The pathology of multiple sclerosis (MS) is characterized by breakdown of the blood-brain barrier (BBB), accompanied by infiltration of macrophages and T lymphocytes into the central nervous system (CNSMultiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS), characterized by neurological symptoms caused by impaired nerve conduction. Clinical signs of MS are a result of inflammatory lesions in the CNS. Early in lesion development there is breakdown of the blood-brain barrier (BBB), allowing mononuclear cells to enter the CNS. These cells form perivascular cell infiltrates (cuffs) and migrate into the parenchyma of the brain. The monocytes become activated to parenchymal macrophages, which engulf and degrade myelin, and oligodendrocyte death occurs.

Objective: This study evaluated the psychological effects of a pre-surgical stress management training (SMT) in cancer patients.Methods: Stress management training comprised four sessions in total: on 5 days and 1 day pre-surgery and on 2 days and 1 month post-surgery. Patients also received audio CDs with relaxation and coping skills exercises. Patients were randomly assigned to the SMT (N = 34) or a regular care condition (N = 36). Depression, anxiety, quality of life, perception of control, fatigue, pain, sleep problems, and surgery-related somatic symptoms were measured at Day 6 and Day 1 pre-surgery, and Day 2, 5, 30 and 90 post-surgery.Results: Depression and fatigue decreased in the intervention group and increased in the control group, leading to significant group differences at Day 2 (fatigue) and Day 5 post-surgery (fatigue and depression). It also appeared that surgery-related symptoms had increased more in the control group 3 months post-surgery than in the SMT group. No intervention effects were observed for anxiety, pain, and sleep problems.Conclusion: The use of a short psychological intervention is effective in reducing depression and fatigue in the post-surgical period, although the effects are of short duration.

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Metastasis to the liver is a common event in clinicaloncology. Blood-borne tumor cells (TCs) arriving to the coined the term metastasis in 1829 in his treatise ''Reliver sinusoids run into a special vascular bed. The lining cherches du Cancer,'' the metastatic cascade has been of liver sinusoids is shared by Kupffer cells (KCs) and exhaustively studied.1,2 Metastases originate from a seendothelial cells. KCs, liver-fixed macrophages, are re-lective population of cells within the great biological sponsible for detection and removal of ''non-self'' parti-heterogeneity of the tumor.3 They must invade the vascles. To investigate their role in arresting blood-borne cular wall to be dislodged into the circulation and surTCs and controlling tumor growth, we injected a synge-vive in the blood stream until they arrest at the distant neic colon carcinoma cell line into a mesenteric vein of vascular bed of the target organ by adherence or metwo groups of rats; one group was without Kupffer cells chanical trapping. Then, they have to proliferate to iniand the other normal controls. We removed the liver of tiate a metastatic colony. these animals at different time intervals and performedLiver metastasis is a common event in cancer paimmunohistochemical analysis with monoclonal antitients. This is of particular relevance for neoplasias of bodies (MoAbs) against our tumor cell line, three macrophage subpopulations, natural killer cells, and B and T the gastrointestinal tract, because the liver is the first lymphocytes. Additionally, we showed in vitro spontane-vascular bed to be encountered by blood-borne tumor ous cytotoxicity of KCs against our tumor cell line. Re-cells (TCs) through the portal system. 4 The lumen of sults suggest that KCs play a relevant role in arresting liver sinusoids differ from the ordinary capillaries in circulating TCs at the liver sinusoid, although it is lim-that, besides endothelial cells, the stellate cells of von ited to a small number of malignant cells. They also seem Kupffer are lining the sinusoid wall.5 Kupffer cells to play a major role in clearing neoplastic cells from the (KCs) represent one of the largest populations of the liver parenchyma, in controlling tumor growth in the mononuclear phagocyte system in the body. Their privery early stages of metastatic development, and in mod-mary function is to discriminate between ''self'' and ulating the host immune response to cancer cells. (HEPA-''non-self'' particles, playing a prominent role as anti-

Laparoscopic surgery preserves the postoperative immunological defenses. In the future, this may imply a lower number of infections, less local recurrence and even fewer distant metastases. Prospective randomized studies are necessary to see whether these suspected advantages can be demonstrated in clinical practice.

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Patients treated with continuous ambulatory peritoneal dialysis (CAPD) may suffer from recurrent peritonitis episodes caused by Staphylococcus epidermidis. Early recruitment of granulocytes from the peripheral blood is important for the peritoneal antibacterial defense of CAPD patients. In this study, human peritoneal mesothelial cells were shown to produce high levels of interleukin-8 (IL-8) in response to IL-1 beta and tumor necrosis factor-alpha (TNF alpha) but not lipopolysaccharide or S. epidermidis. Coculture of peritoneal macrophages with S. epidermidis induced high levels of IL-1 alpha, IL-1 beta, and TNF alpha in 24-h-conditioned medium. Preincubation of this medium with anti-TNF alpha, anti-IL-1 alpha, or anti-IL-1 beta partially blocked stimulation of IL-8 production by mesothelial cells. Added together, these antibodies abolished IL-8 production to a level just above background. Migration of granulocytes to the stimulated mesothelial cell-conditioned medium could be totally blocked with rabbit polyclonal anti-IL-8 antibody. Thus, mesothelial cells are important for the recruitment of granulocytes into the peritoneal cavity.

Scarless wound healing is a unique and intrinsic capacity of the fetal skin that is not fully understood. Further insight into the underlying mechanisms of fetal wound healing may lead to new therapeutic approaches promoting adult scarless wound healing. Differences between fetal and adult wound healing are found in the extracellular matrix, the inflammatory reaction and the levels of growth factors present in the wound. This review focuses specifically on transforming growth factor β (TGF-β), as this growth factor is prominently involved in wound healing and fibroblast-to-myofibroblast differentiation. Although fetal fibroblasts do respond to TGF-β, they lack a proliferative and a contractile response and display short-lived myofibroblast differentiation, autocrine response, and collagen up-regulation in comparison with adult fibroblasts. Curiously, prolonged TGF-β activation is associated with fibrosis, and therefore, this short-lived response in fetal fibroblasts might contribute to scarless healing. This review gives an overview of the current knowledge on TGF-β signaling and the intracellular TGF-β signaling pathway in fetal fibroblasts. Furthermore, this review also describes the various components that regulate the cellular TGF-β response and hypothesizes about the possible roles these components might play in the altered response of fetal fibroblasts to TGF-β.