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Objective: To characterize the pre- and postoperative coagulation profiles of patients undergoing adult-to-adult living donor liver transplantation (LDLT), using various coagulation tests and rotational thromboelastometry (ROTEM). Methods: This single-center observational study evaluated the various coagulation profiles of 22 patients (13 men and 9 women). Blood samples were obtained immediately after the induction of anesthesia (PRE) and on postoperative days (PODs) 1, 3, 5, and 7 after LDLT surgery. Results: Most procoagulant factors (fibrinogen, platelet, and coagulation factors II, VII, VIII, and IX) improved to levels equal to or greater than the PRE levels on POD 7. The levels of von Willebrand factor significantly increased after surgery, whereas those of disintegrin-like and metalloproteinase with thrombospondin type 1 motif 13 decreased. Although the thrombin-antithrombin III complex increased immediately after surgery, the plasmin-α 2 plasmin inhibitor complex increased only on POD 7. The level of plasminogen activator inhibitor-1 increased on POD 1, returning to PRE levels on POD 3. Almost all ROTEM parameters were decreased or prolonged, compared to the PRE levels, on POD 7. Conclusions: The values of most coagulation tests showed the improvement or acceleration of coagulability on POD 7 than at PRE, with almost all the ROTEM parameters decreased or prolonged. Therefore, it cannot be concluded whether ROTEM reflects the net effect of hemostatic balance after liver transplantation. Keywords: Living donor liver transplantation, Postoperative hemostatic balance, Rotation thromboelastometry, Coagulation test, Hypercoagulability

We studied the mechanism of eosinophilia in BALB/c-nu/ + (nu/+) and BALB/c-nu/nu (nu/nu) mice infected with Toxocara canis. Eosinophilia with two peaks on days 11 and 21 of infection was observed in infected nu/+ mice, and with a peak on day 11 in nu/nu mice. Interleukin-5 (IL-5) mRNA was expressed on day 5 of infection in the lung and spleen of nu/+ mice and in the lung of nu/nu mice, but not in the spleen of nu/nu mice. Large numbers of eosinophils and lymphocytes infiltrated the lung of both mice I week after infection. The number of larvae in the lung was the largest on day 5. Anti-IL-5 monoclonal antibody (mAb) treatment completely inhibited eosinophilia of both mice, with no change of larval distribution. Administration of anti-CD4 or anti-CD3 mAb markedly reduced the second peak of eosinophilia on day 21 of infection in nu/+ mice, and slightly reduced the first peak of eosinophilia on day 11 in both mice. Anti-CD8 mAb had no effect on the eosinophilia. These results suggest that eosinophilia in both mice is caused by IL-5, and that IL-5 is produced by cells other than CD4+ T cells, in addition to CD4+ T cells. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) usually develops in patients with an individual or family history of allergic diseases, and is characterized by chronic relapsing inflammation seen especially in childhood, association with IgE hyperproduction and precipitation by environmental factors. However, the exact etiology of AD has been unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is required. We found that skin lesions, which were clinically and histologically very similar to human AD, spontaneously appeared on the face, neck, ears and dorsal skin of inbred NC/Nga mice when they were raised in non-sterile (conventional) circumstances, but not under specific pathogen-free conditions. Plasma levels of total IgE in conventional NC/Nga mice were markedly elevated from 8 weeks of age, correlating with clinical skin severity of dermatitis. Immunohistochemical examination of the skin lesion showed increased numbers of mast cells and CD4+ T cells containing IL-4 necessary for IgE synthesis. Thus, NC/Nga mice suffered from dermatitis very similar to human AD with IgE hyperproduction, which may be triggered by some environmental factor(s). [ABSTRACT FROM AUTHOR]

Adiponectin is an insulin-sensitizing adipocyte-derived adipokine. The decrease in plasma adiponectin level (hypoadiponectinemia) is involved in the development of insulin resistance and the resulting type 2 diabetes. Our previous studies have demonstrated that [gamma]-oryzanol (ORZ) from rice bran suppressed NF-[kappa]B activation and increased adiponectin secretion from adipocyte. In this study, we have evaluated effects of oral administration of animal fat (beef tallow) and palmitate on mouse serum adiponectin level. Oral administrations of beef tallow and palmitate significantly suppressed serum adiponectin levels into around half of the initial level from 48 to 96h after administration compared with the case of corn oil (P<0.05). Coadministration of ORZ successfully remedied mouse hypoadiponectinemia induced by ingestion of beef tallow and the relative adiponectin levels attained to 1.66±0.23 at 96h after administration (mean value±s.e., P<0.05). Diverse physiological functions of ORZ in crop bran might be promising us to prevent chronic inflammations in the pathogeneses of the metabolic or insulin resistance syndromes. [ABSTRACT FROM AUTHOR]

Background Atopic dermatitis is a chronic, relapsing inflammatory disorder characterized by pruritic and eczematous skin lesions. Transforming growth factor (TGF)-β1 has been implicated in the suppression of inflammatory responses. Objective The purpose of this study is to determine whether TGF-β1 suppresses skin lesions in a mouse model of atopic dermatitis. Methods We used the NC/Nga strain of mice as an in vivo model of atopic dermatitis. The effects of exogenous TGF-β1 on atopic dermatitis-like skin lesions in NC/Nga mice were evaluated clinically, histologically and immunologically. Results Subcutaneous injection of recombinant TGF-β1 macroscopically suppressed eczematous skin lesions in NC/Nga mice associated with reduced serum immunoglobulin E (IgE) levels. Histological analysis showed that TGF-β1 significantly inhibited the infiltration of inflammatory cells such as mast cells and eosinophils into the skin of NC/Nga mice. Spontaneous interferon (IFN)-γ production from splenocytes of NC/Nga mice was down-regulated by the treatment with TGF-β1 and neutralizing antibody against IFN-γ inhibited skin lesions in NC/Nga mice. The inhibitory effect of TGF-β1 on the skin lesions lasted at least 1 week after cessation of the treatment. Conclusion These findings indicate that TGF-β1 suppressed atopic dermatitis-like skin lesions in NC/Nga mice at least in part through down-regulation of IFN-γ. These results suggest that TGF-β1 may have a therapeutic potential for atopic dermatitis. [ABSTRACT FROM AUTHOR]