Under these circumstances, www.selleckchem.com/products/Erlotinib-Hydrochloride.html an alternative therapy was instituted (e.g., banding in those on drug therapy, TIPS, or transplantation). The composite endpoint death/LT was preferred over mortality, as it was deemed that, in the specific scenario of advanced liver disease, considering only the latter may lead to important potential bias associated to the impact of LT on the natural history of cirrhosis. Differences between categorical variables were assessed by chi-square test or Fisher’s exact test when necessary. Continuous variables

were compared using the Student t test or Mann-Whitney test as appropriate. A two-sided P value <0.05 was considered statistically significant. Overall rebleeding and death/LT analysis was conducted on an intention-to-treat basis. Kaplan-Meier curves were constructed to evaluate the dynamics of rebleeding and death/LT, and Cox analysis

was conducted to identify independent prognostic indicators for long-term response, rebleeding, and death/LT. Moreover, for the case of rebleeding, in order to describe accurately its cumulative incidence, a competing risk analysis was performed. For Kaplan-Meier analysis, follow-up was censored on the date when the patient was last seen, or the date of death or transplantation. However, in this setting, the occurrence of death or LT (competing risk) may preclude the occurrence of a first rebleeding, modifying its probability and the derived calculations (such as the ones needed for Kaplan-Meier analysis).16, 17 The competing risk model allows differentiating censored patients according to their check details competing risk status (alive versus dead or transplantation) at the end of follow-up. Then, the model calculates first the probability of occurrence of any event (rebleeding or death/LT), and afterward the conditional probability of the event of interest (rebleeding), from which the cumulative incidence is derived. Significance between Kaplan-Meier curves was assessed by log-rank test, and for

the case of competing risks curves, the specific Non-specific serine/threonine protein kinase method described by Gray was used.18 The SPSS (version 15.0; SPSS Inc., Chicago, IL) and STATA (version 10.0; StataCorp, College Station, TX) statistical packages were used for the analysis. During the study period, 304 consecutive patients admitted with acute variceal bleeding were considered. A total of 201 patients were excluded, leaving 103 for hemodynamic assessment. The flow chart of patients in the study is shown in Fig. 1. Basal clinical and hemodynamic features of the 103 patients evaluated are shown in Table 1. The second HVPG measurement was not performed in 13 patients (12.7%). Among these, two patients died from liver failure shortly after the first hemodynamic study, and the remaining 11 patients presented a variceal rebleeding before the second hemodynamic study could be conducted. The remaining 90 patients underwent a second hemodynamic study 14.4 ± 2.5 days after the first study (i.e.

Measures of TL and snout-vent length (SVL; measured to the posterior caudal-most

extent of the vent) were taken to within ±0.5 cm using a standard metric tape measure. Potential performance deviations from isometry were evaluated separately for each species relative to the measures of body size (i.e. body mass, TL and SVL). Interspecific comparisons among these measures and bite forces were also made. Animals missing terminal segments of the tail were noted and not used in the TL comparisons (n = 1). Data were log-transformed and scaling relationships determined using RMA regressions to account for error in both the independent variable (i.e. morphometric) and dependent variable (i.e. bite Napabucasin purchase force), and 95% CIs were constructed (Sokal & Rohlf, 1995) using the open source statistical program R (version 2.15.2; Free Software Foundation, Boston, MA, USA). Comparisons of the C. johnsoni and C. porosus RMA regressions to those of A. mississippiensis were made using the body mass and SVL data from Erickson et al. (2003)

as well as TL data from the same study. The bite-force scaling results for these three species then were used to draw phylogenetic inferences regarding the evolution of ontogenetic bite-force allometry within Crocodylia. Ibrutinib chemical structure In addition, ordinary least squares (OLS) regressions (preferred over RMA for their predictive power; Sokal & Rohlf, 1995) were calculated for all body-size variables versus bite force from

the A. mississippiensis data in order to generate 95% prediction intervals (PIs; Quinn & Keough, 2002), MycoClean Mycoplasma Removal Kit to which the Crocodylus datasets were compared. PIs utilize OLS regressions and the standard deviation about the mean. This metric indicates the range within which 95% of future-sample values are expected to fall. Here we used the PIs to evaluate the utility of our intraspecific bite-force data for predicting performance values in any living or fossil crocodylian based on body-size measurements alone. Bite forces spanning the C. johnsoni developmental series range from 77–1864 N, strongly correlate with body size for all comparisons (R2 ≥ 0.96), and are positively allometric. Bite forces for the C. porosus series range from 118 to 16 143 N (notably, the higher value represents the highest reported value measured for any animal), also strongly correlate with body size for all comparisons (R2 = 0.98), and are positively allometric. The RMA scaling coefficients are reported in Table 1. For eight out of nine of these comparisons (i.e. three taxa for three body size measures), intraspecific bite-force scaling coefficients for C. johnsoni, C. porosus and A. mississippiensis do not differ significantly from one another (as determined by comparing slope and confidence intervals; Table 1). In addition crocodylid bite-force values for all six of the PI comparisons fall within the PI ranges of A.

[13] Based on these results, T12PR48 is recommended for non-responders to previous PR in the USA, Canada and the EU. However, in Japan, generally, T12PR24 is recommended because clinical trials were performed only in the T12PR24 regimen. Therefore, it is unclear whether T12PR48 improves the SVR rate of Japanese non-responders to PR compared to T12PR24. Accordingly, this study investigated which characteristics of non-responders to previous PR EGFR inhibitor are associated with the improvement of SVR rate with extended T12PR48. BETWEEN DECEMBER 2011 and March 2013, 456 consecutive Japanese genotype 1b-infected

CHC patients received TVR-based triple combination therapy at the study hospitals. Among all patients, 103 non-responders to PR were enrolled in this multicenter study. The inclusion criteria were as follows: (i) diagnosis of CHC; (ii) persistently positive sera for HCV RNA for more than 6 months determined by quantitative real-time polymerase chain reaction (PCR) method (COBAS AmpliPrep/COBAS TaqMan HCV Test; Roche Diagnostics, Tokyo, Japan); (iii) HCV genotype 1b confirmed this website by sequence analysis; (iv) non-responders to previous PR in whom HCV RNA never disappeared during PR after 24 weeks of therapy; (v) aged 18–75 years; and (vi) bodyweight of

more than 35 kg at the time of entry into the study. The exclusion criteria were as follows: (i) decompensated cirrhosis; (ii) positive for hepatitis B surface antigen or antibodies against HIV; (iii) previous or current development of hepatocellular

carcinoma; (iv) coexistence of other liver diseases such as autoimmune hepatitis, primary biliary cirrhosis, hemochromatosis, Wilson’s disease and alcoholic liver disease; (v) renal disease or creatinine clearance of 50 mL/min or less at baseline; (vi) hemoglobin level of less than 12 g/dL, white blood cell count of less than 2000/μL, neutrophil count of less than 1500/μL and platelet count of less than 8.0 × 104/μL Temsirolimus at baseline; (vii) depression, schizophrenia or history thereof, or history of suicide attempts; and (viii) pregnancy in progress or planned for either partner during the study period. Liver biopsy was performed in 80 of 103 (77.7%) patients within 12 months of enrollment. The presence or absence of cirrhosis was established according to the METAVIR score.[26] For the remaining 23 patients, the presence or absence of cirrhosis was determined by ultrasonography and/or computed tomography findings. The patients were divided into two categories according to the Japan Society of Hepatology guidelines.[27] Partial responders were defined as having a decrease in HCV RNA of 2 log10 IU/mL or more from baseline at treatment week 12 but detectable at treatment week 24, and null responders were defined as having a decrease in HCV RNA of less than 2 log10 IU/mL at treatment week 12.

Three time intervals between handling and photoactivation were applied: Group 1 = immediately; Group 2 = a 1-minute interval; Group 3 = a 4-minute interval. All specimens were irradiated with a light-emitting diode source for 40 seconds.

Thirty discs of each cement (1 mm thick × 6 mm diameter, n = 10) were prepared for the absorption and solubility tests. These specimens Panobinostat mouse were stored in distilled water at 37°C for 90 days. The results were subjected to ANOVA with two factors (material and activation time intervals) and Tukey’s test (95% significance). The 4-minute interval significantly reduced the degree of conversion of SmartCem2 (30.6% ± 8.3%). No other significant changes were observed for the degree of conversion; however, the time intervals before photoactivation interfered significantly in the water absorption of the RelyX Unicem specimens but not the SmartCem2 specimens. The time intervals did not affect the solubility of either cement. VX-809 clinical trial In all cases, SmartCem2 had higher solubility than RelyX Unicem. The time interval between handling and photoactivation significantly influenced the degree of conversion and water sorption of the resin-based cements. In general, one can say that the self-adhesive resin cements should be photoactivated as soon as possible after the material handling process. “
“The congenitally missing maxillary

lateral incisor is the most common agenesis in the anterior region. There are several treatment options for this anomaly, which causes severe deficiencies: orthodontic space closure, tooth-supported restoration, or single-tooth implant. Each of these solutions has a high degree of success if used in the

correct situation. An implant-supported restoration with an interdisciplinary approach provides a predictable outcome. This article describes the treatment of a patient with agenesis of the maxillary left lateral incisor. After orthodontic space management, it was decided to restore the tooth with an all-ceramic crown cemented on a zirconia custom abutment, which fractured after only 6 weeks of service. Progesterone Fractographic analysis revealed that the failure was due to over-reduction of the buccal wall to correct the labial emergence of the implant. Zirconia abutments should be designed with even wall thicknesses of at least 0.8 mm to avoid areas that may compromise functional success. “
“Purpose: The aim of this study was to measure the in vitro retention force of double conical crowns fabricated using primary galvanoforming and secondary casting techniques and those fabricated using primary casting and secondary galvanoforming techniques under simulated clinical conditions before and after a wear test. Materials and Methods: Primary galvanoformed crowns (n = 10) with non-noble secondary crowns (n = 10; group A) and primary non-noble crowns (n = 10) with secondary galvanoformed crowns (n = 10; group B) were fabricated. Each primary and secondary crown was embedded in acrylic resin and weighed with a digital balance.

Three time intervals between handling and photoactivation were applied: Group 1 = immediately; Group 2 = a 1-minute interval; Group 3 = a 4-minute interval. All specimens were irradiated with a light-emitting diode source for 40 seconds.

Thirty discs of each cement (1 mm thick × 6 mm diameter, n = 10) were prepared for the absorption and solubility tests. These specimens ABT-737 nmr were stored in distilled water at 37°C for 90 days. The results were subjected to ANOVA with two factors (material and activation time intervals) and Tukey’s test (95% significance). The 4-minute interval significantly reduced the degree of conversion of SmartCem2 (30.6% ± 8.3%). No other significant changes were observed for the degree of conversion; however, the time intervals before photoactivation interfered significantly in the water absorption of the RelyX Unicem specimens but not the SmartCem2 specimens. The time intervals did not affect the solubility of either cement. Carfilzomib nmr In all cases, SmartCem2 had higher solubility than RelyX Unicem. The time interval between handling and photoactivation significantly influenced the degree of conversion and water sorption of the resin-based cements. In general, one can say that the self-adhesive resin cements should be photoactivated as soon as possible after the material handling process. “
“The congenitally missing maxillary

lateral incisor is the most common agenesis in the anterior region. There are several treatment options for this anomaly, which causes severe deficiencies: orthodontic space closure, tooth-supported restoration, or single-tooth implant. Each of these solutions has a high degree of success if used in the

correct situation. An implant-supported restoration with an interdisciplinary approach provides a predictable outcome. This article describes the treatment of a patient with agenesis of the maxillary left lateral incisor. After orthodontic space management, it was decided to restore the tooth with an all-ceramic crown cemented on a zirconia custom abutment, which fractured after only 6 weeks of service. Phospholipase D1 Fractographic analysis revealed that the failure was due to over-reduction of the buccal wall to correct the labial emergence of the implant. Zirconia abutments should be designed with even wall thicknesses of at least 0.8 mm to avoid areas that may compromise functional success. “
“Purpose: The aim of this study was to measure the in vitro retention force of double conical crowns fabricated using primary galvanoforming and secondary casting techniques and those fabricated using primary casting and secondary galvanoforming techniques under simulated clinical conditions before and after a wear test. Materials and Methods: Primary galvanoformed crowns (n = 10) with non-noble secondary crowns (n = 10; group A) and primary non-noble crowns (n = 10) with secondary galvanoformed crowns (n = 10; group B) were fabricated. Each primary and secondary crown was embedded in acrylic resin and weighed with a digital balance.

FGF/FGFR-mediated signaling is highly conserved, and downstream pathways include RAS/RAF mitogen-associated protein kinase and phosphoinositide 3-kinase/protein kinase B cascade.12 Several alterations in FGFR signaling correlate with outcomes in patients with HCC.13 A recent clinical study demonstrated FGF8, FGF17, and FGF18 and their receptors, FGFR2, FGFR3, and FGFR4, to be up-regulated in HCC.14 Additional studies also suggested that FGF4, FGF5,

FGF9, and FGF12 may be involved in HCC progression and metastasis.15 Furthermore, FGF up-regulation is one of the proposed escape mechanisms for HCC under sorafenib therapy. In fact, escape from sorafenib treatment by FGF activation was the rationale for an Adriamycin manufacturer international RCT evaluating brivanib as a dual VEGFR/FGF inhibitor in sorafenib progressors. Along this line, BGJ398 order it will be interesting to see whether altered signaling through FGF plays a role for resistance

development under sorafenib in HCC (and other sorafenib-responsive malignancies). Finally, it is important to note that the majority of evaluated sorafenib responders have an underlying viral etiology (11 of 13), and chronic hepatitis C is the most prevalent risk factor in Japan. However, in Europe and North America, other etiologies, in particular, alcoholic and nonalcoholic steatohepatitis have a growing effect. Therefore, transferability of the results to other regions of the world might be limited. The study

by Arao et al. exemplifies a valuable translational research approach (namely, from bedside to bench and back) and, as such, an important next step toward a personalized systemic treatment approach in HCC. A prospective evaluation of the suggested target in a large cohort of patients, including patients from Europe and North America, is clearly warranted. Sorafenib represents the standard treatment for patients with Cytidine deaminase advanced HCC and preserved liver function (stage Child-Pugh A). FGF-signaling alterations have been identified as promising targets in patients with advanced HCC, and already, several novel agents targeting this receptor family, such as brivanib, dovitininb, and intedanib, are being investigated in clinical trials. These new agents will be evaluated in RCTs against sorafenib. This underscores the need for genome-wide sequencing, followed by the functional analysis of targets identified, to personalize molecular targeted therapy in patients with HCC. Development of personalized treatment algorithms has been identified as an urgent medical need and has been proposed as a short-term clinical aim by the investigators of the new EASL/EORTC Clinical Practice Guidelines for HCC.

As shown in Fig. 3B,C, cold-stored Z-VAD-FMK cost and warm-reperfused liver grafts released higher amounts of transaminases and LDH and a lower quantity of bile in comparison to grafts reperfused without previous cold preservation. These detrimental effects were not observed in liver grafts cold stored in UWS supplemented with simvastatin. Figure 4 depicts significantly higher levels of O, ICAM-1, and cleaved caspase-3 in cold-stored and warm-reperfused livers grafts compared with control livers, indicating increased

oxidative stress, inflammation, and apoptosis, respectively. These negative events from cold storage were markedly attenuated, or entirely prevented, in liver grafts cold stored in simvastatin-containing UWS. Livers cold selleckchem stored for 16 hours exhibited a deteriorated microcirculation upon reperfusion, as demonstrated by significantly increased liver vascular resistance as compared to control livers (Fig. 5A). Cold storage-derived increments in liver vascular resistance were not observed in liver grafts cold preserved in the presence of simvastatin. In addition, liver grafts stored for 16 hours in cold UWS exhibit endothelial dysfunction (Fig. 5B,C). As depicted in Fig. 5B, in response to portal flow increments between 35 and 60 mL/min control livers were able to maintain a constant hepatic vascular resistance, thus demonstrating normal flow-dependent vasodilatation of the liver vascular bed. However, cold-stored livers preserved

in UWS did not accommodate portal flow increases, exhibiting a marked and significant increment in their vascular resistance. Remarkably, cold storage-derived endothelial dysfunction was entirely prevented in livers cold preserved in UWS supplemented with simvastatin. Similarly, dose-response

curves to ACH showed that cold-stored livers exhibit significantly reduced endothelial-derived vasodilatation in comparison to not cold-stored livers (Fig. 5C), further demonstrating the development of acute endothelial dysfunction during cold storage. This pathological phenomenon was prevented when livers were cold stored in the presence of simvastatin. Liver microcirculation deterioration and development of endothelial dysfunction after cold preservation were accompanied by significant reductions in eNOS expression and activity and cGMP levels comparing to controls (Fig. 6), with no 3-mercaptopyruvate sulfurtransferase modification in collagen-I expression (1.00 ± 0.16 controls versus 0.92 ± 0.32 cold stored; NS), a known marker of hepatic stellate cell activation. Simvastatin addition to the cold-storage solution maintained hepatic eNOS expression and improved eNOS phosphorylation, which was associated with up-regulation of cGMP levels. The endothelium is the primary target of cold preservation and reperfusion injuries in liver transplantation. Liver sinusoidal endothelial injury involves cell activation, apoptosis, and detachment, leading to hepatic microcirculatory dysfunction.

Analysis of anti-CLDN1 reactivity to chimeric CLDN1/7 expressed on the cell surface of 293T cells

demonstrated that the antibodies interact strongly with CLDN7, where the N-terminal third (N1/3) or half (N1/2) was replaced with the corresponding coding region of CLDN1 (Table 1). In contrast, the antibodies did not exhibit any detectable interaction with CLDN7, where the C-terminal half (C1/2) of EL1 was replaced with the corresponding coding region of CLDN1. A reduced interaction was observed for CLDN7 expressing the entire EL2 of CLDN1 (Table 1). AUY-922 chemical structure These data demonstrate that anti-CLDN1 antibodies recognize epitopes in the N-terminal half of the CLDN1 EL1 which

has been shown to be required for HCV entry9 as well as EL2 epitopes (Table 1). Because antibodies failed to recognize overlapping peptides encoding for linear epitopes comprising the CLDN1 EL1 and 2 in an enzyme-linked immunosorbent assay or an infection assay using peptides as capture antigens (data not shown), it is likely that epitopes targeted by anti-CLDN1 antibodies are conformation-dependent. To study whether anti-CLDN1 antibodies bind to CLDN1 on the cell surface of HCV permissive cells, Huh7.5.1 and primary human hepatocytes were incubated with anti-CLDN1 antibodies and analyzed by flow cytometry. Positive staining of human Huh7.5.1 hepatoma cells and human hepatocytes

with polyclonal KU-57788 purchase anti-CLDN1 antibodies in the absence of permeabilizing reagents demonstrated that these antibodies bind to CLDN1 expressed on the surface of primary hepatocytes and HCV permissive cell lines (Fig. 1C). To further address the specificity of antibodies, we performed CLDN1 knock-down experiments in Huh7.5.1 cells using a pool of three siRNAs described by Evans et al.9 CLDN1 silencing resulted in a decrease of anti-CLDN1 staining in immunoblot analyses (data not shown), further confirming the specificity of the antibodies. Positive staining of native cell Phosphatidylethanolamine N-methyltransferase surface CLDN1 in living and nonpermeabilized Huh7.5.1 cells with anti-CLDN1 antibodies was confirmed using imaging studies. Interestingly, in living native Huh7.5.1 cells, the antibody appeared to localize to certain areas of cell–cell contacts (Fig. 1D), whereas in permeabilized Huh7.5.1 or Caco-2 cells antibody staining showed a polygonal web-like structure (Fig. 1D), which was similar to previous studies using nonneutralizing anti-CLDN1 antibodies.23 CLDN1 staining appeared to be more pronounced in polarized Caco-2 cells than in nonpolarized Huh7.5.1 cells (Fig. 1D). Further imaging studies are ongoing to determine the detailed subcellular localization of CLDN1 recognized by neutralizing anti-CLDN1 antibodies in HCV permissive cells.

Many pathogenic factors have been proposed for FD, including motility abnormalities such as delayed gastric emptying, impaired gastric accommodation and hypersensitivity to gastric distension; psychological factors; excessive gastric acid secretion; H. pylori; genetics; environment in childhood and/or adolescence; diet; lifestyle; and prior GI infection.50–52 The major mechanism thought to induce FD symptoms includes

impaired accommodation, delayed gastric emptying, and visceral hypersensitivity, as well as other complicating factors.51,53 Pharmacological correction of abnormal gastric motility and visceral hypersensitivity has been considered as a valid therapeutic approach in FD; however, changes in motor function and symptomatic outcomes are PARP inhibitor learn more poorly correlated.54 Current evidence suggests that FD is a heterogeneous disorder in which different pathophysiological disturbances are associated with different symptom profiles. Progress in understanding the underlying pathogenetic mechanisms should lead to better targeting of treatment in FD patients.50 Statement 14. Disturbed gastroduodenal motility is one of the pathophysiologic mechanisms in functional

dyspepsia. Grade of evidence: high. Level of agreement: a: 100.0%; b: 0%; c: 0%; d: 0%; e: 0%; f: 0%. Disturbed gastroduodenal motility is considered to be one of the major pathophysiologic mechanisms in FD.4,51 Abnormal gastric motility has been analyzed from different aspects by various measures, and differences in findings between health and diseases have been characterized. We intuitively recognize that delayed gastric emptying may be related to dyspeptic symptoms, especially feelings of retention of ingested food after a meal, which can be abdominal distension, bloating or fullness. There are many reports demonstrating delayed gastric emptying in patients with FD from both Western55,56 and Asian57–63 countries, and about 40% of FD patients

are thought to show delayed gastric emptying after ingestion of solid food.64 However, there are many studies that failed to show a direct connection between delayed gastric emptying and dyspeptic symptoms,65–67 suggesting that the relationship may not be entirely Quinapyramine clear. On the other hand, much attention has recently been paid to impaired gastric accommodation, which is also known as adaptive relaxation. The accommodation reflex is a volume response of the upper part of the stomach after a meal. After ingestion of food, the gastric fundus spontaneously dilates and begins to store food. Such impairment of gastric accommodation is known to correlate well with dyspeptic symptoms, especially early satiety.68,69 However, this relationship has not been confirmed well in studies from some Asian countries.70,71 Statement 15. Visceral hypersensitivity is one of the pathophysiologic mechanisms in functional dyspepsia. Grade of evidence: high. Level of agreement: a: 100.0%; b: 0%; c: 0%; d: 0%; e: 0%; f: 0%.

In 2005, the presence of this disease was reported on black oat (Avena strigosa) at different locations of Parana state. Due to little information of M. grisea that is infecting this host, this work aimed to characterize it at molecular, sexual and pathogenic level. DNA analysis showed that M. grisea from black oat formed a homogenous and genetic distinct group of its own,

different from other hosts, including rice, wheat, triticale and barley. Isolate 15720 was an exception, because selleck kinase inhibitor it was similar to wheat isolate. There was no sexual compatibility between M. grisea from oat and other tested hosts. In pathogenic terms, isolates of M. grisea from oat infected triticale, wheat, rye, millet, barley, sorghum and rice; cross-inoculation was positive with wheat, triticale, rice and barley. “
“Inoculation of cauliflower blossom with Xanthomonas campestris Selleck AZD9668 pv. campestris (Xcc), by brush or pollination with blue bottle flies (Calliphora vomitoria) as a vector, can result in seed infestation. Two years of poly-tunnel experiments with fly inoculation of cauliflower has shown that in approximately 30% of seed batches of a breeding line, high densities of Xcc (>10 000 CFU/g) were found both before and after seed treatment with warm water. The

presence of Xcc in seed derived from fly-inoculated plants was confirmed in a grow-out test. After brush-inoculation, on average 45% of seed batches were contaminated with high densities of Xcc before disinfection and 40% after seed disinfection. A grow-out test, however, did not confirm the presence of internally infected seed. In a 1-year trial, no seed infections were found in warm water-treated seed derived from cv. Opaal, an open pollinated cultivar. No indication of internal

seed infection was found after blossom inoculation with X. c. pv. armoraciae (Xca). To obtain contaminated flies as a vector for Xcc, flies were fed on agar-grown bacteria. Initial populations of Xcc per fly were 105 CFU, but population densities decreased rapidly and survived for 5 days maximum. During the same period, populations of other bacteria associated with flies increased slightly. The implications of blossom infection and the role of pollinating insects in dissemination and transmission of Xcc are discussed. 3-mercaptopyruvate sulfurtransferase “
“Bacterial midrib rot, caused by Pseudomonas cichorii, has become a serious threat to the production of greenhouse butterhead lettuce (Lactuca sativa L. var. capitata) in Belgium. Currently, there are no strategies for controlling this pathogen. Therefore, greenhouse experiments were conducted to obtain more knowledge about the epidemiology of P. cichorii on butterhead lettuce. Greenhouse butterhead lettuce becomes susceptible to lettuce midrib rot infections at head formation, and a single overhead irrigation with water containing 102 CFU/ml P. cichorii was sufficient to cause disease.