But will any single biomarker such as NGAL suffice in AKI? In add

But will any single biomarker such as NGAL suffice in AKI? In addition to early diagnosis and prediction, it would be desirable to identify biomarkers capable of discerning Wnt drug AKI subtypes, identifying aetiologies, predicting clinical outcomes, allowing for risk stratification and monitoring the response to interventions. In order to obtain all of this desired information, a panel of validated biomarkers may be needed. Other AKI biomarker

candidates may include interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), cystatin C and liver-type fatty acid binding protein (L-FABP), to name a few.1–3 The availability of a panel of validated AKI biomarkers, such as those illustrated in Figure 1, could further revolutionize and personalize renal and critical care in the near future. Studies cited in this review that were performed by the author’s laboratory were supported by grants from the NIH (R01 DK53289, RO1 DK069749 and R21 DK070163). Dr Devarajan is a co-inventor on NGAL patents. Biosite(R) Incorporated has signed an exclusive licensing agreement with Cincinnati Children’s Hospital for developing plasma NGAL as a Quizartinib concentration biomarker of acute renal failure. Abbott Diagnostics has signed

an exclusive licensing agreement with Cincinnati Children’s Hospital for developing urine NGAL as a biomarker of acute renal failure. Dr Devarajan has received honoraria for speaking assignments from Biosite(R) Incorporated and Abbott Diagnostics. “
“Date written: June 2008 Final submission: June 2009 Kidney transplant recipients should be advised to take a vitamin D (or analogue) supplement at a dose of at least 0.25 µg daily. (Level I and II) (Suggestions are based on Level III and IV evidence) The treating physician should determine the dose of vitamin D and the necessity of other treatments for minimizing bone mineral density loss, on the basis of available evidence. A rapid decline in bone mineral density occurs in the early post-transplant period.3,4 Though the rate of bone loss may decelerate or cease by around 3 years post-transplant, bone mineral Etomidate density remains below normal.5 The risk of bone fractures

among kidney transplant recipients is four times that among the general population.6 At the time of transplantation, there are usually already significant abnormalities of bone remodelling related to chronic kidney disease.7 Reduced calcium absorption due to prednisone,8 hyperparathyroidism9 and abnormal vitamin D metabolism10 are among the factors contributing to the further weakening of bones and the risk of bone disease post-transplantation. There is an increased risk of bone loss among females, particularly post-menopausal.11 This review set out to explore and collate the evidence to support the use of particular nutrition interventions for the prevention and management of bone disease in kidney transplant recipients, based on the best evidence up to and including September 2006.

7,25 The recognition

of cells by the immune system when u

7,25 The recognition

of cells by the immune system when undergoing redox stress is not well see more defined. Our data suggest that cells undergoing a redox stress that leads to a lowering in the levels of intracellular glutathione may begin to display MHC class I dimers on their cell surface. Such alterations in cellular glutathione levels have been reported to occur during T-cell activation26,27 and also during apoptosis.17,18,28 A more extensive study monitoring both MHC class I dimer formation and the level of glutathione in cells undergoing a variety of stimuli would, we consider, be of some worth. Furthermore, distinguishing whether both apoptotic and necrotic cell death pathways induce dimers would also be informative, alongside other pathological states such as viral infection, Fulvestrant purchase and many others that induce inflammatory responses and the production of reactive oxygen species. This would allow a pattern of conditions to be catalogued under which MHC class I dimer formation is induced. Although various MHC class I dimers have been reported in the literature, their potential biological role remains enigmatic.8,13 Of significant note, however, are the observations that Ig-MHC class I dimers can act to tolerize T cells.29 In this study, Kourilsky and colleagues used a soluble H2-Kd molecule dimerized with a cross-linking antibody to demonstrate

that an antigen-specific T-cell hybridoma was initially activated, followed by a state of unresponsiveness. It has also been demonstrated that antigen-specific occupancy of just one of the two peptide-binding grooves in an

Thymidylate synthase MHC class I dimer can have an effect on T cells,30 which may allow not only the HLA-B dimers we show here, but also the HLA-A-B dimers we describe in Fig. 2 to have some biological activity. Hence, the MHC class I dimers detected on apoptotic cells, and also on exosomes,15 may be capable of providing signal, including tolerogenic signals to immune cells. Similarly, tumour cells undergoing apoptosis, or releasing exosomes containing tumour-associated or tumour-specific antigens may influence T-cell behaviour. Of further interest is the possible recognition of MHC class I dimers by members of the NK cell receptor family. It has been shown that a disulphide-linked engineered version of the KIR2DL1 receptor has an increased affinity for HLA-C,31 and that KIR molecules can form an array of dimers and multimers in a zinc-dependent interaction.32 Hence interactions between dimers of both ligands and receptors may occur, potentially inducing extra stability for the generation of either inhibitory or activatory signals. As indicated above, defining the various conditions under which such dimers form would allow the design of experiments to directly study their potential influence on immune responses.

Therefore, it is important to address whether transfer of immatur

Therefore, it is important to address whether transfer of immature recipient’s DC loaded with donor antigens could also induce anti-allotolerance or even working better than directly transfer donor’s DC. In this study, we generated recipient’s immature DC by adenoviral infection with a kinase-defective dominant negative form of IKK2 (IKK2dn), then loaded with donor antigens and tested their ability to induce anti-allotolerance in an allo-kidney graft rat model. Our results indicated that IKK2dn-transfected DC are capable of inducing tolerance and significantly Lorlatinib in vitro prolonged transplanted allograft survival by reducing B7-1 and B7-2 expression,

increasing IL-10 and decrease IFN-γ production. Animals and reagents.  Male Lewis (LEW/CrlBR), Brown Norway (BN/CrlBR), and Wistar (Crl:(WI)BR) rats, 8–10 weeks, body weight around 180–200 g, were purchased from Charles River (Vital River, Beijing, China) and maintained in the university animal facility. Procedures involving animals and their care were conducted FK228 in vitro in accordance with the institutional guidelines that are in compliance with national and international

laws and policies. The recombinant rrGM-CSF and rrIL-4 were purchased from Peprotech (Rocky Hill, CT, USA). FITC or PE-conjugated mouse anti-Rat CD80, CD86, and MHC-II antibodies were purchased from Serotec (Oxford, UK); IL-2, IL-10, IFN-γ ELISA kits are from R&D (Minneapolis, MN, USA). All other reagents are from Sigma (St. Louis, MO, USA). The replication-deficient adenovirus encoding a kinase-defective dominant negative form of human IKK2 plasmid, pACCMVpLpASR(+)-IKK2dn, was a kind gift from Dr Rain D Martin (University of Vienna, Vienna, Austria). pAdxsi-GFP-IKK2dn and pAdxsi-GFP-0 were constructed by SinoGenoMax Company, Beijing. DC preparation

and gene transfer.  Bone marrow cells were obtained from the tibias and femurs of Lewis rats. Bone marrow cells (2 × 106/ml) were cultured in 6-well plates (Becton Dickinson, Heidelberg, Germany) with recombinant rat granulocyte macrophage-colony Anacetrapib stimulating factor (GM-CSF) (5 ng/ml), in combination with recombinant rat IL-4 (5 ng/ml). On day 3 and every other day after, half of the medium containing the appropriate cytokines was replaced. Recombinant, replication-deficient adenoviral vectors encoding IKK2dn and Adv-0 were constructed as follows: IKK2dn cDNA was cloned into adenovirus transfer vector pShuttle-CMV-GFP(−)TEMP (Sinogenomax, Beijing, China) and analysed by restriction endonuclease KpnI & HindIII digestion. Then, the obtained plasmid, pShuttle-CMV-GFP(−)TEMP-IKK2dn was transferred into pAdxsi vector to construct pAdxsi-GFP-IKK2dn plasmid and was identified by XhoI digestion. The correct adenoviral recombinant was then cleaved with Pac I and transfected into 293 cells to produce and purify viral particles.

02; 95% CI 1 50–12 0; P = 0 0051) As compared with the group wit

02; 95% CI 1.50–12.0; P = 0.0051). As compared with the group without early AKI, the urinary L-FABP level in early AKI group was significantly higher not only on the day of SCT

but also at the baseline. Then, ROC analysis demonstrated the urinary L-FABP level at baseline had good discriminative ability for the early AKI. Conclusion: One-quarter of allogeneic selleck chemical SCT recipients developed the early AKI, which was linked with increased risk of their short-term mortality. Antecedent kidney damage, which can be identified by urinary L-FABP concentration, may portend the emergence of early-onset AKI. YAMASHITA TETSUSHI1, DOI KENT2, TSUKAMOTO MAKI1, NANGAKU MASAOMI1, YAHAGI NAOKI2, NOIRI EISEI3 1Department of Nephrology and Endocrinology, Graduate school of Medicine, The University of Tokyo; GSK1120212 2Department of Critical Care Medicine, The University of Tokyo Hospital; 3Department of Hemodialysis and Apheresis, The University of Tokyo Hospital Introduction: Tissue inhibitor of metalloproteinases-2 (TIMP-2) has recently been reported to detect severe AKI better than new AKI biomarkers that have recently introduced to the clinical such as NGAL. Methods: This study enrolled 98 patients who were admitted to the adult mixed ICU of The University of Tokyo Hospital from July 2011 to October 2011 by consecutive sampling. Urine TIMP-2 and NAG, and plasma NGAL and IL-6 were measured

on ICU admission. This Sitaxentan study was aimed to evaluate whether these biomarkers

could predict AKI and its severity, and mortality by ROC analysis. Results: AKI occurred in 42 (42.9%) patients including 27 (27.6%) severe AKI (KDIGO stage 2 or 3). The area under the ROC curve for each marker was shown in Table. Forty one (41.8%) patients was complicated with sepsis, including 19 (19.4%) severe AKI. In accordance with previous reports, plasma NGAL and IL-6 were increased by sepsis, however urine TIMP-2 and NAG was increased not by sepsis but by the presence of severe AKI (Figure). In-hospital mortality was 15.3% in this cohort and urine TIMP-2 and NAG, and plasma NGAL were significantly higher in the non-survivors than the survivors, whereas plasma IL-6 was not significantly associated with mortality. Conclusion: A new urine biomarker of TIMP-2 is increased especially in severe AKI and associated with mortality. Sepsis appeared to have a smaller impact on urine TIMP-2 and NAG compared with plasma NGAL and IL-6. This distinct feature of biomarkers will enable to evaluate the contribution of sepsis to the development of AKI. TANAKA YUKI1, KUME SHINJI1, MAEDA SHIRO2, OSHIMA ITSUKI3, ARAKI HISAZUMI1, ISSHIKI KEIJI1, ARAKI SHIN-ICHI1, UZU TAKASHI1, MAEGAWA HIROSHI1 1Department of Medicine, Shiga University of Medical Science, Japan; 2Laboratory for Endocrinology, Metabolism and Kidney diseases, RIKEN Center for Integrative Medical Science, Japan; 3Discovery Research Laboratories, Shionogi & Co., Ltd.

Methods: Systolic blood pressure(SBP) was measured at 1-week inte

Methods: Systolic blood pressure(SBP) was measured at 1-week intervals after clipping. Two and 5 weeks after operation, the rats were sacrificed for western-blot and immunohistochemistry. Results: SBP increased in 2K1C rats(n = 12) within 1 week after unilateral renal clipping relative to sham rats(n = 8). Glomerulosclerosis and tubulointerstitial inflammation were aggravated in maintenance phase. From the acute phase, CK showed significant reduction

in ACE2, leading to an increased ratio of ACE/ACE2. Juxtaglomerular(JG) renin was increased in CK and suppressed in NCK, but collecting duct(CD) renin was enhanced in both kidneys beta-catenin inhibitor in immunohistochemistry. In the maintenance phase, medulla in both kidneys presented significantly increased ACE and decreased ACE2, along with up-regulation of renin in medulla of NCK. Immunohistochemistry revealed more intense CD renin staining in both kidneys. Simultaneously AT1R in CK cortex was not suppressed, albeit there was reduced MasR, thus AT1R/MasR ratio was insignificantly elevated in cortex. Conclusion: Even though the reduction of ACE2 along with increase of JG renin in CK could initiate hypertension in the acute phase, eventually a higher stimulation of ACE and suppression of ACE2, according to the activation of CD renin in NCK, are Ibrutinib thought to play key roles for keeping hypertension during

the maintenance phase. In addition, we cautiously presumed the imbalance of AT1R and MasR might have some effects to hypertension in this model. KATSUNO TAKAYUKI, YAMAGUCHI MAKOTO, Dolutegravir purchase TANAKA AKIHITO, YASUDA YOSHINARI, KATO SAWAKO, SATO WAICHI, TSUBOI NAOTAKE, ITO YASUHIKO, MARUYAMA SHOICHI, MATSUO SEIICHI Department of Nephrology, Nagoya University Graduate

School of Medicine Introduction: Albuminuria is known to be a predictive factor for chronic kidney disease (CKD) and cardiovascular disease (CVD). Particularly in the hypertensive patients, albuminuria increases the risk of CKD and CVD. However, little is known about the prevalence of albuminuria among hypertensive patients. The aim of this study is to conduct factual investigation of albuminuria. Methods: The study subjects were 387 individuals who attended a private practice as an outpatient. Semi-quantitative measurement of urinary albumin excretion corrected for the urinary creatinine levels (albumin creatinine ratio: ACR) was conducted by using a urine reagent paper in the hypertensive patients, and cross-sectional analysis was performed. Results: The cohort consisted of 215 males (55.6%) and 172 females (44.4%), with a mean age of 68.3 years (range 28 to 92 years). 367 patients (94.8%) used an antihypertensive agent. 155 patients (40.1%) had a diabetes mellitus. In 57 patients (14.7%) tested, there was evidence of proteinuria by using a test strip. Mean serum creatinine for the entire cohort was 0.83 mg/dL (range 0.4 to 2.1 mg/dL). Among 385 patients, 197 (51.


“We investigated the development

of the other-race


“We investigated the development

of the other-race effect “ORE” in a longitudinal this website sample of 3-, 6-, and 9-month-old Caucasian infants. Previous research using cross-sectional samples has shown an unstable ORE at 3 months, an increase at 6 months and full development at 9 months. In Experiment 1, we tested whether 9-month-olds showed the ORE with Caucasian and African faces. As expected, the 9-month-olds discriminated faces within their own ethnicity (Caucasian) but not within the unfamiliar ethnicity (African). In months. In Experiment 2, we longitudinally tested infants at 3, 6, and 9 months by presenting either the Caucasian or the African faces used in Experiment 1. In contrast to previous cross-sectional studies and Experiment 1, we found that infants discriminated between all stimuli. Hence, we did not find the ORE in this longitudinal study even at 9 months. We assume that the infants in our longitudinal study showed no ORE because of previous repetitive exposure to African faces at 3 and

6 months. We argue that only a few presentations of faces from other ethnic categories sufficiently slow the development of the ORE. selleck inhibitor
“Reduced responsiveness to joint attention (RJA), as assessed by the Early Social Communication Scales (ESCS), is predictive of both subsequent language difficulties and autism diagnosis. Eye-tracking measurement of RJA is a promising prognostic tool because it

is highly precise and standardized. However, the construct validity of eye-tracking assessments of RJA has not been established. By comparing RJA an eye-tracking paradigm to responsiveness to joint attention during the ESCS, the current study evaluated the construct validity of an eye-tracking assessment of RJA for 18-month-old infant siblings of children with autism. Relations between measures of RJA and concurrent language skills and autistic symptomatology were assessed. Correlations between measures of ESCS RJA and eye-tracking RJA were statistically significant, but few relations between either ESCS or eye-tracking assessments of RJA and language or symptoms were observed. This study establishes the construct validity of eye-tracking assessments of RJA. “
“We used eye tracking to examine 4.5- to 12.5-month-old infants’ (N = 92) Leukocyte receptor tyrosine kinase eye movements during 3-s presentations of upright and inverted faces. Scanning of inverted faces was statistically indistinguishable at 4.5, 6.5, 8, and 12.5 months of age; at each of these ages, infants disproportionately scanned the region containing the eyes. Scanning of upright faces changed over this age range. When viewing upright faces, 4.5-month-old and 6.5-month-old infants focused disproportionately on the region containing the eyes, whereas 12.5-month-old and 8-month-old infants distributed looking more broadly, scanning more of the internal area of the faces.

Mismatch negativity (MMN) is an auditory event-related potential

Mismatch negativity (MMN) is an auditory event-related potential elicited when a sequence of repetitive standard sounds is interrupted infrequently by deviant “oddball” stimuli. The MMN is a measure of cortical activity in response to the deviant sound and reflects an automatic, memory-based, comparison process.17-22 It can be rapidly assessed, elicited while the individuals are performing other tasks or sleeping, and reflects preattentive sensory memory and involuntary attention.17 The area under the MMN wave in frontal electrodes is

reduced in patients with schizophrenia, compared to controls, and the area correlates with the degree of cognitive impairment.18 find more click here Baldeweg et al.18 suggested that altered MMN in schizophrenia reflects an impaired attentional trigger, which would be a consequence of deficits in N-methyl-D-aspartate (NMDA) receptor-dependent neural processes underlying it. These and other studies19-22 support that, in schizophrenia, alterations in neurotransmission associated with NMDA receptors lead to impaired attention and cognitive

function, which are reflected in altered MMN, and result in impairment in everyday functioning, including sustained attention impairment. Patients with MHE also show impaired attention (including sustained attention) and cognitive function, which result in impairment in everyday functioning. Altered neurotransmission associated with NMDA receptors is a main contributor to cognitive impairment in animal models of HE.23-26 It is, therefore, likely that altered NMDA-receptor neurotransmission in the cortex could also contribute to attention deficits in MHE. This should be reflected in alterations in MMN. We hypothesized that patients with MHE, similarly Edoxaban to those with schizophrenia, should show alterations in MMN, which would be related with attention deficits. The aim of this work was to assess whether (1) MMN is altered in cirrhotic patients with MHE, compared to those

without MHE and to controls without liver disease, (2) MMN changes in parallel with performance in attention tests and/or with MHE in a longitudinal study; and (3) MMN predicts performance in attention tests and/or in the Psychometric Hepatic Encephalopathy Score (PHES). We performed MMN analysis and attention tests in 34 controls without liver disease, 37 patients with liver cirrhosis without MHE, and 23 with MHE. We used the Stroop and Map search tests to assess selective attention and the Elevator Counting test to assess sustained attention as well as visuomotor and bimanual coordination tests. We analyzed, in the same patients, the critical flicker frequency, proposed as an alternative method to detect MHE.

Conclusion: Placentas of HCV-seropositive mother-child dyads demo

Conclusion: Placentas of HCV-seropositive mother-child dyads demonstrate frequent CD8+ T cells that specifically target HCV epitopes. In particular, the placenta has an enrichment of the TSCM memory phenotype and relatively low frequency of naïve CTLs. The expansion of primordial memory population with enhanced self-renewal and multipotency likely contributes to anti-HCV immunity and

limits HCV transmission. Further characterization of these mechanisms might provide a broader application for novel immunotherapeutic approaches for HCV infection. Disclosures: Michael R. Narkewicz – Consulting: Vertex; Grant/Research Support: BTK inhibitor Novartis, Vertex; Stock Shareholder: Merck The following people have nothing to disclose: Rachel McMahan, Christine

Waasdorp Hurtado, Lucy Golden-Mason, Mona Krull, Hugo R. Rosen Background: The FIB-4 index is a simple SAHA HDAC formula using age, aspartate aminotransferase(AST), alanine aminotransferase (ALT), and platelet counts to evaluate liver fibrosis. We investigated the use of the FIB-4 index in predicting the incidence of hepatocellular carcinoma (HCC) in hepatitis C virus carriers with normal ALT levels. Methods: A total of 516 patients with ALT levels persistently less than or equal to 40 IU/L during the observation period over 3 years were included. None of the patients received antiviral therapy. Factors associated with the cumulative incidence of HCC were determined. Results: HCC developed in 60 of 51 6 patients (1 1.6%). The rates of HCC at 5 and 10 years were 2.6% and 17.6%, respectively. When patients were categorized based

on the FIB-4 index: <2.0 (n=226), >2.0 and <4.0 (n = 169), and >4.0 (n=121), the cumulative incidences Thymidylate synthase of HCC at 5 years were 0.5%, 1.3%, and 8.0%, and those at 10 years were 2.8%, 25.6%, and 37.1 %, respectively. The patients with FIB-4 index > 4.0 was at a highest risk for HCC development (p<0.0001). Factors that were significantly associated with the incidence of HCC by mul-tivariate analysis were FIB-4 index >2.0 (hazard ratio: 7.690 [95% confidence interval, 2.636–22.438]; p<0.001) and FIB-4 index >4.0 (8.991 [3.088–26.178] ; p<0.001), α-fetopro-tein(AFP) >5 ng/ml (2.742 [1.497–5.023] ; p<0.001) and AFP>10ng/ml (4.915 [2.353–10.267] ; p<0.001), and total bilirubin >1.2 mg/dl (2.142 [1.115–4.117]; p=0.022).There were no significant correlation between FIB-4 index and tumor markers(AFP, AFP- Lens culinaris agglutinin-reactive (L3) and des-gamma -carboxyprothrombin (DCP)). Conclusions: The FIB-4 index is closely associated with the risk of HCC in hepatitis C virus carriers with normal ALT levels.

Serum ALT, as a marker of liver injury, was markedly and signific

Serum ALT, as a marker of liver injury, was markedly and significantly raised in OffCon-OD and further increased in OffOb-OD (Fig. 3A). These ALK inhibition increases were paralleled by raised expression of IL-6 and TNF-α messenger RNA (mRNA) (Fig. 3B,C). α-SMA, TGF-β, and collagen were all profoundly up-regulated in OffOb-OD (Fig. 3D-F). Histological assessment of hepatosteatosis revealed greater fat infiltration in OffCon-OD, compared to control, at both 3 (Fig. 4A) and 12 months (Fig. 4B). Previous exposure to maternal obesity (OffOb-OD) exacerbated hepatosteatosis at 3 and 12 months (Fig. 4A,B) which was more advanced at 12 months (Fig.

4B). In parallel, there was, at 12 months, clear evidence of histological liver injury in OffCon-OD, as confirmed by the increased Brunt-Kleiner NAS (Fig. 4D), with more-profound injury in OffOb-OD. There was an independent

effect of maternal and postnatal diet on the NAS. Biochemical evidence of fibrogenic pathway activation was corroborated by clear findings of pericellular fibrosis, Ulixertinib cell line on Masson’s trichrome staining, in OffOb-OD (Fig. 4C,E). We then investigated hepatic nonparenchymal cell fraction. The KC population examined by FACS analyses and corroborated by IHC staining was increased in OffOb-OD, but not in OffCon-OD, compared to OffCon-SC (Fig. 5A,B). Despite the increased numbers, KC phagocytic function was impaired (Fig. 5C) in OffOb-OD, compared to OffCon-SC. In contrast, KC ROS production was significantly increased upon LPS stimulation in OffOb-OD, compared to both OffCon-SC HSP90 and OffCon-OD, with a significant interaction between maternal obesity and postweaning diet (Fig. 5D). Furthermore, hepatic expression of the proinflammatory cytokines, IL-12 and IL-18, were similarly up-regulated

in OffOb-OD, compared to controls. There was an independent main effect of maternal diet on IL-12 expression as well as a significant interaction between maternal obesity and postnatal diet for IL-18 expression (Fig. 6A,B). Interestingly, NKT cell numbers were significantly reduced in OffOb-OD (Fig. 6C,D), and there was a significant interaction between maternal and postweaning diets. A substantial body of literature currently suggests that maternal obesity or a hypercalorific diet may, through perturbation of the intrauterine environment, lead to life-long risk of obesity and related metabolic disorders.7 Animal models in particular have proven invaluable in understanding the mechanisms underlying the persistent effects of maternal obesity on the developing offspring and strongly support the hypothesis of the developmental origins of disease.20, 21 Employing a mouse model of maternal obesity, we have previously demonstrated evidence of offspring hyperphagia, increased adiposity, hypertension, IR, and NAFLD in tandem with reduced hepatic insulin signalling and raised sympathetic tone.

Changes in biochemical parameters under induced blight stress as

Changes in biochemical parameters under induced blight stress as compared with uninoculated control were less in resistant genotypes than that in susceptible genotype. The deviations in biochemical contents were highest in susceptible genotype N-118. Based on the variations of above parameters under stress and non-stress control among

the four tested genotypes, the overall pattern of changes was N-118 > Duradim > Jhankri > DP-25, which is in accordance with the pattern of increasing resistance. The resistant genotypes could be used for commercial cultivation and genetic improvement programme to develop resistant varieties to Phytophthora leaf blight disease. “
“SYBR Green real-time RT-PCR assay was developed and optimized for the sensitive detection of Onion yellow dwarf virus (OYDV), Leek selleck compound yellow stripe virus (LYSV), Garlic common latent virus (GCLV), Shallot latent virus (SLV) and Mite-borne filamentous virus (MbFV). The polyvalence of the designed primers was tested on 50 genotypes of

garlic (Allium sativum L.) which originated from different countries. Plasmid standards were prepared and used as positive standards. The efficiencies of all reactions were 97, 93, 99, 98 and 87% for OYDV, LYSV, SLV, BMN673 GCLV and MbFV standards, respectively. The detection limit for OYDV, LYSV and GCLV was as low as five gene copies, for SLV it was 15 gene copies

and for MbFV it was 130 gene copies. In comparison with ELISA, more virus-positive garlic accessions were detected with LYSV and GCLV by SYBR Green-based real-time RT-PCR assay. This method was shown to be a more suitable tool for the detection of highly variable pathogens, such as garlic viruses. “
“Symptomatic tomato plants exhibiting big bud, proliferation Tacrolimus (FK506) and small leaves of lateral shoots, purplish top leaves, phyllody, enlarged pistils, hypertrophic calyxes and small and polygonal fruit were collected in Yunnan Province of China. Pleomorphic phytoplasma-like bodies were observed in the phloem sieve tube elements of symptomatic plants by transmission electron microscopy. The presence of phytoplasma in collected samples was further analysed and identified by PCR and virtual computer-simulated restriction fragment length polymorphism (virtual RFLP). A 1.2 kb product was amplified by PCR with universal primers R16F2n/R16R2. Sequence comparisons revealed that the tested strains shared 99% 16S rRNA gene sequence similarity with members of ‘Candidatus Phytoplasma aurantifolia’ (16SrII group). Phylogenetic and virtual RFLP analysis of the 16S rRNA gene sequences confirmed that the phytoplasma is a member of the 16SrII group. This is the first report of 16SrII group phytoplasma infecting tomato in China.