No program was ceased due to adverse clinical events. Conclusion: Meal replacements maybe an effective and safe weight loss intervention in CKD (particularly when ordered by the team) and warrants investigation in randomised trials. 214 IMPROVING HEALTH CARE IN DIABETES AND CHRONIC KIDNEY DISEASE: HOSPITAL HEALTH PROFESSIONALS’ VIEWS C LO1, H TEEDE1, D ILIC2, K MURPHY2, G FULCHER3, P KERR4,5, K POLKINGHORNE4,5, M GALLAGHER6,7, R WALKER8, S ZOUNGAS1,7 1Diabetes & Vascular Medicine Research Unit, Monash Centre for Health Research & Implementation, Monash University, Melbourne; 2Department of Epidemiology

& Preventive Medicine, School of Public click here Health & Preventive Medicine, Monash University, Melbourne; 3Department of Diabetes & Endocrinology, Royal North Shore Hospital, Sydney; 4Department of Nephrology,

Monash Health, Melbourne; 5Monash University, Melbourne; 6Concord Clinical School, University of Sydney, Sydney; 7The George Institute for Global Health, Sydney; 8Department of Renal Medicine, Alfred Health, Melbourne, Australia Aim: In this qualitative study we explore how health care can be improved by examining key processes in patients’ management. Background: Diabetes is the commonest cause of chronic kidney disease (CKD). When combined, both selleck screening library conditions increase morbidity and mortality. Despite this, health care of patients with diabetes and CKD is often suboptimal. Methods: Health professionals from 4 major metropolitan hospitals in 2 of Australia’s largest cities were purposively sampled. Thirty-six participants were recruited into 6 focus groups, including endocrine, renal and allied health professionals. Eight Diabetes and Renal unit heads completed semi-structured interviews to triangulate findings. Focus groups and semi-structured interviews were conducted by the same facilitator, until a point of data saturation was reached. Data analysis was completed independently by 2 researchers using an inductive, thematic approach. Results: Both participant

groups agreed on the following key features that were perceived to influence the management of diabetes and CKD: (1) Patient self-management; Histidine ammonia-lyase (2) Patient access to health care; (3) Communication between health care providers and between health care providers and patients; (4) Coordination and integration of care; and (5) Health services having a preventive and early intervention approach. Unit heads also described the importance of quality and improvement measures within a health service. Disparity between health professionals and unit heads was evident regarding the accessibility of tertiary health services and communication between health professionals. Conclusions: The management of patients with diabetes and CKD is an interplay between hospital and community health care and patient self-management.

f (TWHF) which has been applied extensively for treatment of patients with early diabetic nephropathy (DN) in China. Despite this, therapeutic mechanisms remain unclear. Increasing evidences demonstrate renal inflammation is

a determinant during glomerular injurious progress under high-glucose condition. Among them, p38MAPK signaling activity and its related inflammatory factors play pivotal roles respectively. This study aimed to investigate effects and mechanisms in vivo of TP on inflammatory and sclerotic lesions in glomeruli by regulating p38MAPK signaling activity and inflammatory factor expression. Methods: Rats were randomly divided into Trichostatin A 3 groups, Sham-operated group, TP-treated group, and Vehicle given group, and sacrificed at weeks 8 after induction of DN induced by 2 consecutive intraperitoneal injections of streptozotocin (STZ) at 30 mg/kg dose with an interval of 1 week following unilateral nephrectomy. Daily oral administration of TP (0.5 mg/kg/d) and vehicle (saline) was started after the second injection of STZ until sacrifice. Urinary albumin (UAlb), biochemical indicators, glomerular morphology, glomerular macrophage infiltration and protein expressions of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, p38MAPK, phosphorylated p38MAPK (p-p38MAPK) and TGF-beta1 in kidneys were examined, respectively.

Results: Characterizations of glomerular inflammatory damage in DN model rats involved glomerular macrophages (ED1+ cell) infiltration, IL-1beta and TNF-alpha Lumacaftor cost proteins over-expression and p38MAPK signaling molecules activation, especially p-p38MAPK and TGF-beta1 in kidneys,

accompanied by the exasperation of glomerulosclerosis (GS). TP could not only improve the DN model rats’ general state including body weight (BW), kidney weight (KW) and KW/BW, but also attenuate UAlb, GS, glomerular ED1+ cell infiltration and protein over-expressions of IL-1beta, TNF-alpha, p-p38MAPK and TGF-beta1 in kidneys. Selleckchem Sorafenib Conclusion: By means of these DN model rats, we demonstrated that activation of p38MAPK signaling pathway promotes glomerular damage, and that TP, as a natural regulator in vivo, could ameliorate renal inflammation and GS via down-regulating protein over-expressions of p-p38MAPK and TGF-beta1 in p38MAPK signaling pathway. TP may be exploited for therapeutic intervention of DN patients at early stage. TERAMI NAOTO, OGAWA DAISUKE, TACHIBANA HIROMI, HATANAKA TAKASHI, SUGIYAMA HITOSHI, SHIKATA KENICHI, MAKINO HIROFUMI Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Introduction: Trefoil factor (TFF) peptides are coexpressed with mucins in the gastrointestinal tract stomach, colon and are also expressed in kidney tubules. Serum levels of TFF3 have been reported a possible biomarker of gastric cancer.

As shown here, stimulation with CXCL4 induces an increased SphK1 expression in monocytes and rescues these cells from apoptosis. It should be mentioned here that transfection of monocytes either Bcr-Abl inhibitor with empty vector or with SphK1-plasmid resulted in decreased apoptosis but at the same time led to increased necrotic cell death, while overexpression of SphK1 (by transfection) did not further support cell survival (Fig. 6E). This indicates that cell survival in monocytes (non-proliferating cells) requires

at least one additional signal provided by CXCL4 apart from those leading to increased expression of SphK1. Furthermore, this result also might explain why stimulation with exogenous S1P only partially protects monocytes from cell death (Fig. 6A and 7B). In addition to the effects of SphK1 overexpression, Olivera et al. 28, 29 demonstrated that administration of micromolar (but not nanomolar) concentrations of exogenous S1P suppresses apoptosis in a dose-dependent manner, and these effects were independent

of S1P receptors. Similar results were published by Van Brocklyn et al. 24, who could demonstrate that S1P at high concentrations acts not necessarily through binding to S1P receptors, but rather following cellular uptake of the phospho-lipid. Mononuclear phagocytes mainly express two S1P receptors, S1P1 and S1P2 12. While S1P1 exclusively interacts with Gi proteins, S1P2 couples with multiple G proteins 30. In a previous report, we have shown that CXCL4-mediated oxidative burst is only marginally reduced in the presence Selleckchem RG 7204 of PTX, indicating that Gi proteins do not play a relevant role selleck products in this context 2. Furthermore, CXCL4-mediated rescue from apoptosis is not affected in PTX-pretreated cells (Fig. 7B). Although we

cannot fully exclude a minor role of S1P receptors coupled to PTX-insensitive G proteins, the lack of S1P in culture supernatants of CXCL4-stimulated cells argue against the involvement of any S1P surface-expressed receptors. We, thus, conclude that CXCL4 effects are transduced predominantly by intracellularly generated S1P. Monocytes or macrophages undergo spontaneous apoptosis in the absence of serum and/or survival factors. In these cells apoptosis is accompanied by an increase of caspase-9 and caspase-3 activity 31–34. As shown here, stimulation with CXCL4 not only rescues monocytes from apoptosis but also resulted in a nearly complete block of caspase activation (Fig. 4 and 6C). In addition, also treatment with high dosages of S1P resulted in reduction of caspase activity, and cell death. The protective effect of CXCL4 on apoptosis and caspase activation is partially reversed in the presence of SphK or MEK/Erk inhibitors (Fig. 3B and 4, or published earlier by our group 3), indicating that caspase activity is regulated by these kinases in monocytes. Our results support previous findings by Edsall et al.

CD137−/− mice were provided by Professor Dr Robert Mittler from Emory University (Atlanta, GA, USA). C57BL/6J control mice

were purchased from Charles River (Sulzfeld, Germany). The animal protocols were constructed according to institutional and state guidelines and approved by the local animal welfare committee. Eight to 10-week-old age- and sex-matched mice were immunized with ovalbumin [OVA, lipopolysaccharide (LPS) content-reduced <10 EU/mg protein, as described previously [28]] using two protocols (Fig. 1), as follows. Allergy protocol.  Mice were sensitized twice intraperitoneally (i.p.) with OVA (20 µg in 200 µl 0·9% NaCl) in adjuvant (Imject IWR-1 research buy Alum®, PerbioScience, Bonn, Germany) followed by six challenges in which 20 µg OVA in 40 µl of 0·9% NaCl was given intranasally (i.n.) (allergy protocol). Control mice (Alum) received injections and challenges of 0·9% NaCl. Mice were killed 24 h after the last local allergen provocation. Tolerance protocol.  To induce respiratory tolerance, Ivacaftor order WT and CD137−/− mice were pretreated twice i.n. with 500 µg OVA in 40 µl of 0·9% NaCl. Thereafter, mice underwent allergy protocol as described above. BALF from each individual mouse was obtained by flushing the lungs with PBS/2 mM ethylenediamine tetraacetic acid (EDTA); the total number and

differentiation of BALF cells were then determined as described previously [28]. Lung histological sections and computer-based quantification of the degree of pulmonary inflammation [haematoxylin and eosin (H&E)] and mucus production [periodic acid-Schiff (PAS)] were performed as described previously

[28]. Serum levels of OVA-specific IgE, IgG1 and IgG2a were measured by enzyme-linked immunosorbent assay (ELISA), according to standard protocol. IgE concentrations Meloxicam (pg/ml) were calculated using a standard curve for mouse anti-OVA IgE (AbD Serotec, Oxford, UK). Data for IgG1 and IgG2a are presented as titre values derived from analysis of optical density (OD) values versus factors of serum dilution series using a logarithmic curve-fitting model. Spleen and bronchial lymph node (bLN) isolated cells were restimulated in vitro with OVA (200 µg/ml) in RPMI-1640 containing 10% fetal calf serum (FCS), 100 U/ml penicillin and 100 µg/ml streptomycin. Cytokines (IL-4, IL-5, IL-13, IFN-γ) were measured in supernatants after 3 days using DuoSet ELISA kits (R&D Systems, Minneapolis, MN, USA), according to the manufacturer’s instructions. Cell cultures were pulsed with 3[H]-thymidine and incorporated activity was measured in a Betaplate scintillation counter. Single-cell suspensions from spleen, lung and bLN were incubated with fluorescently labelled antibodies for 20 min at 4°C in phosphate-buffered saline (PBS)/0·5% bovine serum albumin (BSA). Intracellular staining of forkhead box protein 3 (FoxP3) was performed using the eBioscience kit, according to the manufacturer’s instructions. Briefly, cells were surface-stained, fixed and incubated with antibody to FoxP3 for 30 min at 4°C.

Thus, hookworms may release molecules that actively Pembrolizumab manufacturer attract and expand NK cells during infection and stimulate IFN-γ release through an undefined NK receptor. This has been proposed as an immune evasion strategy as the IFN-γ released could cross-regulate the otherwise protective TH2 response. The first hookworm vaccine was developed in 1965 against the dog hookworm A. caninum and consisted of irradiated larvae (50). Although this vaccine gave good protection against experimental and field challenge, it was withdrawn

from veterinary use after concerns with efficacy and shelf life were raised. In the 1980s, David Grove and Simon Carroll switched their focus from human immunity to vaccines using A. ceylanicum infection in dogs selleck as a model for the human disease. They showed that dogs that were chronically infected then treated with an anthelmintic were resistant to reinfection (51), highlighting for the first time that immunity to reinfection could occur, at least in the A. ceylanicum/dog relationship. Carroll and Grove then went on to explore the protective efficacy of hookworm extracts and showed that protection against A. ceylanicum infection in dogs by vaccination with adult worm aqueous somatic extracts when formulated with Freund’s adjuvants (52), kicking off efforts to develop vaccines based on soluble molecules

rather than whole parasites. More recently, recombinant vaccines have been found to exert partial efficacy in the dog hookworm model using A. caninum, stimulating human trials with orthologous N. americanus antigens presently underway. The first recombinant vaccine to show efficacy against hookworm was ancylostoma secreted protein-1 (Ac-ASP-1), which conferred partial protection in mice challenged with A. caninum (53,54). ASPs are a large family of proteins, which are the most highly expressed products of in vitro activated PAK5 larvae (55),

with the related ASP-2 protein discovered shortly after ASP-1 (56). However, mice are not a permissive host for hookworms, and ASP-1 did not confer protection in permissive hosts including hamsters (57) and dogs (58). ASP-2, by contrast, appeared to show similar protection to that of irradiated larvae (57), and in human hookworm-endemic populations, IgE specific to ASP-2 negatively correlated with hookworm burden, thus highlighting its potential as a vaccine candidate in animal models and endemic regions (12). An Na-ASP-2 vaccine is currently in development: it has been shown to raise effective and safe immune responses in unexposed individuals (59) and is currently in phase I clinical trials in Brazil being conducted by researchers (including ourselves) at The Human Hookworm Vaccine Initiative – see http://www.sabin.org/vaccine-development/vaccines/hookworm.

Therefore, the attenuating effect of AZM on GVHD might be due partly to its control of bacteria. Concerning the timing and dose of oral AZM, we chose a regimen of 100 mg/kg orally for 5 days starting from day −2 to day 2. Amsden et al. [55] reported that the blood concentration of the drug in humans became stable (0·5–1·0 mg/ml) after 3 or 5 days of oral AZM. The 100 mg/kg/day Target Selective Inhibitor Library dosage was used because

it corresponds to the human dosage after size correction [56]. Accumulating evidence indicates that early interaction between allogeneic T lymphocytes and residual recipient APCs immediately after allo-BMT is critical for eliciting acute GVHD [6, 10]. Zhang et al. [57] studied the kinetic window during which recipient APCs elicited acute GVHD in a murine model and demonstrated that recipient DCs were activated and aggregated rapidly in T lymphocyte-rich areas of the spleen within 6 h after lethal irradiation. By 5 days after irradiation, <1% of recipient DCs were detectable, but the activated donor CD8+ T lymphocytes had already undergone as many as seven divisions. This indicates that, although recipient DCs disappear rapidly after allo-BMT, they first prime donor

T lymphocytes and play a critical role in check details triggering donor CD8+ T lymphocyte-mediated GVHD. In our transplantation model, AZM-treated recipients developed GVHD in the later phase. Although Zhang et al. [57] demonstrated the critical, early role of DCs in initiating acute GVHD, they also found that a small number of radio-resistant recipient DCs remained even at 4 months after allo-BMT

and pointed out the possibility that they might be important in amplifying the GVHD response. Further studies are necessary to elucidate later events in the induction of acute GVHD. Taken together, 4��8C our results suggest that blockade of DC–T lymphocyte interaction by inactivating DCs with AZM, i.e. DC targeting, might require administration of the drug for a short period before and after BMT. It is this period that should be targeted in an attempt to attenuate acute GVHD. Moreover, this treatment might not be accompanied by suppression of the beneficial GVL effect, as oral AZM had no effect on the lymphocyte functions of mice. AZM already has a history of use in the treatment of bacterial infections, so its administration should also be safe in patients undergoing BMT for haematological disorders. Similarly to bortezomib [23], AZM could be used singly or in conjunction with immunosuppressants to prevent acute GVHD in various clinical settings. AZM also seems to have potential for use in treating already developed GVHD. Further studies of the in-vivo effects of AZM in allogeneic BMT are clearly warranted. We thank Dr Takashi Iwamoto of Chubu College of Life and Health Sciences for technical advice and Miyuki Namikata for technical assistance.

Indeed, morphological examination of the mucosa shows epithelial cells in various states of degradation in the vicinity of the schistosome egg (56). Alternatively, the diminished secretion could result from adaptation of the ileal mucosa to the infection. Such an adaptive response has been described for N. brasiliensis-infected rats Regorafenib in vitro and is directed by a neurally mediated mechanism possibly aimed at preventing excessive fluid loss (57). Likewise, in T. spiralis infected ferrets,

basal and stimulated jejunal secretions were attenuated during the enteric stage of infection (58). In these models, the reduced secretion was accompanied by a shift from cholinergic to noncholinergic regulation of secretion, which was associated with an increase in substance P immunoreactivity within

the mucosa. Interestingly, in this context, S. mansoni infection in the mouse results in increased immunoreactivity for the neuropeptide CGRP in close apposition to MMC within the ileum (6,7). Although the role of CGRP in S. mansoni infection remains to be elucidated it is likely that CGRP is involved in neuro-immune interactions between local primary afferent nerve fibres and mast cells (7). Extrapolation of these murine data to man involves a large number of uncertain assumptions, partly arising out of the lack of adequate human data [for reviews see (59,60)] but also since schistosome infection in mice differs in many respects

from that in humans (60). In both human and murine, however, the majority of pathology develops VX809 at the sites of maximal accumulation of eggs: the intestine and the liver (59,60). Gastrointestinal schistosomiasis is characterized by chronic abdominal pain and discomfort, loss of appetite and diarrhoea that commonly contains occult blood (60). The present results show that in mice, in addition to the previously described impairment of sugar and fluid transport (61), the basal secretion and the maximal secretory capacity of the ileal epithelium are severely reduced 8 weeks after schistosome infection. OSBPL9 If and how this finding relates to the patient symptoms cannot be inferred at present, but a derangement of fluid transport may explain some of these. The reported impairment of the mucosal barrier in the murine ileum suggests that translocation of bacteria from the gut lumen to extra-intestinal sites (62) might be increased during schistosomiasis. At present, only limited information is available on the effects of schistosomiasis on murine intestinal function (63). The present results suggest, however, that use of murine models may be of importance for the dissection of the intestinal pathologies. In summary, in S. mansoni-infected mice, the intestinal barrier is severely impaired both in WT and in Mcpt-1−/− mice and egg excretion takes place independently of mMCP-1.

2). The data imply that radiotherapy upregulates the expression of Akt in the Tregs of BCa. A portion of the isolated cells in Fig. 1 was analysed by flow cytometry for the frequency of apoptotic Tregs. The results showed that much less frequency of apoptotic Tregs was detected in RA group than in the

nRA group (Fig. 3). The results implicate that radiation promotes the Treg survival in the cancer that may be via preventing the apoptotic activities in the Tregs. To further investigate the mechanism by which radiation promotes the survival of Tregs in BCa tissue, we generated CD4+ CD25+ Foxp3+ Tregs from human peripheral mononuclear cells. After treated with radiation (RA group), the levels of Akt were markedly increased in activated Tregs in a radiation dose-dependent manner. The frequency of apoptotic Tregs was also less among the Tregs of RA group than nRA group; the latter learn more was activated, but not treated with radiation. Considering the increase in Akt might protect the Tregs from becoming apoptosis during radiation, some cells were treated with Akt inhibitor during the activation and radiation. Indeed, the frequency of apoptotic Tregs in RA group was similar to that of the nRA group (Fig. 4). The results indicate that RA can significantly increase the expression of Akt in Tregs that efficiently prevents Tregs to be apoptotic. This study revealed a side effect of radiotherapy

in the treatment for BCa. After radiation, Buparlisib research buy the frequency of the tumour infiltration Tregs significantly

increased in the BCa tissue. The levels of Akt were increased in the Tregs, which suppressed the sensitivity to apoptosis in Tregs. The tumour-infiltrating T cells play an important role in tumour growth. CD8+ T cells can inhibit Resminostat tumour growth by inducing tumour cell death or apoptosis. However, Tregs can inhibit CD8+ T cells in the tumour tissue that facilitates the tumour survival. Kaycer et al. [11] analysed a group of tumour-infiltrating T lymphocytes in non-small cell lung cancer and found that high numbers of Tregs were of beneficial prognostic influence in patients with non-small cell lung cancer. Boorjian et al. [12] observed a group of patients with liver cancer and found that the high frequency of Tregs in the tumour tissue was correlated with poor survival rate of the patients. Thus, to elucidate the causative factors increasing Tregs in tumour tissue is of significance. Yang et al. [13] found that colorectal cancer expressed high levels of integrin alpha versus beta 6, which had positive correlation with the frequency of Tregs in the tumour tissue. Our data have contributed one more novel evidence that radiotherapy also favours the increase in Treg in Bca tissue. Radiotherapy is an important therapeutic remedy in the treatment for malignant tumours. Because of its side effects, high doses of radiation should be avoided.

baumannii expression properties that augment the organism’s ability to transition from exponential to stationary phase, as opposed to strain-dependent characteristics. Moreover, characterizing conserved biological processes may, in turn, provide rationale for developing strategies check details for the therapeutic intervention of A. baumannii infections. Accordingly, each strain was cultured in LB medium, aliquots were removed during each growth phase, and RNA

was isolated and subjected to microarray analysis. The results presented here are refined to only those changes in gene expression that are conserved across both strains; individual strain expression properties are provided in Supporting Information, Table S1. Results revealed that the gene expression profiles of exponential- and stationary-phase A. baumannii differ dramatically and these differences are relatively well conserved

across the two strains studied. A total of 502 ORFs were determined to exhibit at least a twofold increase (t-test; P ≤ 0.05) in expression during exponential as opposed to stationary phase of growth regardless of the strain studied. Most of these genes belonged to distinct clusters of orthologous functional groups that are related to aspects of cell growth (Fig. 1). For instance, genes associated with amino acid metabolism (n = 43), translation (n = 93), cell wall/envelope Neratinib concentration biogenesis (n = 43), nucleotide transport (n = 28), transcription (n = 22), and replication (n = 21) were upregulated during exponential as opposed to stationary phase growth. Conversely, the mRNA levels of 175 genes were upregulated during stationary as opposed to exponential phase

in both strains. Of these, the majority were associated with energy production and conversion (n = 23), lipid transport Pregnenolone and metabolism (n = 15), and post-translational modification (n = 11). As described below, a more elaborate analysis of the data indicated that several genes that are likely to contribute to the organism’s ability to cause disease were found to be differentially expressed in a growth phase-dependent manner. Acinetobacter baumannii possesses the ability to survive on common hospital surfaces for weeks at a time, due in part to its ability to tolerate desiccation and form biofilms, subsequently providing a means for the organism to persist in the environment and act as a source for bacterial transmission to susceptible patients (Wendt et al., 1997; Jawad et al., 1998; Espinal et al., 2012). Our microarray data provided potential insight with regard to the biological systems that may contribute to the organism’s ability to form biofilms. More specifically, two members of the trehalose metabolic pathway, trehalose-6-phosphate synthase (A1S_0803), and trehalose-6-phosphate phosphatase (A1S_0804) were among the most highly upregulated stationary phase genes.

Both LVH and arterial stiffness are independent determinants of CVD in patients Talazoparib mw with ESRD. The aim of this study is to evaluate the relationship between post-transplant new-onset diabetes and arterial stiffness and LVMI in kidney transplant recipients.

Methods: 159 kidney transplant recipients (57 patients with new onset diabetes) with minimum one year post transplant period were enrolled into the study. All patients’ standard clinical and biochemical parameters, pulse wave velocity (PWv) levels and echocardiographic measurements were analyzed. PWv was determined from pressure tracing over carotid and femoral arteries using the SphygmoCor system. All patients underwent echocardiographic examinations and left ventricular mass was calculated according to the Devereux formula and indexed for body surface area to give LVMI. Results: The percentage of patients with high LVMI (>130 g/m2) was significantly higher in patients with post-transplant new-onset diabetes (63.2% vs 21.6%, p:0.0001).

Patients Angiogenesis antagonist with new onset diabetes were significantly older than patients without diabetes. Serum creatinine, calcium, phosphorus, PTH, hemoglobin, lipid levels and systolic and diastolic blood pressure were similar in both groups. The body mass indices of patients with new onset diabetes was significantly higher (25.0 ± 5.5 vs 27.5 ± 4.1, p:0.002). In patients with new onset diabetes, serum HbA1c levels are significantly correlated with LVMI Axenfeld syndrome (p:0.05). In patients with high LVMI (LVMI > 130 g/m2, n:57); serum HbA1c levels (7.36 ± 1.5 vs 6.68 ± 1.3,

p:0.001), systolic and diastolic blood pressures (p:0.0001) and age (p:0.007) were significantly higher than in patients with low LVMI. Linear regression analysis revealed that HbA1c was the major determinant of LVMI (P:0.026, b:0.361). Conclusion: Post-transplant increased LVMI is associated with new-onset diabetes after renal transplantation. HbA1c is the major determinant of LVMI, so strict control of serum glucose levels is essential for preventing cardiovascular disease. MUSO ERI1, GU JINGWEN2, NAKAMURA HAJIME3, YOSHII TERUKO4, NAGAOKA MASAMI4, TANAKA MEGUMI4, FUKUYA YUKARI4, IWASAKI YUKAKO1, ZOU HEGIAN2 1Division of Nephrology and Dialysis, Kitano Hospital The Tazuke Kofukai Medical Research Institute; 2Huashan Hospital World Wide Medical Center, Shanghai, China; 3Department of Preventive Medicine, Kitano Hospital, The Tazuke Kofukai Medical Research Institute; 4Department of Nursing, Kitano Hospital, The Tazuke Kofukai Medical Research Institute Introduction: In China, especially in Shanghai, a number of companies in Japan sends their employees some of whom have chronic diseases such as hypertension (HT), hyperlipidemia (HL) chronic kidney disease (CKD) and Diabetes mellitus (DM).