Existing criteria are geared towards the diagnosis of type 1 AIP. At present, pancreatic histology is a requirement for the definitive diagnosis of type 2 AIP. AIP can mimic most other pancreatic diseases in its presentation, but

Cabozantinib in clinical practice, it often has to be differentiated from pancreatic cancer. There are established criteria and algorithms not only to diagnose AIP, but also to differentiate it from pancreatic cancer. The utility of these algorithms and the approach to management are discussed here. Autoimmune pancreatitis (AIP) is a rare but distinct form of chronic pancreatitis. Although the first report of an autoimmune process affecting the pancreas can be attributed to the French group led by Henri Sarles, the term “AIP” was not coined until 1995.1–3 Most early case reports originated in Japan. A critical milestone was reached when Hamano et al. in 2001 described the association between serum immunoglobulin G (IgG)4 and AIP.4 To this day, this has proven to be the most useful serum marker for diagnosing AIP. In 2004, Kamisawa et al. showed that that there is an intense IgG4-positive cell Deforolimus order infiltration, not only in the pancreas, but also in the other organs affected by AIP. Thus, the term “IgG4-associated systemic diseases” was coined.5 Over the years, various other names

have been used to describe AIP, such as lymphoplasmacytic sclerosing pancreatitis (LPSP), idiopathic duct destructive pancreatitis, selleck compound and granulocyte epithelial

lesion (GEL)-positive pancreatitis. The reason for such a plethora of terminology is partly due to the fact that AIP is a heterogenous disease. Observations from Asia differ from those from Europe and the US with regards to clinical presentation and histology. Specifically, reports from Asia predominantly described a disease affecting elderly males, with pancreatic histology showing a lymphoplasmacytic infiltrate. Reports from Europe described a disease which affected both sexes equally, and a pancreatic histology showing a neutrophilic infiltrate called GEL. These differences delayed the formulation of a consensus definition for AIP. This issue was recently addressed during an international consensus meeting for AIP in 2011 under the auspices of the Autoimmune Pancreatitis International Study Group.6 This group gathered leading AIP researchers from around the world, and among other things, the need for uniformity in nomenclature used to describe AIP was addressed. It was agreed upon that LPSP be called type 1 AIP, and GEL-associated AIP be called type 2 AIP. In this review, we will follow this nomenclature, and unless otherwise specified, the generic term “AIP” refers to type 1 AIP. There are numerous diagnostic criteria that can aid the clinician in establishing the diagnosis of AIP. More recently, algorithms for differentiating AIP from pancreatic cancer have been published.

However, environmental factors such as diet and exercise have been shown to significantly influence PB gene expression.24, 25 In summary, we have demonstrated down-regulation of mitochondrial genes, most prominently in the oxidative phosphorylation pathway, in PB cells after a single supratherapeutic but not overtly toxic APAP dose.

VX-770 cost The gene expression changes are supported by our metabolomic finding of a concurrent increase in serum lactate. The basis for these changes are unclear, but they are consistent with known mechanisms underlying APAP liver injury and support our earlier rat work suggesting that certain blood transcripts might provide earlier detection of potential DILI. Further studies will be needed to determine if there are blood transcriptome “signatures” that could be used to both diagnose DILI and potentially identify specific culprit drugs. Additional Supporting Information

may be found in the online version of this article. ICG-001 price “
“Aim:  Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer deaths worldwide. Hepatic resection is the mainstay of curative treatment for early stage HCC. Although c-Jun N-terminal kinase (JNK) activation contributes to hepatocyte proliferation and HCC development in mice, the extent of involvement of JNK in human HCC development is unknown. The aim of this study is to assess the predictive value of JNK for postoperative recurrence in HCC. Methods:  From April 2005 to March 2008, 159 patients underwent curative resection for HCC. From the 159 patients, 20 patients each matched for age, gender and etiology were registered as three groups: (i) click here without recurrence (no recurrence group), (ii) with recurrence within one year after surgery (early recurrence group), and (iii) with recurrence at one year or more after surgery (late recurrence group) (a cross-sectional control study). We investigated factors

contributing to postoperative early and late phase recurrence. Results:  Multivariate analysis using a Logistic regression model showed that JNK activity in non-cancerous liver tissue was correlated with postoperative late recurrence. (P = 0.02, odds ratio; 5.79, 95% confidence interval [CI]; 1.33–25.36). Conclusions:  JNK activity in non-cancerous liver tissue is considered as a reliable predictive biomarker for post-operative recurrence in HCC. “
“Little is known about the clinical features of cardia varices (CV). The aim was to examine the background, bleeding risk, and post-treatment outcomes of CV in patients with portal hypertension. The subjects of this retrospective study were 277 patients (179 males, 98 females, 62.9 ± 11.5 years) with esophageal varices (EV). In patients with CV, there were 65 bleeders, and 95 patients received endoscopic treatment for primary or secondary prophylaxis. There were 147 patients with CV (53.1%). The higher grade of EV (P < 0.01) and the lower grade of gastric fundal varices (FV) (P = 0.046) were significant factors for the presence of CV.

The fecal samples were collected into the stool collection devices and suspended in the diluent buffer. Peroxidase-conjugated MAb 21G2 BGJ398 clinical trial was combined with 50 µL of diluted bacterial antigen sample or one drop of the suspended stool sample. The mixture was added to the MAb 21G2-immobilized EIA plates and incubated for 60 min at room temperature.

After washing the plate, the substrate solution was added and incubated for 10 min at room temperature. The reaction was stopped by the stop reagent, and the optical density was measured with a microplate reader (Model 550: Bio-Rad Laboratories, Tokyo, Japan) at dual wavelengths (450 and 630 nm). Absorbance values greater than 0.100 were considered positive. The principle of Rapid TPAg is based on immunochromatography. MAb 21G2 and anti-mouse IgG polyclonal antibody (MP Biomedicals LLC, Irvine, CA, USA) were immobilized onto nitrocellulose membranes (Millipore Corporation, Billerica, MA, USA) as shown in Figure 1 (test line and control line). selleckchem MAb 21G2 was conjugated with red latex particles (Thermo Scientific Inc., Waltham, MA, USA) and dipped onto a glass fiber pad. The concentration of H. pylori and other bacterial antigens was adjusted with the diluent buffer. The fecal samples were collected into stool collection devices and suspended. Fifty microliters of the prepared antigen or one drop of the stool sample suspension was placed on the specimen application region

of the test strip. If native catalase H. pylori antigens were present in the samples, they would form immune complexes with the red latex-labeled MAb 21G2 and migrate by capillary action, where they would be captured by the solid-phase, MAb 21G2 to form a red test line. The labeled 21G2-native catalase H. pylori antigens immune complex or not forming the complexes migrate further up to be captured by solid-phase anti-mouse IgG rabbit polyclonal antibodies forming a red control line. After 10 min,

the results were considered positive for H. pylori if both the control and test lines were red and the results were considered negative if only the control line was red. Fecal samples were obtained from 111 patients with gastrointestinal diseases: 75 patients with gastric ulcers; 11, duodenal ulcers; 6, atrophic gastritis; 5, non-ulcer dyspepsia; 4, gastric MALT lymphoma; 3, selleck products esophagitis; 2, gastric cancer; 2, gastric polyps; 2, ulcerative colitis; and, 1, Crohn’s disease. The clinical diagnosis and H. pylori status were determined at General Medicine and Community Health Science, Sasayama Medical Center, Hyogo College of Medicine, Nishinomiya, Japan. H. pylori status was diagnosed on the basis of culture, histological examination, and rapid urease test (RUT: Helicocheck; Otsuka Pharmaceutical Co. Ltd, Tokyo, Japan). H. pylori status was defined as positive if H. pylori were cultured or both of the histology and RUT were positive. H.

The fecal samples were collected into the stool collection devices and suspended in the diluent buffer. Peroxidase-conjugated MAb 21G2 Protease Inhibitor Library manufacturer was combined with 50 µL of diluted bacterial antigen sample or one drop of the suspended stool sample. The mixture was added to the MAb 21G2-immobilized EIA plates and incubated for 60 min at room temperature.

After washing the plate, the substrate solution was added and incubated for 10 min at room temperature. The reaction was stopped by the stop reagent, and the optical density was measured with a microplate reader (Model 550: Bio-Rad Laboratories, Tokyo, Japan) at dual wavelengths (450 and 630 nm). Absorbance values greater than 0.100 were considered positive. The principle of Rapid TPAg is based on immunochromatography. MAb 21G2 and anti-mouse IgG polyclonal antibody (MP Biomedicals LLC, Irvine, CA, USA) were immobilized onto nitrocellulose membranes (Millipore Corporation, Billerica, MA, USA) as shown in Figure 1 (test line and control line). PARP inhibitors clinical trials MAb 21G2 was conjugated with red latex particles (Thermo Scientific Inc., Waltham, MA, USA) and dipped onto a glass fiber pad. The concentration of H. pylori and other bacterial antigens was adjusted with the diluent buffer. The fecal samples were collected into stool collection devices and suspended. Fifty microliters of the prepared antigen or one drop of the stool sample suspension was placed on the specimen application region

of the test strip. If native catalase H. pylori antigens were present in the samples, they would form immune complexes with the red latex-labeled MAb 21G2 and migrate by capillary action, where they would be captured by the solid-phase, MAb 21G2 to form a red test line. The labeled 21G2-native catalase H. pylori antigens immune complex or not forming the complexes migrate further up to be captured by solid-phase anti-mouse IgG rabbit polyclonal antibodies forming a red control line. After 10 min,

the results were considered positive for H. pylori if both the control and test lines were red and the results were considered negative if only the control line was red. Fecal samples were obtained from 111 patients with gastrointestinal diseases: 75 patients with gastric ulcers; 11, duodenal ulcers; 6, atrophic gastritis; 5, non-ulcer dyspepsia; 4, gastric MALT lymphoma; 3, selleck kinase inhibitor esophagitis; 2, gastric cancer; 2, gastric polyps; 2, ulcerative colitis; and, 1, Crohn’s disease. The clinical diagnosis and H. pylori status were determined at General Medicine and Community Health Science, Sasayama Medical Center, Hyogo College of Medicine, Nishinomiya, Japan. H. pylori status was diagnosed on the basis of culture, histological examination, and rapid urease test (RUT: Helicocheck; Otsuka Pharmaceutical Co. Ltd, Tokyo, Japan). H. pylori status was defined as positive if H. pylori were cultured or both of the histology and RUT were positive. H.

AE, adverse event; AUC, area under the curve; BID, twice daily; CI, confidence interval; Cmax, maximum plasma concentration within the dosing interval; EC50, median effective

concentration; HCV, hepatitis C virus; NNI, non-nucleoside inhibitor; NS, nonstructural protein; pegIFN, pegylated interferon; PK, pharmacokinetic; RBV, ribavirin; SVR, sustained virological response; TE, treatment-experienced; TID, Z-VAD-FMK mouse three times daily; TN, treatment-naive; Tmax, time to Cmax. All patients provided written informed consent before study participation. The protocol and informed-consent forms were approved by independent ethics committees at all study centers in accordance with national procedures. The studies were conducted according to the ethical principles in the Declaration of Helsinki and in compliance with all Good Clinical Practice guidelines, local see more laws, and regulations.17 In study 1, 32 TN patients were enrolled between January 2007 and May 2008 in three European centers: one in Belgium and two in Germany. In study 2, 20 patients were enrolled between April 2008 and December 2008 in a single center in Florida, USA. Both studies were conducted in chronic HCV genotype 1–infected patients, of either sex, aged 18-65 years with a

body mass index of 18-34 kg/m2. Other key eligibility criteria included HCV RNA detectable in serum for ≥6 months and ≥100,000 IU/mL at screening. Women of childbearing potential or who were premenopausal were

excluded, as were patients who were coinfected with hepatitis B or human immunodeficiency virus, who had evidence of severe or decompensated liver disease, or who had liver disease unrelated to HCV infection. Study 1: This was a randomized, double-blind, placebo-controlled, sequential dose escalation study of orally administered filibuvir. Four cohorts of eight patients were randomized (6:2) to receive filibuvir (100, 300, or 450 mg every 12 hours [BID] or 300 mg every 8 hours [TID]) or placebo under fasted conditions for 8 days; treatments were given BID or TID on days 1 through 7, selleck inhibitor and once on day 8. The random allocation sequence used to assign patients was computer-generated. The sponsor generated the allocation sequence, and an investigator assigned participants to their groups sequentially as each patient was screened and in accordance with their randomization numbers. Patients and investigators were blinded but the sponsor was not. Study 2: This was a nonrandomized, open-label, sequential group study of orally administered filibuvir in two cohorts. In cohort A, TE patients received filibuvir 450 mg every 12 hours (BID) for 10 days in a fasted state; in cohort B, TN patients received filibuvir 700 mg every 12 hours (BID) for 3 days in a fed state.

“
“(Headache 2011;51:734-743) Background.— Neck muscle nociception mediated by nitric oxide may play a role in the pathophysiology of tension-type headache. Objective.— The present study addresses the involvement of neuronal nitric oxide synthase (nNOS) in the facilitation of neck muscle nociception after local application of nerve growth factor (NGF). Methods.— After administration of NGF into semispinal neck muscles, the impact of neck muscle noxious input on brainstem processing was monitored by the jaw-opening reflex in anesthetized mice. The modulatory effect of preceding and subsequent administration of an inhibitor of neuronal nitric oxide synthase on central facilitation

was addressed in a controlled study. Results.— With preceding i.p. application of saline or 0.096 mg/kg of selleck inhibitor the specific nNOS inhibitor Nω-propyl-L-arginine

(NPLA), NGF induced a sustained reflex facilitation within 60 minutes. MDV3100 Preceding injection of 0.96 mg/kg or 1.92 mg/kg NPLA completely prevented the potentially facilitatory effect of NGF. Subsequent administration of 0.96 mg/kg NPLA did not affect established NGF-evoked reflex facilitation. Thus, NPLA prevents facilitation of brainstem processing by noxious myofascial input from neck muscles in a dose-dependent manner. Conclusion.— These findings suggest that nNOS is involved in the induction but not the maintenance of NGF-evoked facilitation of nociception in the brainstem. These results from an experimental animal model may support the idea of NOS and nNOS as potential targets for pharmacological treatment of tension-type headache. “
“To assess the decay of the conditioned pain modulation (CPM) response along repeated applications as a possible expression of subtle pronociception in migraine. One of the most explored mechanisms underlying the

pain modulation system is “diffuse noxious inhibitory controls,” which is measured psychophysically in the lab by the CPM paradigm. There selleck are contradicting reports on CPM response in migraine, questioning whether migraineurs express pronociceptive pain modulation. Migraineurs (n = 26) and healthy controls (n = 35), all females, underwent 3 stimulation series, consisting of repeated (1) “test-stimulus” (Ts) alone that was given first followed by (2) parallel CPM application (CPM-parallel), and (3) sequential CPM application (CPM-sequential), in which the Ts is delivered during or following the conditioning-stimulus, respectively. In all series, the Ts repeated 4 times (0-3). In the CPM series, repetition “0” consisted of the Ts-alone that was followed by 3 repetitions of the Ts with a conditioning-stimulus application. Although there was no difference between migraineurs and controls for the first CPM response in each series, we found waning of CPM-parallel efficiency along the series for migraineurs (P = .

98 ± 0.07, 2.30 ± 0.08 mmol/L respectively). We found no difference of serum level of Cu\Fe\Zn, vitamin B12, folic acid, and Hb\MCV\MCH between the two groups. Higher serum Gastrin (109.7 pg/ml) than normal range (100 pg/ml) and controls (79.9 pg/ml) were found in the study group (t = -4.16, P = 0.000). Conclusion: Long term use of PPIs may relate with decrease of hip density, increase of serum gastrin, and slight changes of trace mineral elements. Key Word(s): 1. PPI; 2. long term use; 3. side effects; Presenting Author: WANG DAN Additional Authors: ZHANG XIAOTIAN, XU HONG, WANG FANG Corresponding Author: XU HONG, WANG FANG Affiliations: JiLin University Objective: Nucleotide-binding

oligomerization domain-Like Receptor BMS-777607 cell line with a Pyrin domain 3 (NLRP3) is found to be a key part among innate immune

responses. Caspase-1, an enzyme that proteolytically cleaves other proteins, could be activated by NLRP3. Active caspase-1 then initiates the process which precursor of IL-1β and IL-18 were activated to inflammatory cytokines. Reported information was showed NLRP3 inflammasome was activated during infection with Helicobacter PLX3397 pylori in mice. We think NLPR3 is an important innate immune molecular in the infection by Helicobacter pylori,it could differently expressed in Helicobacter pylori infectious diseases in human.This study aimed to address a possible role for NLRP3 and its substrates in the disease of gastric ulcer (GU) infected by Helicobacter pylori. Methods: 20 Patients of GU, 15 healthy adults were selected. All the patients and normal controls were detected with Helicobacter pylori by endoscopy and rapid urease test. Patients of GU received standard triple therapy (pantoprazole

40 mg,for 6 weeks, clarithromycin 0.5 g and amoxicillin 1 g, for 2 weeks, each administered twice daily),2 weeks after drug-withdrawal reexamined by endoscopy and rapid urease test. This research includes three groups: normal control, patients of GU before and after treatment. NLRP3 and its cytokine check details substrates caspase-1, IL-1β and IL-18 were examined by Real-time RT-PCR and cytokine ELISAs in three groups. Results: Patients of GU were found with activation of NLRP3, caspase-1 and IL-1β in the level of mRNA and protein compared with normal control (p < 0.05), but IL-18 showed no significant difference (p > 0.05). After triple therapy, Expression of NLRP3, caspase-1 and IL-1β showed decrease (P < 0.05). Conclusion: In conclusion,NLRP3,caspase-1 and IL-1β showed differential expression in human when Helicobacter pylori infection. NLRP3 inflammasome could be a key factor in GU when Helicobacter pylori infection. Therefore, targeting NLRP3 inflammasome may be effective for prevention and treatment of GU caused by Helicobacter pylori infection. Key Word(s): 1. NLRP3 inflammasome; 2. Helicobacter pylori; 3. caspase-1; 4.

Clearly, HSCs were again inferior to LSECs in cross-presentation of circulating antigen ingested in vivo (Fig. 1B). These results demonstrate that HSCs do not possess antigen-processing capability similar to DCs, suggesting that if already antigen uptake is inefficient, downstream mechanisms, such as peptide trimming in the endoplasmic reticulum (ER), are unlikely to improve APC function. A recent report also showed that primary HSCs have little, if any, APC function for CD4 T cells, even after stimulation with exogenous interferon gamma.8 Taken together, these results demonstrate a hierarchy in the performance

of APC function for DCs being ICG-001 chemical structure most efficient in antigen processing, macrophages and LSECs compensating for inefficient antigen processing by high antigen uptake, and HSCs showing low antigen uptake and inefficient antigen processing. These data call into question a prominent role for HSCs as liver-resident APCs. Frank

A. Schildberg*, Christian Kurts*, Percy A. Knolle MD*, * Institutes of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms-Universität Bonn, Bonn, Germany. “
“Several studies have indicated that primary biliary cirrhosis (PBC) may be associated with increased risk of some cancers, but Ensartinib research buy the results are controversial. We conducted a systematic review of studies to examine the association of PBC with cancer risk by meta-analysis. We searched the PubMed and EMBASE databases for English-language studies published before November 2011.

Studies were included if they reported relative risk estimates with 95% confidence intervals (CIs) or related data for the association between PBC and cancer risk. Approximately 16,300 PBC patients from several countries were included in this analysis. Of the 3510 titles identified, 16 publications involving 17 studies meeting the inclusion criteria were included in the meta-analysis. Compared with the general population, PBC patients had a significantly higher risk of overall cancer (pooled rate ratio [RR], 1.55; 95% CI, 1.28-1.83) and hepatocellular carcinoma (HCC) (pooled RR, 18.80; 95% CI, 10.81-26.79). For stomach and pancreas cancers, the results of one study learn more that only examined male patients with PBC indicated that PBC patients had increased risk of stomach cancer and pancreatic cancer, whereas the results of other studies of mixed-sex patients showed no significant association. Therefore, despite inconsistent results, the meta-analysis could not be conducted for assessing the association. PBC was not significantly associated with increased risk of other cancers. Conclusion: The present systematic review and meta-analysis demonstrate that PBC is closely associated with a greater risk of overall cancer and HCC, but not with other cancers. The data regarding the association between PBC and risks of several cancers need to be further confirmed in future studies.

Age for herring and sprat was determined using length-at-age regression models that are derived during routine pelagic trawl surveys for stock assessment (Saunders et al. 2010). Carbon and nitrogen isotope composition of whale skin was determined using continuous flow elemental analysis isotope ratio mass spectrometry (CF-EA-IRMS) at the University of Southampton using a EuroVector EA 3000 (EA) combined

with a PDZ Europa Scientific 20-20 (IRMS). Isotope ratios are presented in delta notation as parts per thousand differences from an internal standard (ACROS L-Glutamic Acid) according to the following equation: δYX = [(Rsample/Rstandard) − 1] BAY 57-1293 × 10−3, where R denotes the heavier:lighter isotope ratio and Y is the atomic mass of the stable isotope X (δ13C or δ15N). Internal standards calibrated with International Atomic Energy Agency IAEA (Vienna, Austria), i.e., Vienna Pee Dee Belemnite (for C), atmospheric N2 (for N), were routinely analyzed between samples in order to determine instrument precision. Based on the two standard deviations of these standards, the analytical precision of two runs at separate laboratories was similar 0.4‰ and 0.2‰ for nitrogen, and 0.2‰ and 0.1‰ for carbon for Southampton and University Erastin of California

Davis respectively. Prey items (fish muscle and homogenized krill) were analyzed at UC Davis by CF-EA-IRMS using a PDZ Europa ANCA-GSL (EA) combined with a PDZ Europa 20-20 (IRMS). The analytical precision at Southampton, calculated as the standard deviation of routinely measured bovine liver and glutamic acid standards, was 0.40‰ for nitrogen, and 0.20‰ for carbon. At the UC Davis laboratory, this was 0.15‰ and 0.06‰ for nitrogen and carbon, respectively. In exoskeletons of crustaceans such as krill, carbonates (CaCO3) are derived from isotopically heavy HCO3− ions from the environment, selleck chemicals llc and

are thus a nondietary fraction and must also be removed as their enriched 13C affects whole-body δ13C values (Søreide et al. 2006). Lipids are depleted in 13C, thus altering the δ13C values of tissues. The elemental carbon to nitrogen ratio (C:N) is a useful proxy for lipid content (McConnaughey and McRoy 1979) and was used to assess lipid effects on isotopic values in light of those previously published species- and tissue-specific values for lean tissue. Lipid-free C:N values for whole zooplankton (range) are 3.30–4.03 for marine zooplankton (Kiljunen et al. 2006, Søreide et al. 2006), (± SD) 3.6 ± 0.1 for M. norvegica (Bentaleb et al. 2011) and 3.3 ± 0.1 for white muscle in sprat and herring of (Kiljunen et al. 2006, Caut et al. 2011). These were used as a threshold lipid-free and/or carbonate-free values for each species, which if exceeded indicated that all δ13C values for that species should be corrected arithmetically (i.e., lipid-normalized) to correct for the presence of isotopically lighter lipid (Table 1).

One isolate with cryptic, barely visible plastids lacked detectable chlorophyll and exhibited an apparent loss-of-function mutation

in psbA, indicating the presence of nonphotosynthetic plastids. The other isolate that lacked visible chloroplasts lacked both detectable chlorophyll and an amplifiable psbA sequence. The results demonstrate mixotrophy quantitatively for the first time in a freshwater dinoflagellate, as well as apparent within-clade loss of phototrophy along with a correlated mutation sufficient to explain that phenotype. Phototrophy is a variable trait in Esoptrodinium; further study is required to determine if this represents an inter- or intraspecific (allelic) characteristic in this taxon. Esoptrodinium Javornický and Obeticholic Acid cell line Bernardinium Chodat are genera of freshwater dinoflagellates currently consisting of a small number of similar species (E. gemma, B. bernardinense) originally described from observations Talazoparib in vivo of field material (Chodat 1924, Javornický 1997). Esoptrodinium/Bernardinium-like dinoflagellates are relatively small (<20 μm), naked (athecate), and possess an indistinct sulcus and incomplete cingulum that does not fully encircle the flagellate cell. Field specimens have reportedly varied in features such as the presence or absence of chloroplasts and cingulum orientation, with the latter being used

as the sole generic character to differentiate Esoptrodinium (normal leftward cingulum) from Bernardinium (unusual rightward cingulum) in the most recent taxonomic description of the group (Javornický 1997). All cultured specimens studied thus far have shown the canonical leftward-oriented cingulum, and it has see more been argued based on circumstantial

evidence and systematic utility that Esoptrodinium and Bernardinium should be considered synonymous unless the reported rightward cingulum orientation can be demonstrated as a phylogenetically determinant character in the group (Fawcett and Parrow 2012). In the present work, we refer to the dinoflagellates under study as Esoptrodinium sp. (sensu Javornický) because of their leftward-oriented cingulum, but regard this as synonymous with Bernardinium sp. (sensu auct. non sensu Javornický). Based on molecular and ultrastructural data, Esoptrodinium has been classified as a third genus along with Jadwigia and Tovellia in the Tovelliaceae, a thus far freshwater dinoflagellate family that exhibits a distinctive extraplastidal eyespot as an apparent synapomorphy (Calado et al. 2006, Moestrup et al. 2006). Esoptrodinium-like dinoflagellates appear to have a widespread distribution, being reported in freshwater field samples from Europe (Chodat 1924, Javornický 1962, 1997), North America (Thompson 1951), and South America (Bicudo and Skvortzov 1970, misidentified therein (figs.