Identification of the cell(s) of origin and the signaling pathway

Identification of the cell(s) of origin and the signaling pathways involved are challenging issues in liver cancers with pivotal implications in the clinicopathological and therapeutic perspectives. VINCENZO CARDINALE, M.D.1 “
“A 17-year-old girl presented with a history of elevated alkaline phosphatase and gamma-glutamyl transpeptidase AZD8055 clinical trial (γGT) levels for several years. She was asymptomatic and did not have jaundice, pruritus, abdominal pain, nausea, vomiting, weight loss, rashes,

or diarrhea. Viral hepatitis serologies, autoimmune serologies, and thyroid studies were all normal. γGT, gamma-glutamyl transpeptidase; MRCP, magnetic resonance cholangiopancreatography. She had a past medical history of anxiety, which was treated with Celexa. Otherwise, she was healthy and had no major childhood illnesses or history of substance abuse. She had traveled extensively with her family during her childhood, notably to Northern and Eastern Africa and Southeast Asia. Her physical examination was unremarkable. An abdominal

ultrasound examination was performed, and the findings were normal. Magnetic resonance cholangiopancreatography (MRCP) showed mild beading of the intrahepatic ducts Maraviroc concentration consistent with the diagnosis of primary sclerosing cholangitis involving the small ducts. The patient was started on ursodiol (300 mg three times per day), and her alkaline phosphatase and γGT levels promptly normalized. Subsequently, colonoscopy was performed to

rule out concomitant inflammatory bowel disease. The mucosa appeared normal on endoscopic examination, but random biopsy samples were taken to rule out quiescent colitis. The pathology specimens revealed schistosoma eggs, and stool studies were positive for Schistosomamansoni. Percutaneous liver biopsy was then performed to evaluate hepatic involvement. There were portal intravenular find more granulomas in two triads with a schistosoma egg with otherwise minimal lobular fibrosis There was no evidence of mucopolysaccharide production or hyperplasia of the ductular epithelium (Fig. 1). An endoscopic examination was negative for esophageal varices. She was treated with praziquantel, and ursodiol was continued. One year later, repeat MRCP showed minimal changes with resolution of duct dilation in segment 6. Schistosomiasis, which is also known as bilharzia, affects more than 207 million people worldwide, with 1 of every 30 people infected with the trematode. Free cercariae penetrate the skin, travel to the pulmonary vessels, and then eventually lodge in the liver; there, they mature, mate, and migrate distally against the venous flow in the portal system. Eggs pass through the intestinal wall into the bowel lumen. Chronic disease results from the ongoing host response to accumulating tissue-trapped eggs.

55, P = 0007) Similarly, there was a significant correlation be

55, P = 0.007). Similarly, there was a significant correlation between the levels of claudin

and occludin and the slope of HCV-RNA increase during the first week after LT (r = 0.63, P = 0.005). Occludin and claudin-1 levels increased significantly 12 months after LT (P = 0.03 and P = 0.007, respectively). The expression pattern of both proteins, however, remained unchanged, colocalizing strongly (60%-94%) at the apical membrane of hepatocytes. Conclusions. HCV receptor levels at the time of LT seem to modulate early HCV kinetics. Hepatitis C recurrence after LT was associated with increased levels of claudin-1 and occludin in the hepatocyte cell membrane, although it did not alter http://www.selleckchem.com/products/torin-1.html their localization within the tight junctions. (HEPATOLOGY 2011;.) Hepatitis C virus (HCV) is the leading cause of chronic liver disease

in many regions of the world. Chronic hepatitis C progresses to cirrhosis and endstage liver failure in a significant proportion of patients over the years and is the main indication for liver transplantation (LT) in the Western world and Japan.1 Major advances have been achieved in the last few years towards a better understanding of the HCV life cycle. The development of a retroviral pseudoparticle system (HCVpp)2 and the ability of an HCV strain (JFH-1)3 to replicate and Gamma-secretase inhibitor release infectious particles in cell culture have been very relevant to the study of HCV entry into hepatocytes. Virus entry is commonly a complex event that requires sequential interactions

between viral surface proteins and cellular factors.4-10 The exact mechanisms by which HCV reaches the cytoplasm of liver cells and initiates replication are not yet completely understood. The fact that HCV needs several receptors with different membrane distributions favors the hypothesis of a coordinated entry process, such as what occurs with other viruses (i.e., Coxackie virus B).7, 10, 11 Ploss et al.10 recently proposed that HCV may initially interact with the luminal (sinusoidal) surface of the hepatocyte by contact with scavenger receptor B1 (SR-B1) and CD81. Thereafter a virus-receptor this website complex might migrate to the biliary pole (apical membrane), where the virus-receptor complex reaches the tight junctions and uptake into the cytoplasm would occur. The recent discovery that the tight junction proteins claudin-1 and occludin are essential factors for HCV entry into cells suggests a role for these proteins in HCV cell-cell transmission, a route of spread that is still under investigation.7 Recent studies have analyzed the potential role of HCV infection in the regulation of its putative receptors, particularly those located in the tight junctions. In one study, HCV infection appeared to down-regulate claudin-1 and occludin in Huh7 cells.

Non-English

Non-English NVP-LDE225 price articles were translated by a medical specialist fluent in the respective languages. All prospective, controlled, experimental (randomized), and observational (nonrandomized) studies in which IL-2Ra induction therapy in liver transplant recipients was compared with placebo or no treatment were included. For comparison

1, we included only studies in which IL-2Ra was compared to placebo or no treatment with otherwise the same immunosuppressive treatment in both study arms. For comparison 2, we included studies with reduced and/or delayed CNI in combination with IL-2Ra; and in comparison 3, we included studies with reduced corticosteroids in combination with IL-2Ra. Other immunosuppressive medication, e.g., mycophenolate mofetil, had to be the same in both treatment arms. Studies with historical controls were also included, but we excluded studies in which both cohorts were assessed retrospectively. We also

excluded noncontrolled studies and pharmacological studies that did not provide data on clinical outcome measures because of their very short follow-up time. With regard to patient selection, we excluded trials with patients undergoing multiorgan transplantation or retransplantation. The primary outcomes analyzed were graft loss, acute rejection, steroid-resistant rejection, and death. Other outcome measures assessed were renal dysfunction selleck compound (serum creatinine and/or estimated glomerular filtration rate [eGFR]), de novo malignancy (excluding recurrence of hepatocellular

carcinoma), PTLD, infectious complications, including cytomegalovirus (CMV) infection, new onset of metabolic and cardiovascular disorders, such as hypertension, hyperlipoproteinemia, and posttransplant diabetes mellitus (PTDM), and all other adverse reactions (as a direct consequence of drug treatment). There were four reviewers (A.D.G., A.O., N.H., N.B.). The literature search strategy was designed and selleck chemical performed by three reviewers (A.D.G., A.O., N.H.). The search results were combined in an open source reference management software (JabRef v. 2.6.0). Publications were screened independently by three reviewers (A.D.G., N.H., N.B.). Disagreement and any discrepancies were resolved by discussion (A.O. with A.D.G., N.H., N.B.). Data extraction was performed by two reviewers (A.D.G., N.H.), using a standardized form. A training set was used to validate data extraction. Quality of studies was assessed independently by two reviewers (A.D.G., N.H.) without blinding to journal and authorship. The quality items assessed were blinding, randomization, allocation concealment, intention-to-treat analysis (ITT), completeness of follow-up, and the method of handling missing values. Assessment was performed according to definitions stated in the Cochrane Handbook.8 Furthermore, completeness of follow-up was defined as the number of patients that were not lost to follow-up.

, MD (Early Morning Workshops) Advisory Committees or

, MD (Early Morning Workshops) Advisory Committees or Selleck Dasatinib Review Panels: Roche/Genentech, Merck, HepC Connection,

Roche/Genentech, Merck, HepC Connection Board Membership: HepQuant LLC, PSC Partners, HepQuant LLC, PSC Partners Consulting: Roche/Genentech, BMS, Gilead, Roche/Genentech, Bristol-Myers Squibb, Abbott Grant/Research Support: Roche/Genentech, Pharmassett, Vertex, GSK, Schering-Plough, Bristol-Myers Squibb, Tibotec, GlobeImmune, Pfizer, Abbott, Conatus, Zymogenetics, PSC Partners, Roche/Genentech, Pharmassett, Vertex, GSK, Schering-Plough, Tibotec, GlobeImmune, Pfizer, Gilead, Conatus, Zymogenetics, PSC Partners, Abbott Management Position: HepQuant LLC, HepQuant LLC Patent Held/Filed: Univ of Colorado, Univ of Colorado Content of the presentation does not include discussion of off-label/investigative Doxorubicin chemical structure use of medicine(s), medical devices or procedure(s)

Fan, Jian-Gao, MD, PhD (AASLD/IASL Symposium) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Farias, Alberto Q., MD, PhD (AASLD/IASL Symposium) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Feld, Jordan J., MD (Parallel Session, SIG Program) Advisory Committees or Review Panels: Roche, Merck, Vertex, Gilead, Abbott, Tibotec, Theravance, Achillion Speaking and Teaching: Merck, Roche, Abbott Feldstein, Ariel E., MD (Early Morning Workshops, Parallel Session, SIG Program) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Feng, Sandy, MDPhD (Parallel Session) Nothing to disclose Feranchak, Andrew P., MD (Parallel Session) Nothing to disclose Ferenci, Peter, MD (Early

Morning Workshops) Advisory Committees or Review Panels: Roche, Idenix, Roche, MSD, Vertex, Salix, Madaus Rottapharm, Tibotec, B√∂hringer Ingelheim, check details Achilleon, GSK Grant/Research Support: MSD, Vertex, Madaus Rottapharm Patent Held/Filed: Madaus Rottapharm Speaking and Teaching: Roche, Gilead, Roche, Gilead, Salix Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Fernandez, Javier, MD (SIG Program) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Fitz, J. Gregory, MD (Global Forum, Plenary Session, President’s Choice) Nothing to disclose Fix, Oren K.

No DR1104-restricted T cells were detected in total CD4+ T-cell c

No DR1104-restricted T cells were detected in total CD4+ T-cell cultures (Fig. 3a).

However, tetramer-positive responses to peptide pool 2 were observed for 0.7% of the cells when the total CD4+ fraction was depleted of CD4+CD25+ T cells (Fig. 3b). This small but above-background T-cell response to peptide pool 2 was seen on analysis of two separate blood samples collected three months apart. Decoding identified FVIII2202–2221 (peptide sequence: TWSPSKARLHLQGRSNAWRP), BKM120 purchase which is adjacent to the A2201P missense substitution site, as the immunodominant DR1104-restricted T-cell epitope (Fig. 3c). The possibility of additional minor T-cell epitopes being present cannot be dismissed because of the above-background staining by tetramers loaded with FVIII2186–2205 and FVIII2194–2213. No DR0901-restricted T-cells were detected in total CD4+ or CD4+CD25+-depleted T-cell cultures (data not shown). Subject II-3, the great-uncle of IV-1 and IV-2 and great-grandfather of IV-3, has HLA alleles DRB1*0404 and DRB1*1501; Cisplatin cost despite prior FVIII infusions, he has shown no evidence of an inhibitor. A blood sample was obtained from him several months after his last FVIII exposure and TGEM was carried out as above

using his total CD4+ and CD4+CD25+-depleted T-cell fractions to screen for DR0404- and DR1501-restricted T-cell epitopes. Staining above background (0.9% tetramer-stained CD4 cells) was seen for total CD4 cells cultured with DR0404 tetramers loaded with pool 4 peptides. However, when tetramer binding was plotted versus CD25 staining the learn more tetramer-positive cells did not form a distinct cell

population, suggesting that this signal included significant non-specific binding, so we concluded that this staining did not indicate a legitimate epitope. Similar results were observed for the CD4+CD25+-depleted cultures (data not shown). No DR1501-restricted T cells were detected in total CD4+ or in CD4+CD25+-depleted T-cell cultures (data not shown). Subject III-2, the obligate carrier mother of IV-1 and IV-2, is HLA-DRB1*0101, 0901, and subject III-4, the obligate carrier mother of subject IV-3, is HLA-DRB1*1104, 1501. Blood samples from each were screened for FVIII T-cell epitopes using TGEM with pooled peptides as above. Neither total CD4+ cells or CD4+CD25+-depleted CD4+ cells from the carrier mothers showed T-cell responses to the pooled peptides restricted by their respective HLA-DR allelic proteins (data not shown). T cells from the first blood draw of haemophilic subject IV-2 that were stimulated with peptide pool 2 were next stained using DR0101 tetramers carrying FVIII2194–2213 and then were single-cell sorted into 96-well plates as described above. Cells in 21 wells expanded sufficiently to be tested for tetramer binding, and 20/21 wells contained expanded T cells that were 99–100% tetramer-positive (data not shown). Six of these clones were cryo-preserved.

Excess serum or hepatic iron

Excess serum or hepatic iron Metformin order is a relatively frequent finding in HCV-infected patients, and has been associated with poor response to treatment, greater disease severity, and an increased risk of hepatocellular carcinoma.31, 34-38 Despite the presence of chronic inflammation, hepcidin levels in HCV patients are relatively reduced, thus preventing the appropriate regulation of iron absorption and release, leading to systemic

and hepatic iron excess.39, 40 In vitro studies have suggested that iron may enhance HCV replication,41, 42 although this has recently been challenged.43 Moreover, several reports have suggested an improved disease course and augmented treatment response following iron reduction therapy.31,

32 Weekly PEG-IFN-α administration, with hepcidin induction and the subsequent iron redistribution, may be of similar benefit to HCV patients. Indeed, reduced hepatic iron and an amelioration of hepcidin suppression have been reported following successful HCV eradication.44-46 Novel data from this study extends these clinical observations. Conversely, chronic hepcidin induction may contribute to the anemia associated with PEG-IFN-α therapy, through the development of iron-restricted erythropoiesis.47 IFN-α treatment exerts its antiviral effect through the induction of interferon-stimulated genes (ISGs) by way of activation of the Jak/STAT pathway.4, 5 Although ISG induction is predominantly by buy CH5424802 way of the STAT1 and STAT2 transcription factors, STAT3 activation, which mediates the inflammatory induction of hepcidin, is also critical to the antiviral effect

of IFN-α.48, 49 The significant correlation seen between serum hepcidin and CRP levels in HCV patients likely reflects STAT3 activation following PEG-IFN-α initiation.28, 50 Interestingly, disruption of STAT signaling by way of the suppressor of cytokine signaling-3 (SOCS3) has been reported in nonresponders to treatment in HCV, whereas this molecule also inhibits the induction of hepcidin by inflammation, and potentially its downstream effects on iron regulation.23, 51 This interference may be reflected in the differences in the check details ability of hepcidin to regulate iron levels between treatment responders and nonresponders seen here (Fig. 3D,E). In summary, hepcidin, the master regulator of iron homeostasis, is identified here as an IFN-α-responsive gene. IFN-α induces hepcidin production by way of the Jak/STAT3 signaling pathway, with increased serum hepcidin seen in HCV patients following a single PEG-IFN-α dose. The consequent systemic iron withdrawal was greatest in those with the most marked viral response to PEG-IFN-α, implicating hypoferremia as a surrogate marker of immediate PEG-IFN-α efficacy. The authors thank Dr. Jennifer Russell, Dr. Flavia D’Alessio, and Dr. Katarzyna Mleczko-Sanecka for excellent technical assistance and advice, and Dr.

It is estimated that 1 million patients in the United States suff

It is estimated that 1 million patients in the United States suffer from cirrhosis, and > 10% suffer from chronic encephalopathy. Early results indicate safety and tolerability of GPB in patients with cirrhosis.9 Moreover, GPB contains no sodium, compared to almost 2.4 g of sodium in a standard adult dose of NaPBA. Thus, this remarkable clinical trial in ultraorphan UCDs may eventually expand treatment options for more frequently encountered patients with cirrhosis suffering

from chronic encephalopathy. “
“Background and Aim:  This study aimed to determine the clinical characteristics of immunoglobulin G4 (IgG4)-associated sclerosing cholangitis (ISC) and provide clinical clues differentiating ISC from primary RG-7388 sclerosing cholangitis (PSC) or hilar cholangiocarcinoma (CCC). Methods: 

Sixteen patients with ISC manifesting as hilar/intrahepatic strictures were analyzed for clinical characteristics and compared with patients with PSC and hilar CCC as disease controls for histology and serum IgG4 levels. Results:  Distinguished biliary imaging findings of ISC included multifocal biliary tree involvement (n = 14), concentric bile duct thickening with preserved luminal patency (n = 13), and relatively mild proximal dilatation, despite prominent bile duct thickening VX-770 nmr (n = 11). Serum IgG4 levels were elevated in 12 patients (75%), but not in any of the 25 patients with hilar CCC. Ten patients (63%) had a past or concurrent history of autoimmune pancreatitis (AIP). The significant infiltration of IgG4-positive cells was observed with endobiliary or liver biopsy in 11 of 16 patients (69%) with ISC, but not in any patients with PSC or hilar CCC. Extrabiliary organ involvement, including sialadenitis, inflammatory pseudotumor of the liver and kidney, and retroperitoneal fibrosis, was present in seven patients. Marked improvement of biliary strictures and/or extrabiliary involvement was

observed in all ISC patients after steroid therapy. Conclusions:  ISC should be considered in the differential diagnosis of hilar/intrahepatic biliary strictures. Past or concurrent AIP or extrabiliary organ involvement strongly check details suggests the possibility of ISC. Significant infiltration of IgG4-positive cells on endobiliary or liver biopsy specimens, and/or elevated serum IgG4 levels, highly support the diagnosis of ISC and provide the rationale for steroid therapy. Hilar or intrahepatic biliary strictures are caused by diverse etiologies from benign to malignant, including iatrogenic bile duct injury, primary sclerosing cholangitis (PSC), bile duct stone, other fibroinflammatory cholangitis, and malignancy. The most important issue is how to differentiate benign from malignant strictures.

Another study conducted by Wang et al combined sorafenib with in

Another study conducted by Wang et al. combined sorafenib with interferon (IFN)-α, a type I interferon cytokine that activates the JAK-STAT pathway.[38] IFN-α has been commonly used in renal cell carcinoma, melanoma and chronic myelogenous leukemia because it inhibits angiogenesis and tumor cell proliferation. The combination produced a synergistic effect: it decreased HCC cell viability, blocked the progression Venetoclax of the cell cycle, and promoted apoptosis in vitro. In vivo, the combination also inhibited tumor growth and induced apoptosis. The combination of sorafenib and panobinostat is another promising treatment

for HCC. Panobinostat is a drug that inhibits histone deacetylases, which are frequently dysregulated in cancer. When combined with sorafenib, panobinostat decreased cell viability and proliferation, and increased apoptosis and autophagy in vitro.[39] HCC xenografts also had decreased tumor volumes and lived longer when treated with the combination. In a phase II clinical trial, sorafenib was combined with 5-fluorouracil (5-FU) in patients with advanced HCC (www.clinicaltrials.gov, NCT00619541).[40] 5-FU has cytotoxic effects in HCC cells and xenograft models, and it is commonly used to treat gastrointestinal cancers. Thirty-nine patients were given sorafenib at 400 mg b.i.d. and an infusion of 5-FU at 200 mg/sqm/daily from days 1–14 every 3 weeks. The median time

to progression was 8 months, and the median survival U0126 purchase time was 13.7 months. The combination was deemed safe, with promising efficacy. Transarterial chemoembolization (TACE) is a common treatment for moderate HCC, and clinical trials aimed to discover if it could be safely combined with sorafenib to produce better outcomes.

TACE can sometimes upregulate VEGF, which can increase HCC growth, invasion and metastasis.[41] In a phase II trial, 50 patients with Barcelona Clinic Liver Cancer stage B or C were treated with sorafenib (median dose, 68.7% of 800 mg daily) 3 days after TACE treatment (www.clinicaltrials.gov, NCT00919009).[41] The overall median time to progression was 7.1 months, and 52% of patients survived at least 6 months. The concurrent treatment 上海皓元医药股份有限公司 was deemed safe, and the trial promised efficacy. A phase III study analyzed the efficacy of sorafenib when given to Japanese and Korean patients who had already positively responded to TACE treatment.[42] Patients were given either 400 mg of sorafenib b.i.d. or a placebo, and most of the patients began the treatment more than 9 months after TACE. Patients taking sorafenib had a median time to progression of 5.4 months, while those taking the placebo progressed in 3.7 months. The study concluded that sorafenib did not significantly increase the time to progression for patients who had already reaped benefits from TACE. However, low doses of sorafenib and the extended time between sorafenib and TACE treatment may have contributed to this result.

8, 9 Studies in viral and bacterial infections, tumor rejection a

8, 9 Studies in viral and bacterial infections, tumor rejection and autoimmunity demonstrated that Tregs suppress proliferation, cytokine production and cytotoxic activity of naïve and antigen-specific CD4+ and CD8+ effector T cells and are able to interfere with the activity of antigen-presenting cells as well as B cells.3

Studies addressing the role of Tregs in HBV infection mostly rely on correlation of Treg frequencies in peripheral blood of patients with different disease stages and have been somewhat contradictory.10-12 Therefore, we aimed at defining the overall effect that Tregs impose on the adaptive and innate immune response against HBV and at determining how they selleckchem may influence the outcome of infection. For our study, we used DEREG mice. DEREG mice are transgenic C57BL/6 mice that express an enhanced green

fluorescent protein-human diphtheria toxin receptor fusion protein under control of the foxp3-promotor.13 Foxp3+ Tregs can be depleted in DEREG Z VAD FMK mice by injecting diphtheria toxin (DTX) systemically and specifically, albeit only transiently.13 Because HBV cannot infect murine hepatocytes, we used an adenoviral vector transferring a 1.3-fold overlength HBV-genome (AdHBV) across the species barrier.14 Following Ad-HBV infection, HBV replicates in hepatocytes and infectious HBV virions are secreted into the bloodstream. Depending on the dose of the inoculum, induction of T cell responses leads to an acute, self-limiting or a persistent HBV infection.14, 15 This study investigates the regulatory effects of Tregs on the intrahepatic HBV-specific T cell and innate immune response, and on the B cell response in the early phase of HBV infection. ALT, alanine aminotransferase; BFA, brefeldin 上海皓元医药股份有限公司 A; DC, dendritic cell; DTX, diphtheria toxin; HBc, HBV core protein; HBeAg, hepatitis B e antigen; HBs, HBV small

surface protein; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; IFNγ, interferon-γ; i.u., infectious units; k/o, knockout; LAL, liver-associated lymphocyte; MHC, major histocompatibility complex; NK, natural killer; PCR, polymerase chain reaction; RPMI 1640, Roswell Park Memorial Institute 1640; TNF, tumor necrosis factor; Tregs, regulatory T cells. AdHBV and AdHBV knockout (k/o) were constructed, produced, purified, and titrated as described.14, 15 All animal experiments were approved by the local authorities and animals received human care in accordance to the National Institutes of Health guidelines. Eight-week-old female DEREG mice received a single injection of 109 i.u. AdHBV intravenously. For depletion of Tregs, 1 μg diphtheria toxin (Merck, Darmstadt, Germany) was injected intraperitoneally on 3 consecutive days. Mice were sacrificed at indicated time points.

aeruginosa FACHB 469, and the green microalga Chlamydomonas micro

aeruginosa FACHB 469, and the green microalga Chlamydomonas microsphaera FACHB 52. In monocultures, the growth of all three strains was inhibited by UVB. In mixed cultures, enhanced UVB radiation resulted in decreased percentages of the two M. aeruginosa strains (19%–22% decrease on d 12 of the competition experiment). UVB radiation resulted in increased contents of chlorophyll a, b, and carotenoids (CAR) in C. microsphaera, and decreased contents of allophycocyanin (APC) or phycocyanin in the two Microcystis strains. All Wnt inhibitor three strains showed increased levels of UVabsorbing compounds and intracellular reactive oxygen species

under 0.372 W · m−2 UVB radiation, and decreased light compensation points, dark respiratory rates, and maximal quantum efficiency of PSII. After a 20 h recovery, the photosynthetic oxygen evolution of C. microsphaera was restored to its maximum value, but that of Microcystis strains continued to decrease. Nonphotochemical quenching was increased by UVB radiation in C. microsphaera, but was unaffected in the two M. aeruginosa strains. Our results indicated that C. microsphaera has a competitive advantage relative to Microcystis during exposure to UVB irradiation. “
“The mechanisms of microalgal senescence may play an important role in nutrient recycling and enhanced survival. However, the aging physiology of microalgae is an understudied phenomenon. To investigate

the patterns of conditional senescence in Chlamydomonas reinhardtii P. A. Dangeard, we used MCE a cell wall-less strain, transformed PXD101 with a reporter gene to infer changes in photosynthetic gene expression. We examined plastid ultrastructure, photosynthetic function, and photoprotective mechanisms during aging in batch cultures. LHCII transcription levels decreased before the population entered stationary phase, and the characteristic transcriptional light-shift response was lost. A decline in

photosynthetic proteins with a concomitant increase in the photoprotective protein, LHCSR, was observed over time. However, nonphotochemical quenching remained stable during growth and stationary phase, and then declined as alternative quenching mechanisms were up-regulated. Photosynthetic efficiency declined, while Fv/Fm remained stable until the death phases. As the culture progressed through stationary phase, disorganization of the chloroplast was observed along with an increase in cytoplasmic oil bodies. We also observed a partial recovery of function and proteins during the final death phase, and attribute this to the release of nutrients into the medium from cell lysis and/or active secretion while cells were senescing. Allowing open gas exchange resulted in high levels of sustained starch production and maintained maximum cell density, prolonging the stationary phase. “
“Dimethyl sulfide (DMS) and dimethylsulfoniopropionate (DMSP) are sulfur compounds that may function as antioxidants in algae.