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Objectives: Immunoglobulin treatment is known to suppress atherosclerosis in apolipoprotein E-deficient mice. In addition, immunoglobulin inhibits atherosclerosis via the Fc receptors. However, the effect of immunoglobulin treatment at the advanced stage of atherosclerosis is still unclear. This study examined the effects of immunoglobulin on apolipoprotein E-deficient mice at the advanced stage of the disease., Methods: Atherosclerosis was induced in mice fed a high-fat diet containing 0.3% cholesterol. After confirming the presence of atherosclerotic lesions at 11 weeks, mice were intraperitoneally treated with injections of either intact type of immunoglobulin (1 g/kg/day) or F (ab') 2 fragments of immunoglobulin (1 g/kg/day) on alternate days over 4 weeks. Oil red-O staining and immunohistochemical staining with CD4+ cells were performed of the aorta, and atherosclerotic lesions was evaluated and compared between the groups., Results: Fatty streak lesion was significantly suppressed by intact immunoglobulin compared with saline, and inflammatory cell infiltration and expression of CD4+ cells were less in mice treated with intact immunoglobulin compared with the control., Conclusions: Immunoglobulin treatment even at the advanced stage of atherosclerosis suppressed the development of fatty lesions and may stabilize atherosclerotic plaques by inhibiting inflammatory cell expression. Immunoglobulin suppression of atherosclerosis was confirmed to act via the Fc receptors.

Aim: The relationships among behavioral and psychological symptoms of dementia (BPSD), cognitive impairment of Alzheimer's disease (AD) patients and the caregiver burden of their caregivers were investigated in an outpatient memory clinic., Methods: Forty-six pairs of AD patients and their family caregivers were involved in this study. Neuropsychiatry Inventory (NPI) was used to estimate BPSD, to which memory symptoms were added as a subcategory of BPSD. MMSE, word fluency, clock drawing test and category-cued memory test were used for cognitive measurement. Zarit burden interview (ZBI) and CES-D were used to assess caregiver burden., Results: Among 11 BPSD subcategories, memory symptoms, apathy, depression, delusion, aggression and anxiety were prevalent BPSD was a strong determinant of caregiver burden. Among BPSD symptoms, anxiety, aggression and aberrant motor behavior were significantly related to ZBL In terms of the relationship between BPSD and cognitive impairment, the scores for delusion and apathy were significantly related to the cognitive decline. On the other hand, patients who showed symptoms related to memory and depression had higher cognitive function than those who did not., Conclusion: These analyses will contribute to better assessment of AD patients and their caregivers, hopefully resulting in better support for them.

In this study, we focused on acceptance of memory impairment and satisfaction with life in patients with mild to moderate Alzheimer's disease (AD). We interviewed 71 consecutive patients with AD and asked (1) whether they had memory loss, (2) whether they found trouble in life, and (3) how their daily life was. We categorized the patients into three groups based on awareness of memory loss and reference to the cause of memory loss. Cognitive functions were lower in patients who were not aware of memory loss. The rate of satisfaction with life was the highest in patients who were not aware of memory loss, and was the lowest in patients who complained of memory loss with reference to the cause of memory loss, indicating that patients could hardly accept their lives when memory impairment was a serious issue. However, in these patients, depression scores were not high, suggesting that they may somehow adapt themselves to their current status by defining the reason for memory loss. In patients who complained of memory impairment but did not refer to the cause of memory loss, there was a variation in awareness of memory loss and satisfaction with life. The present study indicated that we have to provide individual care and support for AD patients considering their level of acceptance of memory impairment.

One of the critical events in the early stage of atherosclerosis is the focal accumulation of lipid-laden foam cells derived from macrophages. In various cholesterol-fed animal models of atherosclerosis, it was found that localized attachment of circulating monocytes to arterial endothelial cells appears to precede the formation of foam cells. It has been suggested that monocyte recruitment into early lesions is depend upon the endothelial adhesiveness for monocytes and lymphocytes. In vivo and in vitro experiments have identified molecules, such as ICAM-1, VCAM-1 and P-selecin, those can support the adhesion of monocytes and lymphocytes. Moreover oxidized LDL, lysophosphatidylcholine and oxidized fatty acids induce the expression of not only these adhesion molecules but also scavenger receptors, such as CD-36, SR-A and LOX-1. Recently we isolated and characterized the novel receptors for oxidized LDL, named LOX-1 and SR-PSOX. The expression of LOX-1 is found on endothelial cells, smooth muscle cells and macrophages. Whereas SR-PSOX expresses on macrophages. We address in this paper on the significance of hyperlipidemia, especially oxidized LDL and its receptors in terms of atherosclerosis.

A microemulsion formulation of cyclosporin (Neoral) has been developed to overcome the problems of poor and variable absorption of cyclosporin. Neoral is a potent immunosuppressive agent that is highly bound in the plasma. It has been proposed that low-density lipoprotein (LDL) delivers cyclosporin (CsA) to T-lymphocytes via the LDL receptor pathway, where it produces its therapeutic effects. Herein, we report a case of minimal change nephrotic syndrome with type 2 diabetes mellitus treated by Neoral and fluvastatin. A 65-year-old male with a 10-year history of type 2 diabetes mellitus suddenly developed nephrotic syndrome. The potential causative drugs, such as NSAIDs and antibiotics, had not been administered. The laboratory findings were as follows: proteinuria 23 g/day, serum albumin 1.9 g/dl, total cholesterol 629 mg/dl, LDL-Cho 1,930 mg/dl. Renal biopsy was normal on light microscopy, and immunofluorescence demonstrated no staining. Due to the risk of deterioration of diabetes by administering prednisolone, he was given Neoral at 2.0 mg/kg/day. He was also given fluvastatin (40 mg/day) for hyperlipidemia after the renal biopsy. At four weeks after the start of Neoral and fluvastatin, his nephrosis continued, but his LDL-Cho and total cholesterol decreased. At six weeks after treatment, proteinuria gradually reduced. At eight weeks after treatment, the proteinuria had disappeared. Nephrotic syndrome is often associated with abnormal lipid metabolism, and many patients with nephrotic syndrome show high levels of LDL-Cho. It has been reported recently that LDL apheresis is effective against nephrotic syndrome. However, in the present case, it can be speculated that the improvement of hyperlipidemia by fluvastatin probably augmented the effect of Neoral, presumably through the increased cellular uptake of Neoral. This suggests that fluvastatin may be considered as the treatment of choice for the disturbed lipoprotein profile in patients with nephrotic syndrome.