Recent studies showed that repositioning the hands in visible space, or making visual events more distant, can modulate such crossmodal extinction. Here, in a detailed single-case study, we implemented a novel spatial manipulation when assessing crossmodal extinction. This was designed not only to hold somatosensory inputs and hand/arm-posture

constant, but also to hold (retinotopic) visual inputs constant, yet while still changing the spatial relationship of tactile and visual events in the external world. Our right hemisphere patient extinguished left-hand touches due to visual stimulation of the right visual Dabrafenib research buy field (RVF) when tested in the usual default posture with eyes/head directed straight ahead. But when her eyes/head were turned to the far left (and any visual events shifted along with this), such that the identical RVF retinal stimulation now fell at the same external location as the left-hand touch, crossmodal extinction was FK228 cell line eliminated. Since only proprioceptive postural cues could signal this changed spatial relationship for the critical condition, our results show for the first time that such postural cues alone are sufficient to modulate crossmodal extinction. Identical somatosensory and retinal inputs can lead to severe crossmodal extinction, or none, depending on current

posture. “
“Both real action control and execution and motor imagery abilities require knowledge selleck of the spatial location of body parts, in other words efference copy information and feedbacks from the sensory system (Frith et al., 2000, Philos. Trans. R. Soc. Lond. B. Biol. Sci., 355, 1771). Spinal cord injuries induce severe motor disability, due to a

damage of the descending motor pathways (Cramer et al., 2007, Exp. Brain. Res., 177, 233). Patients’ motor imagery competences are variably reported as either normal or defective (Decety & Boisson, 1990, Eur. Arch. Psychiatry Clin. Neurosci., 240, 39; Lacourse et al., 1999, Behav. Brain Sci., 104, 73). We explored biomechanical constraint effects in Spinal Cord Injury (SCI) patients, as they are considered the most reliable indexes of motor imagery abilities (Parsons, 1987b, Cogn. Psychol., 19, 178). Sixteen spinal cord injuries patients and 16 neurologically unimpaired subjects have been administered with (1) the Hand Laterality Task (HLT), in which subjects were asked to judge the laterality of a rotated hand; and (2) the Mirror Letter Discrimination Task (MLD), in which subjects were asked to judge if a rotated character was in its correct upright position or mirror-reversed form. Our patients did not present the effect of stimulus orientation, neither did they show any effect related to biomechanical constraints. Based on these data, the hypothesis is that SCI patients’ performance may be ascribed to the use of a different strategy to solve the tasks, based on memory rather than on mental rotation.

Two expert liver pathologists evaluated biopsy slides in tandem.

Grading was scored using the Nakanuma system (cholangitis activity, hepatitis activity) and the Ishak system. Staging was scored using the Nakanuma system (fibrosis, bile duct loss, CBP deposition) the Ishak system and the Ludwig system. Association of grading and staging with transplant-free survival, as well as time to liver transplantation (Ltx) selleck chemicals alone was estimated using Kaplan Meier survival curve and log-rank test. Results Sixty-four patients were included, with a median follow up of 112 months (IQR 71-179). Mean age at diagnosis was 38 years (±14), 63% were male. Forty-four patients (69%) had large duct PSC and 43 (67%) had concomitant inflammatory bowel disease (IBD). A total of 9 patients reached an endpoint (7 Ltx, 2 death from CCA) in a median time of 103 months (IQR 34-160). During grading and staging of biopsies, consensus was reached in 100% of cases. Histologic grading according to Ishak was highly significantly associated with time to Ltx (p=0.007). Histologic staging of fibrosis and CBP deposition (dichotomized), according to Nakanuma was significantly associated with transplant-free survival ( p=0.006 and p=0.01 respectively). Ishak and Ludwig staging scores also showed a statistically significant

association with transplant-free survival ( p<0.001 and p<0.001 respectively). Conclusion The Nakanuma, Ishak and Ludwig scoring systems are applicable to PSC liver biopsies. A significant association was shown between Ishak Selleck FK506 grade and time to Ltx. Staging of PSC using all three systems

is highly associated with transplant-free survival. Our observations suggest that these staging systems may be useful in the evaluation of disease severity and as response parameters to therapeutic interventions in PSC patients. Disclosures: Ulrich Beuers – Consulting: Intercept, Novartis; Grant/Research Support: Zambon; click here Speaking and Teaching: Falk Foundation, Gilead, Roche, Scheringh, Zambon Cyriel Y. Ponsioen – Consulting: AbbVIE; Grant/Research Support: AbbVIE, Schering Plough, Dr. Falk Pharma, Tramedico Netherlands The following people have nothing to disclose: Elisabeth M. de Vries, Joanne Verheij, Stefan G. Hubscher, Mariska M. Leeflang, Kirsten Boonstra Background and aim: Gallbladder enlargement is frequent in primary sclerosing cholangitis (PSC). In mice, bile acid homeostasis can be modified by a gallbladder shunt. The aim of this study was to assess the potential cause and influence of gallbladder enlargement on bile acid homeostasis and disease course in PSC. Patients and methods: The study population comprised 77 PSC patients who underwent a three-dimensional magnetic resonance cholangiography (3D-MRC) and a mass spectrometry analysis of serum bile acids within less than a month. Patients were followed for 9±5 years.

Two expert liver pathologists evaluated biopsy slides in tandem.

Grading was scored using the Nakanuma system (cholangitis activity, hepatitis activity) and the Ishak system. Staging was scored using the Nakanuma system (fibrosis, bile duct loss, CBP deposition) the Ishak system and the Ludwig system. Association of grading and staging with transplant-free survival, as well as time to liver transplantation (Ltx) Talazoparib order alone was estimated using Kaplan Meier survival curve and log-rank test. Results Sixty-four patients were included, with a median follow up of 112 months (IQR 71-179). Mean age at diagnosis was 38 years (±14), 63% were male. Forty-four patients (69%) had large duct PSC and 43 (67%) had concomitant inflammatory bowel disease (IBD). A total of 9 patients reached an endpoint (7 Ltx, 2 death from CCA) in a median time of 103 months (IQR 34-160). During grading and staging of biopsies, consensus was reached in 100% of cases. Histologic grading according to Ishak was highly significantly associated with time to Ltx (p=0.007). Histologic staging of fibrosis and CBP deposition (dichotomized), according to Nakanuma was significantly associated with transplant-free survival ( p=0.006 and p=0.01 respectively). Ishak and Ludwig staging scores also showed a statistically significant

association with transplant-free survival ( p<0.001 and p<0.001 respectively). Conclusion The Nakanuma, Ishak and Ludwig scoring systems are applicable to PSC liver biopsies. A significant association was shown between Ishak Roxadustat grade and time to Ltx. Staging of PSC using all three systems

is highly associated with transplant-free survival. Our observations suggest that these staging systems may be useful in the evaluation of disease severity and as response parameters to therapeutic interventions in PSC patients. Disclosures: Ulrich Beuers – Consulting: Intercept, Novartis; Grant/Research Support: Zambon; find more Speaking and Teaching: Falk Foundation, Gilead, Roche, Scheringh, Zambon Cyriel Y. Ponsioen – Consulting: AbbVIE; Grant/Research Support: AbbVIE, Schering Plough, Dr. Falk Pharma, Tramedico Netherlands The following people have nothing to disclose: Elisabeth M. de Vries, Joanne Verheij, Stefan G. Hubscher, Mariska M. Leeflang, Kirsten Boonstra Background and aim: Gallbladder enlargement is frequent in primary sclerosing cholangitis (PSC). In mice, bile acid homeostasis can be modified by a gallbladder shunt. The aim of this study was to assess the potential cause and influence of gallbladder enlargement on bile acid homeostasis and disease course in PSC. Patients and methods: The study population comprised 77 PSC patients who underwent a three-dimensional magnetic resonance cholangiography (3D-MRC) and a mass spectrometry analysis of serum bile acids within less than a month. Patients were followed for 9±5 years.

Real-time PCR and western blotting analyses showed that FoxC1 up-regulated NEDD9 expression in SMMC7721 cells, whereas the knockdown of FoxC1 expression decreased NEDD9 expression in HCCLM3 cells (Fig. 5A). To determine whether FoxC1 regulates NEDD9 transcription, a NEDD9 promoter luciferase construct, (−2056/+121) NEDD9, was cotransfected with pCMV-FoxC1. A luciferase reporter assay showed that FoxC1 transactivated NEDD9 promoter activity (Fig. 5B1). Sequence analysis revealed four putative FoxC1-binding sites in the NEDD9 promoter.

Serial deletion and site-directed mutagenesis showed that the third and fourth FoxC1-binding sites were critical for FoxC1-induced NEDD9 transactivation (Fig. 5B2). A ChIP assay further confirmed that FoxC1 binds directly to the NEDD9 promoter in HCC cells (Fig. 5B3). Furthermore, binding activity of FoxC1 to the NEDD9 promoter was much higher in HCC tissues than in healthy liver tissues (Supporting Fig. 9). Carfilzomib These results suggested that NEDD9 was a direct transcriptional target of FoxC1. Western blotting analysis showed that NEDD9 expression was much higher in highly metastatic HCC cells than in weakly metastatic HCC cells (Fig. 5C). To determine whether NEDD9 regulates the invasive capacity of HCC cells, SMMC7721 Talazoparib cells were infected with the lentivirus, LV-NEDD9. Up-regulation of NEDD9 expression was confirmed by western blotting analysis, and the click here resulting stable

cell line was named SMMC7721-NEDD9. NEDD9 overexpression significantly increased the invasion ability of SMMC7721 cells (Fig. 5D). BLI showed the presence of lung metastases in mice implanted with

SMMC7721-NEDD9 cells, but no lung metastases occurred in mice implanted with SMMC7721-control cells (Fig. 5E1). Histological analysis (Fig. 5E5) confirmed that 7 mice in the SMMC7721-NEDD9 group developed lung metastases. However, only 1 mouse in the SMMC7721-control group developed lung metastasis (Fig. 5E2). The number of metastatic lung nodules in the SMMC7721-NEDD9 group was significantly increased, compared to that in the SMMC7721-control group (Fig. 5E3). Furthermore, the SMMC7721-NEDD9 group had a shorter OS time than the control group (Fig. 5E4). These results suggested that NEDD9 overexpression promoted HCC invasion and metastasis. Additionally, NEDD9 knockdown markedly decreased the invasion and metastasis of HCCLM3 cells (data not shown). IHC results showed that NEDD9 was significantly up-regulated in HCC tissues, compared to adjacent nontumor tissues, and that NEDD9 was mainly localized in the cytoplasm (Fig. 6D1). NEDD9 overexpression was significantly correlated with poor tumor differentiation and more-advanced TNM stage (Table 1). HCC patients with positive NEDD9 expression had shorter OS and higher recurrence rates than those with negative expression of NEDD9 (Fig. 6E1). These results suggested that NEDD9 promoted HCC metastasis and correlated with poor prognosis.

Real-time PCR and western blotting analyses showed that FoxC1 up-regulated NEDD9 expression in SMMC7721 cells, whereas the knockdown of FoxC1 expression decreased NEDD9 expression in HCCLM3 cells (Fig. 5A). To determine whether FoxC1 regulates NEDD9 transcription, a NEDD9 promoter luciferase construct, (−2056/+121) NEDD9, was cotransfected with pCMV-FoxC1. A luciferase reporter assay showed that FoxC1 transactivated NEDD9 promoter activity (Fig. 5B1). Sequence analysis revealed four putative FoxC1-binding sites in the NEDD9 promoter.

Serial deletion and site-directed mutagenesis showed that the third and fourth FoxC1-binding sites were critical for FoxC1-induced NEDD9 transactivation (Fig. 5B2). A ChIP assay further confirmed that FoxC1 binds directly to the NEDD9 promoter in HCC cells (Fig. 5B3). Furthermore, binding activity of FoxC1 to the NEDD9 promoter was much higher in HCC tissues than in healthy liver tissues (Supporting Fig. 9). MK-1775 ic50 These results suggested that NEDD9 was a direct transcriptional target of FoxC1. Western blotting analysis showed that NEDD9 expression was much higher in highly metastatic HCC cells than in weakly metastatic HCC cells (Fig. 5C). To determine whether NEDD9 regulates the invasive capacity of HCC cells, SMMC7721 http://www.selleckchem.com/PD-1-PD-L1.html cells were infected with the lentivirus, LV-NEDD9. Up-regulation of NEDD9 expression was confirmed by western blotting analysis, and the this website resulting stable

cell line was named SMMC7721-NEDD9. NEDD9 overexpression significantly increased the invasion ability of SMMC7721 cells (Fig. 5D). BLI showed the presence of lung metastases in mice implanted with

SMMC7721-NEDD9 cells, but no lung metastases occurred in mice implanted with SMMC7721-control cells (Fig. 5E1). Histological analysis (Fig. 5E5) confirmed that 7 mice in the SMMC7721-NEDD9 group developed lung metastases. However, only 1 mouse in the SMMC7721-control group developed lung metastasis (Fig. 5E2). The number of metastatic lung nodules in the SMMC7721-NEDD9 group was significantly increased, compared to that in the SMMC7721-control group (Fig. 5E3). Furthermore, the SMMC7721-NEDD9 group had a shorter OS time than the control group (Fig. 5E4). These results suggested that NEDD9 overexpression promoted HCC invasion and metastasis. Additionally, NEDD9 knockdown markedly decreased the invasion and metastasis of HCCLM3 cells (data not shown). IHC results showed that NEDD9 was significantly up-regulated in HCC tissues, compared to adjacent nontumor tissues, and that NEDD9 was mainly localized in the cytoplasm (Fig. 6D1). NEDD9 overexpression was significantly correlated with poor tumor differentiation and more-advanced TNM stage (Table 1). HCC patients with positive NEDD9 expression had shorter OS and higher recurrence rates than those with negative expression of NEDD9 (Fig. 6E1). These results suggested that NEDD9 promoted HCC metastasis and correlated with poor prognosis.

A 64-gene profile reproducibly differentiated severe NAFLD from mild NAFLD, and a 20-gene subset within this profile correlated with NAFLD severity, independent of other factors known to influence NAFLD progression. Multiple genes involved with tissue repair/regeneration and certain metabolism-related genes

were induced in severe NAFLD. Ingenuity Pathway Analysis and IHC confirmed deregulation of metabolic and regenerative pathways in severe NAFLD and revealed overlap among the gene expression patterns of severe NAFLD, cardiovascular disease, and cancer. Conclusion: By demonstrating specific metabolic and repair pathways that are differentially activated in livers with severe NAFLD, gene profiling identified novel targets that can be exploited to improve diagnosis and treatment of patients who are at greatest risk for NAFLD-related BGB324 morbidity and mortality. (Hepatology 2014;59:471–482) “
“Obstructive cholestasis induces liver injury, postoperative complications, and mortality after surgery. Adaptive control of cholestasis, including bile salt homeostasis, is necessary for recovery and survival. Peripheral serotonin is a cytoprotective neurotransmitter also associated with liver regeneration. The effect of serotonin on cholestatic liver

injury is not known. Therefore, we tested whether serotonin affects the severity of cholestatic liver injury. We induced cholestasis by ligation of the bile duct (BDL) in either wild-type (WT) mice or mice lacking peripheral selleck inhibitor serotonin (Tph1−/− and immune thrombocytopenic [ITP] mice). Liver injury was assessed by the levels of plasma aspartate aminotransferase (AST), alanine aminotransferase JNK signaling pathway inhibitor (ALT) and tissue necrosis. Bile salt–regulating genes were measured by quantitative polymerase chain reaction and confirmed by western blotting and immunohistochemistry. Tph1−/− mice displayed higher levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days of BDL than WT mice. Likewise, liver injury

was disproportional in ITP mice. Moreover, severe cholestatic complications and mortality after prolonged BDL were increased in Tph1−/− mice. Despite the elevation in toxic bile salts, expression of genes involved in bile salt homeostasis and detoxification were not affected in Tph1−/− livers. In contrast, the bile salt reabsorption transporters Ostα and Ostβ were up-regulated in the kidneys of Tph1−/− mice, along with a decrease in urinary bile salt excretion. Serotonin reloading of Tph1−/− mice reversed this phenotype, resulting in a reduction of circulating bile salts and liver injury. Conclusion: We propose a physiological function of serotonin is to ameliorate liver injury and stabilize the bile salt pool through adaptation of renal transporters in cholestasis. (HEPATOLOGY 2012;56:209–218) Bile salts are biological detergents produced primarily by hepatocytes for digestion and absorption of fatty nutrients in the intestines.

A 64-gene profile reproducibly differentiated severe NAFLD from mild NAFLD, and a 20-gene subset within this profile correlated with NAFLD severity, independent of other factors known to influence NAFLD progression. Multiple genes involved with tissue repair/regeneration and certain metabolism-related genes

were induced in severe NAFLD. Ingenuity Pathway Analysis and IHC confirmed deregulation of metabolic and regenerative pathways in severe NAFLD and revealed overlap among the gene expression patterns of severe NAFLD, cardiovascular disease, and cancer. Conclusion: By demonstrating specific metabolic and repair pathways that are differentially activated in livers with severe NAFLD, gene profiling identified novel targets that can be exploited to improve diagnosis and treatment of patients who are at greatest risk for NAFLD-related R428 cell line morbidity and mortality. (Hepatology 2014;59:471–482) “
“Obstructive cholestasis induces liver injury, postoperative complications, and mortality after surgery. Adaptive control of cholestasis, including bile salt homeostasis, is necessary for recovery and survival. Peripheral serotonin is a cytoprotective neurotransmitter also associated with liver regeneration. The effect of serotonin on cholestatic liver

injury is not known. Therefore, we tested whether serotonin affects the severity of cholestatic liver injury. We induced cholestasis by ligation of the bile duct (BDL) in either wild-type (WT) mice or mice lacking peripheral click here serotonin (Tph1−/− and immune thrombocytopenic [ITP] mice). Liver injury was assessed by the levels of plasma aspartate aminotransferase (AST), alanine aminotransferase BMS-777607 manufacturer (ALT) and tissue necrosis. Bile salt–regulating genes were measured by quantitative polymerase chain reaction and confirmed by western blotting and immunohistochemistry. Tph1−/− mice displayed higher levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days of BDL than WT mice. Likewise, liver injury

was disproportional in ITP mice. Moreover, severe cholestatic complications and mortality after prolonged BDL were increased in Tph1−/− mice. Despite the elevation in toxic bile salts, expression of genes involved in bile salt homeostasis and detoxification were not affected in Tph1−/− livers. In contrast, the bile salt reabsorption transporters Ostα and Ostβ were up-regulated in the kidneys of Tph1−/− mice, along with a decrease in urinary bile salt excretion. Serotonin reloading of Tph1−/− mice reversed this phenotype, resulting in a reduction of circulating bile salts and liver injury. Conclusion: We propose a physiological function of serotonin is to ameliorate liver injury and stabilize the bile salt pool through adaptation of renal transporters in cholestasis. (HEPATOLOGY 2012;56:209–218) Bile salts are biological detergents produced primarily by hepatocytes for digestion and absorption of fatty nutrients in the intestines.

For each source, we selected the best available and most current estimate of migraine or headache prevalence, and selected associated measures of disability, health care http://www.selleckchem.com/products/ldk378.html use, and treatment patterns. Compared with a slightly higher proportion of 22.7% in the National Health and Nutrition Examination Survey, 16.6% of adults 18 or older reported having migraine or other severe headaches in the last 3 months in the 2011 National Health Interview Survey. In contrast, the AMPP study found an overall prevalence of migraine

of 11.7% and probable migraine of 4.5%, for a total of 16.2%. Data from National Ambulatory Medical Care Survey/National Hospital Ambulatory Medical Care Survey showed that head pain was the fifth leading cause of ED visits overall in the US and accounted for 1.2% of outpatient visits. The burden of headache was highest

in females 18-44, where the 3-month prevalence of migraine or severe headache was 26.1% and head pain was the third leading cause of ED visits. The prevalence and burden of headache was substantial even in the least affected subgroup of males 75 or older, where 4.6% reported experiencing severe headache or migraine in the previous 3 months. Triptans accounted for almost 80% of antimigraine analgesics prescribed at office visits in 2009, nearly half of which were for sumatriptan. Migraine is associated with increased risk for other physical and psychiatric

comorbidities, buy XL765 and this risk increases with headache frequency. This report provides the most current available estimates of the prevalence, impact, and treatment selleck compound patterns of migraine or severe headache in the United States. Migraine and other severe headaches are a common and major public health problem, particularly among reproductive-aged women. Data about prevalence and disability from the major government-funded surveillance studies are generally consistent with results of studies such as the American Migraine Studies 1 and 2, and the AMPP study. Migraine and other benign recurrent headache disorders are a major public health problem. They are associated with substantial personal suffering, disability, and societal expense.[1] In the United States, a number of public health surveillance systems and privately funded studies have collected information on the prevalence, impact, and treatment of headache and migraine. Locating and interpreting the most up-to-date statistics from these sources can be time-consuming. In this article, we provide an overview of current data from a variety of governmental and other sources. We searched PubMed and the National Center for Health Statistics websites for summary data from population-based or nationally representative survey studies performed in the United States from 1999 to 2011.

Only one isolate formed strong heterokaryons with the reference isolates of VCG 0423. Five isolates were heterokaryon self-incompatible. Restriction fragment analysis with six different enzymes revealed 13 IGS types among 75 F. oxysporum isolates from Galunisertib solubility dmso Turkey as well as 16 reference isolates

from Colorado, USA. The majority of single-member VCGs produced identical RFLP banding patterns with minor deviations, considerably different from those of the reference VCG isolates. These results suggested that isolates of F. oxysporum f.sp. cepae in Turkey derived from distinct clonal lineages and mutations at one or more vegetative compatibility loci restrict heterokaryon formation. “
“A novel soil-less method Temozolomide in vitro was developed to define susceptibility of developing potato tubers accurately to infection with Streptomyces scabiei the causal agent of common scab disease. Hydroponic production enabled precise identification of individual tuber development. Direct inoculation of tubers with a spore suspension of S. scabiei

resulted in disease development, demonstrating that infection could be initiated in a soil-less media. Tubers were most susceptible to infection between 3 and 20 days after tuber initiation, confirming that this early period of tuber formation is critical to disease development. Common scab caused by pathogenic Streptomyces spp. is one of the most important diseases of the potato (Solanum tuberosum L.) worldwide (Loria et al. 2006). Annual losses in Tasmania, Australia alone are estimated at c. 4% of the industry value (Wilson et al. 2009). The disease primarily reduces tuber quality, through the production of unsightly lesions with yield rarely affected. Deep-pitted lesions can also cause losses for processing (French fry and chipping). Pathogenic Streptomyces spp. produce a phytotoxin, thaxtomin A that is a key pathogenicity determinant in this disease system (Lawrence et al. 1990; Tegg et al. 2005). Epidemics of common scab disease can be sporadic and are strongly influenced by environmental conditions. Enclosed pot-based systems containing inocula have been developed for improving

selleck screening library consistency of infection (McIntosh 1970) enabling the testing of disease management strategies (e.g. resistant cultivars; soil or tuber applied chemicals; irrigation treatments; Lapwood et al. 1970; Wilson et al. 1999, 2009; Wilson 2001; Tegg et al. 2008). It is believed that most infections occur during early tuber development yet in field and pot-based systems precise identification of tuber initiation and development is difficult as tubers are underground. Destructive processes that compromise the experiments are necessary to uncover and identify tuber development stages which also hinder precise measurement. The objectives of this study were to develop a methodology enabling precise identification of tuber development and successful infection of tubers in a non-destructive manner.

Only one isolate formed strong heterokaryons with the reference isolates of VCG 0423. Five isolates were heterokaryon self-incompatible. Restriction fragment analysis with six different enzymes revealed 13 IGS types among 75 F. oxysporum isolates from RGFP966 Turkey as well as 16 reference isolates

from Colorado, USA. The majority of single-member VCGs produced identical RFLP banding patterns with minor deviations, considerably different from those of the reference VCG isolates. These results suggested that isolates of F. oxysporum f.sp. cepae in Turkey derived from distinct clonal lineages and mutations at one or more vegetative compatibility loci restrict heterokaryon formation. “
“A novel soil-less method selleck chemicals was developed to define susceptibility of developing potato tubers accurately to infection with Streptomyces scabiei the causal agent of common scab disease. Hydroponic production enabled precise identification of individual tuber development. Direct inoculation of tubers with a spore suspension of S. scabiei

resulted in disease development, demonstrating that infection could be initiated in a soil-less media. Tubers were most susceptible to infection between 3 and 20 days after tuber initiation, confirming that this early period of tuber formation is critical to disease development. Common scab caused by pathogenic Streptomyces spp. is one of the most important diseases of the potato (Solanum tuberosum L.) worldwide (Loria et al. 2006). Annual losses in Tasmania, Australia alone are estimated at c. 4% of the industry value (Wilson et al. 2009). The disease primarily reduces tuber quality, through the production of unsightly lesions with yield rarely affected. Deep-pitted lesions can also cause losses for processing (French fry and chipping). Pathogenic Streptomyces spp. produce a phytotoxin, thaxtomin A that is a key pathogenicity determinant in this disease system (Lawrence et al. 1990; Tegg et al. 2005). Epidemics of common scab disease can be sporadic and are strongly influenced by environmental conditions. Enclosed pot-based systems containing inocula have been developed for improving

this website consistency of infection (McIntosh 1970) enabling the testing of disease management strategies (e.g. resistant cultivars; soil or tuber applied chemicals; irrigation treatments; Lapwood et al. 1970; Wilson et al. 1999, 2009; Wilson 2001; Tegg et al. 2008). It is believed that most infections occur during early tuber development yet in field and pot-based systems precise identification of tuber initiation and development is difficult as tubers are underground. Destructive processes that compromise the experiments are necessary to uncover and identify tuber development stages which also hinder precise measurement. The objectives of this study were to develop a methodology enabling precise identification of tuber development and successful infection of tubers in a non-destructive manner.