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Notes: The crystal structure of metastable phase in Ag added Al-Mg-Si alloy was investigatedby comparing the β’-phases in Al-Mg-Si alloy without Ag, using images of high resolutiontransmission electron microscope (HRTEM), selected area electron diffraction patterns (SADPs)and an energy dispersive X-ray spectroscopy (EDS). SADPs and HRTEM images obtained frommetastable phase in the Ag added Al-Mg-Si alloy showed similar to those of β’-phase in Al-Mg-Sialloy without Ag and had different lattice spacings because of the effect of Ag. According to ourcareful analysis on obtained HRTEM images and SADPs, it includes more complicated crystallattice of distorted hexagons

Notes: The purpose of this study is to identify the crystal structure of metastable phase in Agadded Al-Mg-Si alloy to compare the formation of β’-phases in Al-Mg-Si alloys without Ag, usingimages of high resolution transmission electron microscope (HRTEM), selected area electrondiffraction (SAED) patterns and an energy dispersive X-ray spectroscopy (EDS). The result ofSAED patterns and HRTEM images have been simulated and compared with images then SAEDpatterns obtained from actual precipitates. SAED patterns and HRTEM images obtained frommetastable phase in the Ag added Al-Mg-Si alloy showed similar to those of β’-phase in Al-Mg-Sialloy without Ag and the lattice spacings changed because of the effect of Ag

Notes: The purpose of this study is identity the crystal structure of metastable phase in Ag addedAl-Mg-Si alloy by comparing the β’-phases in Al-Mg-Si alloy without Ag, using images of highresolution transmission electron microscope (HRTEM), selected area electron diffraction patterns(SADPs) and an energy dispersive X-ray spectroscopy (EDS). The result of SADPs and HRTEMimages have been simulated and compared with images and SADPs obtained from actualprecipitates. SADPs and HRTEM images obtained from metastable phase in the Ag added Al-Mg-Sialloy showed similar to those of β’-phase in Al-Mg-Si alloy without Ag and had different latticespacings because of the effect of Ag

Notes: It is well known that two different photobiologic processes mainly take place when the human skin is exposed to ultraviolet (UV) light. The long waves of UVA and visible light (320–400 nm) irradiation causes skin tanning by melanocytic activation and the short waves of UVB (280–320 nm) can elicit variety of biologic action in cutaneous keratinocytes, melanocytes and other skin component cells. The sensitivity to the UV lights is generally depending on the three kinds of the skin type classified by the proposal of Pathak et al. [1]. The skin sensitivity of Japanese population, however, seems to be different from that of Caucasian's population because of the differences in genetic background and skin color, as indicated by Satoh and Kawada [2]. They tried to classify into three groups as J-I (always burn and rarely tan), J-II (moderately burn and moderately tan) and J-III (never burn and always tan) by the skin types to UV lights for the sun-tanning and sun-burning. Comparing these two criteria, a general concern indicates that J-I–III may correspond to the skin type II–IV of the Fitzpatrick's classification, respectively. Based on the Japanese skin types, the incidence of skin cancers and precancerous lesions related to the long-term exposure of sun-light was epidemiologically estimated by Araki et al. [3]. According to their results for several years (1992–1998), the overall number of skin cancers and precancerous states in Japanese was demonstrated to be small in comparison with the incidence of Caucasian's population, even though the people sets in areas of higher ambient solar radiation. However, working outdoors having J-I and/or a history of severe sunburn during childhood were found to be important risk factors, particularly among people of over 60 years of age. Regarding skin cancers and sun-exposed areas, we compared between 20 patients with skin cancers (males 13 and females seven) (average 65 years old) (〈link href="#t1-14"〉Table I) and 24 controls (males 10 and females 14), who were selected as similar ages to the patients at random, in their skin types and life environments by a questionnaire system. The skin types of the patients were J-I (15%), J-II (40%), and J-III (35%) and those of controls were J-I (4.2%), J-II (62.5%), and J-III (4.2%), respectively. The patient group tended not to protect from sun exposure and most of them were farmers. UV exposure is known to induce modulation of the skin immune system which Langerhans cells decrease in number in the epidermis, and on the other hand it is supposed that interleukin IL-10 producing macrophages (CD11b+) expand in the dermis. Not only IL-10, but also tumor necrosis factor (TNF)-α from macrophages and mast cells in the dermis seem to increase and suppress Th1 immune responses of the epidermis and Th2 immune responses might be induced by UV irradiation [4]. Recently, it has been reported, however, that in patients with polymorphous light eruption (PLE), the expression of TNF-α, IL-4, and IL-10 is reduced by UVB irradiation and that PLE appearance is related to UVB-induced immunosuppression [5].〈tabular xml:id="t1-14"〉I〈title type="main"〉 Twenty patients with skin cancers (average ages: 65 years old) (Department of Dermatology, Fukushima Medical University Hospital, 2001–2002) 〈table frame="topbot"〉〈tgroup cols="2" align="left"〉〈colspec colnum="1" colname="col1"/〉〈colspec colnum="2" colname="col2"/〉〈thead valign="bottom"〉〈row rowsep="1"〉Skin cancersNumber of patients〈tbody valign="top"〉Malignant melanoma8Squamous carcinoma4Bowen's disease4Basal cell carcinomas3Eccrine porocarcinoma1Location of skin cancersSun-exposed areas9Non-exposed areas11Then, we attempted to study UVB effects on atopic disease and chronic inflamed skin diseases in the therapeutic advantage, although it is harmful for the patients to be cutaneous carcinogenesis. The epidermal keratinocytes are capable of producing CC chemokines in the local Th2 response, as seen in atopic dermatitis, mycosis fungoides, etc. [6]. Thymus and activated-related chemokine (TARC) is one of the chemokines produced by keratinocytes which selectively activate lymphocytes of Th2 subset expressing CCR4 (receptor for TARC) [7]. Accumulating evidence has suggested that these chemokines have primary pathogenic importance in Th2 skin diseases. In order to find the effects of UVB irradiation on the production of TARC, we used a human keratinocyte HaCaT cell line. As assessed by RT-PCR and ELISA, UVB irradiation significantly decreased the expression of TARC mRNA and protein in HaCaT cells stimulated with interferon-γ (IFN-γ) and TNF-α in a dose-dependent manner. The down-regulation of TARC expression may be mediated in part by activation of the particular transcription, signal transducer and activator of transcription 1 (STAT 1), since it has shown that STAT 1 DNA-binding was down-regulated by UVB irradiation. Our results suggest that STAT 1 and other transcription factors play an important biological role in immune system of human skin irradiated by UVB and may support the results of Kolgen et al. [5].In this point of view, UVB irradiation will be a therapeutic tool for skin diseases related to Th2 type reaction, such as atopic dermatitis, mycosis fungoides, etc., although we need to optimize adequately the use of UVB in patients with J-I skin type or those of whom have the episode of severe sun-burn after UVB irradiation.〈section xml:id="abs1-1"〉〈title type="main"〉References1. Pathak, M.A., Nghiem, P. and Fitzpatrick, T.B. Acute and chronic effects on the skin. In: Fitzpatrick's Dermatology in General Medicine, 5th edn (Freedberg, I.M., Eisen, A.Z., Wolf, K., Austen, K.F., Goldsmith, L.A., Katz, S.I. and Fitzpatrick, T.B. eds), pp. 1598–1607. McGraw-Hill, New York (1999).2. Satoh, Y. and Kawada, A. Action spectrum for melanin pigmentation to ultraviolet light, and Japanese skin typing. In: Brown Melanoderma: Biology and Diseases of Epidermal Pigmentation (Fitzpatrick, T.B., Wick, M.M. and Toda, K. eds), pp. 87–95. University of Tokyo Press, Tokyo (1986).3. Araki, K., Nagano, T., Ueda, M., Washio, F., Watanabe, S., Yamaguchi, N. and Ichihashi, M. Incidence of skin cancers and precancerous lesions in Japanese- Risk factors and prevention. J. Epidemiol. 9, S14–S21 (1999).4. Teunissen, M. B., Piskin, G., Nuzzo, S. et al. Ultraviolet B radiation induces a transient appearance of IL-4+ neutrophils, which support the development of Th2 responses. J Immunol. 168, 3732–3739 (2002).5. Kolgen, W., van Meurs, M., Jongsma, M. et al. Differential expression of cytokines in UVB-exposed skin of patients with polymorphous light eruption. Arch. Dermatol. 140, 295–302 (2004).6. Kakinuma, T., Sugaya, M., Nakamura, K., Kaneko, F., Wakugawa, M., Matsushima, K. and Tamaki, K. Thymus and activation-regulated chemokine (TARC/CCL17) in mycosis fungoides: serum TARC levels reflect the disease activity of mycosis fungoides. J. Am. Acad. Dermatol. 48, 23–30 (2003).7. Imai, T., Nagira, M., Tkagi, S. et al. Selective recruitment of CCR4-binding Th2 cells toward antigen-presenting cells by the CC chemokins thymus and activation-regulated chemokine and macrophage-derived chemokine. Int. Immunol. 11, 81–88 (1999).

Notes: Chorea-acanthocytosis (CHAC) is a hereditary neurodegenerative disorder with autosomal recessive transmission, in which selective degeneration of striatum has been reported in brain pathology. Clinically, CHAC shows Huntington's disease-like neuropsychiatric symptoms and red blood cell acanthocytosis. Recently, we identified the gene, CHAC, encoding a novel protein, chorein, in which a deletion mutation was found in Japanese families with CHAC. In the present study, we have identified the mouse CHAC cDNA sequence and the exon–intron structures of the gene and produced a CHAC model mouse introducing no. 60–61 exon deletion corresponding to a human disease mutation by a gene-targeting technique. The mice began to show acanthocytosis and motor disturbance in old age. In behavioral observations, locomotor activity was significantly decreased and the contact time at social interaction test was decreased significantly in the model mice. In the brain pathology, many apoptotic cells were observed in the striatum of the mutant mice. In neurochemical determinations, the dopamine metabolite, homovanillic acid, concentration decreased significantly in the portion including the midbrain of the mutant mice. These findings are consistent with the human results reported elsewhere and indicate that the CHAC model mice showed a mild phenotype with late adult onset. The CHAC model mouse therefore provides a good model system to study the human disease.

Notes: Aims:  Lymphomatous polyposis (LP) is considered to represent mantle cell lymphoma (MCL) of the gastrointestinal (GI) tract. However, a few reports have suggested that some are follicular lymphoma (FL) or mucosa-associated lymphoid tissue (MALT) lymphomas. In this study, we analysed 35 patients and clarified the clinicopathological features of LP.Methods and results:  Paraffin-embedded tissue samples were stained immunohistochemically and analysed by tissue-fluorescence in situ hybridization (T-FISH) for IGH/CCND1 (cyclin D1) and IGH/BCL2. The average age of the patients was 58.3 years. Over half of the cases showed gastric, duodenal, small intestinal, ileocaecal and sigmoid colonic lesions (15, 19, 15, 16 and 16 cases, respectively). Phenotypically, cases were classified into three types of MCL (cyclin D1+ CD5+ CD10–) (n = 12), FL (cyclin D1– CD5– CD10+) (n = 14) and MALT (cyclin D1– CD5– CD10–) (n = 9). T-FISH identified 11 of the 11 examined cases with MCLs to have IGH/CCND1, while seven of 10 cases with FL had IGH/BCL2, and none of the MALT cases were positive for IGH/CCND1 or IGH/BCL2. At the study endpoint, five of 12 patients with MCL were dead, two of 14 with FL and one of nine with MALT were dead of other disease. Event-free survival analysis showed significantly poorest outcome in MCL, followed by FL, while MALT was associated with a favourable outcome (P = 0.0040).Conclusions:  Our study emphasizes the importance of differentiating MCL, FL and MALT of LP in evaluating prognosis and hence the most suitable therapeutic regimen.

Notes: Fever is induced by a neuronal mechanism in the brain. Prostaglandin (PG) E2 acts as a pyrogenic mediator in the preoptic area (POA) probably through the EP3 subtype of PGE receptor expressed on GABAergic neurons, and this PGE2 action triggers neuronal pathways for sympathetic thermogenesis in peripheral effector organs including brown adipose tissue (BAT). To explore pyrogenic efferent pathways from the POA, we determined projection targets of EP3 receptor-expressing POA neurons with a special focus on rat hypothalamic regions including the dorsomedial hypothalamic nucleus (DMH), which is known as a center for autonomic responses to stress. Among injections of cholera toxin b-subunit (CTb), a retrograde tracer, into hypothalamic regions at the rostrocaudal level of the DMH, injections into the DMH, lateral hypothalamic area (LH) and dorsal hypothalamic area (DH) resulted in EP3 receptor immunolabelling in substantial populations of CTb-labeled neurons in the POA. Bilateral microinjections of muscimol, a GABAA receptor agonist, into the DMH and a ventral region of the DH, but not those into the LH, inhibited thermogenic (BAT sympathetic nerve activity, BAT temperature, core body temperature and expired CO2) and cardiovascular (arterial pressure and heart rate) responses to an intra-POA PGE2 microinjection. Further immunohistochemical observations revealed a close association of POA-derived GABAergic axon swellings with DMH neurons projecting to the medullary raphe regions where sympathetic premotor neurons for febrile and thermoregulatory responses are localized. These results suggest that a direct projection of EP3 receptor-expressing POA neurons to the DMH/DH region mediates febrile responses via a GABAergic mechanism.

Notes: Bone morphogenetic protein (BMP) is known as a protein that induces new bone in heterotopic sites. This study was conducted to assess the cell-biological effects of crude porcine BMP and 3 pulp-capping materials by implantation and cell culture methods. The following results were obtained: a new bone site of approx 5mm in diameter were induced in the hind limbs, which confirmed the osteoinductive activity of the crude BMP. The pulp-capping materials hardly influenced the calcification of rat dental pulp (RDP) cells. Our data also suggest that the effect ofthe crude BMP on the proliferation and calcification depended on its quantity. The finding of a large increase in the ALPase activity and the formation of mineralized nodules caused by the crude BMP , suggests that the crude BMP enhanced the calcification by RDP cells. Consequently, it is quite possible that crude porcine BMP could be used as a pulp-capping material

Notes: We investigated the immediate response in the vicinity of the implanted polarizedhydroxyapatite (HA). One of the important immediate events was found to be the fibrin adsorption on the implanted HA. The activation of the fibrin adsorption on the polarized HA was confirmed by the observation by SEM observation and immunohistochemical detection. After the implantation, the coagulation cascade induced the wound healing. The adsorbed fibrin was formed network structure and worked for later cell responses as the scaffolds. The acceleration offibrin scaffolds formation in the vicinity of the implanted polarized HA contributed to the stimulation and activation of plate ets and osseous cells. The platelets were activated from the results of the signal transduction and cytoskeleton changes and released growth factors. The growth factors released from platelets led to bone regeneration by stimulating migration and proliferation of the osseous cells. In the vicinity of the implanted HA samples, the coagulation cascade reaction to repair wound healing led to the new bone formation by mediation of the platelets and osseous cells. The mechanism of osteoconduction at earlier stage had closerelationships to the electrostatic properties of the implant

Notes: [Auszug] Inflammation is now considered critical in the pathogenesis of myocardial infarction. One of the mechanisms regulating the inflammatory process is the ubiquitin-proteasome system. We investigated whether variants of the 20S proteasome are associated with susceptibility to myocardial infarction and ...