bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recovery characteristics and post‐operative delirium after long‐duration laparoscope‐assisted surgery in elderly patients: propofol‐based vs. sevoflurane‐based anesthesia
Authors: Nishikawa K. , Nakayama M. , Omote K. , Namiki A. 
Published: January 2004

Background:  Post‐operative mental dysfunction may be an important problem in elderly patients. This study was designed to compare the effects of propofol and sevoflurane anesthesia on recovery characteristics and the incidence of post‐operative delirium (POD) in long‐duration laparoscopic surgery for elderly patients.Methods:  Fifty ASA physical status I–II patients over the age of 65 scheduled for laparoscopic surgery lasting 3 h or more randomly received propofol (group P, n = 25) or sevoflurane (group S, n = 25) for both induction and maintenance of general anesthesia. Both groups were combined with continuous perioperative epidural analgesia. The level of primary anesthetics was adjusted to maintain changes in mean arterial pressure within 20% of the pre‐anesthetic values. The emergence times from anesthesia (eye opening, extubation, response to command, and orientation) were recorded, and the occurrence of POD was assessed by the delirium rating scale (DRS) during the first 3 days after surgery. All patients received oxygen and continuous epidural analgesia postoperatively.Results:  Immediate emergence, i.e. eye opening and extubation was significantly faster after sevoflurane (P < 0.05). There was no significant difference between the incidences of POD in the two groups during the first 3 days after surgery. The scores for DRS on day 2 and 3 after surgery, however, were significantly higher in group P than in group S (P < 0.01).Conclusion:  Sevoflurane may be preferable to propofol for general anesthesia in combination with epidural analgesia with respect to less effect on mental function during the early postoperative period for long‐duration laparoscopic surgery in elderly patients.
The angiotensin II receptor blocker candesartan improves survival and mesenteric perfusion in an acute porcine endotoxin model
Authors: Laesser M. , Oi Y. , Ewert S. , Fändriks L. , Åneman A. 
Published: January 2004

Background:  Blockade of the angiotensin II type 1 (AT1) receptor has been demonstrated to ameliorate splanchnic hypoperfusion in acute experimental circulatory failure. This study focused on hemodynamic changes and survival in pigs treated with AT1 blockade prior to or during acute endotoxinemia.Methods:  Escherichia coli lipopolysaccharide endotoxin was infused in anesthetized and mechanically ventilated pigs. Systemic, renal, mesenteric and jejunal mucosal perfusion as well as systemic oxygen and acid‐base balance were monitored. The selective AT1 receptor blocker candesartan was administered prior to as well as during endotoxinemia. Control animals received the saline vehicle.Results:  Pre‐treatment with candesartan resulted in higher survival rate (83%, 10 out of 12 animals) compared with 50% (6 of 12) in control animals and 27% (3 of 11) in animals treated during endotoxinemia. Pre‐treatment with candesartan resulted in higher cardiac output, mixed venous oxygen saturation, arterial standard base‐excess, portal venous blood flow during endotoxin infusion compared with controls and animals treated during endotoxinemia. No adverse effects were found on neither systemic nor renal circulation.Conclusion:  The favorable results of AT1 receptor blockade prior to endotoxinemia are lost when blockade is established during endotoxinemia demonstrating the importance of the renin‐angiotensin system and its dynamic involvement in acute endotoxinemic shock.
Effect of desflurane/remifentanil anaesthesia on glucose metabolism during surgery: a comparison with desflurane/epidural anaesthesia
Authors: Schricker T. , Galeone M. , Wykes L. , Carli F. 
Published: January 2004

Background:  The aim of this study was to investigate the effect of general anaesthesia combined with remifentanil or epidural blockade on glucose metabolism during surgery.Methods:  We randomly assigned patients undergoing elective colorectal surgery to receive either desflurane anaesthesia supplemented with intravenous remifentanil (n = 7) or desflurane anaesthesia supplemented with epidural bupivacaine (n = 7). Plasma concentrations of glucose, lactate, free fatty acids (FFA), insulin, glucagon and cortisol were measured before and after 2 h of surgery. Pre‐ and intraoperative whole body glucose production and glucose clearance, an indicator of glucose uptake, were determined by an isotope dilution technique using [6,6–2H2]glucose.Results:  In both groups intraoperative glucose production ( P< 0.05) and uptake ( P< 0.05) decreased. Plasma glucose concentrations ( P< 0.05) increased during surgery but did not exceed the normal range (remifentanil group: 5.7 ± 0.7 mmol l−1, epidural group: 5.8 ± 0.4 mmol l−1). The plasma concentrations of lactate, FFA, insulin and glucagon remained unchanged during the operation. The plasma cortisol concentration in both groups increased intraoperatively (P< 0.05).Conclusion:  Both desflurane/remifentanil and desflurane/epidural anaesthesia decrease the intraoperative rate of whole body glucose production, thereby attenuating the hyperglycaemic response to colorectal surgery.
Are there reliable predictors of postoperative pain?
Authors: Mamie C. , Bernstein M. , Morabia A. , Klopfenstein C. E. , Sloutskis D. , Forster A. 
Published: January 2004

Background:  The purpose of this study was to identify the preoperative determinants of severe postoperative pain.Methods:  Potential predictors were assessed using a questionnaire submitted on the day before surgery. Pain at rest, and pain during coughing/mobilization, were measured using visual analog scales on the day of surgery and on the following 2 days. The type of postoperative pain management was not standardized and was prescribed by the anesthesiologist in charge. Multivariate logistic regression models explaining postoperative pain were developed in Group I, comprising 304 consecutive patients undergoing orthopedic or intraperitoneal surgery, and validated in Group II, comprising 145 independent patients.Results:  Of the 62 variables examined by univariate analysis, only five were found to increase the risk of severe postoperative pain in Group I at rest and six factors during cough/mobilization. In the multivariate model for pain at rest, general anesthesia, expectation of postoperative pain, and chronic sleeping difficulties increased the risk of severe postoperative pain. In Group II, only chronic sleeping difficulties remained (OR: 3.97, 95% Cl: 1.69–9.29). In the multivariate model during cough/mobilization, intraperitoneal surgery, fear of postoperative pain, and having a relative with a history of pain increased the risk of severe postoperative pain in Group I. Intraperitoneal surgery OR 2.45 (95% Cl = 1.01–4.50) and having a relative with a history of pain OR 2.06 (95% Cl = 1.005–4.50) remained in Group II.Conclusion:  Of the many factors that may influence postoperative pain, chronic sleeping difficulties emerge in this population of patients as the strongest determinant of pain at rest. Intraperitoneal surgery and having a relative with a history of pain are the strongest determinants of pain during cough/mobilization. These findings make physiological sense and deserve more attention by anesthesiologists.
Phagocytosis of opsonized apoptotic cells: roles for ‘old-fashioned’ receptors for antibody and complement
Authors: HART S P , SMITH J R , DRANSFIELD I 
Published: January 2004

SUMMARYEfficient phagocytic clearance of apoptotic cells is crucial in many biological processes. A bewildering array of phagocyte receptors have been implicated in apoptotic cell clearance, but there is little convincing evidence that they act directly as apoptotic cell receptors. Alternatively, apoptotic cells may become opsonized, whereby naturally occurring soluble factors (opsonins) bind to the cell surface and initiate phagocytosis. Evidence is accumulating that antibodies and complement proteins opsonize apoptotic cells, leading to phagocytosis mediated by well-defined ‘old-fashioned’ receptors for immunoglobulin-Fc and complement. In this review we summarize the evidence that opsonization is necessary for high capacity clearance of apoptotic cells, which would render putative direct apoptotic cell receptors redundant.
High dose interleukin-12 exacerbatesBordetella pertussisinfection and is associated with suppression of cell-mediated immunity in a murine aerosol challenge model
Authors: CARTER C R D , DAGG B M , WHITMORE K M , KEEBLE J R , ASOKANATHAN C , XING D , WALKER K B 
Published: January 2004

SUMMARYThe in -vivo clearance of Bordetella pertussis infections in murine models in naive mice and animals vaccinated with whole-cell vaccine is considered to be via a Th-1-dependent mechanism in which interleukin-12 (IL)-12 may play a prominent role. It has also been demonstrated clearly that the treatment of animals with macrophage-derived IL-12 administered with an acellular vaccine can increase the efficacy of this vaccine preparation to levels seen with the whole-cell vaccine. However, the effects of exogenously added IL-12 on immune responses in non-vaccinated B. pertussis-challenged mice remain unclear, with two studies giving contradictory findings. In this study we have treated mice with escalating doses of mIL-12 (0·1–10 µg/mouse) prior to challenge with B. pertussis (using an aerosol challenge model of infection). The ability of mice to clear infection was assessed in IL-12 treated and in phosphate buffered saline (PBS) control animals at days 6 and 13 post-challenge. Lymphoid cells were isolated from spleen and cell-mediated immune responses assessed at days 1, 6 and 13 post-challenge. In addition, the direct effects of high-dose IL-12 on challenged mice was assessed by checking natural killer (NK) activity from isolated lung and spleen lymphoid cells as well as interferon-γ (IFN-γ) generation from isolated cells and serum at day 1 post-challenge. The results from this study show that bacterial colonization of the lungs is actually enhanced following treatment with high-dose IL-12. This is associated with impaired cellular immune responses. The mechanisms associated with the immunosuppressive effects of IL-12 are discussed.
Generation of B220low B cells and production of autoantibodies in mice with experimental amyloidosis: association of primordial T cells with this phenomenon
Authors: KAWABE S , ABE T , KAWAMURA H , GEJYO F , ABO T 
Published: January 2004

SUMMARYTo investigate the immunological state in amyloidosis, mice were twice intraperitoneally injected (2-week interval) with casein emulsified in complete Freund's adjuvant. Two weeks after the treatment, amyloid deposits were detected in the spleen and other organs of these mice. The number of lymphocytes yielded by the liver and spleen increased significantly. The most affected lymphocyte subset was found to be B cells, namely, the total number of B cells increased and unusual B220low B cells were newly generated in the liver and spleen. In other words, not only normal B220high B cells but also unusual B220low B cells were detected in these organs of mice with amyloidosis. In parallel with this phenomenon, autoantibodies against denatured DNA were detected in sera. Since such autoantibodies are known to accompany the functional activation of NKT cells, NKT cell-deficient mice were used for the induction of amyloidosis. Such mice showed less formation of amyloidosis and lower levels of autoantibodies in sera. Athymic nude mice were NKT cell-deficient but NK1·1–TCRint cells were present. These athymic mice showed an intermediate induction of amyloidosis. The cytokine profile seen in mice with amyloidosis was the Th0 type, showing simultaneous production of IL-4 and IFNγ. These results suggest that the generation of B220low B cells and the production of autoantibodies in aid of primordial T cells may be major immunological mechanisms in amyloidosis mice.
Blocking B7 and CD40 co-stimulatory molecules decreases antiviral T cell activity
Authors: VERMEIREN J , CEUPPENS J L , HAEGEL-KRONENBERGER H , DE BOER M , BOON L , VAN GOOL S W 
Published: January 2004

SUMMARYInhibition of co-stimulatory signals for T cells by interrupting CD80/CD86–CD28 and CD40–CD154 interactions is a promising approach to prevent transplant rejection and to induce graft tolerance. However, this tolerizing treatment might affect T cell reactivity towards all the antigens to which the immune system is exposed during treatment. We addressed the question whether such inhibition of co-stimulatory ligands on human antigen presenting cells (APC) would affect T cell reactivity against a virus. This was tested in an in vitro system with freshly isolated human monocytes transduced with adenovirus (ad) containing either murine interferon-γ (mIFN-γ) or green fluorescent protein (GFP) as marker transgene. T cells co-cultured with transduced monocytes proliferated and produced cytokines. These ‘primed’ T cells had strong antiviral activity as they subsequently killed ad/GFP-transduced monocytes and reduced mIFN-γ accumulation in coculture with ad/mIFN-transduced monocytes. However, if priming had occurred in the presence of blocking anti-CD40/CD80/CD86 MoAbs, generation of this antiviral activity was completely prevented. Moreover, T cells primed in the absence of co-stimulatory cells failed to proliferate upon restimulation with adenovirus-transduced monocytes. The results confirm that co-stimulatory signals from APC are required for efficient induction of antiviral T cell activity and point to a potential infectious risk of blocking co-stimulatory signals.
Dietary soy phytoestrogens and ERαsignalling modulate interferon gamma production in response to bacterial infection
Authors: CURRAN E M , JUDY B M , NEWTON L G , LUBAHN D B , ROTTINGHAUS G E , MACDONALD R S , FRANKLIN C , ESTES D M 
Published: January 2004

SUMMARYDiets rich in soy phytoestrogens have many potential health benefits but isoflavones such as genistein may suppress cell mediated immune function. The effect of dietary phytoestrogens on the host response to infection has not been extensively examined. Mice were fed a diet containing soy phytoestrogens and infected with Mycobacterium avium to establish a chronic infection and inflammatory response. As phytoestrogens may act through classical oestrogen receptors (ER), mice deficient in ERα signalling and wild type mice were evaluated for a panel of Type 1-associated cytokines (IFNγ, IL-12 and IL-18) in the spleen. IFNγ production in the spleen was increased approximately 4-fold in ERα-deficient mice fed a casein-based diet over wild type mice fed a casein-based diet (P &lt; 0·05), suggesting a role for ERα in suppressing IFNγ production. IL-18 levels in spleens of wild type mice were decreased compared to ERα-deficient mice on a casein diet. Splenic IL-12 and IL-18 levels were not affected in wild type and ERα-deficient mice on the phytoestrogen containing diets, with the exception that whole soy increased IL-12 levels in the tissues of ERα deficient mice. We conclude that ERα and dietary phytoestrogens can influence production of key regulatory cytokines in response to chronic bacterial infection.
Endotoxin stimulates monocyte–endothelial cell interactions in mouse intestinal Peyer's patches and villus mucosa
Authors: ISHII N , TSUZUKI Y , MATSUZAKI K , MIYAZAKI J , OKADA Y , HOKARI R , KAWAGUCHI A , NAGAO S , ITOH K , MIURA S 
Published: January 2004

SUMMARYAlthough monocyte–endothelial cell interactions represent an initial step in controlling the recruitment of monocytes in inflamed tissues, their dynamic processes in microvessels of lymphoid (Peyer's patches) and non-lymphoid (villus) regions in gut-associated lymphoid tissue remain poorly understood. We monitored the migration of fluorescence-labelled monocytes derived from the spleen in intestinal microvessels with or without lipopolysaccharide (LPS) treatment and investigated the role of adhesion molecules, P-selectin, vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). In control mice, there were few interactions between infused monocytes and the endothelium of intestinal microvessels. The monocyte–endothelial interactions (both rolling and adhesion) were significantly increased in intestinal microvessels of LPS-treated mice compared with those in controls. Anti-P-selectin monoclonal antibody (MoAb) significantly suppressed the LPS-induced increase in monocyte rolling in postcapillary venules of Peyer's patches and submucosal venules. Anti-VCAM-1 MoAbs significantly suppressed the LPS-induced increase in monocyte adhesion to postcapillary venules (PCVs) of Peyer's patches, submucosal venules, and villus capillaries. In contrast, anti-ICAM-1 MoAb significantly suppressed the number of adherent monocytes in PCV of Peyer's patches but not in submucosal venules or villus capillaries. These observations demonstrated that LPS treatment resulted in a significant increase in recruitment of monocytes both in microvessels of lymphoid and non-lymphoid regions and that P-selectin, VCAM-1 and ICAM-1 appeared to play important roles in LPS-induced interactions.
Desferrioxamine modulates chemically induced T helper 2-mediated autoimmunity in the rat
Authors: WU Z , HOLWILL S D J , OLIVEIRA D B G 
Published: January 2004

SUMMARYA rise in interleukin (IL) 4-dependent immunoglobulin E (IgE) is a hallmark of the mercuric chloride (HgCl2)-induced Th2-mediated autoimmune syndrome in the Brown Norway (BN) rat, and one of the mediators in allergic asthma in human. Oxidative stress, a potential factor related to the pathogenesis of allergy and asthma, has been shown to up-regulate IL-4 in mast cells and predispose to degranulation in vitro. However, it remains unknown whether oxidative/antioxidative imbalance plays a role in this Th2-driven model of autoimmunity in the rat. Here we show that administration of the non-sulphydryl-containing antioxidant desferrioxamine i.p. and s.c. to BN rats reduces HgCl2-enhanced IL-4 gene expression and inhibits HgCl2-induced Th2-mediated autoimmunity. Desferrioxamine treatment suppresses significantly IgE production and lymphoproliferation, and reduces tissue injury in the form of caecal vasculitis in the HgCl2-induced autoimmune syndrome. These results support a role for oxidative stress in the pathogenesis of the HgCl2-induced Th2-dominated autoimmune syndrome. This finding might have implications for understanding the mechanisms involved in Th2 cell responses as seen in allergy and asthma and thereby aid the development of new therapeutic strategies for these diseases.
Mycobacterial heat shock protein 70 induces interleukin-10 production: immunomodulation of synovial cell cytokine profile and dendritic cell maturation
Authors: DETANICO T , RODRIGUES L , SABRITTO A C , KEISERMANN M , BAUER M E , ZWICKEY H , BONORINO C 
Published: January 2004

SUMMARYCytokines are key modulators of the immune responses that take place in the inflamed synovium of arthritis patients. Consequently, substances that can reverse the inflammatory profile of the inflamed joint are potential tools for clinical management of the disease. Mycobacterial heat shock protein 70 (MTBHSP70) has been found to protect rats from experimentally induced arthritis through the induction of interleukin (IL)-10-producing T cells. In this study, we have demonstrated that MTBHSP70 induces IL-10 production in synoviocytes from arthritis patients and peripheral blood monoculear cells (PBMCs) from both patients and healthy controls. IL-10 production was accompanied by a decrease in tumour necrosis factor (TNF)-α production by synovial cells. Separation studies showed that the target cells were mainly monocytes. Accordingly, we observed that MTBHSP70 delayed maturation of murine bone marrow-derived dendritic cells. Our results suggest that MTBHSP may act on antigen-presenting cells (APCs) to modulate the cytokine response in arthritis and support an anti-inflammatory role for this protein, suggesting that it may be of therapeutic use in the modulation of arthritis.
High levels of type 2 cytokine-producing cells in chronic fatigue syndrome
Authors: SKOWERA A , CLEARE A , BLAIR D , BEVIS L , WESSELY S C , PEAKMAN M 
Published: January 2004

SUMMARYThe aetiology of chronic fatigue syndrome (CFS) is not known. However, it has been suggested that CFS may be associated with underlying immune activation resulting in a Th2-type response. We measured intracellular production of interferon (IFN)-γ and interleukin (IL)-2; type 1 cytokines), IL-4 (type 2) and IL-10 (regulatory) by both polyclonally stimulated and non-stimulated CD4 and CD8 lymphocytes from patients with CFS and control subjects by flow cytometry. After polyclonal activation we found evidence of a significant bias towards Th2- and Tc2-type immune responses in CFS compared to controls. In contrast, levels of IFN-γ, IL-2 and IL-10-producing cells were similar in both study groups. Non-stimulated cultures revealed significantly higher levels of T cells producing IFN-γ or IL-4 in CFS patients. Concluding, we show evidence for an effector memory cell bias towards type 2 responsiveness in patients with CFS, as well as ongoing type 0 immune activation in unstimulated cultures of peripheral blood cells.
Immune responses to glutamic acid decarboxylase and insulin in patients with gestational diabetes
Authors: FÜCHTENBUSCH M , BONIFACIO E , LAMPASONA V , KNOPFF A , ZIEGLER A-G 
Published: January 2004

SUMMARYPregnancy is a natural state of immunoprotection and tolerance. We studied subjects with gestational diabetes (GDM) to evaluate the influence of pregnancy on the humoral immune response to the autoantigen GAD and to injected insulin. Antibodies against glutamic acid decarboxylase (GADA) subclasses and epitope reactivity were determined in 34 GADA-positive pregnant patients with GDM, in 20 GADA-positive relatives of people with TID and in 25 GADA-positive patients with newly diagnosed TID. Partum levels of insulin antibodies (IA), IgG1- and IgG4-IA were measured in 131 women with GDM treated with human insulin from the time of diabetes diagnosis (including 22 with GADA) and were compared to 19 patients with TID after 3 months of insulin treatment. GADA titre and subclasses were similar among all groups. GADA in GDM patients bound fewer epitopes than GADA in relatives of patients with TID (all epitopes being present in 23%versus 65%, P &lt; 0·01). In particular, antibodies to the minor GADA epitopes GAD6596–249, GAD651–100 and GAD67 were less frequent in patients with GDM compared to relatives (P &lt; 0·01). Antibodies to insulin (IA) were found in 17% of patients with GDM. They were more frequent in GDM patients with GADA compared to GADA-negative patients (41%versus 12%, P &lt; 0·005). IgG1 was the dominant insulin antibody subclass response in both patients with GDM and TID but levels of IgG1-IA and IgG4-IA were significantly lower in patients with GDM compared to patients with TID (P &lt; 0·004). Antibody responses in women with gestational diabetes appear to be dampened and restricted, but without change in subclass usage.