These intriguing results were confirmed in a diet-induced obesity and insulin resistance model. Liver-specific knockout of Lrh-1 had no effect on development of obesity and diabetes

when a high-fat diet was applied over 15 weeks. However, DLPC treatment substantially improved Selleck PLX4032 glucose homeostasis, and decreased hepatic glucose production, and serum glucose and insulin levels. Improved hepatic insulin sensitivity may have been caused by increased insulin-dependent phosphorylation of the insulin receptor IRS2. Despite unchanged food intake, total body weight, and liver weight, hepatic triglycerides and NEFAs were reduced following DLPC administration and mouse livers showed reduced steatosis. Mechanistically, DLPC markedly decreased expression of genes associated with de novo lipogenesis, especially the lipogenic transcription factor Srebp-1c and its key downstream targets Acc-2, Scd-1, and Fasn. However, no effects of DLPC were observed on hepatic expression of a number of genes controlling glucose homeostasis. It is noteworthy that both serum and hepatic bile salts nearly doubled following DLPC treatment, alongside an induction of Cyp7a1 and Cyp8b1 in the liver. All reported effects of DLPC

were absent when LRH-1 was conditionally deleted in the liver. DLPC thus proved to be of potential selleckchem therapeutic benefit in both genetic and diet-induced models of insulin resistance. Encouraged by these results, Lee et al. suggest that DLPC might be a promising therapeutic agent for the treatment of metabolic these disorders. Consequently, the group has initiated a clinical trial to explore the effect of DLPC in prediabetic

patients. How does DLPC improve insulin sensitivity and reduce steatosis? The authors reason that the beneficial effect of DLPC on steatosis might be a result of the markedly decreased expression of Srebp-1c and/or decreased insulin levels. They propose the following regulatory loop (Fig. 1): Lrh-1-dependent repression of Srebp-1c expression may improve steatosis, increase insulin sensitivity, and hence decrease serum insulin; and decreased insulin levels in turn may reinforce repression of Srebp-1c,5 further ameliorating steatosis. This model is supported by previous data from other groups: the repression of Srebp-1c by way of Lrh-1 is consistent with a functional antagonism of SREBP-1c transactivation by LRH-16 and Srebp-1c target genes Acc-2 and Scd-1 have been shown to modulate β-oxidation, hepatic steatosis, and insulin resistance.1 Do bile salts contribute to the antidiabetic and antisteatotic effects of DLPC? Upon DLPC treatment, bile salts in serum and more strikingly in liver tissue were markedly increased. This is remarkable because hepatic bile salt levels are tightly controlled. Feeding a 1% cholate (w/w) diet only induces an increase of hepatic bile salts by approximately 50% in mice.

These intriguing results were confirmed in a diet-induced obesity and insulin resistance model. Liver-specific knockout of Lrh-1 had no effect on development of obesity and diabetes

when a high-fat diet was applied over 15 weeks. However, DLPC treatment substantially improved Selleckchem Venetoclax glucose homeostasis, and decreased hepatic glucose production, and serum glucose and insulin levels. Improved hepatic insulin sensitivity may have been caused by increased insulin-dependent phosphorylation of the insulin receptor IRS2. Despite unchanged food intake, total body weight, and liver weight, hepatic triglycerides and NEFAs were reduced following DLPC administration and mouse livers showed reduced steatosis. Mechanistically, DLPC markedly decreased expression of genes associated with de novo lipogenesis, especially the lipogenic transcription factor Srebp-1c and its key downstream targets Acc-2, Scd-1, and Fasn. However, no effects of DLPC were observed on hepatic expression of a number of genes controlling glucose homeostasis. It is noteworthy that both serum and hepatic bile salts nearly doubled following DLPC treatment, alongside an induction of Cyp7a1 and Cyp8b1 in the liver. All reported effects of DLPC

were absent when LRH-1 was conditionally deleted in the liver. DLPC thus proved to be of potential HSP assay therapeutic benefit in both genetic and diet-induced models of insulin resistance. Encouraged by these results, Lee et al. suggest that DLPC might be a promising therapeutic agent for the treatment of metabolic Baf-A1 in vivo disorders. Consequently, the group has initiated a clinical trial to explore the effect of DLPC in prediabetic

patients. How does DLPC improve insulin sensitivity and reduce steatosis? The authors reason that the beneficial effect of DLPC on steatosis might be a result of the markedly decreased expression of Srebp-1c and/or decreased insulin levels. They propose the following regulatory loop (Fig. 1): Lrh-1-dependent repression of Srebp-1c expression may improve steatosis, increase insulin sensitivity, and hence decrease serum insulin; and decreased insulin levels in turn may reinforce repression of Srebp-1c,5 further ameliorating steatosis. This model is supported by previous data from other groups: the repression of Srebp-1c by way of Lrh-1 is consistent with a functional antagonism of SREBP-1c transactivation by LRH-16 and Srebp-1c target genes Acc-2 and Scd-1 have been shown to modulate β-oxidation, hepatic steatosis, and insulin resistance.1 Do bile salts contribute to the antidiabetic and antisteatotic effects of DLPC? Upon DLPC treatment, bile salts in serum and more strikingly in liver tissue were markedly increased. This is remarkable because hepatic bile salt levels are tightly controlled. Feeding a 1% cholate (w/w) diet only induces an increase of hepatic bile salts by approximately 50% in mice.

001) and Nkg2d+ NK cells (IL-1R1–/–: 4±0.4 vs WT: 6±1 %; P<0.01). RXDX-106 Conclusions: Disruption of the inflammasome by the loss of IL-1R1 signaling suppressed the activation of DCs and their ability to activate NK cells, and prevented obstruction of bile ducts in experimental biliary atresia. These data identify a regulatory role of IL-1R1 in pathogenesis of bile duct injury, and

as a potential novel therapeutic approach to treat the disease. Disclosures: Jorge A. Bezerra – Grant/Research Support: Molecular Genetics Laboratory, CHMC The following people have nothing to disclose: Tatsuki Mizuochi, Pranavkumar Shivakumar, Reena Mourya, Stephanie Walters, Bryan Donnelly, Shiva K. Shan-mukhappa Background: Hepatic macrophage activation by endotoxin (LPS) absorbed from injured intestine promotes Parenteral Nutrition Associated Cholestasis (PNAC) in mice (Hepatol-ogy. 2012;55:1518-28). Furthermore, intestinal microbiota and TLR4 signaling promote transcriptional suppression of hepatic bile salt export pump Abcb11/BSEP, bilirubin exporter Abcc2/MRP2 and sterol exporter Abcg5/8, which is associated with accumulation of cholestatic PN-derived phytosterols (Sci. Transl. Med. 2013 Oct 9;5(206):206ra137). However, the signaling pathways regulating these alterations in Selleck FK506 gene expression

in mice with PNAC remain undefined. The aim of this study was to elucidate the role of cytokine signaling pathways as mediators in PNAC. Methods and Results: Wild type (WT) C57/B6 mice that were exposed to dextran sulfate sodium (DSS) (to induce intestinal injury) for 4 days followed by infusion of phytosterol-containing (soy lipid) PN solution through a central venous catheter for 14 days (DSS-PN mice) developed cholestasis (increased serum bile acids and bili-rubin) and hepatocyte injury (increased AST and ALT) compared to controls (including mice treated Liothyronine Sodium with DSS only, PN only, or untreated chow fed). Compared to controls, DSS-PN mice displayed significantly reduced hepatic

mRNA amounts of Abcb11, Abcc2, Abcg5/8, paralleled by increased mRNA for Il1b while mRNA for Tnfα and Il6 were not increased. To further elucidate the role of IL-1β signaling in these pathways, mice with genetic deletion of the receptor for IL-1 (IL-1Rko) and syngeneic wild type mice were exposed to DSS-PN for 14 days or control treatments. Compared to DSS-PN wild type mice, DSS-PN treated IL-1Rko mice had significantly reduced serum AST, ALT, bile acids, and bilirubin. Moreover, hepatic gene expression of Abcb11, Abcc2, and Abcg5/8 was not reduced in DSS-PN IL1R-ko mice. To determine if IL-1β had a direct effect on hepatocytes, wild type mice were injected with recombinant IL-1β and sampled after 4 hrs, and HuH7 and HepG2 cells (human hepatocyte cell lines) were incubated with IL-1β for 4 hrs and gene expression was measured.

5 Thus, our observations suggest that risk factor–based screening of incarcerated adults, in addition to community screening of those born in the birth cohort, would be effective selleck screening library complementary strategies for national HCV testing and treatment initiatives. Our findings may be influenced by several limitations. First, initial screening was not performed by trained research staff, which enhances the probability of errors. Second, only ∼28% of all newly incarcerated inmates were screened; however, the racial/ethnic distribution of those screened was similar to the overall population. Importantly, we have likely underestimated the true prevalence of acute HCV for several reasons: (1) high-risk inmates who

did not undergo complete evaluation were not included

as potential cases, even if they had abnormal aminotransferase levels; (2) inmates may have underreported IDU due to stigma, fears of recrimination, or loss of confidentiality43; (3) inmates may have incorrectly reported their HCV serostatus; and (4) inmates already found to be seropositive would have been classified as having past infection, but may, in fact, have been recently infected or reinfected.44 We also could not determine the prevalence of acute check details HCV among low-risk individuals due to limitations in resources. Our real-life screening approach should be validated in additional health care settings, such as emergency rooms, opiate substitution clinics, detoxification clinics, needle exchange programs, and other correctional facilities. As one modeling

study suggests, this risk factor–based screening approach might also be cost-effective in finding new diagnoses.45 Implementation of screening protocols for acute HCV in high-risk populations represents a promising component of a comprehensive nationwide strategy for HCV prevention and surveillance.10 Furthermore, enough identification of those with chronic HCV infection in the prison setting would provide a golden opportunity for evaluating liver disease and providing therapeutic interventions.22 We thank the individuals who consented to take part in this study. We acknowledge Arthur Brewer, Thomas Groblewski, and Warren Ferguson of University of Massachusetts Medical School Correctional Health and the providers at MCI-Framingham and MCI-Concord for their support, especially Patricia Casella, Jessica Laprel, Jennifer O’Keefe, and Laura Smith (MCI-Framingham) and Rosalie Berry, Amie Dunbar, Jessica Fabry, Deirdre Kells, Khalid Mohammed, Joanne Pomerancz, and Edith Quintinella (MCI-Concord). We thank Daniel Church, Kimberly Page, and Rochelle Walensky for careful review of the manuscript. “
“Inflammatory myofibroblastic tumor of the liver (IMTL) is a very rare benign disease with a good prognosis. To determine the clinical, radiological, and pathological characteristics of IMTL. The diagnosis and treatment strategies were discussed.

Davis et al selleck compared ketorolac 60 mg IM with promethazine 25 mg IM plus meperidine 75 mg IM and found that there was no difference between the 2 groups in percentage pain free at 30 minutes (promethazine/meperidine 20.8% vs ketorolac 22.3%).7 Harden et al found no difference in headache relief between ketorolac 60 mg IM (44.4%), meperidine 50 mg plus promethazine 25 mg IM (60%), or placebo/NS IM (54.5%).9 Duarte et al found no difference in pain reduction (VAS) for

ketorolac 60 mg IM compared with meperidine 100 mg IM plus hydroxyzine 50 mg IM (−33.5 vs −33.7, P = .76); the percentage complaining of nausea and drowsiness was not significantly less for ketorolac (28% vs 48%, P = .15).8 Larkin and Prescott compared ketorolac 30 mg IM with meperidine 75 mg IM; the percentage pain free at 1 hour was greater for meperidine (30% vs 6%, P < .05), as was sustained pain freedom at 24 hours (44% vs 13%, P < .02), and no adverse events were reported in either group.11 Klapper and Stanton found that ketorolac 60 mg IM was less effective in treating migraine than DHE 1 mg IV plus metoclopramide 5 mg IV; headache relief (4-PPS) at 1 hour was greater for DHE/metoclopramide (78% vs 33%, P = .031).22 Bigal et al compared metamizole (MMZ, also called dipyrone and not available in the USA) 1000 mg IV with placebo/NS Atezolizumab in vivo IV.23 For migraineurs without aura, pain reduction (11-PPS) with

MMZ was more effective than placebo at 30 and 60 minutes (−4.0 vs −1.2, P < .01 and −6.0 vs −3.0, P < .01). For patients with aura, the reduction was also significantly greater with MMZ at 30 and 60 minutes (−4.9 vs −0.9, P < 0.01 and −6.4 vs −1.9, P < .01). Krymchantowski et al then compared MMZ 1000 mg IV with lysine clonixinate (LC, an NSAID not available in the USA) 200 mg IV, delivered as a 25 mL infusion over 5 minutes.24 The percentage pain free at 60 and 90 minutes was greater with LC (60 minutes: 33% vs 13%, P < .001; 90 minutes: 86.7% vs 73%, P < .001). There was no follow-up post-discharge. Patients receiving

LC had more injection-site pain than those receiving MMZ (13/15 vs 3/15, P < .0001). Engindeniz et al compared diclofenac sodium 75 mg IM with tramadol 100 mg IM. Headache relief at 2 hours was the same for both groups (80%).16 Ellis et al Liothyronine Sodium compared ibuprofen 600 mg oral (PO) with metoclopramide 10 mg IV and placebo; pain reduction (VAS) was similar for metoclopramide and metoclopramide/ibuprofen (−75 vs −50) but was greater in both these groups (P < .01) than in the ibuprofen or placebo groups, which were the same (−25).25 Table 2 summarizes the studies involving ketorolac, diclofenac, ibuprofen, LC, and MMZ (the last not an NSAID). The rate of headache recurrence within 24-72 hours following discharge from the ED can exceed 50%, and corticosteroids typically are used in the ED in an attempt to reduce the frequency of such recurrence.

Davis et al PLX3397 order compared ketorolac 60 mg IM with promethazine 25 mg IM plus meperidine 75 mg IM and found that there was no difference between the 2 groups in percentage pain free at 30 minutes (promethazine/meperidine 20.8% vs ketorolac 22.3%).7 Harden et al found no difference in headache relief between ketorolac 60 mg IM (44.4%), meperidine 50 mg plus promethazine 25 mg IM (60%), or placebo/NS IM (54.5%).9 Duarte et al found no difference in pain reduction (VAS) for

ketorolac 60 mg IM compared with meperidine 100 mg IM plus hydroxyzine 50 mg IM (−33.5 vs −33.7, P = .76); the percentage complaining of nausea and drowsiness was not significantly less for ketorolac (28% vs 48%, P = .15).8 Larkin and Prescott compared ketorolac 30 mg IM with meperidine 75 mg IM; the percentage pain free at 1 hour was greater for meperidine (30% vs 6%, P < .05), as was sustained pain freedom at 24 hours (44% vs 13%, P < .02), and no adverse events were reported in either group.11 Klapper and Stanton found that ketorolac 60 mg IM was less effective in treating migraine than DHE 1 mg IV plus metoclopramide 5 mg IV; headache relief (4-PPS) at 1 hour was greater for DHE/metoclopramide (78% vs 33%, P = .031).22 Bigal et al compared metamizole (MMZ, also called dipyrone and not available in the USA) 1000 mg IV with placebo/NS CT99021 price IV.23 For migraineurs without aura, pain reduction (11-PPS) with

MMZ was more effective than placebo at 30 and 60 minutes (−4.0 vs −1.2, P < .01 and −6.0 vs −3.0, P < .01). For patients with aura, the reduction was also significantly greater with MMZ at 30 and 60 minutes (−4.9 vs −0.9, P < 0.01 and −6.4 vs −1.9, P < .01). Krymchantowski et al then compared MMZ 1000 mg IV with lysine clonixinate (LC, an NSAID not available in the USA) 200 mg IV, delivered as a 25 mL infusion over 5 minutes.24 The percentage pain free at 60 and 90 minutes was greater with LC (60 minutes: 33% vs 13%, P < .001; 90 minutes: 86.7% vs 73%, P < .001). There was no follow-up post-discharge. Patients receiving

LC had more injection-site pain than those receiving MMZ (13/15 vs 3/15, P < .0001). Engindeniz et al compared diclofenac sodium 75 mg IM with tramadol 100 mg IM. Headache relief at 2 hours was the same for both groups (80%).16 Ellis et al FER compared ibuprofen 600 mg oral (PO) with metoclopramide 10 mg IV and placebo; pain reduction (VAS) was similar for metoclopramide and metoclopramide/ibuprofen (−75 vs −50) but was greater in both these groups (P < .01) than in the ibuprofen or placebo groups, which were the same (−25).25 Table 2 summarizes the studies involving ketorolac, diclofenac, ibuprofen, LC, and MMZ (the last not an NSAID). The rate of headache recurrence within 24-72 hours following discharge from the ED can exceed 50%, and corticosteroids typically are used in the ED in an attempt to reduce the frequency of such recurrence.

The amelioration of liver damage by systemic application of Cxcl9 might offer a novel therapeutic approach for chronic liver diseases associated with increased neoangiogenesis. (HEPATOLOGY 2012) The pathophysiology

of liver fibrosis is a complex biological process which includes features of abnormal inflammatory wound healing, the deposition of extracellular matrix proteins, and increased neoangiogenesis. 1-3 At advanced stages, liver fibrosis leads to liver failure, portal hypertension, and represents the main risk factor for hepatocellular carcinoma. 4 Therefore, novel therapies that target key molecules involved in this website fibrosis progression are clinically warranted. A chemokine receptor that has been implicated in many pathophysiological processes of fibroproliferative disorders, including liver fibrosis, is CXCR3. 5, 6 The main ligands of

this receptor are the interferon-γ-inducible chemokines CXCL9, CXCL10, and CXCL11 and the platelet-derived chemokine CXCL4 in humans. In experimental murine liver fibrosis models, genetic deletion of Cxcr3 (Cxcr3−/−) leads to a see more reduced hepatic infiltration of interferon-γ-positive T-cells, 7 which are considered part of an antifibrotic immune response. 8 These results are congruent with the main role of CXCL9 for transendothelial migration of T helper 1 (Th1)-polarized cells into the liver. 9 Furthermore, Cxcr3 has been shown to be important for recruitment of CD4+CD25+ T regulatory cells into the liver, which might limit inflammatory hepatic injury. 10, 11 In vivo, the absence of Cxcr3 leads to pronounced liver fibrosis 7 and an exacerbated liver damage after Concanavalin A administration. 11 These findings are in line with previous studies showing an enhanced fibrogenic response of Cxcr3-deficient mice in the lung 12 and the kidney. 13 Neoangiogenesis and Teicoplanin the development of an abnormal angioarchitecture in the liver are strongly linked with progressive fibrogenesis, although the direct interaction between both processes is not yet fully understood. 14 Among

molecules involved in angiogenesis, vascular endothelial growth factor (VEGF) has been identified to play potent angiogenic as well as profibrogenic role during liver fibrogenesis. 2, 15 In line with these findings, receptors for VEGF (VEGFR) are expressed in liver sinusoidal endothelial and stellate cells. 14 Interestingly, the CXC family of chemokines is also known to be crucially involved in angiogenesis. Members of the CXC family that contain an ELR motif (ELR+ chemokines) promote angiogenesis, whereas ELR− chemokines, which are all ligands of CXCR3, antagonize the formation of new blood vessels. 5, 16 Notably, the angiostatic CXCR3 ligand CXCL4 directly interferes with VEGF signaling in human cells.

This therapeutic modality was selected based on the large prosthetic space and the patient’s maxillary bone width and height condition, mainly on the right area, which would require bone grafts to obtain a ridge augmentation. The patient was informed about the possible therapeutic modalities and opted for the related treatment. This therapeutic alternative was less complex and time-consuming. In addition,

the use of dental implants in the maxilla would not significantly change the treatment planning for the anterior teeth regarding their periodontal condition. Even if an attachment-retained RPD was not used, these teeth would be splinted to form a stabilized polygon, achieving better long-term prognosis. As regards the periodontal health of the abutments and condition of the residual ridge, mandibular rehabilitation was performed using six dental implants selleck and a full-arch fixed prosthesis. The maxillomandibular relationship, including reestablishment of the curves

of Spee and Wilson and the OVD, was recorded with occlusion rims and an acrylic resin template, according to the metric, phonetic, and esthetic methods (Fig 3). The maxillary cast was oriented on the semiadjustable articulator with a facebow record and the mandibular cast was mounted. The artificial teeth were positioned for an esthetic and functional clinical evaluation. After this, maxillary interim prostheses (anterior crowns and RPD) were obtained. Considering the extensive caries lesions Ferroptosis activation and the inflammatory pulpal response or pulp breakdown, the maxillary left central incisor, lateral incisor, and canine were endodontically treated. The maxillary right central incisor was submitted to root canal retreatment. According to Torabinejad and Goodacre,[23] it appears that more than 95% of teeth Idoxuridine that have undergone endodontic treatment remain functional over time. Besides the success rates of endodontically

treated teeth used as abutments in RPDs, the maintenance of the remaining teeth present advantages such as proprioception and bone level preservation. Patient psychological factors must also be considered. Considering the absence of coronal dental tissue, which may compromise the bonding procedures for composite cores, only the left central incisor was restored with cast dowel and core. The other teeth were restored using a two-piece dowel/core system (prefabricated metallic dowel/composite core). When the presence of at least 1.5 to 2.0 mm of hard dental tissue structure is limited, and a cervical ferrule may not be gained, the definitive crown seems to be unable to support the masticatory loads.

flaccumfaciens pv. flaccumfaciens, the causal agent of cowpea bacterial wilt in Iran. “
“Evolutionarily conserved ecto-nucleoside triphosphate diphosphohydrolases (referred to ‘NTPDases’ below) are important ecto-nucleotidases that are able to hydrolyse NTPs and NDPs in the environment to the monophosphate form. NTPDases are found in a variety of eukaryotic organisms including medical pathogens. However, pathogenic roles of these NTPDases in medical and plant pathogens are still very obscure. Here, we demonstrate that conidial germination, appressorium formation and pathogenicity of rice blast fungus Magnaporthe oryzae that had been pretreated with NTPDase-specific inhibitors

were significantly reduced, suggesting that NTPDases of M. oryzae play an important role in its infection. Our findings may

provide a new avenue for powerful fungicide development and Selleckchem Target Selective Inhibitor Library the control of rice blast. “
“Cauliflower mosaic virus (CaMV) with a high incidence and widespread distribution on Brassica crops in Iran reduces the yield and quality of these crops. The complete sequences of three open reading frames (ORFs) 2, 4 and 6 coding for aphid transmission (AT), coat protein (CP) and inclusion body protein/translation transactivator (TAV) genes, respectively, were determined GSI-IX clinical trial for two Iranian CaMV isolates from Kerman (south Iran). They induced latent or mild mottle (L/MMo) infection in Brassica oleracea var. capitata so are considered as the (L/MMo) biotype. Clear recombination breakpoints were detected between ORF2 and ORF6 in two Kerman isolates using concatenate fragments. Phylogenetic analysis revealed three Iranian CaMV pheromone subpopulations in which the two Kerman isolates in the new subgroup C were added to the two previously reported Iranian subpopulations A (central and west Iran) and B (north-east Iran). Also three regions of pairwise identity were detected which representing: 97.1–100, 93.8–97.1 and 90.6–93.8% for subgroups A, C and B, respectively. Our

analysis showed the high variability of Iranian CaMV population and provided valuable new information for understanding the diversity and evolution of caulimoviruses. Furthermore, star phylogeny was found in the subgroup C with overall lack of nt diversity and high haplotype diversity as evidence of a recent population expansion after a genetic bottleneck although this may have been modified subsequently by clinal genetic drift. The appearance of new genetic types demonstrates a high potential of risks and should be considered in the planning of efficient control programmes. “
“In recent years, leaf necrosis and twig dieback in the olive crop have been detected in Sicily (Italy). In this article, we identify the predominant fungal species associated with symptomatic leaves and twigs, using morphological features and DNA sequencing of the internal transcribed spacer (ITS) region, as Alternaria alternata, Arthrinium phaeospermum, Phoma cladoniicola and Ulocladium consortiale.

flaccumfaciens pv. flaccumfaciens, the causal agent of cowpea bacterial wilt in Iran. “
“Evolutionarily conserved ecto-nucleoside triphosphate diphosphohydrolases (referred to ‘NTPDases’ below) are important ecto-nucleotidases that are able to hydrolyse NTPs and NDPs in the environment to the monophosphate form. NTPDases are found in a variety of eukaryotic organisms including medical pathogens. However, pathogenic roles of these NTPDases in medical and plant pathogens are still very obscure. Here, we demonstrate that conidial germination, appressorium formation and pathogenicity of rice blast fungus Magnaporthe oryzae that had been pretreated with NTPDase-specific inhibitors

were significantly reduced, suggesting that NTPDases of M. oryzae play an important role in its infection. Our findings may

provide a new avenue for powerful fungicide development and CHIR-99021 order the control of rice blast. “
“Cauliflower mosaic virus (CaMV) with a high incidence and widespread distribution on Brassica crops in Iran reduces the yield and quality of these crops. The complete sequences of three open reading frames (ORFs) 2, 4 and 6 coding for aphid transmission (AT), coat protein (CP) and inclusion body protein/translation transactivator (TAV) genes, respectively, were determined SCH727965 for two Iranian CaMV isolates from Kerman (south Iran). They induced latent or mild mottle (L/MMo) infection in Brassica oleracea var. capitata so are considered as the (L/MMo) biotype. Clear recombination breakpoints were detected between ORF2 and ORF6 in two Kerman isolates using concatenate fragments. Phylogenetic analysis revealed three Iranian CaMV Reverse transcriptase subpopulations in which the two Kerman isolates in the new subgroup C were added to the two previously reported Iranian subpopulations A (central and west Iran) and B (north-east Iran). Also three regions of pairwise identity were detected which representing: 97.1–100, 93.8–97.1 and 90.6–93.8% for subgroups A, C and B, respectively. Our

analysis showed the high variability of Iranian CaMV population and provided valuable new information for understanding the diversity and evolution of caulimoviruses. Furthermore, star phylogeny was found in the subgroup C with overall lack of nt diversity and high haplotype diversity as evidence of a recent population expansion after a genetic bottleneck although this may have been modified subsequently by clinal genetic drift. The appearance of new genetic types demonstrates a high potential of risks and should be considered in the planning of efficient control programmes. “
“In recent years, leaf necrosis and twig dieback in the olive crop have been detected in Sicily (Italy). In this article, we identify the predominant fungal species associated with symptomatic leaves and twigs, using morphological features and DNA sequencing of the internal transcribed spacer (ITS) region, as Alternaria alternata, Arthrinium phaeospermum, Phoma cladoniicola and Ulocladium consortiale.