bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuroimmunomodulatory Effects of Morphine in <i>Leishmania donovani</i>-Infected Hamsters
Authors: Singal Priya , Kinhikar Arvind G. , Singh Savita , Singh Prati Pal 
Published: May 2003

<i>Objective:</i> The effect of morphine on host defense during <i>Leishmania donovani</i> infection in golden hamsters was studied. <i>Methods:</i> Hamsters were intracardially infected with <i>L. donovani</i> amastigotes and then monitored by spleen touch print microscopic examination. Morphine and naloxone were administered subcutaneously and intraperitoneally, respectively. Leukocytes were counted by a hemocytometer, and ex vivo phagocytosis was determined by the examination of stained adherent macrophages. <i>Results:</i> Low doses of morphine, 1.75 and 2.5 mg/kg × 2, administered subcutaneously on day 0 and day 15 significantly (p < 0.05) suppressed the infection, whereas high doses (20.0 and 50.0 mg/kg × 2) exacerbated the infection. On day 30, hamsters treated with low doses of morphine showed a significant (p < 0.05) increase in the number of circulating leukocytes and the pool size and phagocytic activity of peritoneal macrophages ex vivo; in hamsters treated with high doses, all these parameters appeared to be diminished. The bone marrow of morphine-treated hamsters showed a fall in total cellularity and no change in the number of monocytes; however, in those treated with low doses, the infection was completely eliminated by day 30, and paradoxically, a significant (p < 0.05) potentiation of infection was observed in hamsters treated with high doses. The spleens of hamsters treated with both low and high doses of morphine showed a significant (p < 0.05) decrease and increase in weight, respectively; treatment with low doses also caused an almost 2-fold increase in the percentage of monocytes. Morphine apparently exerted its protective effects via naloxone-sensitive opioid receptors; naloxone pretreatment did not affect the potentiation of infection. <i>Conclusion:</i> Conditional doses of morphine apparently biphasically modulated the course of <i>L. donovani</i> infection in hamsters, at least in part through macrophage-mediated mechanisms.
Noninvasive Monitoring of Cerebral Oxygenation during Vasomotor Reactivity Tests by a New Near-Infrared Spectroscopy Device
Authors: Terborg Christoph , Birkner Thomas , Schack Bärbel , Weiller Cornelius , Röther Joachim 
Published: May 2003

<i>Background:</i> Spatially resolved spectroscopy is a recently developed technique for noninvasive monitoring of cerebral tissue oxygenation using the photon diffusion theory. <i>Methods:</i> We studied this technique with a new, commercial near-infrared spectroscopy (NIRS) device during vasomotor reactivity tests in 28 healthy volunteers (mean age 31.0 years; SD 10.6 years) and compared it with values assessed by the modified Beer-Lambert law and indices from simultaneous transcranial Doppler sonography of both middle cerebral arteries. We measured O<sub>2</sub> reactivity as percentage change of cerebral blood flow velocity (CBFV), as absolute change in the concentrations (measured in µmol/l) of oxygenated (HbO<sub>2</sub>), deoxygenated (Hb) and total hemoglobin (HbT), and as change in the tissue oxygenation index (TOI) during inhalation of 100% oxygen. CO<sub>2</sub> reactivity was calculated as percentage change of CBFV (NCR), as absolute change in the concentrations of HbO<sub>2</sub>, Hb, and HbT (µmol/l), and as change in TOI (%) per 1% increase in end-tidal CO<sub>2</sub>. <i>Results:</i> One hundred percent oxygen inhalation lead to a decrease in CBFV (mean ± SD: left –8.0 ± 7.0%, p = 0.000; right –9.6 ± 7.6%, p = 0.000), an increase in HbO<sub>2</sub> (0.99 ± 1.07 µmol/l), Hbdiff (2.23 ± 1.72 µmol/l), and TOI (3.1 ± 1.5%), and a decrease in Hb (–1.22 ± 0.74 µmol/l), significant from baseline values (p = 0.0000). CO<sub>2</sub> reactivity was: NCR left 25.4 ± 14.7%; NCR right 25.9 ± 13.4%; HbO<sub>2</sub> 1.99 ± 0.97 µmol/l; Hb –1.24 ± 0.81 µmol/l; HbT 0.81 ± 1.0 µmol/l, and TOI 3.7 ± 2.2%. O<sub>2</sub> reactivity in TCD did not correlate with NIRS reactivities (Pearson p > 0.05), but NCR did correlate with changes in HbO<sub>2</sub>, Hb, and TOI (Pearson p < 0.01). TOI was closely related to indices derived from the Beer-Lambert law (Pearson p < 0.03), but not with mean arterial blood pressure or skin blood flow during vasomotor reactivity tests. <i>Conclusion:</i> Spatially resolved spectroscopy provides an encouraging, noninvasive new tool to study cerebral tissue oxygenation during vasomotor reactivity tests consistent with physiological changes.
Imipramine-Induced Antinociception in the Formalin Test
Authors: Zarrindast Mohammad-Reza , Vousooghi Nasim , Sahebgharani Mousa 
Published: May 2003

This study concerned the effect of swim stress on imipramine-induced antinociception in mice. The data showed that intraperitoneal (i.p.) administration of different doses of imipramine (10–40 mg/kg) and 0.5–3 min of swim stress (17°C) induced antinociception in the first and second phases of the formalin test. Low period of swim stress (10 s) with low doses of imipramine (2.5, 5 and 10 mg/kg i.p.), which did not have any effect by themselves, in combination showed antinociception in the second phase of the test. Either yohimbine (0.5 mg/kg i.p.) or naloxone (1 mg/kg i.p.) reversed the response induced by the combination of low doses of imipramine plus swim stress. Yohimbine (1 mg/kg i.p.) decreased the response of imipramine (20 mg/kg i.p.) but not that of 30 s swim stress in the second phase. However, naloxone (1 mg/kg i.p.) reduced the antinociception induced by imipramine (20 mg/kg i.p.) or 30 s swim stress in the second phase of the test, the combination of imipramine with swim stress was not altered by yohimbine or naloxone. Prazosin induced antinociception by itself in the first phase of the test and increased swim-stress-induced antinociception with no interaction. It is concluded that antinociception induced by imipramine in the second phase of formalin test may be mediated through α<sub>2</sub>-adrenoceptor antagonists. The results indicate that the responses of swim stress and imipramine may be mediated by an opioid mechanism, but the combination of both drugs induced higher antinociceptive effects.
Regulation of Gonadotropin Releasing Hormone Release by Neuropeptide Y at the Median Eminence during the Preovulatory Period in Ewes
Authors: Advis J.P. , Klein J. , Kuljis R.O. , Sarkar D.K. , McDonald J.M. , Conover C.A. 
Published: May 2003

The median eminence (ME) of the hypothalamus is known to be an important brain site where hypophysiotropic release might be regulated by excitatory and inhibitory signals impinging on their neuronal terminals. Since a role for neuropeptide Y (NPY) on preovulatory luteinizing hormone (LH) release has been suggested, we hypothesized that NPY might act at the ME to control preovulatory gonadotropin-releasing hormone (GnRH) release and thus the onset of the preovulatory surge of LH. To examine this possibility, we used the ewe as an animal model to determine: (a) immunocytochemical distribution of GnRH and NPY in the ewe ME; (b) changes in in vivo release of NPY and GnRH using ME push-pull cannula (PPC) perfusate samples, as well as in plasma LH, during the luteal, follicular and preovulatory phases of a synchronized estrous cycle, and (c) effects of ME perfusion of NPY or a Y1-NPY antagonist, or an NPY antiserum on in vivo release of ME-GnRH and plasma LH during a synchronized follicular phase. Immunolocalization reveals a dense plexus of beaded GnRH-containing neurites in the arcuate nucleus and in its vicinity, the pituitary stalk and the palisade. In contrast, a dense plexus of NPY-containing neurites occurs in the internal layer, with occasional fibers found in the intermediate and lateral external zone of the ME. In the area between the lateral internal and lateral external layers, both NPY and GnRH-containing processes were found, thus providing opportunities for synaptic and/or paracrine interactions between NPY- and GnRH-containing neurons. Hormonal analysis indicated that a synchronized preovulatory surge of LH is elicited within a 2-hour window by the sequential implantation and removal of silastic-encased estradiol (E2) or progesterone (P4) implants. In this paradigm, there was a parallel increase in ME release of both NPY and GnRH preceding the synchronized LH surge. The onset of this synchronized LH surge was advanced by ME perfusion of exogenous NPY and was both delayed and blunted by ME perfusion with the NPY antagonist (both were perfused through the PPC probe for 2 h, starting 2–3 h before the expected onset of the LH surge). In addition, NPY perfusion in the ME increases, while perfusion of the Y1-NPY antagonist or of the NPY antiserum decreases ME-PPC GnRH content and plasma levels of LH in early follicular ewes. Finally, perfusion of NPY antiserum during an ongoing LH surge disrupted LH release. These results suggest that interactions between NPY and GnRH neurons are important in controlling the timing, magnitude and maintenance of the preovulatory LH surge.
Embryonic Blastemic Changes in Retinoic Acid-Induced Hindlimb Deformity
Authors: Santos-Alvarez Inmaculada , Martos-Rodríguez Antonia , Delgado-Baeza Emilio 
Published: May 2003

In this study we analyzed, on an experimental model, blastemic changes occurring during the embryonic period that may later cause fetal hindlimb deformity. Experimental induction of clubfoot-like deformity in rat fetuses was performed by maternal administration of retinoic acid (RA) (120 mg/kg body weight) as a single intragastric dose on day 10 of pregnancy (previous phase of this assay). The caudal and hindlimb blastemic changes were studied by mitosis count and stereological, immunohistochemistry and AgNOR techniques in the hindlimbs of 15-day embryos and in the caudal somites of 11-day embryos. In 15-day embryos from the assay group, hypoplasia and misorientation of hindlimbs were present in 90% of the cases. The histological study showed a blastemal defect as follows: (a) reduction in mesenchymal cell activity (mitotic and AgNOR activities); (b) increase of volume of vascular lumen; (c) reduction in volume of nerve structures, and (d) reduction in the percentage of pre-rhabdomyoblastic cells. In 11-day embryos from the assay group, caudal somites showed disruption, including loss of usual morphology. Moreover, somitic AgNOR activity decreased compared to the control group. The greatest reduction in the number of black-dots per cell was in the myotome. These findings suggest that a certain pathology of the somites, very little studied to date, might be involved in clubfoot pathogenesis.
Stimulation of Bronchus-Associated Lymphoid Tissue in Rats by Repeated Inhalation of Aerosolized Lipopeptide MALP-2
Authors: Lührmann A. , Tschernig T. , Pabst R. 
Published: May 2003

<i>Objective:</i> Bronchus-associated lymphoid tissue (BALT) is a part of the integrated mucosal immune system. It may play an important functional role for antigen uptake and induction of specific immune reactions. The aim of this study was to investigate whether it is possible to induce or modulate BALT by the repetitive inhalation of the synthetic lipopeptide MALP-2. <i>Methods:</i> Female Lewis rats (245 ± 19 g) inhaled 25 µg of MALP-2 six times at intervals of 1 week. One week after the last inhalation, they were sacrificed. Cells of the bronchoalveolar lavage and the left lung were investigated by flow cytometry. The middle lobe of the right lung was embedded in paraffin. BALT was semiquantitatively measured in 15 serial cross sections per animal. <i>Results:</i> After repetitive inhalation of the diluent as well as MALP-2, BALT was found. The total area was increased after repetitive treatment with MALP-2. In addition, the preferential incidence of BALT was higher after MALP-2 application, in association with a bronchial diameter of 0.6–1 mm. The cellular analysis revealed no differences in the number of leukocyte subsets between the control and MALP-2 group. <i>Conclusion:</i> MALP-2 is a potent local stimulator and can be used to modulate BALT by repetitive inhalant treatment. The functional significance of enlarged or activated BALT has to be elucidated in future studies.
Acceptability for the Use of Postpartum Intrauterine Contraceptive Devices: Assiut Experience
Authors: Mohamed Safwat A. , Kamel Momen A. , Shaaban Omar M. , Salem Hossam T. 
Published: May 2003

<i>Objectives:</i> To evaluate the acceptance of postpartum intrauterine contraceptive devices (PPIUCD) among the inhabitants of Assiut governorate, Egypt and to study the factors that influence this acceptance. <i>Subjects and Methods:</i> Contraceptive counseling was given to 3,541 clients: 1,880 and 1,661 during the antenatal visits and postpartum hospitalization, respectively. Acceptors during antenatal counseling were to receive IUCDs via postplacental insertion in the case of vaginal delivery or transcesarean insertion in case of abdominal delivery. The clients who refused PPIUCD and chose interval IUCD insertion were referred to the Family Planning Clinic after the end of puerperium. Among postpartum counselees, PPIUCD acceptors received predischarge insertion within 48 h of delivery and the interval IUCD were referred to have IUCD inserted after the end of puerperium. The acceptance rate of both PPIUCD and interval IUCD and the percentage of actual insertions were recorded. The causes of both acceptance and refusal were also recorded. <i>Results:</i> Of the 3,541 clients, 1,024 (28.9%) accepted the use of IUCD after delivery. Acceptance was approximately the same during antenal and postpartum counseling: 26.4 and 31.8%, respectively. Verbal acceptance was higher among women with formal education than among illiterate women. Planning another pregnancy in the near future, preference for another contraceptive method, namely lactational infertility, and complications from previous use of IUCD were the most common reasons for refusing the use of IUCD. Of the 1,024 verbal acceptors, only 243 (23.7%) had the actual insertion of IUCD. <i>Conclusion:</i> Both the acceptance and actual insertion of IUCD were low probably because the use of IUCD is a new concept in the community. For these women, the only opportunity to receive information about contraceptives is during childbirth when they are in contact with medical personnel. Hence, it is suggested that family planning should be integrated with maternal and child-care services in order to effectively promote the use of contraceptive devices in these women who otherwise would not seek the use of such a device.
Angiogenin: A Novel Inhibitor of Neutrophil Lactoferrin Release during Extracorporeal Circulation
Authors: Schmaldienst Sabine , Oberpichler André , Tschesche Harald , Hörl Walter H. 
Published: May 2003

Degranulation of polymorphonuclear leukocytes (PMNL) occurs during extracorporeal circulation. A degranulation-inhibiting protein identical to angiogenin was recently isolated from high-flux dialyzer ultrafiltrate. This protein inhibits the release of lactoferrin and metalloproteinases from PMNL in vitro. In the present study, we investigated end-stage renal disease patients undergoing regular hemodialysis treatment with either high-flux dialyzers (n = 51) or low-flux dialyzers (n = 44), and chronically uremic patients undergoing hemodiafiltration (n = 30). Hemodialysis therapy with low-flux polysulfone or cellulose triacetate membranes caused no or only minimal reduction (≤8%) of plasma angiogenin levels within 2 h of dialysis treatment associated with a 1.6-fold lactoferrin release from PMNL. Hemodialysis therapy with high-flux membranes (e.g. cellulose triacetate, polymethylmethacrylate) or hemodiafiltration resulted in a reduction of plasma angiogenin levels by 20–40% after 2 h associated with a nearly 4-fold PMNL lactoferrin release. The release of PMNL elastase was not affected by the different treatment modalities used. We conclude that high angiogenin plasma levels protect against lactoferrin release from PMNL during extracorporeal circulation in chronically uremic patients. A decrease of plasma angiogenin between 20 and 40% during extracorporeal circulation, however, results in marked PMNL lactoferrin release. This novel mechanism may explain, at least in part, PMNL degranulation also in non complement activating high-flux membranes.
Activation of CR3-mediated phagocytosis by MSP requires the RON receptor, tyrosine kinase activity, phosphatidylinositol 3-kinase, and protein kinase C ζ
Authors: Lutz Michael A , Correll Pamela H 
Published: May 2003

Abstract
Macrophage-stimulating protein (MSP) promotes the phagocytosis of C3bi-coated erythrocytes by resident peritoneal macrophages, although the mechanism by which this occurs is largely unknown. We show that MSP-induced complement-mediated phagocytosis requires the RON receptor tyrosine kinase and the αMβ2 integrin, as evidenced by the inability of RON−/− and αM−/− peritoneal macrophages to augment phagocytosis of complement-coated sheep erythrocytes in response to MSP. MSP stimulation of macrophages results in tyrosine phosphorylation and AKT activation, and inhibitor studies demonstrate a phagocytic requirement for tyrosine kinase and phosphatidylinositol 3-kinase (PI-3K) activity as well as activity of the atypical protein kinase C (PKC) isoform ζ, which localizes to MSP-induced phagosomes containing complement-coated beads. Additionally, MSP augments the ability of peritoneal macrophages to bind to intercellular adhesion molecule-1 (ICAM-1) via the αMβ2 integrin. MSP-induced ICAM-1 adhesion is also dependent on tyrosine kinase activity, PI-3K, and PKC ζ, indicating that these signaling requirements are upstream of complement receptor 3 activation.
Up-regulated expression of MICA on activated T lymphocytes involves Lck and Fyn kinases and signaling through MEK1/ERK, p38 MAP kinase, and calcineurin
Authors: Molinero Luciana L , Fuertes Mercedes B , Fainboim Leonardo , Rabinovich Gabriel A , Zwirner Norberto W 
Published: May 2003

Abstract
Major histocompatibility complex class I-related chain (MICA) is a cell stress-regulated molecule recognized by cytotoxic cells expressing the NKG2D molecule. MICA can be induced on T cells after CD3 or CD28 engagement. Here, we investigated the intracellular pathways leading to activation-induced expression of MICA. The Src kinase inhibitor PP1 inhibited up-regulated expression of MICA on anti-CD3-stimulated T cells. Downstream signaling routes involved mitogen-activated protein kinase (MAPK) kinase (MEK)1/extracellular signal-regulated kinase (ERK), p38 MAPK, and calcineurin, as MICA expression was prevented by U0126, SB202190, cyclosporin A, and FK506. Also, Lck and Fyn as well as MEK1/ERK and p38 MAPK were found to regulate MICA expression in anti-CD28/phorbol 12-myristate 13-acetate-stimulated T cells. Expression of MICA on activated T cells involved interleukin-2-dependent signaling routes triggered by Janus tyrosine kinases/signal transducer and activators of transcription and p70S6 kinase, as it could be inhibited by AG490 and rapamycin. This is the first demonstration of the intracellular pathways involved in activation-induced expression of MICA, which may reveal potential targets for immune intervention to modulate MICA expression in pathological disorders.
Essential involvement of IL-6 in the skin wound-healing process as evidenced by delayed wound healing in IL-6-deficient mice
Authors: Lin Zi-Qing , Kondo Toshikazu , Ishida Yuko , Takayasu Tatsunori , Mukaida Naofumi 
Published: May 2003

Abstract
To clarify interleukin (IL)-6 roles in wound healing, we prepared skin excisions in wild-type (WT) and IL-6-deficient BALB/c [knockout (KO)] mice. In WT mice, the wound area was reduced to 50% of original size at 6 days after injury. Microscopically, leukocyte infiltration was evident at wound sites. Furthermore, the re-epithelialization rate was ∼80% at 6 days after injury with increases in angiogenesis and hydroxyproline contents. The gene expression of IL-1, chemokines, adhesion molecules, transforming growth factor-β1, and vascular endothelial growth factor was enhanced at the wound sites. In contrast, the enhanced expression of these genes was significantly reduced in KO mice. Moreover, in KO mice, the reduction of wound area was delayed with attenuated leukocyte infiltration, re-epithelialization, angiogenesis, and collagen accumulation. Finally, the administration of a neutralizing anti-IL-6 monoclonal antibody significantly delayed wound closure in WT mice. These observations suggest that IL-6 has crucial roles in wound healing, probably by regulating leukocyte infiltration, angiogenesis, and collagen accumulation.
Ly49E expression points toward overlapping, but distinct, natural killer (NK) cell differentiation kinetics and potential of fetal versus adult lymphoid progenitors
Authors: Stevenaert Frederik , Van Beneden Katrien , De Creus An , Debacker Veronique , Plum Jean , Leclercq Georges 
Published: May 2003

Abstract
Using a new antibody, we found previously that contrary to adult natural killer (NK) cells, fetal NK cells have a unique phenotype, as they exclusively express Ly49E. This can be explained by an intrinsic different NK differentiation potential of fetal versus adult lymphoid progenitors, by immaturity of fetal NK cells or by instability of Ly49E expression. Here, we show that adult progenitor cells were still capable of differentiating into Ly49E-expressing NK cells but at a much lower frequency. Surprisingly, Ly49E expression in vitro did not require stromal cells. Kinetic analysis in vivo showed that Ly49E was expressed early, together with CD94/NKG2 and Ly49G2, followed by Ly49C, and finally Ly49D. Transfer of sorted Ly49E-positive fetal NK cells showed stable Ly49E expression, and later, part of these cells up-regulated other Ly49 members. These data indicate that although there are intrinsic differences, there is no strict fetal and adult wave of NK cell differentiation.
The effect of phosphatases SHP-1 and SHIP-1 on signaling by the ITIM- and ITAM-containing Fcγ receptors FcγRIIB and FcγRIIA
Authors: Huang Zhen-Yu , Hunter Sharon , Kim Moo-Kyung , Indik Zena K , Schreiber Alan D 
Published: May 2003

Abstract
Inositol and tyrosine phosphatases have been implicated in inhibitory signaling by an Fc receptor for immunoglobulin G, FcγRIIB, in B cells, mast cells, and monocytes. Here, we propose a role for the Src homology 2 (SH2)-containing tyrosine phosphatase-1 (SHP-1) in FcγRIIB-mediated inhibition of FcγR signaling. Coexpression of SHP-1 enhances FcγRIIB-mediated inhibition of FcγRIIA phagocytosis in COS-1 cells. SHP-1 also enhances the reduction in FcγRIIA tyrosine phosphorylation that accompanies this inhibition. Significantly, tyrosine phosphorylation of Syk kinase is substantially inhibited by SHP-1. Furthermore, the activation of SHP-1 tyrosine phosphorylation is observed following stimulation of FcγRII in COS-1 cells and in human monocytes. The SH2 domain containing inositol phosphatase (SHIP), SHIP-1 also enhances FcγRIIB-mediated inhibition of FcγRIIA, indicating that FcγRIIB can use more than one pathway for its inhibitory action. In addition, SHP-1 and SHIP-1 can inhibit FcγRIIA phagocytosis and signal transduction in the absence of FcγRIIB. The data support emerging evidence that SH2-containing phosphatases, such as SHP-1 and SHIP-1, can modulate signaling by “activating” receptors.