4) and confirmed the dose-dependency of HCV RNA reduction. The analysis suggests a plateau in the response to filibuvir and that increasing the filibuvir

dose beyond 700 mg BID is unlikely to produce greater HCV RNA reductions. The log of baseline plasma HCV RNA concentration (normalized to 6) was identified as an influential covariate describing the Emax. There appeared to be no effect of genotype (1a versus 1b) on the Emax, E0, or AUC24,50 parameters (95% CI included null value). However, given that these studies were not powered to detect such differences, further exploration of the covariate–parameter AZD6738 molecular weight relationships will be performed when new data emerge. The parameter estimates, their relative Palbociclib ic50 standard errors, and the associated 95% CIs are presented in Table 4. Filibuvir was well tolerated at all doses evaluated in these two studies. The most frequently reported AEs were headache, flatulence, and fatigue in study 1 (Table 5); headache and dyspepsia (four patients each) were reported in study 2, cohort A, and headache (three) and dry mouth (two) were reported in study 2, cohort B. There were no trends toward increasing frequency or

severity of AEs with increasing doses of filibuvir. All AEs were mild or moderate in severity (one moderate AE in the 450 mg BID group in both studies). No temporary discontinuations or withdrawals due to AEs were required, and no serious AEs or deaths were reported. No clinically significant changes in vital signs, electrocardiogram parameters, or laboratory values were reported during treatment. Mutations in NS5B at position Met423 were the preferred resistance pathway selected following filibuvir therapy. Before treatment, all patients were infected with virus encoding wild-type methionine

at position 423 in NS5B. After treatment, virus from 29 of the 38 patients who received filibuvir >100 mg BID encoded amino medchemexpress acid variants at NS5B residue Met423. There was no significant difference in the frequency of appearance of position 423 mutations between subtype 1a (19 of 25; 76%) and subtype 1b (10 of 13; 77%) viruses (Fisher’s exact test; P = 1.00). Mutations at residue 423 were consistently associated with virologic breakthrough (>0.5 log increase in HCV RNA from nadir) in patients receiving >100 mg BID. Sequence analysis of the day 28 follow-up samples indicated that reversion toward baseline methionine at position 423 was common (24 of 29 patients, 83%). One patient who received filibuvir 450 mg BID, who did not respond to treatment at all time points, was infected with a virus encoding an Arg422Lys variant. This is the first report of the antiviral activity and safety of filibuvir in HCV-infected patients. Data from these two phase 1b studies showed that filibuvir potently inhibited viral replication in a dose-dependent manner in patients infected with HCV genotype 1.

This stood in contrast to results obtained when an AAV vector expressing canine factor X under the control of the ubiquitously expressing CMV promoter was injected into skeletal muscle in the same dog model; these animals invariably developed inhibitors unless

immunosuppression (IS) was administered concomitantly [32], suggesting that the target organ, and perhaps the tissue-specificity of the promoter (here ref#7), influenced inhibitor formation in the gene transfer setting. Recent work from Brown et al. shows that lentivirus-driven transgene expression in cells of the haematopoietic lineage (dendritic cells, DC) plays an important role in transgene immunogenicity [33] and detargeting Selleck STI571 of expression from DCs results in tolerance to the FIX transgene in haemophilia B mice [34,35]. Similarly, the use of self-complementary AAV expression cassettes may increase the overall vector immunogenicity by increasing the efficiency of DC transduction [36]. Mingozzi et al. sought to explore the mechanism for the absence of inhibitor formation following AAV-mediated gene transfer to liver, and showed in mice that induction of immune tolerance to the secreted transgene product human

FIX was favoured by higher levels of transgene expression as determined by promoter Pembrolizumab research buy strength, vector dose and mouse strain. Moreover, they showed that hepatocyte-derived expression of human FIX induced regulatory CD4+ T cells that could suppress anti-human FIX formation after adoptive transfer [37]. Subsequent studies have further delineated the role of regulatory T MCE cells (Tregs) in induction of tolerance to the transgene product following AAV-mediated gene

transfer. A number of different T cell subsets with suppressor activity have been described; perhaps the most well-characterized are CD4+CD25+FoxP3+ Treg, which originate during thymic development (natural Treg) and constitutively express CD25 (the α chain of the IL-2 receptor), CTLA-4, and FoxP3, a transcription factor critical to the development and function of regulatory T cells. Cao et al. showed in a mouse model that hepatic AAV-mediated gene transfer induces transgene product-specific CD4+CD25+Tregs, which are similar to natural Tregs in terms of expression of FoxP3, GITR and CTLA-4 [38]. Matsui et al. also described the expansion of a population of CD4+CD25+FoxP3+Treg after lentiviral gene transfer for FVIII in neonatal haemophilia A mice [39]. An interesting aspect of this work is that basal levels, undetectable in plasma, of transgene product expression in a developing immune system are sufficient to induce long-term tolerance to FVIII. The likely clinical relevance of the Treg subset was shown by Mingozzi et al. in a series of experiments in which AAV-human FIX was administered to liver in non-human primates.

The stent delivery system passed

all cardias, and the stent placement was successful in all of patients under the guidance of fluoroscopy. The stent was retained approximately 3–7 days after insertion. All stents, including the two stents that migrated into stomach, were successfully removed via endoscopy. After the stent removal, all of the patients were able to ingest semisolid Venetoclax supplier or solid foods. Stent insertion or removal procedure-related complications included pain, reflux, bleeding, stent migration, or esophageal perforation. In this group, pain occurred in 27 patients (42.9%), reflux in eight (12.7%), bleeding in 10 (15.9%), and stent migration in two (3%), and there was no statistical difference (P = 0.057, P = 0.276, P = 0.361, respectively) compared to that in Group A. However, total adverse events occurred in 17 patients (44.7%) in Group A and in 35 patients (55.6%) in Group B, which presented a statistical difference (P = 0.0305). No esophageal perforation occurred. TSS and esophageal manometry improved from 6.22 ± 2.26–0.89.74 ± 0.88 and 58.92 ± 8.47 mmHg to 9.03 ± 4.45 mmHg, respectively, which was a significant statistical difference (P < 0.0001) (Figs 2,3). The barium column height and width improved from 12.82 ± 2.51 and 6.10 ± 1.68 cm to 1.15 ± 1.41 and 0.93 ± 1.01 cm, respectively, which also indicated a significant improvement (P < 0.0001)

(Fig. 4). The improvement of TSS, LES pressure, and barium column height or width post-treatment was more conspicuous in Group B than in Group A and were statistically 上海皓元医药股份有限公司 significant (P < 0.0001). The mean follow-up period was 71.26 ± 40.9 months (range: 15–137 months) in Group A Ku-0059436 cell line and 53.92 ± 36.22 months (range: 13–133 months) in Group B. During the regularly-scheduled interval follow up, TSS and LES pressure in both groups presented gradual aggravation compared to those measurements post-treatment. At the end of follow up, TSS and LES pressure in Group B were 4.00 ± 1.00 and 43.67 ± 12.66 mmHg, respectively, compared to the post-procedure values of 0.89.74 ± 0.88 (P < 0.0001) and 9.03 ± 4.45 mmHg (P = 0.042), respectively. In Group A, TSS and LES pressure at the end of follow up were 10.20 ± 0.45

and 58.60 ± 8.65 mmHg, respectively, compared with the post-procedure values of 1.74 ± 1.06 (P < 0.0001) and 15.63 ±  6.88 mmHg (P = 0.0004), respectively (Figs 2,3). TSS in Group A at the end of follow up had a significant statistical difference to those in Group B (P = 0.0096), while LES pressure in Group A was not significantly different (P = 0.1687) compared with Group B. However, at the 8–10-year follow up, the statistical difference was apparent in the TSS and LES pressure difference between the two groups (P < 0.0001) (Figs 2,3). The recurrence rate in Group A was 50% (19 out of 38) at the 8–10-year follow up and at 57.9% (22 out of 38) at the > 10 year follow up, but the corresponding recurrence rates in Group B were 9.5% (6 out of 63) (P < 0.0001) and 11.

The real novelty and probably the most important finding of this study is the association between serum vitamin A deficiency and the condition of nonresponse to antiviral therapy, suggesting that vitamin A could be an important buy RO4929097 and modifiable factor interfering with IFN sensitivity in patients with chronic hepatitis C. This finding, together with the data suggesting an antiviral activity against HCV of ATRA, suggests that vitamin A supplementation and normalization of its serum levels, before antiviral treatment, could enhance

the responsiveness to INF-based antiviral therapy. These considerations seem to confirm those derived from in vitro experiments that provided evidence of a pivotal role of retinol in enhancing the expression of IFN receptor and IFN signaling, linking vitamin A deficiency Nutlin3 to IFN unresponsiveness. The fact that vitamin A and vitamin D serum levels are not reciprocally influenced suggests that they can exert an additive and probably synergistic effect on viral response. Indeed, the analysis showed that a concomitant vitamin A and D deficiency strongly impairs the responsiveness to antiviral therapy and that its impact is not so far from that exerted by IL-28B polymorphisms. The major and obvious

difference is that, instead of IL-28B polymorphisms, vitamins serum levels might be modified. Moreover, it is important to note that a strong additive effect in determining nonresponse was observed in patients with concomitant carriage of the IL-28B T/* genotype and vitamin A serum levels ≤100 ng/mL. A possible

concern in terms of the use of vitamin A supplementation in clinical practice is represented by its possible hepatotoxicity.22 However, the experiences concerning the use of polyprenoic acid, a synthetic vitamin MCE公司 A derivate, in the prophylaxis of HCC in patients with chronic viral hepatitis23 and the study by Bocher et al.9 did not support this assumption. The main limitations of the present study lie in its retrospective design and in the lack of data concerning the dietary intake of both vitamin A and D. It is conceivable that vitamin D serum levels could be greatly influenced by the season, since sunlight exposure is recognized as a key factor in determining vitamin D synthesis. Nevertheless, it cannot be excluded that season-related dietary variations could influence vitamin A intake and serum levels. Nevertheless, the multicenter design of the study supported the external validation of data that have been confirmed in each center. In conclusion, a high percentage of patients with chronic HCV infection presented serum vitamin A deficiency. This condition is strongly associated with nonresponse to antiviral therapy, suggesting that vitamin A serum levels could modulate the responsiveness to IFN-based antiviral therapy.

The real novelty and probably the most important finding of this study is the association between serum vitamin A deficiency and the condition of nonresponse to antiviral therapy, suggesting that vitamin A could be an important Palbociclib concentration and modifiable factor interfering with IFN sensitivity in patients with chronic hepatitis C. This finding, together with the data suggesting an antiviral activity against HCV of ATRA, suggests that vitamin A supplementation and normalization of its serum levels, before antiviral treatment, could enhance

the responsiveness to INF-based antiviral therapy. These considerations seem to confirm those derived from in vitro experiments that provided evidence of a pivotal role of retinol in enhancing the expression of IFN receptor and IFN signaling, linking vitamin A deficiency Selleck Decitabine to IFN unresponsiveness. The fact that vitamin A and vitamin D serum levels are not reciprocally influenced suggests that they can exert an additive and probably synergistic effect on viral response. Indeed, the analysis showed that a concomitant vitamin A and D deficiency strongly impairs the responsiveness to antiviral therapy and that its impact is not so far from that exerted by IL-28B polymorphisms. The major and obvious

difference is that, instead of IL-28B polymorphisms, vitamins serum levels might be modified. Moreover, it is important to note that a strong additive effect in determining nonresponse was observed in patients with concomitant carriage of the IL-28B T/* genotype and vitamin A serum levels ≤100 ng/mL. A possible

concern in terms of the use of vitamin A supplementation in clinical practice is represented by its possible hepatotoxicity.22 However, the experiences concerning the use of polyprenoic acid, a synthetic vitamin 上海皓元医药股份有限公司 A derivate, in the prophylaxis of HCC in patients with chronic viral hepatitis23 and the study by Bocher et al.9 did not support this assumption. The main limitations of the present study lie in its retrospective design and in the lack of data concerning the dietary intake of both vitamin A and D. It is conceivable that vitamin D serum levels could be greatly influenced by the season, since sunlight exposure is recognized as a key factor in determining vitamin D synthesis. Nevertheless, it cannot be excluded that season-related dietary variations could influence vitamin A intake and serum levels. Nevertheless, the multicenter design of the study supported the external validation of data that have been confirmed in each center. In conclusion, a high percentage of patients with chronic HCV infection presented serum vitamin A deficiency. This condition is strongly associated with nonresponse to antiviral therapy, suggesting that vitamin A serum levels could modulate the responsiveness to IFN-based antiviral therapy.

Combining all animals in each group, LC/MS/MS analysis of carbonylated proteins using streptavidin purified biotin hydrazide treated mitochondrial fractions identified 156/148 SV PF/EtOH, and 212/215 GSTA4−/− PF/EtOH proteins respectively. Using bioinformatics, 2.1-fold (PF) and 1.75-fold (EtOH-fed) more carbonylated proteins were identified in 5/5 GSTA4−/− PF-EtOH animals

when compared to their respective SV controls. Using pathway analysis, chronic Etoh consumption significantly increased carbonylation of proteins involved in glutathione homeostasis, fatty acid metabolism and in glucose metabolism. Using immunoprecipitation analysis and Western blotting, carbonylation of ACSL1, ALDH2 and ACADL was verified. Conclusions: Stem Cell Compound Library These data suggest that increased mitochondrial carbonylation of key proteins involved AUY-922 clinical trial in fatty acid/glutathione homeostasis in PF/EtOH fed contributes to increases in hepatocellular damage and steatosis. This work was funded by NIH 5R37 AA009300-18

(D.R.P.). Disclosures: The following people have nothing to disclose: Colin T. Shearn, Kelly E. Mercer, Kristofer S. Fritz, James J. Galligan, Bridgette Engi, David J. Orlicky, Piotr Zim-niak, Martin J. Ronis, Dennis R. Petersen BACKGROUND & AIMS: Neutrophil infiltration is a hallmark of alcoholic steatohepatitis (ASH) and has been shown to correlate with the severity of alcoholic liver disease (ALD) in humans. Toll-like receptor (TLR) signaling regulates synthesis of neutrophil-attracting chemokines through the adaptor molecule MyD88. However, in vivo role of the TLR2 and TLR9-depen-dent neutrophil infiltration and liver injury in ALD has not been elucidated. METHODS: ALD was induced by feeding of Lieb-er-DeCarli diet (Bio-Serv) containing 6.6 % (vol/vol) ethanol plus binge drink (5g/kg BW) in wild-type (WT), TLR2-deficient, TLR9-deficient mice, Kupffer cell (KC)-depleted mice, and mice treated with a CXCR2 antagonist (SB225002) and a MyD88 上海皓元 inhibitor. RESULTS: Upon alcohol treatment, TLR2 and TLR9-deficient mice showed less liver injury than WT mice

as demonstrated by a decrease in serum ALT levels and TUNEL-positive cells. Notably, induction of neutrophil-attracting chemokines including CXCL1, CXCL2 and CXCL5 was significantly suppressed in TLR2 and TLR9-deficient mice compared with WT mice. Consistently, neutrophil infiltration was suppressed in both deficient mice as demonstrated by quantification of Ly-6G-positive cells in the liver. Interestingly, similar production of proinflammatory cytokines (IL-6, TNF-a) was seen in WT and both deficient mice. In vivo KC depletion with treatment with clodronate liposome reduced the levels of ALT and proinflam-matory cytokines, but did not affect the expression of neutro-phil-attracting chemokines, suggesting that KCs are not major source of neutrophil-attracting chemokines in ALD.

Combining all animals in each group, LC/MS/MS analysis of carbonylated proteins using streptavidin purified biotin hydrazide treated mitochondrial fractions identified 156/148 SV PF/EtOH, and 212/215 GSTA4−/− PF/EtOH proteins respectively. Using bioinformatics, 2.1-fold (PF) and 1.75-fold (EtOH-fed) more carbonylated proteins were identified in 5/5 GSTA4−/− PF-EtOH animals

when compared to their respective SV controls. Using pathway analysis, chronic Etoh consumption significantly increased carbonylation of proteins involved in glutathione homeostasis, fatty acid metabolism and in glucose metabolism. Using immunoprecipitation analysis and Western blotting, carbonylation of ACSL1, ALDH2 and ACADL was verified. Conclusions: Palbociclib cell line These data suggest that increased mitochondrial carbonylation of key proteins involved click here in fatty acid/glutathione homeostasis in PF/EtOH fed contributes to increases in hepatocellular damage and steatosis. This work was funded by NIH 5R37 AA009300-18

(D.R.P.). Disclosures: The following people have nothing to disclose: Colin T. Shearn, Kelly E. Mercer, Kristofer S. Fritz, James J. Galligan, Bridgette Engi, David J. Orlicky, Piotr Zim-niak, Martin J. Ronis, Dennis R. Petersen BACKGROUND & AIMS: Neutrophil infiltration is a hallmark of alcoholic steatohepatitis (ASH) and has been shown to correlate with the severity of alcoholic liver disease (ALD) in humans. Toll-like receptor (TLR) signaling regulates synthesis of neutrophil-attracting chemokines through the adaptor molecule MyD88. However, in vivo role of the TLR2 and TLR9-depen-dent neutrophil infiltration and liver injury in ALD has not been elucidated. METHODS: ALD was induced by feeding of Lieb-er-DeCarli diet (Bio-Serv) containing 6.6 % (vol/vol) ethanol plus binge drink (5g/kg BW) in wild-type (WT), TLR2-deficient, TLR9-deficient mice, Kupffer cell (KC)-depleted mice, and mice treated with a CXCR2 antagonist (SB225002) and a MyD88 MCE公司 inhibitor. RESULTS: Upon alcohol treatment, TLR2 and TLR9-deficient mice showed less liver injury than WT mice

as demonstrated by a decrease in serum ALT levels and TUNEL-positive cells. Notably, induction of neutrophil-attracting chemokines including CXCL1, CXCL2 and CXCL5 was significantly suppressed in TLR2 and TLR9-deficient mice compared with WT mice. Consistently, neutrophil infiltration was suppressed in both deficient mice as demonstrated by quantification of Ly-6G-positive cells in the liver. Interestingly, similar production of proinflammatory cytokines (IL-6, TNF-a) was seen in WT and both deficient mice. In vivo KC depletion with treatment with clodronate liposome reduced the levels of ALT and proinflam-matory cytokines, but did not affect the expression of neutro-phil-attracting chemokines, suggesting that KCs are not major source of neutrophil-attracting chemokines in ALD.

The second explanation is the way patients were classified (definitive NASH versus non selleck chemical NASH) for survival comparison. As discussed by the authors, the NASH-CRN scoring system takes into account only the presence and severity of steatosis, hepatocyte ballooning, and lobular inflammation to differentiate between patients with and without definitive NASH.11 The reported inter-rater agreement on lobular inflammation and hepatocyte ballooning was as low as 0.1 and 0.14 (poor to fair) respectively in one series,12 and increased to only 0.45 and 0.56 (moderate to good) respectively in another series.11 Similarly, the intra-rater agreement on lobular inflammation and hepatocyte ballooning was 0.37

and 0.62 (moderate to good) respectively in one series13 and 0.60 and 0.66 (good), respectively, in another series.11 These levels of agreement indicate that mandating lobular inflammation and hepatocyte ballooning for the diagnosis of NASH would make the diagnosis often difficult, if not impossible to reproduce from one pathologist to the next, or from one reading to another reading of the same slides even if the reading is done by the same pathologist. In addition, a

series of individuals who had undergone paired liver biopsy with two samples of liver tissue taken simultaneously reported an inter-biopsy agreement on lobular inflammation selleck inhibitor and hepatocyte ballooning as low as 0.13 and 0.45, respectively.13 Thus, the diagnosis of NASH may or may not be established in subjects with NAFLD depending on where in the liver parenchyma the biopsy needle is inserted. Furthermore, there are no data from long-term follow-up studies on whether lobular inflammation or hepatocyte ballooning would indicate a greater likelihood of disease progression, and there are no compelling data that lobular inflammation or hepatocyte ballooning per se are of any prognostic significance. MCE公司 As discussed by Soderberg et al.,4

the NASH-CRN scoring system also does not take into account the presence and severity of fibrosis for NASH classification; so not surprisingly, a good proportion of individuals classified as non NASH would be expected to have increased fibrosis. In fact, 45 of 67 (67.2%) patients classified as non NASH in the study by Soderberg et al.4 had increased liver fibrosis, with 8 of them having septal fibrosis or even well established cirrhosis. If all these patients with increased liver fibrosis would have been labeled definitive NASH, the mortality most definitively would have been significantly higher in the NASH group. Indeed, if we extend the analysis of the data to consider the presence and severity of fibrosis on long-term mortality regardless of other histological features, the study would provide additional and more clinically relevant conclusions. For instance, 40 of 47 (89.

The second explanation is the way patients were classified (definitive NASH versus non JQ1 manufacturer NASH) for survival comparison. As discussed by the authors, the NASH-CRN scoring system takes into account only the presence and severity of steatosis, hepatocyte ballooning, and lobular inflammation to differentiate between patients with and without definitive NASH.11 The reported inter-rater agreement on lobular inflammation and hepatocyte ballooning was as low as 0.1 and 0.14 (poor to fair) respectively in one series,12 and increased to only 0.45 and 0.56 (moderate to good) respectively in another series.11 Similarly, the intra-rater agreement on lobular inflammation and hepatocyte ballooning was 0.37

and 0.62 (moderate to good) respectively in one series13 and 0.60 and 0.66 (good), respectively, in another series.11 These levels of agreement indicate that mandating lobular inflammation and hepatocyte ballooning for the diagnosis of NASH would make the diagnosis often difficult, if not impossible to reproduce from one pathologist to the next, or from one reading to another reading of the same slides even if the reading is done by the same pathologist. In addition, a

series of individuals who had undergone paired liver biopsy with two samples of liver tissue taken simultaneously reported an inter-biopsy agreement on lobular inflammation selleck compound and hepatocyte ballooning as low as 0.13 and 0.45, respectively.13 Thus, the diagnosis of NASH may or may not be established in subjects with NAFLD depending on where in the liver parenchyma the biopsy needle is inserted. Furthermore, there are no data from long-term follow-up studies on whether lobular inflammation or hepatocyte ballooning would indicate a greater likelihood of disease progression, and there are no compelling data that lobular inflammation or hepatocyte ballooning per se are of any prognostic significance. MCE As discussed by Soderberg et al.,4

the NASH-CRN scoring system also does not take into account the presence and severity of fibrosis for NASH classification; so not surprisingly, a good proportion of individuals classified as non NASH would be expected to have increased fibrosis. In fact, 45 of 67 (67.2%) patients classified as non NASH in the study by Soderberg et al.4 had increased liver fibrosis, with 8 of them having septal fibrosis or even well established cirrhosis. If all these patients with increased liver fibrosis would have been labeled definitive NASH, the mortality most definitively would have been significantly higher in the NASH group. Indeed, if we extend the analysis of the data to consider the presence and severity of fibrosis on long-term mortality regardless of other histological features, the study would provide additional and more clinically relevant conclusions. For instance, 40 of 47 (89.

Our current evidence suggests www.selleckchem.com/products/CAL-101.html that the source of this Ca2+ is intracellular. “
“The processes that produce and maintain genetic structure in organisms operate at different timescales and on different life-history stages. In marine macroalgae, gene flow occurs through gamete/zygote dispersal and rafting by adult thalli. Population

genetic patterns arise from this contemporary gene flow interacting with historical processes. We analyzed spatial patterns of mitochondrial DNA variation to investigate contemporary and historical dispersal patterns in the New Zealand endemic fucalean brown alga Carpophyllum maschalocarpum (Turner) Grev. Populations bounded by habitat discontinuities were often strongly differentiated from adjoining populations over scales of tens of kilometers and intrapopulation diversity was generally low, except for one region of northeast New Zealand (the Bay of Plenty). There was evidence of strong connectivity between the northern and eastern regions of New Zealand’s North Island and between the North and South Islands of New Zealand and the Chatham Islands (separated by 650 km of open PLX-4720 solubility dmso ocean). Moderate haplotypic diversity was found in Chatham Islands populations, while other southern populations showed low diversity consistent with Last Glacial Maximum (LGM) retreat and subsequent recolonization. We suggest that ocean current patterns and prevailing westerly winds facilitate long-distance

dispersal by floating adult thalli, decoupling genetic differentiation of Chatham Island populations from dispersal potential at the gamete/zygote stage. This study highlights the importance of encompassing the entire range of a species when inferring dispersal patterns from genetic differentiation, as realized dispersal distances can be contingent on local or regional oceanographic and historical processes. “
“Kuwait Institute for Scientific Research (KISR), Salmiya, Kuwait A new photosynthetic, sand-dwelling marine dinoflagellate, Ailadinium reticulatum gen. et sp. nov., is described from the Jordanian coast in the Gulf of Aqaba,

northern Red Sea, based on detailed morphological and molecular data. A. reticulatum is a large (53–61 μm long and 38–48 μm wide), dorsoventrally compressed species, with the epitheca smaller than the hypotheca. 上海皓元 The theca of this new species is thick and peculiarly ornamented with round to polygonal depressions forming a foveate-reticulate thecal surface structure. The Kofoidian thecal tabulation is APC (Po, cp), 4′, 2a, 6′′, 6c, 4s, 6′′′, 1p, 1′′′′ or alternatively it can be interpreted as APC, 4′, 2a, 6′′, 6c, 4s, 6′′′, 2′′′′. The plate pattern of A. reticulatum is noticeably different from described dinoflagellate genera. Phylogenetic analyses based on the SSU and LSU rDNA genes did not show any supported affinities with currently known thecate dinoflagellates. “
“Three species of phytoplankton, Rhodomonas sp.