The cause of PGCH is unknown and probably multifactorial; possibilities include a virus,8,

9 drugs and herbal remedies,10 and autoimmune changes.11, 12 In addition, reports have been published about patients who have undergone liver transplantation.13, 14 Our patient received Pil-Food. Severe changes in liver function tests occurred, she was positive for antinuclear antibody autoreactivity, and a histological examination found abundant see more areas of multinucleate giant cells with marked periportal and parenchymal hepatocellular necrosis and inflammation. Because all the aforementioned alterations appeared during the long-term ingestion of Pil-Food [a composition developed by Synthelabo that contains D,L-methionine, IDH inhibitor cancer L-(+)-cysteine hydrochloride, L-cysteine, enzymes and animal protein hydrolysates, millet extract, calcium pantothenate, vitamin B2 phosphate, vitamin B6, biotin (vitamin H), and vitamin E] and a successful corticosteroid response was attained, we speculate that this hepatic autoreactivity could be related to the Pil-Food treatment.15, 16 Moreover, just like patients with drug-induced AIH,1 our patient did not require long-term immunosuppressive therapy. We believe that this case highlights (1) that the breakdown of immune tolerance by drugs is able to trigger liver autoreactivity and (2) that some cases of PGCH may present a rapid and effective response

to corticosteroid therapy instead of a fulminant or progressive course. Ricardo Moreno-Otero M.D.* ‡, Maria Trapero Marugán M.D.* ‡, Luisa García-Buey M.D.* ‡, Asunción García-Sancchez selleck chemical M.D.†, * Digestive Diseases Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain, † Pathology Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid,

Madrid, Spain, ‡ Centro de Investigación Biomédica en Red, Instituto de Salud Carlos III, Madrid, Spain. “
“A 53 year-old man presented with a 5-month history of severe diarrhoea and abdominal cramping immediately occurring after tube feeding. The Percutaneous Endoscopic Gastrostomy (PEG) tube was inserted 2 years previously, for enteral feeding, following diagnosis of an oropharyngeal carcinoma. The patient had no signs or symptoms of peritonitis. The skin surrounding the tube was inflamed with brown odorous fluid exuding. Upon checking the tube position using upper endoscopy no inner bumper was seen within the stomach. A fistulogram through the feeding tube revealed typical haustration of the colon rather than expected gastric appearances (Figure 1A). CT confirmed misplacement, localizing the position of the bumper in the transverse colon (Figure 1B, arrow). A gastrocolic fistula could not be visualized. Colonoscopy showed the inner bumper located near the splenic flexure (Figure 2A).

The cause of PGCH is unknown and probably multifactorial; possibilities include a virus,8,

9 drugs and herbal remedies,10 and autoimmune changes.11, 12 In addition, reports have been published about patients who have undergone liver transplantation.13, 14 Our patient received Pil-Food. Severe changes in liver function tests occurred, she was positive for antinuclear antibody autoreactivity, and a histological examination found abundant Alectinib datasheet areas of multinucleate giant cells with marked periportal and parenchymal hepatocellular necrosis and inflammation. Because all the aforementioned alterations appeared during the long-term ingestion of Pil-Food [a composition developed by Synthelabo that contains D,L-methionine, BIBW2992 manufacturer L-(+)-cysteine hydrochloride, L-cysteine, enzymes and animal protein hydrolysates, millet extract, calcium pantothenate, vitamin B2 phosphate, vitamin B6, biotin (vitamin H), and vitamin E] and a successful corticosteroid response was attained, we speculate that this hepatic autoreactivity could be related to the Pil-Food treatment.15, 16 Moreover, just like patients with drug-induced AIH,1 our patient did not require long-term immunosuppressive therapy. We believe that this case highlights (1) that the breakdown of immune tolerance by drugs is able to trigger liver autoreactivity and (2) that some cases of PGCH may present a rapid and effective response

to corticosteroid therapy instead of a fulminant or progressive course. Ricardo Moreno-Otero M.D.* ‡, Maria Trapero Marugán M.D.* ‡, Luisa García-Buey M.D.* ‡, Asunción García-Sancchez selleck compound M.D.†, * Digestive Diseases Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain, † Pathology Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid,

Madrid, Spain, ‡ Centro de Investigación Biomédica en Red, Instituto de Salud Carlos III, Madrid, Spain. “
“A 53 year-old man presented with a 5-month history of severe diarrhoea and abdominal cramping immediately occurring after tube feeding. The Percutaneous Endoscopic Gastrostomy (PEG) tube was inserted 2 years previously, for enteral feeding, following diagnosis of an oropharyngeal carcinoma. The patient had no signs or symptoms of peritonitis. The skin surrounding the tube was inflamed with brown odorous fluid exuding. Upon checking the tube position using upper endoscopy no inner bumper was seen within the stomach. A fistulogram through the feeding tube revealed typical haustration of the colon rather than expected gastric appearances (Figure 1A). CT confirmed misplacement, localizing the position of the bumper in the transverse colon (Figure 1B, arrow). A gastrocolic fistula could not be visualized. Colonoscopy showed the inner bumper located near the splenic flexure (Figure 2A).

Additional Supporting Information may be found in the online version of this article. “
“Refractory hepatic encephalopathy (HE) remains a major cause of morbidity in cirrhosis patients. Large spontaneous portosystemic shunts (SPSSs) have been previously suggested to sustain HE in these patients. We aimed to retrospectively

assess the efficacy and safety of patients treated with embolization of large SPSSs for the treatment of chronic therapy-refractory HE in a European multicentric working group and to identify patients who may benefit from this procedure. Between July 1998 and January 2012, 37 patients (Child A6-C13, MELD [Model of Endstage Liver Disease] 5-28) with refractory HE were diagnosed with single large SPSSs that were considered eligible for embolization. On a

BGB324 cell line short-term basis (i.e., within 100 days after embolization), 22 out of 37 patients (59.4%) were free of HE (P < 0.001 versus before embolization) of which 18 (48.6% of patients overall) remained HE-free over a mean follow-up period of 697 ± 157 days (P < 0.001 versus before embolization). Overall, we noted improved autonomy, decreased number of hospitalizations, and severity of the worst HE episode after embolization in three-quarters of the patients. Logistic regression identified the MELD score as strongest positive predictive factor of HE recurrence with a cutoff of 11 for patient selection. As to safety, we noted one major nonlethal procedure-related complication. There was no significant increase in selleck chemicals llc de novo development or aggravation of preexisting varices, portal hypertensive gastropathy, or ascites. Conclusion: This multicenter European cohort study demonstrated a role for large SPSSs in chronic protracted or recurrent HE learn more and substantiated

the effectiveness and safety of embolization of these shunts, provided there is sufficient functional liver reserve. (HEPATOLOGY 2013;57:2448–2457) Hepatic encephalopathy (HE) is a major complication of cirrhosis and refers to potentially reversible alterations in autonomy, consciousness, behavior, and psychomotor functions related to an accumulation of toxins due to hepatocellular dysfunction and portosystemic shunting.1-5 While in some patients HE is initiated abruptly by a precipitating event such as infection or gastrointestinal bleeding (the so-called episodic HE), other patients have persistent HE characterized by continuous high levels of ammonia, chronic electrophysiological abnormalities, and recurrent or persistent incapacitating alterations in mental status, often without evident precipitating events.1, 3, 4 In this latter group, medical treatment is usually unsatisfactory, with subsequent need of frequent hospitalization.1, 6 This impacts not only the quality of life of these patients but also puts a weight on health economics due to significant resource use.

Additional Supporting Information may be found in the online version of this article. “
“Refractory hepatic encephalopathy (HE) remains a major cause of morbidity in cirrhosis patients. Large spontaneous portosystemic shunts (SPSSs) have been previously suggested to sustain HE in these patients. We aimed to retrospectively

assess the efficacy and safety of patients treated with embolization of large SPSSs for the treatment of chronic therapy-refractory HE in a European multicentric working group and to identify patients who may benefit from this procedure. Between July 1998 and January 2012, 37 patients (Child A6-C13, MELD [Model of Endstage Liver Disease] 5-28) with refractory HE were diagnosed with single large SPSSs that were considered eligible for embolization. On a

see more short-term basis (i.e., within 100 days after embolization), 22 out of 37 patients (59.4%) were free of HE (P < 0.001 versus before embolization) of which 18 (48.6% of patients overall) remained HE-free over a mean follow-up period of 697 ± 157 days (P < 0.001 versus before embolization). Overall, we noted improved autonomy, decreased number of hospitalizations, and severity of the worst HE episode after embolization in three-quarters of the patients. Logistic regression identified the MELD score as strongest positive predictive factor of HE recurrence with a cutoff of 11 for patient selection. As to safety, we noted one major nonlethal procedure-related complication. There was no significant increase in click here de novo development or aggravation of preexisting varices, portal hypertensive gastropathy, or ascites. Conclusion: This multicenter European cohort study demonstrated a role for large SPSSs in chronic protracted or recurrent HE learn more and substantiated

the effectiveness and safety of embolization of these shunts, provided there is sufficient functional liver reserve. (HEPATOLOGY 2013;57:2448–2457) Hepatic encephalopathy (HE) is a major complication of cirrhosis and refers to potentially reversible alterations in autonomy, consciousness, behavior, and psychomotor functions related to an accumulation of toxins due to hepatocellular dysfunction and portosystemic shunting.1-5 While in some patients HE is initiated abruptly by a precipitating event such as infection or gastrointestinal bleeding (the so-called episodic HE), other patients have persistent HE characterized by continuous high levels of ammonia, chronic electrophysiological abnormalities, and recurrent or persistent incapacitating alterations in mental status, often without evident precipitating events.1, 3, 4 In this latter group, medical treatment is usually unsatisfactory, with subsequent need of frequent hospitalization.1, 6 This impacts not only the quality of life of these patients but also puts a weight on health economics due to significant resource use.

Our study provides novel lines of evidence that parenchymal cells are the main producers of Type I IFNs in response to alcohol/LPS exposure, and that IRF3 is a dominant signaling

molecule inducing Type I IFN in alcoholic liver disease. First, chimeric mice containing IRF3-deficient liver parenchymal cells and WT BM-derived cells show a similar reduction selleck chemicals llc in baseline and ethanol-induced expression of Type I IFNs as mice with global IRF3 deficiency. Second, no decrease in liver expression of Type I IFNs was observed in mice with selective deficiency of IRF3 in BM-derived cells. Third, ex vivo stimulation of WT primary mouse hepatocyte isolates with LPS resulted in phosphorylation of IRF3 and in a significant up-regulation of Type I IFNs, in contrast to hepatocyte isolates from IRF3KO mice that failed to induce Type I IFNs. In addition, phenotypic analysis of hepatocyte isolates employed in our study indicated that the IRF3-dependent Type I IFN induction indeed originates from hepatocytes, PLX4032 mouse whereas the role of other cell types remains negligible. Our study defines induction of

Type I IFNs by way of IRF3 in hepatocytes and down-regulation of inflammatory cytokines in BM-derived cells as two complementary, yet independent mechanisms by which TLR4 controls the extent of alcohol-induced liver inflammation and injury. Kupffer cells stimulated by way of TLR4 are a main source of inflammatory cytokines in the liver and promote tissue inflammation, injury, and fibrosis.22 Thus, TLR4 seems to activate IRF3 in both parenchymal and nonparenchymal liver cells: here we demonstrate that, whereas the signaling pathways are shared, we observed a cell-specific response to LPS, with a distinct outcome. find more Studies by Zhao et al.21 suggested that IRF3, activated by TLR4/TRIF and ethanol, induces inflammatory cytokines in macrophages, thereby playing a proinflammatory role. We observed no induction of inflammatory cytokines in mice with BM-specific deficiency of IRF3; however, our novel data show that this effect was not sufficient to prevent alcohol-induced liver injury. These findings suggest that both myeloid and parenchymal

cell-specific IRF3 contribute to ALD, i.e., that the solo contribution IRF3 in BM-derived cells is not sufficient for the development of ALD. The type of signal in IRF3 deficient BM-derived cells that improves ALD in the global IRF3 knockouts, and the reason why this signal requires the absence of IRF3 in parenchymal cells remains to be further investigated. Recently, Klein et al.23 and Kennedy and Abkowitz24 reported that in chimeric mice two populations of liver macrophages coexist: radioresistant macrophages that show tolerogenic properties, and radiosensitive macrophages that are immunogenic; the latter macrophages are rapidly replaced by BM transplantation and expected to be the dominant subtype that participates in the immunoinflammatory reactions in the liver posttransplant.

Our study provides novel lines of evidence that parenchymal cells are the main producers of Type I IFNs in response to alcohol/LPS exposure, and that IRF3 is a dominant signaling

molecule inducing Type I IFN in alcoholic liver disease. First, chimeric mice containing IRF3-deficient liver parenchymal cells and WT BM-derived cells show a similar reduction Selleck EPZ-6438 in baseline and ethanol-induced expression of Type I IFNs as mice with global IRF3 deficiency. Second, no decrease in liver expression of Type I IFNs was observed in mice with selective deficiency of IRF3 in BM-derived cells. Third, ex vivo stimulation of WT primary mouse hepatocyte isolates with LPS resulted in phosphorylation of IRF3 and in a significant up-regulation of Type I IFNs, in contrast to hepatocyte isolates from IRF3KO mice that failed to induce Type I IFNs. In addition, phenotypic analysis of hepatocyte isolates employed in our study indicated that the IRF3-dependent Type I IFN induction indeed originates from hepatocytes, AG-014699 supplier whereas the role of other cell types remains negligible. Our study defines induction of

Type I IFNs by way of IRF3 in hepatocytes and down-regulation of inflammatory cytokines in BM-derived cells as two complementary, yet independent mechanisms by which TLR4 controls the extent of alcohol-induced liver inflammation and injury. Kupffer cells stimulated by way of TLR4 are a main source of inflammatory cytokines in the liver and promote tissue inflammation, injury, and fibrosis.22 Thus, TLR4 seems to activate IRF3 in both parenchymal and nonparenchymal liver cells: here we demonstrate that, whereas the signaling pathways are shared, we observed a cell-specific response to LPS, with a distinct outcome. see more Studies by Zhao et al.21 suggested that IRF3, activated by TLR4/TRIF and ethanol, induces inflammatory cytokines in macrophages, thereby playing a proinflammatory role. We observed no induction of inflammatory cytokines in mice with BM-specific deficiency of IRF3; however, our novel data show that this effect was not sufficient to prevent alcohol-induced liver injury. These findings suggest that both myeloid and parenchymal

cell-specific IRF3 contribute to ALD, i.e., that the solo contribution IRF3 in BM-derived cells is not sufficient for the development of ALD. The type of signal in IRF3 deficient BM-derived cells that improves ALD in the global IRF3 knockouts, and the reason why this signal requires the absence of IRF3 in parenchymal cells remains to be further investigated. Recently, Klein et al.23 and Kennedy and Abkowitz24 reported that in chimeric mice two populations of liver macrophages coexist: radioresistant macrophages that show tolerogenic properties, and radiosensitive macrophages that are immunogenic; the latter macrophages are rapidly replaced by BM transplantation and expected to be the dominant subtype that participates in the immunoinflammatory reactions in the liver posttransplant.

Communal nursing is unlikely, however, because unweaned ice rats nipple cling to the mother only (Willan, 1990). Ice rats occupy underground burrows and accrue the benefits of huddling (Hinze & Pillay, 2006), as occurs in alpine marmots Marmota marmota (Arnold, 1988). Therefore, group living in ice rats, as for many other small mammals (Canals et al., 1998), could be explained by the social thermoregulation hypothesis; huddling occurs belowground even in summer when burrow

temperatures regularly drop to 0°C at night (Hinze et al., 2006). Another benefit is the reduced per capita cost of burrow construction (i.e. the burrow-sharing hypothesis) because the construction and maintenance of the burrow system involve the collective efforts of all colony members (Hinze et al., 2006). We tested two other hypotheses, resource dispersion, as seen in Blanford’s fox Vulpes cana (Geffen et al., 1992), and food competition, as seen in the striped field mouse Apodemus agrarius (Gliwicz, selleck chemicals llc 1981), which could also explain group living in ice rats. Despite mutual avoidance aboveground, colony members overlapped spatially, indicating that they forage

in the same areas but at different times. This is a key assumption of the resource dispersion hypothesis. The patchiness of food resources in the alpine environment of the Maluti mountains indicates high environmental heterogeneity, and utilizing the same resources at different times possibly reduces direct competition Venetoclax order (Carr & MacDonald, 1986), although we cannot rule out the possibility of exploitation competition as we did not measure fitness of individuals. Spatial overlap with minimal temporal overlap resembles temporal territoriality (Leyhausen, 1965). Temporal avoidance may be phylogenetically constrained in ice rats because temporal territoriality occurs

click here in the related vlei rat (Davis, 1972). Members of an ice rat colony competed aggressively for a prized food (apple) in winter. Mutual avoidance and/or aggression may be related to defence of limited resources (Ostfeld, 1990). Despite having a wide diet of green food plants, ice rats feed selectively from particular food patches, preferring wetland sedges (Schwaibold & Pillay, 2010); such selectivity may drive competition to forage alone. Ice rats also displayed mutual avoidance in summer, almost never occurring within 4 m of one another. The alpine environment is characterized by short growing seasons (Schwaibold & Pillay, 2010) and ice rats possibly defend food patches to obtain sufficient energy to meet reproductive demands (Schwaibold & Pillay, 2003). Therefore, like other larger mammals (e.g. Ethiopian wolves Canis simensis; Sillero-Zubiri et al., 2004), the food competition hypothesis is likely to be a driver of solitary foraging in ice rats. The main functional consequences of group living in mammals involve reducing predation risk (Schradin, 2004), acquiring and defending resources and enhancing reproductive success (Silk, 2007).

Communal nursing is unlikely, however, because unweaned ice rats nipple cling to the mother only (Willan, 1990). Ice rats occupy underground burrows and accrue the benefits of huddling (Hinze & Pillay, 2006), as occurs in alpine marmots Marmota marmota (Arnold, 1988). Therefore, group living in ice rats, as for many other small mammals (Canals et al., 1998), could be explained by the social thermoregulation hypothesis; huddling occurs belowground even in summer when burrow

temperatures regularly drop to 0°C at night (Hinze et al., 2006). Another benefit is the reduced per capita cost of burrow construction (i.e. the burrow-sharing hypothesis) because the construction and maintenance of the burrow system involve the collective efforts of all colony members (Hinze et al., 2006). We tested two other hypotheses, resource dispersion, as seen in Blanford’s fox Vulpes cana (Geffen et al., 1992), and food competition, as seen in the striped field mouse Apodemus agrarius (Gliwicz, Metformin mouse 1981), which could also explain group living in ice rats. Despite mutual avoidance aboveground, colony members overlapped spatially, indicating that they forage

in the same areas but at different times. This is a key assumption of the resource dispersion hypothesis. The patchiness of food resources in the alpine environment of the Maluti mountains indicates high environmental heterogeneity, and utilizing the same resources at different times possibly reduces direct competition Napabucasin mouse (Carr & MacDonald, 1986), although we cannot rule out the possibility of exploitation competition as we did not measure fitness of individuals. Spatial overlap with minimal temporal overlap resembles temporal territoriality (Leyhausen, 1965). Temporal avoidance may be phylogenetically constrained in ice rats because temporal territoriality occurs

learn more in the related vlei rat (Davis, 1972). Members of an ice rat colony competed aggressively for a prized food (apple) in winter. Mutual avoidance and/or aggression may be related to defence of limited resources (Ostfeld, 1990). Despite having a wide diet of green food plants, ice rats feed selectively from particular food patches, preferring wetland sedges (Schwaibold & Pillay, 2010); such selectivity may drive competition to forage alone. Ice rats also displayed mutual avoidance in summer, almost never occurring within 4 m of one another. The alpine environment is characterized by short growing seasons (Schwaibold & Pillay, 2010) and ice rats possibly defend food patches to obtain sufficient energy to meet reproductive demands (Schwaibold & Pillay, 2003). Therefore, like other larger mammals (e.g. Ethiopian wolves Canis simensis; Sillero-Zubiri et al., 2004), the food competition hypothesis is likely to be a driver of solitary foraging in ice rats. The main functional consequences of group living in mammals involve reducing predation risk (Schradin, 2004), acquiring and defending resources and enhancing reproductive success (Silk, 2007).

g., Fuscifolium S.C. Lindstrom, Lysithea W.A. Nelson, Minerva W.A. Nelson) were distinguished from related genera strictly by molecular sequence differences. Interestingly, when discussing the newly reinstated Pyropia J. Agardh, Sutherland et al. (2011) demonstrated that it contained a number of clades

that “would require the recognition of at least an additional eight genera.” They declined to create those taxa in their paper, writing that these should be clarified by additional data sets and analyses. Using rbcL sequence data, Arakaki et al. (2011) took a broad look at Pacific-American species of Callophyllis, and found significant intrageneric genetic variation. These workers, however, did not divide the genus despite genetic data that would have warranted it. Another paper in which the genus Laurenciella Cassano, Gil-Rodríguez, Sentíes, Díaz-Larrea, M.C. selleck chemicals llc Oliveira et M.T. Fujii was erected solely on the basis of molecular differences, was recently published by Cassano et al. (2012) as a segregate genus in the Laurencia complex. While Sutherland et al. (2011) and Cassano et al. (2012) created “molecular” genera without unique morphological characteristics, others have used molecular evidence to reassess existing genera

lacking distinct morphological markers from closely related genera. Sheng et al. (2012) relegated the recently described genus Sinotubimorpha Selleckchem BGB324 Li and Ding (1998) to Grateloupia C. Agardh after finding them impossible to distinguish morphologically. Sinotubimorpha formed a monophyletic subclade within the larger Grateloupia

clade of the Halymeniales (Sheng et al. 2012). It remains to be seen whether their results will stand as Wynne (2005) (note 248) pointed out that Sinotubimorpha was typified by a West Indian species and the molecular results of the study were based upon Asian material. Earlier, Faye et al. (2004) subsumed Meristiella D.P. Cheney in Meristotheca J. Agardh based upon inconsistent anatomical and reproductive characteristics within the monophyletic rbcL learn more clade including species of both genera. We have struggled with this same issue in the current paper and reason that a default to the established norms of alpha taxonomy should be followed to render this decision. Do we have two monophyletic clusters differing in morphological attributes consistent with other generic level distinctions in this family? In establishing Psaromenia, D’Archino et al. (2010) used morphology and geographic distribution to differentiate their new genus from Meredithia. Prior to our present report, Meredithia was restricted to the Northeast Atlantic and Mediterranean, while Psaromenia was endemic to New Zealand. Now, with the numerous species found in Bermuda, Western Australia, Tasmania, Lord Howe Is., and Norfolk Is. (Table 1; Figs.

g., Fuscifolium S.C. Lindstrom, Lysithea W.A. Nelson, Minerva W.A. Nelson) were distinguished from related genera strictly by molecular sequence differences. Interestingly, when discussing the newly reinstated Pyropia J. Agardh, Sutherland et al. (2011) demonstrated that it contained a number of clades

that “would require the recognition of at least an additional eight genera.” They declined to create those taxa in their paper, writing that these should be clarified by additional data sets and analyses. Using rbcL sequence data, Arakaki et al. (2011) took a broad look at Pacific-American species of Callophyllis, and found significant intrageneric genetic variation. These workers, however, did not divide the genus despite genetic data that would have warranted it. Another paper in which the genus Laurenciella Cassano, Gil-Rodríguez, Sentíes, Díaz-Larrea, M.C. PLX4032 order Oliveira et M.T. Fujii was erected solely on the basis of molecular differences, was recently published by Cassano et al. (2012) as a segregate genus in the Laurencia complex. While Sutherland et al. (2011) and Cassano et al. (2012) created “molecular” genera without unique morphological characteristics, others have used molecular evidence to reassess existing genera

lacking distinct morphological markers from closely related genera. Sheng et al. (2012) relegated the recently described genus Sinotubimorpha Z-VAD-FMK chemical structure Li and Ding (1998) to Grateloupia C. Agardh after finding them impossible to distinguish morphologically. Sinotubimorpha formed a monophyletic subclade within the larger Grateloupia

clade of the Halymeniales (Sheng et al. 2012). It remains to be seen whether their results will stand as Wynne (2005) (note 248) pointed out that Sinotubimorpha was typified by a West Indian species and the molecular results of the study were based upon Asian material. Earlier, Faye et al. (2004) subsumed Meristiella D.P. Cheney in Meristotheca J. Agardh based upon inconsistent anatomical and reproductive characteristics within the monophyletic rbcL click here clade including species of both genera. We have struggled with this same issue in the current paper and reason that a default to the established norms of alpha taxonomy should be followed to render this decision. Do we have two monophyletic clusters differing in morphological attributes consistent with other generic level distinctions in this family? In establishing Psaromenia, D’Archino et al. (2010) used morphology and geographic distribution to differentiate their new genus from Meredithia. Prior to our present report, Meredithia was restricted to the Northeast Atlantic and Mediterranean, while Psaromenia was endemic to New Zealand. Now, with the numerous species found in Bermuda, Western Australia, Tasmania, Lord Howe Is., and Norfolk Is. (Table 1; Figs.