The specific diagnosis was also recorded. SPSS was used to analyze the data. Descriptive statistics were used to explore demographic data and survey responses. Chi-square tests of independence were conducted to examine associations among variables. A total of 72 patients completed surveys. Three (4.2%) patients were under the age of 25, 23 (31.9%)

were between the ages of 26 and 35, 18 (25%) were between the ages of 36 and 45, 17 (23.6%) were between the ages of 46 and 55, and 9 (12.5%) were over the age of 55. Two (2.7%) patients did not report their age. Out of the 72 patients, 32 (44%) reported that they had pelvic region pain brought on by sexual activity. Thirteen (18%) indicated they had pelvic region pain that prevented them from engaging in sexual activity. Of this website the patients who reported pelvic pain, 1 (3.2%) indicated they had pain for less than 1 year, 12 (35.4%) reported they had

pain from 1 to 5 years, 9 (29%) indicated they had pain from 6 to 10 years, and 10 (32.3%) said the pain was present for over 10 years. A chi-square test of independence was conducted to examine whether there was an association between the frequency of pelvic region pain brought on by or preventing sexual activity, and the type of headache (chronic medication overuse headache, INCB024360 order chronic migraine, or a combination of the 2). There was no significant association

between pelvic pain brought on by sexual activity and the type of headache, χ2(2) = 0.65, P > .05. However, a pattern emerged suggesting that a greater percentage of patients reported pelvic pain brought on by sexual activity if they reported both chronic medication overuse headache and migraine (57.1%) compared with patients who reported either chronic medication overuse headache (41.7%) or chronic migraine (41.2%). There was no significant association between pelvic pain that prevents sexual activity and the type of headache, χ2(2) = 0.65, P > .05. When patients were asked whether they had discussed their pelvic region pain with an HCP, 16 (50%) indicated they had, while the remaining 16 (50%) did not. Of the patients why who had discussed their pain with an HCP, 5 (31%) indicated they had not received treatment at all, 6 (37.5%) reported they were currently in treatment, 5 (31.2%) said they had received treatment in the past, and 1 (6.2%) did not give a response regarding whether they had treatment. Of those patients who had discussed their pain with a HCP but indicated that they did not receive treatment (n = 6), the reasons provided included: no treatment was offered (n = 2); pain went away on its own (n = 2); pain was not severe enough to warrant care (n = 1); and too embarrassed to pursue treatment (n = 1).

Phosphorylation of both Y705 and S727 residues was reduced in PTPRO-overexpressing cells, indicating that PTPRO expression inhibited STAT3 activity (Fig. 5A). Moreover, STAT3 Y705 and S727 phosphorylation was detected in tissue proteins from ptpro−/− and WT mice. Both western blotting and IHC staining exhibited escalated phosphorylation

levels of Y705 and S727 (Fig. 5B,C). In addition, cyclin D1 and Bcl-2 were found to be down-regulated in PTPRO-overexpressing HCC cells; these findings serve to explain the modified cell proliferation and apoptosis. We further evaluated the correlation between PTPRO level and STAT3 activity with 50 paraffin-embedded human HCC tissue slices. Two cases of HCC with different PTPRO expression levels are shown in Fig. 5D: case selleck screening library 1 (weak positive) and case 2 (negative). phosphorylated STAT3 (p-STAT3) Selleck PF2341066 levels were extensively down-regulated in case 1. Pearson’s

correlation analysis demonstrated the inversely linear relationship between p-STAT3 and PTPRO levels in HCC (Fig. 5E; PTPRO and p-STAT3 [Y705]: r2 = 0.3536, P < 0.001; PTPRO and p-STAT3 [S727]: r2 = 0.4464, P < 0.001). Taken together, these findings indicated that PTPRO suppressed HCC by control of STAT3 activation. Because PTPRO exhibited an effective role in STAT3 inactivation, we further investigated PTPRO-mediated signaling, through which STAT3 phosphorylation was directly regulated. Published data indicated that JAK2 played the role of a typical activator of STAT3; because p-JAK2 (Y1007) phosphorylation has been demonstrated

to be associated with JAK2 activity, we assessed its expression in HCC cells and mice using western blotting and IHC staining. p-JAK2 level was decreased in PTPRO-overexpressing HCC cells and increased in ptpro−/− mice (Fig. 6A,D). We then treated HCC cells with JAK2 inhibitor (AG490)40 and found that PTPRO-overexpressing HCC cells exhibited a higher level of Y705 phosphorylation and a lower level in S727 (Fig. 7B). This finding suggested that PTPRO controlled STAT3 Y705 phosphorylation through JAK2. Because STAT3 Y705 dephosphorylation was potentially the result of inactivated Benzatropine JAK2, we were intent to identify the pathway of S727 dephosphorylation regarding PTPRO regulation. Because c-Src-mediated JNK, MAPK p38, and ERK pathways activated STAT3 at both the Y705 and S727 sites, we determined the level of p-c-Src (Y527), p-c-Src (Y416), p-JNK1, p-p38, and p-ERK in PTPRO-overexpressing cells and ptpro−/− mice. p-c-Src (Y527) and p-c-Src (Y416) levels were both decreased in PTPRO-overexpressing HCC cells and increased in ptpro−/− mice (Fig. 6B,D). However, our findings confirmed that Y527 and Y416 phosphorylation levels were divergent in terms of kinase activity.

1B). The authors deduct from this finding that increased proliferation is a consequence of increased apoptosis. However, the direct link between these two separate cellular fates is not entirely clear. It is known that some primarily apoptotic proteins including caspases or FADD (Fas-associated protein with death domain) exert nonapoptotic functions like cellular activation, proliferation, and differentiation (reviewed in Lamkanfi et al.6 and Strasser et al.7). However, the findings are somewhat contradictory, especially in the liver. The detailed understanding of nonapoptotic functions of caspases Fulvestrant purchase (or FADD) including the precise mechanisms, upstream

activators, and downstream targets will tremendously help cell death researchers and potentially foster future antineoplastic drug development Decitabine manufacturer (reviewed in Strasser et al.7). Another possible explanation of how increased apoptosis translates into carcinogenesis might be found in the up-regulation of Survivin, an inhibitor of apoptosis (IAP) family member that the authors found to be up-regulated

in hepatocytes lacking Mcl-1 (see figure 2, C and D, in Weber et al.1). Survivin is involved in cell cycle progression, proliferation, assembly of the mitotic spindle, but also apoptosis (reviewed in Altieri8). Survivin is highly expressed in a multitude of cancers, independently of their mitotic index, indicating that it is an interesting candidate to drive cell division and cell cycle entry. Its expression, however, might be a consequence (or unrelated effect) of increased proliferation rather than its cause. The study by Weber et al. would benefit from functional data on the role of Survivin; however, genetically accurate testing involves breeding Survivin-deficient mice into the Mcl-1fl/fl–AlbCre background. Defining the key players that drive proliferation in Mcl-1–deficient hepatocytes constitutes an intriguing and difficult task ahead. Solving the key components of potential caspase-mediated

proliferation will offer a variety of new insights into liver homeostasis and probably other tissues as well. What is the apoptotic stimulus that kills Oxalosuccinic acid Mcl-1–deficient hepatocytes in unchallenged mice? The mitochondrial permeabilization by active Bak or Bcl-2–associated X protein (Bax) within hepatocytes is critical for intrinsic cell death progression. Although it is not clear which prosurvival Bcl-2 family members exactly neutralize Bax, its homologue Bak is subject to negative regulation specifically by Mcl-1 and Bcl-x(L) but not other prosurvival family members.9 Mcl-1 guards Bak and shields the outer mitochondrial membrane from apoptotic stimuli transmitted by BH3-only proteins such as Bim, Puma, and Noxa (Fig. 1A). The report by Weber et al. presents data on apoptosis (together with data from Vick et al.2) but does not provide evidence on the upstream stimuli that induce cell death.

2 It is proposed that the condition of DPM arises from a persistence or lack of remodeling of the embryonic ductal plate normally observed during IHBD formation. ARPKD, autosomal recessive polycystic kidney disease;

DPM, ductal plate malformation; HNF, hepatocyte nuclear factor; IHBD, intrahepatic bile duct; PDS, primitive ductal structure; SOX9, SRY-related HMG box transcription factor 9; TβRII, transforming growth factor receptor type II; ZO-1, zonula occludens-1. From a developmental point of view, the cells that contribute to the IHBD system are a subpopulation of hepatoblast bipotential progenitors located near portal veins. This subpopulation of hepatoblasts forms a band of potential cholangiocytes, termed a ductal plate, encircling the portal veins. Remodeling of ductal plates into IHBDs start at the oldest ductal plates surrounding the larger Autophagy Compound Library portal veins near the hilum and is thought to move toward the periphery of liver following the portal vein system. The ductal plate cells

that remain unincorporated into an IHBD then involute. If the unincorporated ductal plate cells do not receive or are deaf to the proper signals, they may contribute selleck compound to DPM. Thus, there is a level of coordination that must regulate sequential tubulogenesis and regression of the ductal plates along portal veins within the three-dimensional space of the liver check details to connect the entire IHBD system to the extrahepatic ductal system. This indicates that careful orchestration of signals between epithelial and mesenchymal cells is required to guide IHBD formation.3 In this issue of HEPATOLOGY, the report by Raynaud et al.4 gives the general term DPM a new set of classifications according

to distinct defects in biliary tubulogenesis. This article reassesses how DPM observed in human congenital liver disease might result from various tubulogenesis defects in light of a defined transient asymmetry step identified during the process of mouse IHBD maturation.5 This step delineates the structure surrounding a forming lumen as either a primitive ductal structure (PDS) or a mature duct. PDS is composed of two cell types as distinguished by the presence or absence of marker expression (SRY-related HMG box transcription factor 9 [SOX9], hepatocyte nuclear factor 4 [HNF4], and transforming growth factor receptor type II [TβRII]) compared to a mature duct. The PDS is asymmetrical; cells on the portal vein side of the lumen express the marker SOX9, compared to cells on the parenchymal side that express HNF4 and TβRII. A mature duct is symmetrical, composed of cells expressing SOX9. To evaluate DPM, the authors focused their investigation on differentiation, polarity, and ciliogenesis in mouse models and human cases of DPM. Raynaud et al.

The following primary antibodies were used: anti-thrombin (clone 12, BD Biosciences, Franklin Lakes, NJ), anti-OPN (R&D Systems, Minneapolis, MN), anti-FAK, Phospho-FAK (Tyr397), or anti-GAPDH (Cell Signal

Tech, Danvers, MA). Values are expressed as the mean ± standard deviation. P < 0.05 was considered statistically significant. Both the mRNA and protein expression levels of thrombin in six established HCC cell lines were found to be significantly increased in comparison to nontransformed hepatic cell lines (L-02 and Chang liver cell U0126 price lines) detected by real-time PCR (Fig. 1A) and western blot (Fig. 1B). Among these HCC cell lines, HepG2, PLC, and MHCC97-L cells had relatively lower invasive and metastatic capabilities (low-metastatic group), whereas MHCC97-H, HCCLM3, and HCCLM6 had higher invasive and metastatic potential (high-metastatic group). Both the mRNA and protein

Belnacasan order expression levels of thrombin in these three high-metastatic HCC cell lines were much higher than those of the three low-metastatic HCC cell lines (P < 0.01, Fig. 1A,B). These data indicate that expression of thrombin is up-regulated in HCC cell lines, and its increased expression is positively correlated with the malignant phenotype of HCC cells. The mRNA expression levels of thrombin were evaluated in 72 human HCC tumors, in their adjacent nontumor liver tissues, and 20 normal liver tissues. The amount of thrombin mRNA was significantly increased in HCC tissues (2-&Dgr;Ct, 46.4 ± 23.5) compared with their adjacent nontumor liver tissues (19.6 ± 8.1, P = 0.005; Fig. 2A, Supporting Information PDK4 Table S2). Moreover, the higher amount of thrombin mRNA in HCC tissue was significantly positively correlated with tumor recurrence (P = 0.037; Fig. 2A). These findings were confirmed by elevated thrombin protein levels in eight out of the above 72 HCC tissue samples using western blot analyses (Fig. 2B). The mRNA level of OPN in HCC tissues (2-&Dgr;Ct,

137.4 ± 69.1) were also significantly higher than that in nontumor liver tissues (2-ΔCt, 22.2 ± 7.6, P = 0.043) and normal liver tissues (19.9 ± 8.7) (Supporting Information Table S2). A scatterplot of thrombin and OPN expression revealed no correlation between thrombin and OPN mRNA levels in HCC tissues (r = −0.17, P = 0.15) (Supporting Information Fig. S1). To determine whether thrombin influences OPN-related prognosis, we divided the HCC patients into low-OPN and high-OPN groups using the median OPN expression level as the cutoff. As shown in Fig. 2C, among the HCC tissues in the high-OPN group the expression level of thrombin was significantly increased in HCCs from the patients with tumor recurrence compared with those without recurrence (P = 0.027). Importantly, this difference was not statistically significant in the low-OPN group (P = 0.457).

2, 8, 9 Moreover, it remains unclear whether the degree of steatohepatitis www.selleckchem.com/products/GDC-0941.html depends more upon total adiposity per se (i.e., body mass index; BMI) or the severity of

adipose tissue dysfunction and resistance to insulin action (i.e., liver exposure to elevated plasma free fatty acids; FFA). Adipose tissue is important under normal living conditions, being the primary source of FFA (∼70%) for hepatic triglyceride (TG) synthesis.10 Excess release of FFA plays a key role in the development of hepatic “lipotoxicity” in NAFLD.7, 11-13 Failure of insulin to inhibit TG lipolysis in insulin-resistant states leads to the oversupply of FFA to the liver, excess hepatic TG synthesis, and intracellular accumulation of toxic lipid products that impair insulin signaling and activate inflammatory pathways (i.e., nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor/nuclear factor kappa light-chain enhancer of activated B cells and Jun N-terminal kinase pathways, Toll-like receptor 4, and others). Adaption to this metabolic stress involves hepatic IR, dyslipidemia and

steatohepatitis with mitochondrial dysfunction, endoplasmic reticulum stress, release of reactive oxygen species, and hepatocellular damage.14 Whether the degree of hepatic IR and steatohepatitis is proportional to the magnitude of adipose tissue IR has not been carefully examined. Only one study has reported that Selleck LY294002 the severity of adipose tissue IR is closely correlated with histological damage in patients with nonalcoholic steatohepatitis (NASH) as well as its improvement with a thiazolidinedione (TZD) to the reversal of dysfunctional fat.9 To better understand the relationship between the degree of adipose tissue IR, hepatic steatosis, and NASH, we studied in depth the metabolic and

histological profiles of patients with and without NAFLD. If liver disease mirrors adipose tissue dysfunction, future therapies aimed at dysregulated adipose tissue may hold particular promise in NAFLD. A1c, test for glycated hemoglobin; Adipo-IR, Glutathione peroxidase Adipo-IRi, adipose tissue insulin resistance index; ALT, alanine aminotransferase; ANOVA, analysis of variance; AST, aspartate aminotransferase; BMI, body mass index; DXA, dual-energy X-ray absorptiometry; EGP, endogenous glucose production; FFA, free fatty acids; FPI, free plasma insulin; HDL-C, high-density lipoprotein cholesterol; HIRi, hepatic insulin resistance index; HSCs, hepatic stellate cells; IR, insulin resistance; LDL-C, low-density lipoprotein cholesterol; MetS, metabolic syndrome; MHO, metabolically healthy obese; MRI, magnetic resonance imaging; MRS, magnetic resonance imaging and spectroscopy; NAFLD, nonalcoholic fatty liver disease; NAS, NAFLD activity score; NASH, nonalcoholic steatohepatitis; OGTT, oral glucose tolerance test; Rd, insulin-stimulated glucose disposal; T2DM, type 2 diabetes mellitus; TG, triglyceride; TZD, thiazolidinedione. We recruited a total of 229 subjects.

“
“Summary.  Persistence of inhibitors against factor VIII (FVIII) may be a risk factor that increases physical disability in haemophilia A (HA) patients. This study aimed to evaluate prevalence of FVIII inhibitors in previously treated children with severe HA and the impact of persistent inhibitors

on knee joint status and lumbar bone mineral density (BMD). Fifty children with severe HA, FVIII <1%; aged 5–16 years were enrolled in this study; they received plasma-derived FVIII on-demand treatment for 50–250 exposure days (EDs). Inhibitors were checked at Selleckchem BMS 907351 basal visit and were followed up for 1 year, using Bethesda assay. Cross-sectional clinical scoring and radiological evaluation of the knee joint (by Arnold-Hilgartner staging and Pettersson score), along with lumbar BMD by Dual Energy X-ray Absorptiometry (DEXA) were performed. Patients with persistent inhibitors for 1 to 5 years, median 2.5 years, were 10 (20%). Six had high titre and none of them had completely normal knees, seven had advanced knee arthropathy and six had low lumbar BMD in comparison to 2 and 8 of the 40 patients without inhibitors respectively (P < 0.05). Persistence of inhibitors for more than 2 years without immuno-prophylaxis was a risk factor for joint damage. Low lumbar BMD was found in

88.9% of patients with stages four and five knee arthropathy and in 66.7% of patients with positive hepatitis C. Severe HA children in this Egyptian study had a relatively low prevalence of persistent FVIII inhibitors, which, if not VX-770 mouse treated, may increase the risk of knee arthropathy and lumbar osteopenia. “
“The increasing emphasis on home-based treatment for the management of children with haemophilia has meant that many of these children no longer regularly report to a medical facility. Consequently, it is difficult to monitor incidence of bleeding episodes. The aim of this study was to assess the feasibility of using a short message service (SMS) to monitor incidence of bleeding episodes in children with haemophilia. One hundred

and four children with moderate and severe Resveratrol haemophilia A or B took part in a 1-year prospective study between 2008 and 2010. Children or their parents were asked to maintain a bleeds diary. They received a weekly SMS asking whether there had been a bleeding episode in the preceding week. Response rates were calculated. Children were followed for a total of 4839 person-weeks. SMS replies were received for 4201 weeks. Thus, the rate of follow-up was 86.8%. Median responses rates were 94.2% (IQR: 86.1–100%). Weekly SMS is a feasible reporting tool for documenting bleeding episodes in children with haemophilia. It is associated with high response rates and minimal expense and intrusion. The use of SMS could be extended to encourage compliance to prophylactic treatment, particularly in adolescents with haemophilia. “
“Summary.

CPA showed significant reduction of collagen deposition in the abstinent group compared to the recent drinkers (1 4.2 % vs 25.6 %, p= 0.04).

Significant over-expression of MMP-9 was observed in the abstinent group as compared to the recent drinkers (2.0 vs 0.33, p=0.013). Immunostains for TIMP-1 &2 and MMP-2 were negative in both groups. Conclusions: This study demonstrates evidence of fibrosis regression in liver transplanted patients after a long period of alcohol abstinence. IHC study further supports the role of MMP-9 in this fibrosis regression. Comparison of immunohistoloical features of abstinent liver transplant patients and recent sobriety   M:F Age Steatosis (%) Mallory-Denk hyalines CPA (%) MMP-9 expression * p < 0.05, ns: not significant Disclosures: The following people have nothing to disclose: Hongfa Zhu, Xuchen Zhang, Fal-guni Parikh, HaiShan Wu, Neil D. Theise, Stephen see more C. Ward, Swan N. Thung, Thomas D. Schiano, M. Isabel Fiel Background/Aim: Cirrhosis is a long-term consequence of chronic hepatic injury with fibrosis and no

effective therapy except liver transplantation is currently available for decom-pensated cirrhosis. However, some practical limitations in liver transplantation lead us to a need for new therapeutic paradigm in this field. Recent reports have shown that the mesenchymal stem cells(MSCs) have the plasticity to differentiate into some kinds of tissue cells and improve organ function. Hence, STA-9090 price we investigated the effect of direct inoculation of human bone marrow derived MSCs(BM-MSCs) in thioacetamide(TAA)-induced cirrhosis in a rat model. Methods: Adult Sprague-Daw-ley rats were allocated into three groups (each group, n = 15) as follows: G1, shame; G2, TAA-control; G3, TAA+BM-MSC. To induce cirrhosis, 200mg/kg TAA injection was done twice a week for 12weeks in G2 and G3. 2×106 cells of amplified human BM-MSCs were injected directly into the right liver lobe twice, at weeks 6 and 8 in G3. At 12 weeks, the effect of BM-MSCs on cirrhosis was analyzed histomorphologically using

Laennec scores. α-Smooth muscle actin(α-SMA) expression by immunohistochemical staining, relative expression of collagen type 1, and transforming growth factor β (TGF-β) were also evaluated by real-time ifenprodil reverse transcriptase-polymerase chain reaction. Results: Laennec scores were 0, 5.4±0.7 and 3.7±1.06 in G1, G2 and G3, respectively. Histologically, BM-MSCs injected group (G3) showed significant suppression of hepatic fibrosis compared with TAA-control group (G2)(P < 0.001). Expressions of α-SMA(%) were significantly lower in G3 than in G2 (3.08±1 .26 vs. 7.00±4.12, P < 0.05). Also, the relative expression of collagen type 1 and TGF-β1 in RT-PCR were 0.64±0.24, 2.06±0.51, 1.32±0.31 and 0.62±0.28, 5.89±3.05, 2.22±1.41 in G1, G2 and G3, respectively P < 0.005).

2003, Karczmarski

et al. 2005). Bottlenose dolphins in the Bahamas lost 30% of their resident individuals, with an influx of almost the same number of immigrants after two major hurricanes impacted the area (Elliser and Herzing 2011). This resulted in a split of the community into two Idelalisib solubility dmso units, which were distinct and more homogenous in nature (Elliser and Herzing 2011). After the extreme environmental disturbance of the oil spill from the Exxon Valdez, killer whales suffered similar losses and a split in a matriline occurred (Matkin et al. 2008). It is evident that demographic and/or environmental factors can help shape the social structure of a given population. How individuals adjust

to these changes may depend on the species, habitat, and social structure of the population. This study reports on a large loss of individuals from a small stable, resident, community of Atlantic spotted dolphins and the subsequent effects on their social structure. This community has been studied since 1985 (Herzing 1997, Herzing and Brunnick 1997). Long-term association patterns reveal a society remarkably similar to well-studied coastal bottlenose dolphin societies, including female networks, male alliances, and no long-term associations between sexes (Elliser and Herzing, in press). This community is divided into three Copanlisib ic50 social Aprepitant clusters with overlapping ranges where mixed-cluster groups occur, but associations are stronger within clusters than between (Elliser and Herzing 2012). In 2004 this community was impacted by two major hurricanes within three weeks of each other. Following the hurricanes this community had a decrease in community size, either through mass mortality, displacement, or other correlated events. Due to the synchronous and sharp decline and lack of resightings of individuals that disappeared after 2004 (as of 2012 none have been

resighted), the reduction in community size was most likely due to the hurricanes. The goal of the present study was to quantitatively describe the differences in social structure of this community of spotted dolphins before and after the hurricanes in 2004. Little Bahama Bank (LBB) is about 64 km from the east coast of Florida, and just north of West End, Grand Bahama Island. The study area spans 60 km north to south and 8 km east to west and encompasses 480 km2. The sandbank is shallow, between 6 and 16 m deep, and is surrounded by deep water (steep drop off to over 500 m into the Gulf Stream). It has a mostly sandy bottom, scattered with areas of rock, reef, and patches of seagrass (Thalassia testudimum). The entire study area was divided into six sections, A–F (Fig. 1). Effort was not evenly distributed throughout every area (% of total effort: A = 3.5%, B = 10.2%, C = 31.8%, D = 51.4%, E&F = 3.

The PCR-negative samples were also subjected to dsRNA and mechanical transmission tests. PCR Roxadustat manufacturer results indicated that c. 86% of the trees were infected with at least one virus, whereas visible bands were shown by 3 of 24 PCR-negative samples in dsRNA analysis. OLYaV was the most prevalent virus (49.1%), followed by OLV-1 (34.3%), CMV (25.7%), OLRSV

(16.6%), CLRV (13.1%), SLRSV (7.4%) and OLV-2 (6.9%), whereas ArMV was not detected. Very high infection rates were found in the two main oil cvs. Chemlali (84.6%) and Chétoui (86.9%). “
“In 2012 and 2013, watermelon (Citrullus lanatus) plants from commercial crops in São Paulo State were found showing mosaic, necrotic lesions, leaf deformation and necrotic spots on the fruits, suggestive of tospovirus infection. Leaf and fruit samples were separately tested by PTA-ELISA and reverse transcription

polymerase chain reaction (RT-PCR) against tospovirus was performed. The virus was identified as Groundnut ringspot virus (GRSV) and was sap transmissible. The host range was similar to isolates of GRSV found naturally infecting Solanaceae, except that this isolate infected watermelon systemically but did not infect tomato cvs. Santa Clara and Mariana. Thrips collected in the field transmitted GRSV to watermelon, sweet pepper and Nicotiana species. To our knowledge, this is the first report on the natural infection of watermelon by GRSV. “
“The genus Ditylenchus learn more contains more than 80 recognized nematode species with a very wide host range. The most serious species are Ditylenchus dipsaci and Ditylenchus

destructor. Populations of D. dipsaci species complex were collected from Allium cepa, Cichorium endivia and Phlox paniculata in Poland. The Ditylenchus gigas population was collected from Vicia faba minor, and OSBPL9 populations of D. destructor, from Solanum tuberosum spp. tuberosum. Analyses of the rDNA sequences spanning both ITS1 and ITS2 fragment regions were carried out on the collected populations. The obtained DNA sequences were compared with those DNA sequences deposited in GenBank of populations isolated in other countries. Phylogenetic analysis was performed using the data obtained from the DNA sequence comparisons. The results indicated that there is no clear distinction between European and non-European populations within D. dipsaci. The results also showed no clear distinction between populations isolated from different host plant species, including populations found in Poland. The populations of D. destructor described here constitute a common group together with American and Chinese populations belonging to the haplotype C of the D. destructor species. On the other hand, the D. gigas population was localized separately from those populations that have been described up until now, from Europe and Africa. This is also the first report on the occurrence of D.