-related suppressor activity, and vascular lesions (fibrinoid necrosis), varying in extent, were associated with both scid/scid x scid/scid and +/+ x +/+ pregnancies. TNF-alpha also appeared prematurely in pregnant scid/scid mice, but the levels were lower (and areas of necrosis smaller than in +/+ x +/+ pregnancies). Outcrossing onto a C57B1/6 background dramatically reduced the abortion rate, indicating an important genetic effect on susceptibility with heterogeneity protecting against abortion. CONCLUSIONS: SCID mice on the CB-17 background do not have a high rate of successful syngeneic pregnancies, and a TNF-alpha induced vasculopathy may be responsible. Abortion was not caused by immunodeficiency leading to loss of immunotrophism because immunocompetent non-SCID CB-17 mice had a higher rate of loss. Factors augmenting the abortion rate included the presence of embryos of the +/+ genotype in the uterus and treatment with anti-asialo GM1 antibody. Abortion rates were not reduced by treatments effective in the DBA/2-mated CBA/J mouse model but were reduced by re-establishing a new colony with defined flora (a temporary effect) and by outcrossing mice with a different (C57B1/6) background. Together, the data suggest an infectious trigger (identity uncertain) of the vasculopathy and an important genetic influence on susceptibility with heterozygosity and a SCID mouse mutation providing against abortion a degree of protection.

Abortion, Veterinary↗
PubMed1992

Release of a transforming growth factor (TGF)-beta 2-related suppressor factor from postimplantation murine decidual tissue can be correlated with the detection of a subpopulation of cells containing RNA for TGF-beta 2.

Postimplantation murine decidual tissue from allopregnant C3H mice has been shown to release in vitro a potent immunosuppressive factor closely related to transforming growth factor (TGF)-beta 2 but slightly lower in apparent molecular weight. Decidual suppressor factor (DSF) activity was first detected in decidual tissue supernatant at day 9.5 of gestation and reached a plateau by day 10.5 to 12.5. By Northern analysis of decidual and placental tissue with a simian TGF-beta 2 probe, two characteristic TGF-beta 2 mRNA transcripts were detected in decidual tissue. In situ hybridization analysis of C3H implant sites, with the simian (pGEM-G1G2) TGF-beta 2 riboprobe, revealed a small population of TGF-beta 2+ cells localized to postimplantation decidua basalis and metrial gland cell area after day 8.5. On and before day 8.5, when DSF was not detectable, few TGF-beta 2 mRNA+ cells were detected. To test for TGF-beta release in situ, sections of uterine tissue were stained with antibody specific for TGF-beta 2, that identified DSF in Western blots. In postimplantation tissues (day 9.5, 12.5) patchy anti-TGF-beta 2 staining was seen over decidual tissue. Before day 9.5, slight and diffuse staining over decidual tissue was present with more marked staining of extradecidual tissue. Very little staining was noted over day 9.5 decidual tissue by using anti-TGF-beta 1 antibody as a control; however, some staining was seen over postimplantation fetal trophoblast and myometrial tissue. Fractionation of disaggregated postimplantation decidua by velocity sedimentation revealed that TGF-beta 2 mRNA+ cells were predominantly small and sedimented in the same fraction(s) as those cells previously shown to release DSF in vitro. Thus, the release of TGF-beta 2 related DSF correlates with the in situ detection of TGF-beta 2 mRNA and the in situ release of TGF-beta 2 peptide. These studies suggest that DSF may be a form of TGF-beta 2 released by a population of small lymphocytic decidual suppressor cells.

Animals↗
PubMed1990

Murine pregnancy decidua produces a unique immunosuppressive molecule related to transforming growth factor beta-2.

Non-T small lymphocytic suppressor cells in murine allopregnancy release a potent immunosuppressive factor in vitro that is neutralized by rabbit anti-transforming growth factor (TGF)-beta. Previous studies have suggested that the decidual suppressor factor (DSF) is smaller than TGF-beta 1, and in this paper, we show that DSF on HPLC-sieving columns also elutes later than TGF-beta 2. Nevertheless, DSF has the ability to promote anchorage-independent growth of NRK fibroblasts similar to TGF-beta s. Using turkey antibodies specific for TGF-beta 1 or beta 2, we show that DSF is related to TGF-beta 2 rather than TGF-beta 1, and this relationship was confirmed by using a panel of murine mAb to TGF-subtypes. PAGE and Western blotting showed that the TGF-beta 2-reactive molecules in HPLC-purified DSF was slightly smaller than TGF-beta 2 and approximately 20 to 23 kDa. The DSF molecule is therefore closely related to TGF-beta 2 but as released from decidua, differs in size. The TGF-beta 2-related decidual suppressor factor was also obtained from the decidua of synpregnant C.B.-17 severe combined immune deficiency (SCID) and pregnant SCID-BG (C57BL/6 background) mice, confirming the lack of T or B cell dependence of DSF production and the generality of production of a TGF-beta-related suppressor factor by decidua associated with successful pregnancy in mice.

Animals↗