One investigator per country reviewed all CRFs before its inclusion in the database. Patients were considered lost LY2157299 to follow-up if the last visit preceded the 9 months before

study closure. All national and, if necessary, local ethics committees approved the study, and all patients provided written informed consent to participate. Child-Pugh and Model for End-Stage Liver Disease (MELD) scores were calculated using the data at diagnosis of BCS, as previously reported.12, 13 The Rotterdam score was previously published to predict survival and is defined as follows: 1.27 × encephalopathy + 1.04 × ascites + 0.72 × prothrombin time + 0.004 × bilirubin (where ascites was scored as present “1” or absent “0”). The 5-year survival rate was 89% (95% confidence interval [CI]: 79-99) for class I, 74% (95% CI: 65-83) for class II, and 42% (95% CI: 28-56) for class III.9 The BCS-TIPS prognostic index score (TIPS-BCS PI score) was developed to predict OLT free survival in patients that received TIPS and is defined as follows: age (years) × 0.08 + bilirubin (mg/dL) × 0.16 + international normalized ratio (INR) × 0.63. The cutoff of 7 points EMD 1214063 ic50 had a sensitivity of 58%, a specificity of 99%, a positive predictive

value of 88%, and a negative predictive value of 96% for death or OLT 1 year after TIPS.6 Results are expressed as N (proportions) for categorical variables and as medians (range) for continuous 上海皓元医药股份有限公司 variables. Actuarial transplantation-free and intervention-free survival

rates were calculated by using Kaplan-Meier’s method. Uni- and multivariable Cox’s regression analysis was used to explore the association between different variables and prognosis. New prognostic scores were constructed by combining (in a linear equation) those variables independently associated with the event multiplied by their regression coefficients. To add potential advantages to these models, we did not include subjective parameters (e.g., presence or absence of hepatic encephalopathy; HE) or INR in patients that may have initiated anticoagulation that were integrated in the previously described scores. Statistical significance was defined as a P value less than 0.05. All statistical analyses were conducted with the PASW Statistics 18 program (SPSS, Inc., Chicago, IL). All 163 patients included in the previous EN-Vie study were eligible, and all centers, except one, that took part in the first study agreed to participate. Finally, 157 patients were included in the current study (Belgium, N = 5; France, N = 35; Germany, N = 14; Great Britain, N = 29; Italy, N = 18; Spain, N = 33; Switzerland, N = 4; The Netherlands, N = 19). Overall median follow-up of these 157 patients was 50 months (range, 0.1-74.0). Twenty-six patients (17%) were lost to follow-up after a median time of 25 months (range, 0.

Rat liver specimens were obtained from previous experiments. Healthy livers, pools of liver preneoplastic lesions isolated with

the use of a stereomicroscope, and HCC were used. The transplantation procedure was performed as previously described.19, 20 Briefly, diabetes was induced in adult inbred male Lewis rats (250-300 g) by treatment with a single subcutaneous dose of streptozotocin (80 mg/kg body weight [BW]) and was defined by a nonfasting Deforolimus nmr blood-glucose level higher than 400 mg/dL, manifesting between 1 and 3 days after the administration of streptozotocin. Islets of Langerhans were isolated from nondiabetic littermates and transplanted into the liver of recipient rats through the portal vein. A low number of islets (250-450 islet grafts per animal) was transplanted so that mild hyperglycemia (250-300 mg/dL) persisted for at least 10 months after transplantation. During infusion, the branch supplying the left part of the liver was clamped, thus ensuring that the transplants were embolized only into the right part of

the liver and the left part served as an intraindividual control. As an additional control, the livers of nondiabetic rats not undergoing transplantation were used. However, because there were no significant differences see more in the parameters examined between the intraindividual controls and the nondiabetic rats not undergoing transplantation, the data of these two groups were combined and referred to as the control liver. Animals were sacrificed under anesthesia between 2 days and 24 months after transplantation. Groups of rats were subjected to daily administration

of the phosphoinositide 3-kinase (PI3K)/mTOR dual inhibitor, NVP-BEZ235 (kindly provided by Novartis, Basel, Switzerland), dissolved in 1% methylcellulose at a concentration of 10 mg/kg BW for 4 weeks. Rats were housed, fed, and treated according to the German Animal Protection Law and approved by the Local Government of Mecklenburg-Vorpommern. Transfection of Hep3B and HLE cell lines with short interfering 上海皓元 RNAs (siRNAs) and treatment with specific inhibitors were performed as described in the Supporting Materials and Methods. Hepatic tissue samples were homogenized and processed as previously reported.26 Nitrocellulose membranes were probed with specific primary antibodies (Supporting Table 1). Tukey-Kramer’s test was used to evaluate statistical significance. P < 0.05 was considered significant. Data are expressed as means ± standard deviation (SD). See the Supporting Materials and Methods for detailed descriptions of materials and methods.

Rat liver specimens were obtained from previous experiments. Healthy livers, pools of liver preneoplastic lesions isolated with

the use of a stereomicroscope, and HCC were used. The transplantation procedure was performed as previously described.19, 20 Briefly, diabetes was induced in adult inbred male Lewis rats (250-300 g) by treatment with a single subcutaneous dose of streptozotocin (80 mg/kg body weight [BW]) and was defined by a nonfasting RGFP966 price blood-glucose level higher than 400 mg/dL, manifesting between 1 and 3 days after the administration of streptozotocin. Islets of Langerhans were isolated from nondiabetic littermates and transplanted into the liver of recipient rats through the portal vein. A low number of islets (250-450 islet grafts per animal) was transplanted so that mild hyperglycemia (250-300 mg/dL) persisted for at least 10 months after transplantation. During infusion, the branch supplying the left part of the liver was clamped, thus ensuring that the transplants were embolized only into the right part of

the liver and the left part served as an intraindividual control. As an additional control, the livers of nondiabetic rats not undergoing transplantation were used. However, because there were no significant differences MK-1775 in vitro in the parameters examined between the intraindividual controls and the nondiabetic rats not undergoing transplantation, the data of these two groups were combined and referred to as the control liver. Animals were sacrificed under anesthesia between 2 days and 24 months after transplantation. Groups of rats were subjected to daily administration

of the phosphoinositide 3-kinase (PI3K)/mTOR dual inhibitor, NVP-BEZ235 (kindly provided by Novartis, Basel, Switzerland), dissolved in 1% methylcellulose at a concentration of 10 mg/kg BW for 4 weeks. Rats were housed, fed, and treated according to the German Animal Protection Law and approved by the Local Government of Mecklenburg-Vorpommern. Transfection of Hep3B and HLE cell lines with short interfering 上海皓元医药股份有限公司 RNAs (siRNAs) and treatment with specific inhibitors were performed as described in the Supporting Materials and Methods. Hepatic tissue samples were homogenized and processed as previously reported.26 Nitrocellulose membranes were probed with specific primary antibodies (Supporting Table 1). Tukey-Kramer’s test was used to evaluate statistical significance. P < 0.05 was considered significant. Data are expressed as means ± standard deviation (SD). See the Supporting Materials and Methods for detailed descriptions of materials and methods.

5B). Moreover, the addition of the anti-KLF15 antibody resulted in a supershift, whose intensity positively correlated with the amount of the anti-KLF15 antibody used (lanes 5 and

6). It is noteworthy that the addition of the control antibody could increase the binding of KLF15 to the DNA probe. In addition, despite the appearance of the supershifted signal, the intensity of the original KLF15-DNA complex did not diminish accordingly, which was also observed in another study using the same antibody.24 The reason why the addition check details of the antibodies increased the binding of KLF15 to the DNA probe is unclear. It may have been related to stabilization by protein (antibody or bovine serum albumin [BSA] in the antibody storage buffer) or other components in the antibody storage buffer. To determine whether KLF15 binding to CP35 would be specific, we synthesized CP35-2m, which had mutations in the two potential KLF15-binding sites (Supporting Fig. 1). As shown in Fig. 5C, KLF15-DNA complex was decreased by the nonlabeled CP35 competitor in a dose-dependent manner, whereas CP35-2m failed to compete for KLF15 binding Staurosporine in vivo (Fig. 5C). To further confirm that the binding of KLF15 to DNA would depend on the KLF15 consensus sequence embedded in the core promoter, we performed ChIP assays using cells cotransfected with pKLF15 and the core promoter reporter, pCP, or its mutant, pCP-2m. Our results showed that the anti-KLF15 antibody could

efficiently precipitate pCP, but not pCP-2m (Fig. 5F, upper panel), indicating that KLF15 could, indeed, bind to pCP, and this binding was dependent

on the intact KLF15 consensus sequence. To determine whether KLF15 could also bind to the surface promoter, we performed similar EMSA assays. MCE As shown in Fig. 5D, the incubation of rKLF15 with the labeled surface promoter probe, SP70, resulted in a bandshift, which could be competed off by nonlabeled SP70, but not by a nonspecific competitor. Similarly, a supershift band could be observed when the anti-KLF15 antibody was added in the binding reaction (Fig. 5E). Consistent with these results, ChIP assays showed that KLF15 was able to bind to the S promoter DNA. Further analysis indicated that mutations in the Sp1 sites (i.e., Z1/Z2 mutant; Fig. 5F, middle panel), which prevented the binding of Sp1, reduced the binding of KLF15 to the S promoter by 42% (Supporting Fig. 2). In contrast, mutations in the NF-Y site (i.e., M2 mutant; Fig. 5F, bottom panel) had essentially no effect on the binding of KLF15 to the S promoter, despite suppressing NF-Y binding. Together, the results in Fig. 5 indicated that KLF15 could bind to the HBV core and surface promoters and further suggested the partial overlap of the KLF15 sites with the Sp1 sites or the presence of a cryptic KLF15-binding site elsewhere in the S promoter. Suppression of KLF15 expression in the liver decreases viral gene expression and DNA replication in a HBV mouse model.

23. Neomycin is an alternative choice for treatment of OHE (GRADE II-1, B, 2). 24. Metronidazole is an alternative choice for treatment of OHE (GRADE II-3, B, 2). There are no randomized, placebo-controlled trials of lactulose for maintenance Selleckchem FK228 of remission from OHE. However, it is still widely recommended and practiced. A single-center, open-label RCT of lactulose demonstrated less recurrence

of HE in patients with cirrhosis.[33] A recent RCT supports lactulose as prevention of HE subsequent to upper gastrointestinal (GI) bleeding.[110] Rifaximin added to lactulose is the best-documented agent to maintain remission in patients who have already experienced one or more bouts of OHE while on lactulose treatment after their initial episode of OHE.[101] Once TIPS was popularized to treat complications of PH, its tendency to cause the appearance of HE, or less commonly, intractable persistent HE, was noted. Faced with severe HE as a complication of a TIPS procedure, physicians had a major dilemma. Initially, it was routine to use standard HE treatment to prevent post-TIPS HE. However, one study illustrated that neither rifaximin nor lactulose prevented post-TIPS HE any better than DAPT in vivo placebo.[111] Careful case selection has reduced the incidence

of severe HE post-TIPS. If it occurs, shunt diameter reduction can reverse HE.[112] However, the original cause for placing TIPS may reappear. Another important issue with TIPS relates to the desired portal pressure (PP) attained after placement of stents. Too low a pressure because of large stent diameter can lead to intractable HE, as noted above. There is a lack of consensus on whether to aim to MCE reduce PP by 50% or below 12 mmHg. The latter is associated with more bouts of encephalopathy.[113] It is widely

used to treat post-TIPS recurrent HE as with other cases of recurrent HE, including the cases that cannot be managed by reduction of shunt diameter. Recurrent bouts of overt HE in patients with preserved liver function consideration should lead to a search for large spontaneous PSSs. Certain types of shunts, such as splenorenal shunts, can be successfully embolized with rapid clearance of overt HE in a fraction of patients in a good liver function status, despite the risk for subsequent VB.[114] 25. Lactulose is recommended for prevention of recurrent episodes of HE after the initial episode (GRADE II-1, A, 1). 26. Rifaximin as an add-on to lactulose is recommended for prevention of recurrent episodes of HE after the second episode (GRADE I, A, 1). 27. Routine prophylactic therapy (lactulose or rifaximin) is not recommended for the prevention of post-TIPS HE (GRADE III, B, 1). There is a nearly uniform policy to continue treatment indefinitely after it has successfully reversed a bout of OHE. The concept may be that once the thresholds for OHE is reached, then patients are at high risk for recurrent episodes.

Our group has already proved that both Curcuma Wenyujin and its extracts show great effects

in anti-inflammation and anti-cancer. Methods: Taking SGC7901 as the negative control group, we use MTT to prove Whether SGC7901/VCR is a kind of multidrug resistant cell lines and draw a Volasertib solubility dmso growth curve of SGC7901 and SGC7901/VCR cultivated without VCR, and to choose non-toxic dose of Curcuma Wenyujin ethanol extract (CWEE). Then to prove whether non-toxic dose of Wenyujin can reverse MDR by MTT. Testing CD44 of both SGC7901 and SGC7901/VCR by flow cytometry to see whether it is a mark of cancer stem cell. We also use flow cytometry to test the effect of CWEE on apoptosis rate induced by VCR and cycle arrested by VCR. Through Western blot, we can see if CWEE can regulate the expression of Pgp and LRP. Then we further test the location of Pgp by IHC. To get check details a clear understanding of how CWEE affects the expression of Pgp and MRP1, we use RT-PCR to test the mRNA of Pgp and MRP1. Results: This study has proved that the SGC7901/VCR is a kind of multidrug resistant cell lines which resists Vincristine (VCR), Adriamycin (ADR), 5-fluorouracil (5-FU) and cis-platinum

(DDP). Among these chemotherapeutics, the cell line has a strongest resistance (5259.22 ± 358.08-fold) to the VCR while it has a least resistance (1.37 ± 0.16-fold) to DDP. When it is cultured without VCR, it proliferates just like the nondrug resistant cell line SGC7901 in the first week, but the former proliferates much MCE more quickly in the second week. flow cytometry shows there is no difference of CD44

between SGC7901/VCR and SGC7901. MTT and flow cytometry reveal that CWEE can reverse the resistance of SGC7901/VCR to VCR, ADR and 5-FU which depends on the concentration of CWEE. Flow cytometry shows that CWEE can enhance apoptosis rate of SGC7901/VCR induced by VCR and increase the ratio of cells in G2/M stage arrested by VCR. Both Western blot and IHC show that Pgp and LRP expresses much higher in SGC7901/VCR than in SGVC7901. However, only Pgp can be reduced by WEE. The interesting thing is that RT-PCR reveals CWEE increases the transcription of Pgp. Both Western blot and IHC show that Pgp and LRP expresses much higher inSGC7901/VCR than in SGVC7901. However, only Pgp can be reduced by CWEE. RT-PCR also shows that CWEE can reduce the transcription of MRP1. Conclusion: SGC7901/vcr is a good cell line of MDR for experiments. SGC7901/VCR is more aggressive than SGC7901. CD44 may have no relation with SGC7901/VCR’s drug resistance. To be more exact, CD44 may not be considered as an independent mark of cancer stem cell. we may infer that CWEE reverse MDR mainly by inhibiting the process of translation instead of transcription of Pgp as well as the transcription of MRP1.

Thence the Committee decided our next task of high priority is to produce the practical guidelines for hepatitis B, also a significant burden to the health care system. Here the Committee has launched the Guidelines for the Management of Hepatitis B Virus Infection. As with hepatitis C virus, this is a field that changes rapidly with the accumulation of new evidence, accompanied by changes in the level of evidence, so we have elected not to show evidence levels. We plan to update these guidelines at appropriate intervals, as new evidence comes to hand.

It is estimated that there are 400 million patients of persistent hepatitis B virus (HBV) infection in the world.[1] In Japan, the HBV infection rate is around 1%. HBV infection at birth or during infancy leads to persistent infection in over 90% of cases. Approximately 90% of these undergo seroconversion from HBe antigen (HBeAg) Selleckchem PD98059 positive at the initial stage to anti-HBe antibody Gefitinib price positive and become inactive carriers, and in virtually all cases the condition effectively stabilizes. But in the remaining 10% the virus remains active, leading to chronic hepatitis, and in around 2% of cases annually, there is further progression to liver cirrhosis, with potential for hepatocellular carcinoma (HCC) and liver failure.[2-4] Clinical research on HBV dates back to the discovery of the Australia antigen (later renamed HBs antigen; HBsAg) by Blumberg et al.

in 1964. Prince et al. and Okouchi et al. subsequently reported a link between the Australia antigen and hepatitis. And there have been various other discoveries demonstrating that MCE公司 the existence of an asymptomatic carrier, who does not develop hepatitis following HBV infection and indicating HBV as a cause of chronic liver diseases. The base form of HBV, known as the Dane particle, was discovered in 1970, followed by the identification of HBeAg in 1972. In 1979, the whole HBV genome was successfully cloned from virus particles,

enabling measurement of the virus gene (HBV DNA) for the first time. In Japan, screening for the HBsAg was introduced at blood centers in 1972. 1986 was the year of the introduction of an anti-HBV vaccine and immunoglobulin for newborns designed to prevent vertical (mother-to-child) infection. This was highly effective in arresting the development of new HBV carriers through vertical infection, causing a marked decline in HBsAg positive rates among juveniles. The incidence of acute hepatitis caused by HBV infection, however, has not declined, mainly as a result of horizontal transmission associated with sexual activity. In recent years, there has been an increase in infection rates for the HBV genotype A, which frequently causes persistent infection.[5] HBV in itself is considered to have little or no cytotoxicity. Hepatocellular damages are generally caused by cellular immunity associated with cytotoxic T cells, which represent the host’s immune response attacking HBV infected cells.

This study was to investigate the role of STIM1 on metastatic potential of human CRC. Methods: We examined the expression of STIM1 in four CRC cell lines with different metastatic potentials using real-time PCR and Western Blot, SW620

and LOVO (high metastatic potential), SW480 and HT29 (low metastatic potential). Expression of STIM1 in CRC tissues was explored using immunohistochemisty. The relationships between STIM1 expression and clinicopathologic factors were assessed using theχ2 test. Effects of stable expression of STIM1 and its siRNA inhibitors were studied in the human CRC cell lines SW480 and SW620; transwell experiments were performed to evaluate cellular migration and invasion. Results: Expression of STIM1 was increased in highly invasive CRC cell lines and lymph node-positive CRC specimens. Enhancing the expression of STIM1 promoted CRC cell migration and invasion, while silencing KU-60019 research buy its expression click here resulted in reduced migration and invasion. STIM1 overexpression was significantly associated

with advanced clinicalTNM stage and lymph node metastasis. Conclusion: These results suggest that STIM1 is a novel metastasis marker in CRC and might be a potential target for diagnosis and therapy. Key Word(s): 1. STIM1; 2. SOCE; 3. Colorector cancer; 4. Metastasis; Presenting Author: BANGMAO WANG Additional Authors: HAILONG CAO Corresponding Author: BANGMAO WANG Affiliations: General Hospital, Tianjin Medical University Objective: Berberine, an isoquinoline plant alkaloid, has shown antineoplastic effects on a variety of cancer cells in vitro. The aim of this study was to investigate chemopreventive effects of berberine on intestinal tumor development in APCmin/+ mice. Methods: Four-week old APCmin/+ mice were treated with 0.05% or 0.1% berberine in drinking water for twelve weeks. Parameters of intestinal tumor development, cell proliferation and apoptosis, and tumor promoting signaling pathways were determined. Results: The total number of the intestine tumor was decreased by

39.6% in 0.05% berberine treatment group 18.50 ± 1.51) and by 62.5% in 0.1% treatment group (11.50 ± 2.05) compared with untreated group (30.63 ± 1.69). All sizes of tumor (>2 mm, 1–2 mm, and <1 mm) were significantly reduced in both berberine treatment groups. medchemexpress In 0.1% berberine-treated group, tumors in proximal, middle, distal segments of small intestine were significantly reduced by 53.7%, 55.3%, and 76.5%, and the percentage of PCNA and Ki-67 positive cells were decreased by 32% and 55%, respectively, expression of cyclin Dl was also decreased, and apoptotic cell number was increased by 2.14 fold in the tumors. Gene microarray indicated different gene expression profiles, and Wnt and EGFR pathways may be involved. Furthermore, berberine treatment suppressed β-catenin and epidermal growth factor receptor activation, and down-regulated the expression of cyclooxygenase-2 and prostaglandin E2 production.

Disclosures: The following people have nothing to disclose: Abdelrahman Zekri, Hosny M. Salama, Abeer Bahnassy, Shereen M. Al Alim, Ola Ahmed, Mai Lotfy, Eman Medhat, Rasha Ahmed, Sherief Musa Mesenchymal stem cells (MSC) display a striking immunoregulatory property. This property has been used in several clinical settings; particularly, MSC infusion could resolve severe, acute graft-vs-host disease. Apoptosis Compound Library Most of the data

suggest that this property involves secretion of specific cytokines and mechanisms mediated by cell-cell contact. In addition, MSC are also likely to modulate the differentiation and function of dendritic cells (DC). However, the underlying mechanisms are still poorly understood. In this study, we found that human MSC from umbilical cord (huc-MSC) induced immature dendritic cells (iDC) to differentiate into

a novel tolerogenic DC subset (MSC-DC) with a stable phenotype and function when cocultured. MSC-DC display the low immunogenicity and immune tolerance by triggering a T helper type 2-polarizing program and down-regulating the pro-inflammatory factor production. Further study demonstrates that huc-MSC induce the tolerogenic MSC-DC generation through the IL-6/STAT3/SOCS1/TLR4 signaling network. Huc-MSC induced the higher expression of SOCS1 in MSC-DC, which were activated by secreting a larger number of IL-6 through the JAK-STAT pathway, repressing toll like receptor 4 (TLR4) Ku-0059436 purchase signaling pathway, and ultimately inducing the generation of novel tolerogenic dendritic cells. Moreover, Huc-MSC could increase phophorylation of Akt, but inhibit phophorylation of IRF3. We also observed that amount of microRNAs changed when cocultured. We found that miR-378 was an important factor in the generation of novel tolerogenic

dendritic cells by targeting STAM2. These results indicate that microRNAs could play essential roles in the production of the tolerogenic MSC-DC. Taken together, our data proposed a new 上海皓元医药股份有限公司 molecular mechanism of MSC in regulating tolerogenic DC production and promote the clinical application of MSC in new and broader immune applications, including treatment of allograft rejection and graft-vs-host disease in organ transplantation and autoimmune liver diseases. Disclosures: The following people have nothing to disclose: Guo-Ying Wang, Yi-nan Deng, Yong Zou, Minru Li, Qi Zhang, Gui-Hua Chen Bioengineering of a fully functional tissue reguires precise recapitulate normal tissue development. Specifically for the liver, one may use bipotent human liver progenitor cells (hFLCs) capable of differentiation into hepatocytes and cholangiocytes.

“
“Tibetiella pulchra Y. L. Li, D. M. Williams et Metzeltin is described from River Nujiang. Its main features are heteropolar valves, which are linear with capitate ends; narrow sternum, expanding at its center; 2–5 rimoportulae at each apex; uniseriate striae; two short projections arising on the surface above each apical pore plate; and an ocellulimbus, extending from the edge of the valve margin to the edge of the valve surface. Of these characters, it is defined by the 2–5 rimoportulae at each apex. T. pulchra PCI-32765 clinical trial was common to abundant on rocks in the samples examined herein. “
“Polyadenylation is best known for occurring to mRNA of eukaryotes transcribed

by RNA polymerase II to stabilize mRNA molecules and promote their translation. rRNAs transcribed by RNA polymerase I or III are typically believed not to be polyadenylated. However, there is increasing evidence that polyadenylation occurs to nucleus-encoded rRNAs as part of the RNA degradation pathway. To examine whether the same polyadenylation-assisted degradation pathway occurs in algae, we surveyed representative species of algae including diatoms, chlorophytes, dinoflagellates and pelagophytes using oligo (dT)-primed reversed transcription PCR (RT-PCR). In all the algal species examined, truncated 18S rRNA or its precursor molecules with homo- or hetero-polymeric poly(A) tails were detected. Mining existing algal expressed sequence tag (EST) data revealed

polyadenylated Acalabrutinib manufacturer truncated 18S rRNA in four additional phyla of algae. rRNA polyadenylation occurred at various internal positions along the 18S rRNA and its precursor sequences. Moreover, putative homologs of noncanonical poly(A) polymerase (ncPAP) Trf4p, which is responsible for polyadenylating nuclear-encoded RNA and targeting it for degradation, were detected from the genomes and transcriptomes

of five phyla of algae. Our results suggest that polyadenylation-assisted RNA degradation mechanism widely exists in algae, particularly for the nucleus-encoded rRNA and its precursors. “
“The subfamily Crucigenioideae was traditionally classified within the well-characterized family Scenedesmaceae (Chlorophyceae). Several morpho-logical revisions and questionable taxonomic changes hampered the correct classification of crucigenoid species resulting in a high number medchemexpress of synonymous genera. We used a molecular approach to determine the phylogenetic position of several Tetrastrum and Crucigenia species. The molecular results were correlated with morphological and ontogenetic characters. Phylogenetic analyses of the SSU rDNA gene resolved the position of Tetrastrum heteracanthum and T. staurogeniaeforme as a
age within the Oocystis clade of the Trebouxiophyceae. Crucigenia tetrapedia, T. triangulare, T. punctatum, and T. komarekii were shown to be closely related to Botryococcus (Trebouxiophyceae) and were transferred to Lemmer-mannia.