Through KEGG, 46 and Selleckchem Veliparib 41 enriched pathways were collected for the target genes of upregulated and downregulated miRNA, including apoptosis, fatty acid metabolism and so on. Analysis of common target genes of all

downregulated miRNA revealed potential involvement of ion transport and the membrane structure in steatohepatitis. Conclusion:  We reported the dysregulated miRNA in transition from hepatic steatosis to steatohepatitis and showed potential clinical application in disease differentiation. This study provided data reservoir for miRNA exploration and revealed novel disease-specific Gene Ontology functions and KEGG pathways such as uncoupling-protein-guided membrane change. Our data contributes to further researches on the pathogenesis and treatment of non-alcoholic steatohepatitis. “
“Drinking excessive amounts of alcohol regularly for years is toxic to almost every tissue of the body. On the other hand, epidemiological and clinical evidence shows that light-to-moderate drinking is associated with a reduced risk of coronary heart disease, total and ischemic stroke, and mortality. In the past two decades, metabolic syndrome, the combination of obesity, hypertension, dyslipidemia and hyperglycemia, are all also recognized BGB324 clinical trial as major cardiovascular risk factors, has given rise to much

clinical and research attention, because of its high prevalence in the world. Therefore, it is of interest to evaluate the overall associations of alcohol consumption with the development of metabolic many syndrome. Recently, the protective, detrimental or J-shaped associations have been reported between alcohol consumption and metabolic syndrome. This controversy may be due to the complex mechanistic relation between alcohol consumption and each component of metabolic syndrome, and almost all studies have various

limitations and problem points. Prospective studies are therefore needed to confirm the association between alcohol consumption and prevalence of metabolic syndrome, and to assess the influence of alcohol drinking patterns and other possible factors, such as smoking, physical activity, socioeconomic status, education, occupation, diet and exercise. This article reviews the relation of alcohol consumption and components of metabolic syndrome, and discusses the epidemiological evidence for alcohol’s putative vascular protective effects and plausible underlying biological mechanisms. “
“Background and Aim:  Despite improvements of treatment in hepatocellular carcinoma (HCC), the recurrence rate after curative hepatic resection still remains remarkably high. An immediate recurrence of HCC after surgery is frustrating. We tried to clarify risks of immediate postoperative recurrence of HCC; that is, within 4 months after curative hepatic resection.

Here we report a novel function for FoxQ1 in modifying the tumor microenvironment to promote HCC metastasis. FoxQ1 expression was an independent Acalabrutinib and significant risk factor for the recurrence and survival in two independent cohorts totaling 1,002 HCC patients. FoxQ1 induced epithelial-mesenchymal transition (EMT) through the transactivation of ZEB2 expression by directly binding to the

ZEB2 promoter. Knockdown of ZEB2 decreased FoxQ1-enhanced HCC metastasis, whereas up-regulation of ZEB2 rescued the decreased metastasis induced by FoxQ1 knocking down. Additionally, serial deletion, site-directed mutagenesis, and a chromatin immunoprecipitation assays showed that VersicanV1, which promoted HCC metastasis and macrophage attraction, was a direct transcriptional target of FoxQ1. FoxQ1-induced VersicanV1 expression promoted the secretion of chemokine (C-C motif) ligand 2 (CCL2) from HCC cells. Chemotaxis assay showed that the culture media from FoxQ1-overexpressing HCC cells increased the migratory activity of the macrophages. Inhibition of VersicanV1 and CCL2 expression significantly inhibited FoxQ1-mediated macrophage migration. In animal studies, the up-regulation of FoxQ1 in HCC cells promoted

HCC metastasis and intratumoral tumor associated macrophage (TAM) infiltration, whereas knockdown of VersicanV1 reduced FoxQ1-mediated HCC metastasis and intratumoral TAM infiltration. Depletion of macrophages Erlotinib concentration using clodronate liposomes dramatically decreased FoxQ1-enhanced HCC metastasis. In human HCC tissues, FoxQ1 expression was positively correlated with ZEB2 and VersicanV1 expression and intratumoral TAM infiltration. Patients with positive coexpression of FoxQ1 and ZEB2, FoxQ1, and VersicanV1, or FoxQ1 and intratumoral TAMs were associated with poorer prognosis. Conclusion: FoxQ1 promotes HCC metastasis by transactivating ZEB2 and VersicanV1 expression, resulting in the induction of EMT and the

recruitment of macrophage infiltration. (Hepatology 2014;59:958–973) mafosfamide “
“Clinicians rely upon the severity of liver fibrosis to segregate patients with well-compensated nonalcoholic fatty liver disease (NAFLD) into subpopulations at high- versus low-risk for eventual liver-related morbidity and mortality. We compared hepatic gene expression profiles in high- and low-risk NAFLD patients to identify processes that distinguish the two groups and hence might be novel biomarkers or treatment targets. Microarray analysis was used to characterize gene expression in percutaneous liver biopsies from low-risk, “mild” NAFLD patients (fibrosis stage 0-1; n = 40) and high-risk, “severe” NAFLD patients (fibrosis stage 3-4; n = 32). Findings were validated in a second, independent cohort and confirmed by real-time polymerase chain reaction and immunohistochemistry (IHC).

027).58 This is the first study to suggest that therapy may actually impact the natural history of the disease. More recently, Gluck et

al. described a 20 year experience with endoscopic therapy for 84 symptomatic patients with PSC.59 Similar to the Baluyut study, observed patient survival was higher than expected by the Mayo Risk Score.59 All therapeutic endoscopy comes with risk. In the two largest reported series of patients with long follow-up, the risk of complications was 7.3%–20%. The complications were mild without need for surgical intervention.58, 59 The most common complications were pancreatitis, cholangitis, biliary tract perforation and hemorrhage. Focal Autophagy inhibitor nmr biliary tract obstruction, whether benign or malignant, has been the primary indication for the nontransplant surgical management of PSC. Despite limitations of the accuracy of current diagnostic modalities for malignancy in buy Metformin PSC, diagnostic laparotomy has little clinical value. The rationale for surgical management in PSC is bypass of an obstruction caused by a dominant stricture. Non-transplant surgical approaches include biliary bypass by cholangio-enterostomy or resection of the extrahepatic biliary stricture and Roux

Y hepaticojejunostomy.60, 61 Biliary bypass alone has been employed infrequently because dominant strictures are typically hilar. Moreover, the intrahepatic ducts are variably involved which limits the access and quality of these ducts for bypass.60 Florfenicol Biliary bypass has no role in PSC patients with cirrhosis. Extrahepatic

bile duct resection and Roux Y hepaticojejunostomy with or without stenting for dominant strictures is controversial.53, 61 Current evidence suggests that selected patients with non-cirrhotic stage PSC have an overall survival of 83% at 5 years and 60% at 10 years and a readmission free rate from cholangitis of 57% at 3 years for such an approach.62 Bilirubin levels > 2 mg/dL and cirrhosis are associated with decreased survival. No data regarding surgical management have shown that either bypass or resection of a dominant stricture affect natural history or disease progression. Most patients, who have not had biliary tree instrumented, have negative microbial bile cultures.63, 64 However, dominant strictures can induce stagnation of bile resulting in bacterial colonization and secondary cholangitis. This can be the first presentation of the disease occurring in 6.1% of PSC patients in one recent study.65 Furthermore, severe recurrent cholangitis may play a role in the progression of the disease. The relevance of a bile duct stricture was demonstrated by documenting bacterial infection of the bile in 15 out of 37 PSC patients (40.5%) with a dominant stricture but not in the absence of such stenosis; short-course antibiotic treatment proved not very effective in eradicating bacteria from the bile ducts of patients with dominant strictures.

With disease progression, cardiac output (CO) cannot be further increased resulting in arterial hypotension, stimulation of the sympathetic nervous and renin-angiotensin

system as well as ascites. Tense ascites decreases venous return and thus CO due to compression of the inferior vena cava and right atrium. Finally, hepatorenal syndrome (HRS) is the extreme expression of this hemodynamic dysfunction. Therapeutic paracentesis acutely increases CO which has been previously identified to be an independent risk factor for the development SB203580 ic50 of HRS. However, the determination of CO is difficult in clinical routine due to invasive, operator dependent or time-consuming standard procedures such as right heart catheterization, echocardiography or cardiac magnetic resonance imaging. The aim of our study was to evaluate hemodynamic changes during paracentesis using non-invasive inert gas rebreathing (IGR). Methods: Routine therapeutic paracentesis was performed in the supine position using ultrasound guidance in 28 patients with tense ascites refractory to therapy. In patients with a volume of ascites removed (VA) > 5 liters albumin was administered. Hemodynamic parameters including CO, stroke volume (SV), heart rate

Epacadostat supplier (HR), systolic and diastolic blood pressure (SBP, DBP) were assessed immediately prior to and after Protein kinase N1 the procedure using IGR. Results: The collective (19 men) aged from 42 to 76 years. Mean MELD score was 13 with 15 patients in Child-Pugh class B (CPC) and 13 in C. Most frequent causes of cirrhosis were alcohol (16) and HCV (4) or HBV (3). Mean VA was 4400±1500 ml (range 1900 to 8000 ml). CO significantly increased from 5.7±1.7 to 7.0±2.0 l/min after paracentesis

(p<0.001). SV accordingly increased from 81±26 ml to 97±33 ml (p<0.001). Both SBP and DBP significantly dropped from 122±19 to 117±18 mmHg (p=0.04) and 69±12 to 63±13 mmHg (p<0.001). HR remained unchanged at 73±14 and 74±15 mmHg (p=0.69).There was a moderate correlation between VA and change in CO (r=0.36, p=0.12). We neither found differences between change in CO and CPC (p=0.31) nor the cause of cirrhosis (p=0.25). Conclusion: IGR is safe and feasible in tracking hemodynamic changes non-in-vasively induced by therapeutic paracentesis. Hyperdynamic circulation further increases acutely showing a moderate association with VA. Further studies are warranted as knowledge of hemodynamics may be beneficial in evaluating patients at risk for e.g. HRS, portopulmonary hypertension or hepatopul-monary syndrome. Disclosures: Christoph Antoni – Speaking and Teaching: Roche, MSD, BMS, Janssen, Gilead, Falk Foundation The following people have nothing to disclose: Joachim Saur, Thomas Zimmerer, Nenad Suvajac, Julia D.

Biovigilance has many different aspects that involve a variety of data collection methods, analysis and resolution. In the United States, biovigilance programmes are only now becoming centralized.

Coordinated safety and public health efforts are shared by various divisions of Health and Human Services agencies including the Food and Drug Administration (FDA), the Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH) and Selleckchem U0126 Centers for Medicare and Medicaid Services (CMS), with input from trade, academic, industrial and patient groups. In the US, the CDC has the primary responsibility for conducting national disease surveillance and developing epidemiological and laboratory tools to enhance surveillance. CDC’s emerging infectious disease working group

gathers information from multiple sources, including state health surveillance, Selleck AP24534 literature reports and reports from regulatory authorities worldwide. CDC shares information about pathogens that might affect blood products with relevant offices within the FDA, and other governmental agencies as appropriate, such as the Department of Defense. FDA assesses the risk of potential pathogen transmission by blood products and develops a risk mitigation strategy depending on the nature of the pathogen. The Centers for Disease Control and Prevention’s National Healthcare Safety Network (NHSN) has worked with the AABB (formerly the American Association of Blood Banks), a trade organization, to develop a web-based

haemovigilance system that collects data from hospitals to detect adverse transfusion events such as reactions to blood products, process problems and medical errors. The information, collected using standardized of data collection tools, can be used to create benchmarks for trending purposes, provide opportunities for data-driven intervention, including validation, quality control and impact measurement. The first module of this programme, that became operational in February, 2010, is designed to collect information about recipients of blood product transfusions; a second module on blood donors will be implemented shortly. Other CDC surveillance programmes include the Universal Data Collection project to monitor the safety of the nation’s blood supply for persons with bleeding disorders being treated with blood products, as well as to monitor the occurrence of joint complications experienced by persons with haemophilia. CDC also has a programme to monitor for any emergence of Creutzfeldt–Jakob disease. The Food and Drug Administration has a number of different surveillance programmes for blood products that vary according to the type of product under scrutiny, e.g. blood components such as whole blood, cells or plasma, or manufactured products such as plasma derivatives.

Key Word(s): 1. GERD; 2. extraesophageal manifestations; 3. prevalence Presenting Author: AMIE VIDYANI Additional Authors: UMMI MAIMUNAH, PANGESTU ADI Corresponding Author: NVP-AUY922 clinical trial AMIE VIDYANI Affiliations: Gastroenterology-Hepatology Division, Gastroenterology-Hepatology

Division Objective: The prevalence of gastroesophageal reflux disease (GERD) and obesity are increasing. However, the relationship between body mass index (BMI) and GERD is still controversial. Therefore,we designed a study to evaluate the relationship between BMI and the severity of GERD. Methods: This is an analytic-cross sectional study that involved of GERD patients in one of private clinic in Surabaya. The diagnosis of GERD was based on endoscopic examination. We dichotomized the frequency of heart burn

and acid regurgitation into less than once a week and once a week or more frequent. The BMI was categorized according to World Health Organization (WHO) classification (normal BMI < 25 kg/m 2, overweight 25–30 kg/m 2, and obese >30 kg/m 2). The learn more severity of endoscopic findings based on modification of Los Angeles (LA) criteria (non-erosive reflux disease/NERD, stage A,B,C,D). Spearman correlation and Chi-square test were used to know the relationship between variabels. Results: MicrosoftInternetExplorer4 Result of the 28 GERD patients, there were 16 (57.1%) patients with normal BMI, 9 (32.1%) patients were overweight, and 3 (10.7%) patients were obese. The correlation of BMI with frequency of heart burn and acid regurgitation was not significant (r = 0.19, p = 0.3; r = 0.01, p = 0.94). The correlation of BMI with endoscopic severity was not significant (r = 0.1, p = 0.6). Conclusion: This study suggest there was no relationship between BMI and the severity of GERD. Key Word(s): 1. GERD; 2. BMI; 3. LA criteria Presenting Author: ZHIQIN WONG Additional Authors: UMMI NADIRAH DAUD, JEEVINESH NAIDU, CHAI SOON NGIU, RAJA AFFENDI RAJA ALI, SHANTHI PALANIAPPAN, MAZLAM ZAWAWI, HAMIZAH RAZLAN Corresponding Author: ZHIQIN WONG Affiliations: University

Putra Malaysia, National University of Malaysia, National University of Malaysia, National University of Malaysia, National University of Malaysia, National University of Malaysia, National University Thymidine kinase of Malaysia Objective: Functional dyspepsia (FD) is a common global disorder that causes significant morbidity and time loss from work. Itopride, a prokinetic drug, has been demonstrated to be efficacious in improving FD symptoms compared with placebo. This study was conducted to evaluate the efficacy of itopride as compared to placebo in achieving symptom improvement and improvement in health-related quality of life in a subset of FD patients with post-prandial distress syndrome PDS / PDS overlap symptoms. Methods: This was a randomized double blind placebo controlled trial.

Louis, MO). After incubation, all cells were collected, washed, stained with BGB324 surface markers, and analyzed by FACS. Patterns

of CD69 coexpression were determined by gating on CD3+, CD8+ T-cells. Lymphocytes were labeled with 1 μM carboxyfluorescein succinimidyl ester (CFSE) (Molecular Probes, Eugene, OR) as described previously11 and cultured for 7 days in the presence of HBV core peptide (10 μg/mL) and anti-CD244 (10 μg/mL) or anti-PD-L1/2 (5 μg/2.5 μg/mL). Plain medium, isotype control, and phytohemagglutinin (PHA) (Biochrom, Berlin, Germany) (2.4 μg/mL) served as controls. At day 3, 20 IU/mL recombinant human interleukin 2 (rhIL-2) was added. At day 7, cells were collected, washed, stained with surface markers, and analyzed by FACS. The percentage of proliferating CD8+CFSElow T-cells was determined after gating on CD3+ T-cells. In vitro expansion was performed with 2 × 106 PBMCs diluted in 1 mL culture medium. After preincubation with anti-CD244 (10 μg/mL), anti-CD48 (5 μg/mL), anti-CD244/CD48/anti-PD-L1/2 (5 μg/2.5 μg/mL) for 30 minutes at 37°C, cells were stimulated with HBV core or EBV posttranscriptional regulator protein of

EBV containing a CD8 epitope (BMFL1) peptide (10 μg/mL). At day 7, 20 IU/mL rhIL-2 was added. Isotype control and healthy donors (n = 9) served as controls. At day 21, cells were collected, washed, stained with pentamers, and analyzed by FACS. If the mean value plus 2SD in healthy individuals was exceeded, the increase of virus-specific CD8+ T-cells was defined as positive. After in vitro expansion of 3 × 106 PBMCs with HBV core or EBV peptide in the presence or absence of anti-CD244, cells were re-stimulated with or without antigen (10 μg/mL) in the presence of Monensin (2μM) and anti-CD107a

(15 μg/mL). Anti-CD3/CD28 (10 μg/mL/2 μg/mL) was used as positive control. After 6 hours of incubation, cells were collected, washed, stained with surface markers, fixed, and permeabilized. Cells were then stained with anti-IFN-γ, IL-2, and TNF-α for 20 minutes at room temperature and analyzed by FACS after a wash step. Cells were gated Selleckchem Paclitaxel on CD3+, CD8+ T-cells. Background-corrected data were shown, with subtraction of individual costimulated control sample. Data were shown as mean values. GraphPad Prism was used for analysis of the Mann-Whitney U test, Wilcoxon signed rank test, Fisher’s exact test, and Spearman correlation test. P values of less than 0.05 were considered significant. We first performed a comparative analysis of CD244 on total and HBV core (c)18-27–specific CD8+ T-cells. The characterization of CD244 distribution was done in the peripheral blood of 27 chronically infected patients, 13 acutely infected patients, 8 resolvers, and 15 healthy individuals. CD244 expression was also investigated in the liver tissue of four chronically infected patients. The mean frequency of CD8+Pentc18-27+ T-cells in chronically infected and untreated patients was 0.02%.

In addition, cognitive status was assessed by administration of the Mini Mental State Examination (MMSE; Folstein, Folstein, & McHugh, 1975). Data were analysed using one-way ANOVAs (Table 3). On each trial, two characters, a digit (1–9, except 5 and 0) and a letter from the subset A, E, I, U,

F, C, T, X, were presented. The task-relevant stimuli and task-irrelevant PF-562271 cell line distracters were counterbalanced across each trial type. Distracters were presented either to the left or to the right of the target stimulus, to prevent subjects from adopting a constant search strategy. The Rogers et al. (1998) paradigm contained no stimulus or distracter repetitions, so in the present design the task-relevant stimulus and irrelevant distracter also switched on every trial. In the alternating runs task sequence (AABB), subjects switched task on every second trial. Salient spatial cueing was employed, in the form of stimulus

position in a 2 × 2 grid (Rogers & Monsell, 1995), ensuring a cue switch on each trial and thereby unconfounding cue switches from task switches (Logan & Bundesen, 2003). The task mapping Doramapimod order within the grid was counterbalanced within groups. Since foreperiod preparation has been shown to mask parkinsonian switching deficits (Cools et al., 2003) and reduce sensitivity to frontal activation (Wylie et al., 2004), a short (300 ms) response to stimulus interval duration was utilized to maximize paradigm sensitivity to any such deficits. selleck kinase inhibitor No feedback was given. Subjects switched between categorizing a letter as a vowel or consonant, and categorizing a digit as higher or lower than 5 on every second trial, as fast and as accurately as possible, by emitting vocal responses. Successful performance required selection of the task-relevant stimulus in the face of interference from the irrelevant character in the display, the distracter, and application of the correct response rule. Similar to

our previously published study, these tasks were selected based on the following criteria: (1) the vocal responses mapped directly and naturally onto the judgment outcome (‘high/low’, ‘vowel/consonant’), (2) the vocal responses themselves comprised short vocalizations for ease of triggering the voice key, and (3) the tasks, previously piloted to address task dominance and control for asymmetrical switch costs (Allport, Styles, & Hsieh, 1994; Allport & Wylie, 2000), were relatively easy and based on well-learnt rules. The task sequence followed the alternating runs procedure of AABB, so that subjects switched between two vowel/consonant and two high/low judgments on every second trial. The probability of a response repetition was additionally controlled, since the Rogers et al. (1998) procedure contained by definition no response repetitions because responding to the target comprised vocalization of its identity and there were no stimulus repetitions.

Based on the data presented here,

we hypothesize that the macrophage infiltrate following AALF is derived from an early wave of bone marrow–derived circulating monocytes followed by an expansion of the resident proliferating KC population that is implicated in the resolution of inflammation and tissue repair processes. The protein array analysis reveals an inflammatory microenvironment favoring tissue repair processes in AALF at the time of transplantation. In whole liver tissue, levels of IL-6, IL-10, and TGF-β1 are elevated in AALF compared with pathological controls, whereas concentrations of proinflammatory mediators BIBW2992 purchase (IL-1β, IL-12, IL-17, TNF-α, interferon-γ) remain similar. Higher concentrations of monocyte chemoattractants (CCL2, CCL3) and immunoregulatory cytokines (TNF-α, IL-6, IL-10) are detected in necrotic compared with nonnecrotic areas. These findings concur with data from experimental liver injury models, where CCL2 skews the inflammatory microenvironment to augment levels of

anti-inflammatory/hepatoprotective selleck mediators (IL-6, IL-10, TGF-β1).13, 26, 28 In other inflammatory models, CCL2 induces an IL-10–skewed cytokine profile in murine polymicrobial sepsis and contributes to the recruitment of IL-10–producing, monocyte-derived macrophages during experimental colitis.41-44 Therefore, our data demonstrating increased expression of CCR2 on CD14+CD16+ circulating monocytes may indicate that CCL2 possesses immunoregulatory capabilities in AALF through recruitment of different circulating monocyte subsets.45 Further studies evaluating monocyte subsets at different stages of liver injury are required to address this question. Our data indicate that h-mϕ represent the predominant selleckchem cell population in the inflamed AALF liver and are avidly

proliferating within areas of necrosis, a finding that is associated with hepatic regenerative responses in experimental liver models.7 They express markers associated with enhanced scavenger functions (CD68+HLA-DR+),46-48 preferentially expressed at the resolution stages of experimental liver injury,12, 28 and contain phagocytosed cellular and extracellular debris. Akin to other inflammatory conditions, phagocytosis may be the microenvironmental switch that triggers h-mϕ to secrete immunoregulatory mediators (CCL2, TNF-α, IL-6, IL-10) that are present at higher concentrations within areas of hepatic necrosis.49-51 Equally, the proportion of h-mϕ not expressing HLA-DR in central areas of necrosis could indicate that they are functionally modulated by their microenvironment. Functional and phenotypic analyses of freshly isolated h-mϕ are warranted to explore these observations. These findings also pose further questions as to whether these intra-hepatic events impact on circulating monocyte phenotype and function.

38 μmol photons · m−2 · s−1 at low temperature). Both the photosynthetic light- and carbon-use efficiencies increased with increasing growth or temperatures (from 12°C to 26°C). The results suggested that the thermal acclimation of photosynthetic performance of G. lemaneiformis would have important ecophysiological implications in sea cultivation for improving photosynthesis at low temperature this website and maintaining high standing biomass during summer. Ongoing climate change (increasing

atmospheric CO2 and global warming) may enhance biomass production in G. lemaneiformis mariculture through the improved photosynthetic performances in response to increasing temperature. “
“Clonal kelp taxa may reproduce both sexually and vegetatively resulting in a potential trade-off in the allocation of acquired carbon and nitrogen resources. Such trade-offs may dictate a different response of clonal kelps to varying environmental conditions relative to aclonal kelp taxa. Laboratory temperature and nutrient manipulation experiments selleck kinase inhibitor demonstrated that investment in sexual and vegetative reproduction in Laminaria sinclairii (Harv. ex Hook. f. et Harv.) Farl., C. L. Anderson et D. C. Eaton was regulated by different abiotic

factors. Sorus production (investment in sexual reproduction) and blade growth were significantly higher at 12°C compared to 17°C, regardless of nutrient concentration. Net carbon storage and depletion in rhizomes were observed in the low- and high-temperature treatments, respectively, suggesting that carbon stores were not responsible for increased growth. Rhizome elongation (investment in vegetative reproduction), on the other hand, was significantly higher in 12 μM NO3− than in 2 μM NO3−, irrespective of temperature. This increase in rhizome growth was concurrent

learn more with elevated rhizome percent tissue nitrogen levels also observed in treatments with higher nutrients, again indicating a growth response to treatment independent of previous nutrient stores. These results suggest that regulation of growth and investment in sexual reproduction in L. sinclairii is similar to that in aclonal kelps (i.e., warmer temperatures result in decreased reproductive output). Additionally, depletion of carbon and nitrogen from rhizomes in suboptimal conditions confirms the role of clonal kelp rhizomes in carbon and nutrient storage. “
“The aims of this work were to study cyanobacterial isolates resembling the genus Hydrocoryne using a combination of morphology and phylogeny of 16S rRNA and nifH sequences and to investigate genes involved in cyanotoxin and protease inhibitor production. Four new cyanobacterial strains, isolated from biofilm samples collected from King George Island, Antarctica, were studied.