(Hepatology 2013;58:1461–1473) The development of liver fibrosis constitutes one of the major complications of chronic liver disease, with many clinical consequences such as the development of esophageal varices and ascites being directly related to the presence of liver fibrosis.[1] The hepatic wound healing response is a concerted action of multiple resident and nonresident cell types LY2157299 that not only provides a scaffold for structural stability but also involves the removal of cellular debris by infiltrating hepatic macrophages (HM) and the regeneration of functional

parenchyma.[2, 3] Hepatic stellate cells (HSCs) are considered the main fibrogenic cell type in the liver and are responsible for the production of various types of extracellular matrix.[2, 3] HSCs undergo a well-characterized activation process, during which they lose their characteristic vitamin A and lipid stores and obtain a myofibroblastic phenotype.[2, 3] The activation Neratinib mouse of HSCs is controlled by multiple soluble mediators, including transforming growth factor β and platelet-derived growth factor, and is part of a complex cellular network that controls the hepatic wound healing response. Previous studies have demonstrated that multiple cell populations—including HMs, myeloid-derived suppressor cell, B cells,

T cells, and natural killer cells—influence the development of liver fibrosis.[4-12] Among those, HMs exert a profound effect on HSCs and hepatic fibrosis as shown by genetic or pharmacologic models of macrophage depletion.[6, 7, 13] At the same time, HMs also contribute to fibrosis resolution through MMP13 and matrix remodeling.[6, 14, 15] However, the mechanisms by which HMs promote liver fibrosis remain largely elusive. Dendritic cells

(DCs) are developmentally closely related to macrophages and exert a profound effect on liver fibrosis regression[16] and the cytokine microenvironment during fibrogenesis,[12] but their contribution to liver fibrosis development remains unknown. In the present study, we uncovered the promotion of HSC/myofibroblast survival 上海皓元医药股份有限公司 as a novel mechanism through which macrophages promote fibrosis. Moreover, we demonstrate for the first time that neither classical DCs (cDCs) nor plasmacytoid DCs (pDCs) contribute to fibrogenesis. C57BL/6 mice, Balb/c mice, CD11c-DTR-eGFP mice (in C57Bl/6 background), Tnfrsf1a/Il1r1-deleted (“dko”) mice (in B6.129S background), and B6.129S mice were purchased from The Jackson Laboratory (Bar Harbor, ME) and housed in a specific pathogen-free facility. Collagen–green fluorescent protein (GFP) reporter mice have been described.[17] Hepatic fibrosis was induced in 8- to 12-week-old male mice by ligating the common bile duct for 5 to 15 days as described,[18, 19] via 4 to 20 intraperitoneal injections of carbon tetrachloride (CCl4) (0.125 μL/g to 0.

Total RNA was isolated from liver tissue of Stat5f/f, Stat5f/f;Alb-Cre mice and hepatocytes using an RNeasy mini kit (Qiagen, Valencia, CA) and 1 μg of RNA was reverse-transcribed (complementary DNA reverse-transcription kit; Applied Biosystems, Selleckchem Cabozantinib Foster City, CA). Real-time quantification of messenger RNA (mRNA) transcript levels was performed using the TaqMan Gene Expression Master Mix (Applied Biosystems, Foster City, CA) according to the manufacturer’s instructions. Real-time PCR was performed using an ABI Prism 7900HT (Applied Biosystems, Foster City,

CA). TaqMan probes for Nox4 (Mm00479246_m1), Socs2 (Mm00850544_g1), Puma (Mm00519268_m1), Bim (Mm00437795_m1), and beta-actin (4352341E) were used (Applied Biosystems, Foster City, CA) for real-time PCR. The SYBR primers were as follows: Cdkn2b, 5′-CCCTGCCACCCTTACCAGA-3′ (forward), 5′-CAGATACCTCGCAATGTCACG-3′ Doxorubicin cost (reverse); GAPDH, 5′-AACGACCCCTTCATTGAC-3′ (forward), 5′-TCCACGACATACTCAGCAC-3′ (reverse). All statistical analyses were performed using a two-tailed, unpaired Student t test. P ≤ 0.05 was considered significant. ChIP, chromatin immunoprecipitation; DAPI, 4′,6-diamidino-2-phenylindole; DPI, diphenylene iodonium; GH, growth hormone;

HCC, hepatocellular carcinoma; IgG, immunoglobulin G; MEF, mouse embryonic fibroblast; mRNA, messenger RNA; NIDDK, National Institute of Diabetes and Digestive and Kidney

Diseases; PCR, polymerase chain reaction; ROS, reactive oxygen species; STAT5, signal transducer and activator of transcription 5; TGF-β, transforming growth factor-β. To gain further insight into STAT5′s role as tumor suppressor and understand underlying genetic pathways, we mined microarray-based expression data from liver tissue of control and liver-specific Stat5-null mice and from Stat5+/+ and Stat5−/− mouse embryonic fibroblasts (MEFs) (for GEO accession numbers, see Materials MCE and Methods). In addition to the reduced expression of genuine STAT5 target genes (such as Socs2) in Stat5-null liver tissue, we observed a 2.5- and 3.6-fold reduction of Nox4 and Bim mRNA levels, respectively (Supporting Table 1). Similarly, expression of Nox4 in Stat5−/− MEFs was reduced 3.3-fold (Supporting Table 2). In addition, we observed a 5.7-fold reduction of Puma mRNA in Stat5−/− MEFs. Whereas NOX4 is a reactive oxygen species (ROS)-generating enzyme, BIM and PUMA are proapoptotic proteins. Quantitative real-time PCR and western blots confirmed GH and STAT5 dependency of the Nox4, Puma, and Bim genes in liver tissue. Nox4, Puma, and Bim mRNA levels were reduced in Stat5-null livers (Fig. 1A). The Socs2 gene served as a positive control (Fig. 1A,B).

Results: HERG-siRNA vector was constructed and transfected into gastric cancer cells successfully. The expression of HERG protein and HERG current in gastric cancer cells transfected with HERG-siRNA this website was decreased. HERG-siRNA inhibited proliferation of gastric cancer cells and reduced clone formation ability of gastric cancer cells (P < 0.05). Conclusion: HERG-siRNA can

inhibit proliferation and clone formation of gastric cancer cells. HERG protein is a potential target for gastric cancer biological therapy. Key Word(s): 1. gastric cancer; 2. HERG; 3. potassium channel; 4. proliferation; Presenting Author: YING-CHAO WANG Additional Authors: JI-LIN WANG, XUAN KONG, TIAN-TIAN SUN, HAO-YAN CHEN, JIE HONG, JING-YUAN FANG Corresponding Author: JING-YUAN FANG Affiliations: GI Division, Ren Ji Hospital, School of Medicine, buy RXDX-106 Shanghai Jiao-Tong University; GI Division, Ren Ji Hospital, School of medicine, Shanghai Jiao Tong University Objective: CD24 is associated with invasiveness and poor prognosis in gastric cancer (GC), but the mechanism remains uncertain. Methods: Surgery or biopsy samples from various stages of human GC tumorigenesis were analyzed using immunohistochemistry. Two GC cell lines and one normal gastric epithelial cell line were used.

Differential expressions were validated by real-time PCR and Western blot, and functional studies were performed after transfection of siRNA or lentiviruses. A subcutaneous xenograft mouse model was used for in vivo efficacy. Results: we determined that the expression of CD24 gradually increased in the multistage process of gastric carcinogenesis. The knockdown of CD24 induced significant apoptosis in GC cells via the mitochondrial apoptotic pathway. CD24 may also initiate EMT in GC, as the knockdown of CD24 increased fibronectin

expression and decreased E-cadherin and vitamin D receptor (VDR) expression in GC cells. The signal transducer and activator of transcription 3 (STAT3), may mediate CD24-induced GC survival and EMT. Moreover, CD24 promoted GC progression MCE公司 and STAT3 activation in tumor xenografts both in vivo and in primary GC tissues. Conclusion: CD24 overexpression is an early event in GC carcinogenesis and may promote GC progression by suppressing apoptosis and inducing EMT via STAT3 activation. Key Word(s): 1. CD24; 2. early event; 3. gastric cancer; 4. STAT3; Presenting Author: WEICHUN HUI Additional Authors: LAIMING YU Corresponding Author: LAIMING YU Affiliations: guangxi medical university Objective: TO analysis serum proteomics of intestinal metaplasia patients, dysplasia patients, gastric cancer patients and normal control population, screen serum differential proteins involving in the genesis and development of gastric cancer, and search for specific marks of gastric cancer early diagnosis.

In open-label studies, approximately 70% of ECH and CCH patients have substantial improvement with verapamil therapy.32 In a double-blind placebo-controlled trial of verapamil for maintenance prophylaxis of ECH, 15 patients Bortezomib clinical trial were randomized to 120 mg of verapamil 3 times daily while 15 subjects were randomized to placebo.33 During 2 weeks of treatment, 80% of patients receiving verapamil had a greater than 50% reduction in headache frequency, including 4 patients who became attack free. Verapamil took effect quickly, with one-half of responders having substantial improvement within the first week and

the other one-half responding during the second week. Meanwhile, zero patients receiving placebo had a greater than 50% reduction in headache frequency. Adverse effects due to verapamil were mild, with constipation being the most common and most bothersome. A double-blind, crossover study of verapamil vs lithium carbonate for CCH suggests

that verapamil is a superior treatment.34 In this randomized trial, each of the 24 subjects received verapamil 360 mg per day or lithium carbonate 300 mg 3 times daily for 8 weeks, and then following a 2 week washout period was switched to the other therapy for an additional 8 weeks. Verapamil and lithium both provided similar reductions in both headache index and analgesic consumption. However, verapamil worked more quickly, PD0325901 with over 50% of patients having significant improvement in headache

index within the first week compared with 37% of those taking lithium. Furthermore, only 12% of those taking verapamil reported AEs compared with 29% of those taking lithium. Target dosages of verapamil ranging from 200 mg to 960 mg per day in divided doses are typically used for cluster prophylaxis.35 Most patients will respond to doses of 200 mg to 480 mg per day.36 Immediate or extended out release formulations may be used. Slow titrations up to the target dose may reduce AEs including hypotension, constipation, and peripheral edema. A method of titrating and tapering verapamil dosage in 40 mg intervals is described in a paper by Blau and Engel.36 EKG monitoring is necessary during verapamil therapy because of the risk of heart block and bradycardia, AEs that can develop with initiation of therapy, increases in dose, and even during continued stable dose therapy.37 In our practice, we obtain a baseline EKG before initiating verapamil therapy, repeat EKG with each increase in dose of at least 80 mg, and an EKG each 3 months if the dose has been unchanged. Patients should be informed of the possibility of developing gingival hyperplasia because of long-term use of verapamil. Second-Line Therapy.— Lithium carbonate is a second-line therapy for maintenance prophylaxis of CH.

None of 27 patients of Child B and C liver cirrhosis , developed ATT induced hepatotoxicity after being started on regimen 2. Conclusion: Conclusions -Prevalence of tuberculosis in patients with cirrhosis of liver in our study, was 145.33 per 1000 patients (14.53%) which was 30 times higher than the prevalence of all forms of tuberculosis in general population in India. PZA should be avoided in patients with cirrhosis of liver, even in Child A liver cirrhosis. Combination of RMP, EMB and Ofloxacin is absolutely safe in cirrhosis of liver, even in Child B or C cirrhosis Key Word(s): 1. Tuberculosis; 2. Cirrhosis of liver; 3. ATT; 4. Regimen; Presenting

Author: IOAN SPOREA Additional Authors: SIMONA BOTA, ROXANA SIRLI, ALINA POPESCU, MIRELA DANILA, ANA JURCHIS, OANA GRADINARU-TASCAU Corresponding Author: IOAN SPOREA Affiliations: Department of Gastroenterology and Hepatology, CCI-779 „Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania Objective: To assess the value of liver stiffness (LS) measurements by means of Acoustic Radiation Force Impulse (ARFI) elastography as a predictive selleck chemical factor for the severity of fibrosis. Methods: Our study included 1150 subjects with an median age of 55 years (18-87): 652 patients (56.7%) diagnosed with liver cirrhosis by clinical, ultrasound, endoscopy criteria; 244 subjects (21.2%) without known liver disease, 133 patients (11.6%) with chronic hepatitis C in

whom liver biopsy (LB) was performed, 72 chronic hepatitis B patients (6.3%) with LB and 49 patients (4.2%) with non-cirrhotic ascites. Ten LS valid ARFI measurements were performed in each subject and a median value was calculated, expressed in

meters/second (m/s). Reliable LS measurements were considered the median of 10 valid measurements with a success rate ≥60% and an interquartile range interval <30%. Results: Reliable LS values by means of ARFI measurements Carteolol HCl were obtained in 1076/1150 (93.5%) subjects. In „normal subjects” the mean LS value assessed by ARFI was 1.22 ± 0.31 m/s (median 1.19 m/s). In patients with LB, the best LS ARFI cut-offs values for predicting different stages of liver fibrosis were: F ≥ 2 – 1.48 m/s (AUROC = 0.671), F ≥ 3 – 1.61 m/s (AUROC = 0.709) and F = 4 – 1.75 m/s (AUROC = 0.824). The mean LS values were significantly higher in cirrhotic patients with significant esophageal varices (al least grade 2) as compared with those without or with grade 1 varices: 2.96 ± 0.71 m/s vs. 2.81 ± 0.71 m/s, p = 0,01; also in cirrhotic with ascites as compared with those without ascites: 3.01 ± 0.70 m/s vs. 2.78 ± 0.68 m/s, p = 0.0001. The mean LS values assessed by ARFI were significantly higher in cirrhotic patients with ascites as compared with patients with non-cirrhotic etiology of ascites: 3.01 ± 0.70 m/s vs. 1.43 ± 0.49 m/s, p < 0.0001. Conclusion: ARFI is a good method for noninvasive liver fibrosis assessment. Key Word(s): 1. ARFI; 2.

As shown in Fig. 1A,B, one of the predicted binding sites (2,280–2,286 nt) was highly conserved in human, mouse, rat, chicken, and dog, whereas the other putative site (2,161–2,166 nt) was poorly conserved across species. No predicted miR-196 binding sites were found in the nuclear regulatory factor erythroid 2–related factor 2 and HMOX1 gene, and no putative miR-196 binding sites were found in the coding region of Bach1 gene (data not shown). To click here experimentally verify that the putative miR-196 binding sites are functional,

we transfected 9–13 cells with miR-196–specific mimic and measured Bach1 protein and mRNA levels by way of Western blotting and qRT-PCR, respectively. 9–13 cells transfected with miR-196 mimic showed a significant reduction in the expression of Bach1 protein levels (≈55% after 24 hours’ transfection and ≈64% find more after 48 hours’ transfection) compared with MMNC, whereas

no effects on Bach1 protein levels were detectable in cells transfected with miRNA mimic negative control compared with mock transfection (Fig. 2A). However, no significant effect of miR-196 on Bach1 mRNA levels was observed in 9–13 cells (Fig. 2B). These results demonstrate that the regulation of miR-196 on Bach1 occurs at a translational level in human hepatoma 9–13 cells. Bach1 is a well-established transcriptional repressor of the HMOX1 gene10, 11; therefore, we next determined whether down-regulation of Bach1 protein by miR-196 could increase HMOX1 gene expression. 9–13 cells were transfected with miR-196 mimic or miRNA mimic negative control for 48 hours, after which the levels of HMOX1 and Cullin 3 (Cul 3, nonspecific gene control) mRNA were quantified by way of qRT-PCR. As expected, miR-196 mimic significantly up-regulated HMOX1 mRNA levels by ≈2.4-fold (Fig. 2C),

but not Cul 3 mRNA levels (Fig. 2D) compared with the same amount of miRNA mimic negative control. To further establish that miR-196 targets the 3′-UTR of Bach1 mRNA, which contains two predicted seed match sites for miR-196 (Fig. 3A), (rather than exerting a less direct and specific regulation), a reporter construct, which we called pGL3-Bach1, with Bach1 3′-UTR downstream of the firefly luciferase Staurosporine research buy (f-luc) open reading frame (Fig. 3B), was used. 9-13 cells were cotransfected with pGL3-Bach1 (f-luc), pRL-TK (renilla, to normalize for transfection efficiencies), and miRNA-negative controls, miR-196 mimic, or miR-16 (a negative miR with no predicted binding sites in the 3′-UTR of Bach1 mRNA). Forty-eight hours after transfection, the luciferase reporter activity was assayed. miR-196 mimic transfection significantly decreased reporter activity by ≈53%, whereas miRNA mimic negative control and miR-16 mimic had no effect on reporter luciferase activity (Fig. 3C).

However, we found no significant differences between patient and control groups in the ability to recognize faces and chairs. The inversion effects for bodies and faces were also comparable between the two groups. Conclusions. The current findings suggest that patients

with OCD experience difficulty in perceiving static forms of bodily postures, but are able to adequately recognize human faces. Our data indicate a selective deficit in the perception of bodily postures in those with OCD and suggest that this deficit is probably not related to the abnormal configurational processing of social objects. “
“In cancellation tasks, patients with unilateral spatial neglect typically fail to mark targets within the side of the sheet contralateral to the side of the lesion (contralesional). Moreover, they can show a perseverative behaviour, which Luminespib mw consists in repeatedly cancelling stimuli, mainly in the side of the display ipsilateral to the side of the lesion (ipsilesional). We investigated in 13 right-brain-damaged patients with left spatial neglect and perseverative

behaviour whether and how different densities of horizontal targets modulated Venetoclax price omission and perseverative errors. We found that the density of targets modulated the patients’ distribution of neglect (area of omission), but not its extent, as indexed by the percentage of omissions. Specifically, the area of omissions tightened when target density increased leftwards. On the other hand, target density did not affect the distribution of perseverative behaviour (area of perseveration), as well as its extent,

Lonafarnib in vitro as indexed by the percentage of perseverations. Correlation analyses showed that both the extent and the distribution of omissions were positively correlated to clinical measures of spatial neglect. Conversely, perseverations did not show such a correlation. These findings support the view that two different pathological mechanisms might be involved in left spatial neglect and in ipsilesional perseverative behaviour. “
“Tourette syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics. Tics are repetitive and uncontrolled behaviours that have been associated with basal ganglia dysfunction. We investigated saccadic eye movements in a group of young people with TS but without co-morbid ADHD. Participants performed two tasks. One required them to perform only pro-saccade responses (pure pro-saccade task). The other involved shifting, unpredictably, between executing pro- and anti-saccades (mixed saccade task). We show that in the mixing saccade task, the TS group makes significantly fewer errors than an age-matched control group, while responding equally fast. By contrast, on the pure pro-saccade task, the TS group were shown to be significantly slower to initiate and to complete the saccades (longer movement duration and decreased peak velocity) than controls, while movement amplitude and direction accuracy were not different.

The majority of associations with inhibitor production are related to HLA class

II alleles: HLA-DRB1*14, DRB1*15, HLA-DQB1*06:02, DQB1*06:03. A positive association of the DRB1*15:01/DQB1*06:02 haplotype and inhibitor prevalence was reported in severe haemophilia patients. On the contrary DRB1*16 and DQB1*05:02 alleles were found to lower inhibitor risk [23-26]. The weak association of HLA types with inhibitor development suggests that the ability of a patient’s MHC class II to present one or more FVIII-derived peptides is a necessary but Selleckchem RXDX-106 not sufficient condition to stimulate helper T cells and produce neutralizing antibodies. In attempts to find new markers allowing a stratification of the risk patients to develop inhibitors, single-nucleotide polymorphisms (SNPs) in the regulatory regions of cytokine genes have been studied. Certain polymorphisms, mainly localized in the promoter regions, in the exons or in microsatellites of intron regions can affect the transcription and influence the production of cytokines and subsequently modify the profile of the immune response. Genetic polymorphisms

in immune-response associated genes, i.e. IL1b, IL4, IL10, TNF-α and CTLA4, have been analysed. The association between the −308A/A genotype in TNF-α gene and the formation of inhibitors was evident in several studies. For the cytogene IL10, the −1082G allele and 134 bp allele of a ‘CA’ dinucleotide repeat microsatellite in the promoter region of the IL10 see more gene were found to be more common in patients with inhibitors patients. A clear predominance of the high-producer GCC haplotype (0.55 vs. 0.32) and Methocarbamol a lower frequency of the low-producer ACC haplotype (0.20 vs. 0.32; P = 0.002) was observed in patients with inhibitors [26-28]. Furthermore, several new candidates as potentially predictors for inhibitor development (CD44, CSF1R, DOCK2, MAPK9 and IQGAP2) have been identified in Haemophilia

Inhibitor Genetic Study [29]. Ethnicity and family history have been shown to predispose for the development of FVIII inhibitors. The incidence of inhibitors is high in the subgroup of patients of African descent when compared with Caucasians (55.6% vs. 27.4%). As the F8 mutation spectrum does not differ between races this difference might be based on ethnic-specific genetic variants in immune response determinants. Another hypothesis is related to ethnic-specific F8 gene variants. Four common, non-synonymous SNPs within the F8 have been identified, which occur as six haplotypes in the human population (H1–H6). Three of these haplotypes (H3, H4 and H5) have been associated with an increased risk of inhibitor development and were detected mainly in black people [30]. The risk for the formation of inhibitors increases significantly in patients with a family history of inhibitors, where the absolute risk in such patients is determined to be 48%, whereas the risk in patients with no family history only 15%.

In a variety of cells, the A2aR is known to be coupled with adenylate cyclase, resulting in up-regulation of cAMP and PKA activation. We extend these findings to MSCs, demonstrating an increase in cytosolic cAMP after activation by the non-hydrolyzable adenosine agonist NECA. The ability of forskolin to inhibit HGF chemotaxis demonstrates that elevations in cAMP are sufficient for such inhibition. We also show a requirement for PKA using the specific PKA peptide inhibitor ST-HT31. HGF is known to increase cytosolic Ca++, and we have previously

shown in hepatic stellate cells that signaling via the A2a receptor Ku 0059436 can inhibit increases in cytosolic Ca++. We therefore tested whether NECA can inhibit the HGF-induced increase in cytosolic Ca++. As can be seen from Fig. Selleck LY2606368 5A, HGF induced a significant increase in cytosolic Ca++, and this was inhibited by NECA in a PKA-dependent manner. HGF has been shown to increase Rac1 activity in a Ca++-mediated manner, and we further confirm the requirement for Rac1 in HGF chemotaxis by demonstrating that a Rac1 inhibitor blocks HGF-induced chemotaxis. The inhibition of HGF-induced

cytosolic Ca++ by adenosine and the requirement for an increase in cytosolic Ca++ for Rac1 activation predict that adenosine will inhibit an HGF-mediated increase in Rac1 activity. This was found to be the case (Fig. 3B). To definitively confirm that the inhibition of HGF-induced Rac1 activation by adenosine is the mechanism of inhibition of chemotaxis, we used a well-tested plasmid (RacQL) expressing the constitutively active form of rac1. When MSCs were transfected with RacQL, NECA was unable to block HGF-induced chemotaxis. Rac1 activation is known to for be important in actin stress fiber formation, and to further confirm functional Rac1 inhibition

in response to NECA, we examined actin stress fibers in MSC. HGF increased the prominence of actin stress fibers, and as predicted from its ability to inhibit Rac1, NECA resulted in almost complete loss of actin stress fibers. Collectively, these studies demonstrate a novel action of adenosine on MSC via the A2a receptor, resulting in inhibition of chemotaxis through a cAMP, PKA, Rac1 pathway. This has significant implications for MSCs when they reach an area of cell death or inflammation with high levels of adenosine. The previously described model of chemotaxis of MSCs toward an increasing gradient of HGF is still valid,33, 34 but our data suggest that, on arriving at a site of cellular injury with high adenosine levels, MSC chemotaxis will be inhibited. We propose that the inhibition of chemotaxis will provide a functional stop signal and result in localization of MSC to these sites. Such a model incorporating a stop signal in addition to the known chemotaxis signals has the advantage of localizing MSC to sites of injury, where they are most needed. We propose a schema to describe the interaction between HGF and adenosine (Fig. 8).

Preliminary in vitro tests showed that ammonium bicarbonate, ammonium carbonate, potassium benzoate, potassium sorbate, sodium benzoate and sodium metabisulphite at 2% completely inhibited mycelial growth of the fungus. No significant differences were observed among these salts and disodium EDTA (P ≤ 0.05). However, the ED50, minimum

Carfilzomib mw inhibition concentration (MIC), and minimum fungicidal concentration (MFC) values indicated that sodium metabisulphite was more toxic to Ilyonectria liriodendri than these other six salts. Soil bioassays showed that sodium metabisulphite, sodium benzoate and potassium sorbate at 0.25% completely inhibited mycelial growth of the fungus, whereas potassium benzoate reduced the mycelial growth of fungus learn more by 90.30%; however, the differences in inhibitory effects were statistically insignificant (P ≤ 0.05). Moreover, there was no significant difference between 0.1% sodium metabisulphite and 0.5% ammonium carbonate, 0.75% ammonium bicarbonate and 1.5–2.0% disodium EDTA (P ≤ 0.05). Unlike disodium EDTA, complete inhibitory was observed with ammonium carbonate and ammonium bicarbonate at

higher concentrations. However, in root bioassays, applications of 2% ammonium bicarbonate, 1.5% ammonium carbonate and 2% disodium EDTA were phytotoxic to kiwifruit seedlings, but 0.25% four other salts were neither phytotoxic to kiwifruit seedlings nor did it adversely affect root length, root fresh weight and root dry weight of seedling. This study also showed I. liriodendri to be capable of growth in both acidic and basic environments. However, while the fungus showed uninhibited growth at pH values of 5–11, growth decreased significantly at both higher and lower pH values (P ≤ 0.05) and was completely inhibited at pH 12. “
“Anatomical observations of leaves infected by Taphrina deformans

were studied in tolerant peach trees (TPT) and in very susceptible (VSPT) ones. Leaves from the first sampling (2nd April) showed hyphae penetrating through the stomata or into the cuticle of the host tissue; anatomical structures of leaf sections were similar for both TPT and VSPT. The ultrastructure of the leaves of TPT showed seemingly normal mesophyll cells. In contrast, mesophyll cells of the VSPT showed important signs of degradation. Cells were organelle-free and the middle lamella was expanded and invaded by hyphae of before T. deformans. In some samples, the leaves of TPT showed deformed epidermal cells, loss of some spongy cells and increase of the intercellular spaces and division of the palisade cells. The pathogen proliferation in the leaves of the VSPT was considerably superior. In this case, stimulation of cell division occurred in the abaxial epidermis. Cells showed periclinal and oblique divisions, with an increased number of plasmodesmata; palisade or spongy cells were not differentiable. Leaves from TPT collected on 26th April showed hyphae with a non-cylindrical section and with a squashed aspect.