Systematics of the Platyrrhinus helleri species complex (Chiroptera: Phyllostomidae), with descriptions of two new species

Platyrrhinus is a diverse genus of small to large phyllostomid bats characterized by a comparatively narrow uropatagium thickly fringed with hair, a white dorsal stripe, comparatively large inner upper incisors that are convergent at the tips, and three upper and three lower molars. Eighteen species are currently recognized, the majority occurring in the Andes. Molecular, morphological, and morphometric analyses of specimens formerly identified as Platyrrhinus helleri support recognition of Platyrrhinus incarum as a separate species and reveal the presence of two species from western and northern South America that we describe herein as new ( Platyrrhinus angustirostris sp. nov. from eastern Colombia and Ecuador, north‐eastern Peru, and Venezuela and Platyrrhinus fusciventris sp. nov. from Guyana, Suriname, French Guiana, Trinidad and Tobago, northern Brazil, eastern Ecuador, and southern Venezuela). These two new species are sister taxa and, in turn, sister to Platyrrhinus incarum. © 2010 The Linnean Society of London, Zoological Journal of the Linnean Society, 2010, 159 , 785–812.     

Bargaining theory and cooperative fishing participation on ifaluk atoll

In this paper we examine the merit of bargaining theory, in its economic and ecological forms, as a model for understanding variation in the frequency of participation in cooperative fishing among men of Ifaluk atoll in Micronesia. Two determinants of bargaining power are considered: resource control and a bargainer’s utility gain for his expected share of the negotiated resource. Several hypotheses which relte cultural and life-course parameters to bargaining power are tested against data on the frequency of cooperative sail-fishing participation. Consistent with predictions generated from bargaining theory, we show that (1) age is negatively correlated with cooperative fishing participation, (2) men of highranking clans and men with high levels of education fish less than men of low-ranking clans and less-educated men, (3) men with high expected utility gains from fishing returns fish more than men with low expected utility gains, (4) number of dependents is positively correlated with cooperative fishing participation, and (5) the number of young genetic offspring residing with a man is positively correlated with cooperative fishing participation, whereas the number of genetic offspring more than 13 years old who are residing with a man is negatively correlated with cooperative fishing participation.     

Identification of a cytochrome P4502E1/Bid/C1q-dependent axis mediating inflammation in adipose tissue after chronic ethanol feeding to mice

Chronic, heavy alcohol exposure results in inflammation in adipose tissue, insulin resistance, and liver injury. Here we have identified a CYP2E1/Bid/C1q-dependent pathway that is activated in response to chronic ethanol and is required for the development of inflammation in adipose tissue. Ethanol feeding for 25 days to wild-type (C57BL/6J) mice increased expression of multiple markers of adipose tissue inflammation relative to pair-fed controls independent of increased body weight or adipocyte size. Ethanol feeding increased the expression of CYP2E1 in adipocytes, but not stromal vascular cells, in adipose tissue and Cyp2e1(-/-) mice were protected from adipose tissue inflammation in response to ethanol. Ethanol feeding also increased the number of TUNEL-positive nuclei in adipose tissue of wild-type mice but not in Cyp2e1(-/-) or Bid (-/-) mice. Apoptosis contributed to adipose inflammation, as the expression of multiple inflammatory markers was decreased in mice lacking the Bid-dependent apoptotic pathway. The complement protein C1q binds to apoptotic cells, facilitating their clearance and activating complement. Making use of C1q-deficient mice, we found that activation of complement via C1q provided the critical link between CYP2E1/Bid-dependent apoptosis and onset of adipose tissue inflammation in response to chronic ethanol. In summary, chronic ethanol increases CYP2E1 activity in adipose, leading to Bid-mediated apoptosis and activation of complement via C1q, finally resulting in adipose tissue inflammation. Taken together, these data identify a novel mechanism for the development of adipose tissue inflammation that likely contributes to the pathophysiological effects of ethanol.     

Effect of phytase supplementation on phosphorus digestibility in low-phytate barley fed to finishing pigs

Forty crossbred barrows (Camborough 15 Line female×Canabred sire) weighing an average of 79.6±8.0?kg were used in a factorial design experiment (5 barleys×2 enzyme levels) conducted to determine the effects of phytase supplementation on nutrient digestibility in low-phytate barleys fed to finishing pigs. The pigs were assigned to one of 10 dietary treatments comprised of a normal 2-rowed, hulled variety of barley (CDC Fleet, 0.26% phytate) or 2 low-phytate hulled genotypes designated as LP422 (0.14% phytate) and LP635 (0.09% phytate). A normal, hulless barley (CDC Dawn, 0.26% phytate) and a hulless genotype designated as LP422H (0.14% phytate) were also included. All barleys were fed with and without phytase (Natuphos 5000 FTU/kg). The diets fed contained 98% barley, 0.5% vitamin premix, 0.5% trace mineral premix, 0.5% NaCl and 0.5% chromic oxide but no supplemental phosphorus. The marked feed was provided for a 7-day acclimatization period, followed by a 3-day faecal collection. In the absence of phytase, phosphorus digestibility increased substantially (P<0.05) as the level of phytate in the barley declined. For the hulled varieties, phosphorus digestibility increased from 12.9% for the normal barley (0.26% phytate) to 35.3 and 39.8% for the two low-phytate genotypes (0.14 and 0.09% phytate respectively). For the hulless varieties, phosphorus digestibility increased from 9.2% for the normal barley (0.26% phytate) to 34.7% for the hulless variety with 54% of the normal level of phytate (0.14% phytate). In contrast, when phytase was added to the diet, there was little difference in phosphorus digestibility between pigs fed normal barley and those fed the low-phytate genotypes (significant barley×enzyme interaction, P=0.01). For the hulled varieties, phosphorus digestibility was 50.1% for the barley with the normal level of phytate (0.26% phytate) compared with 51.1 and 52.4% for the varieties with 54 and 35% of the normal level of phytate (0.14 and 0.09% phytate respectively). For the hulless varieties, phosphorus digestibility increased from 47.1% for the normal barley (0.26% phytate) to 54.4% for the hulless variety with 54% of the normal level of phytate (0.14% phytate). In conclusion, both supplementation with phytase and selection for low-phytate genotypes of barley were successful in increasing the digestibility of phosphorus for pigs. Unfortunately, the effects did not appear to be additive. Whether or not swine producers will choose low-phytate barley or supplementation with phytase as a means to improve phosphorus utilization, will likely depend on the yield potential of low-phytate barley and the additional costs associated with supplementation with phytase.     

Mice Lacking C1q Are Protected from High Fat Diet-induced Hepatic Insulin Resistance and Impaired Glucose Homeostasis

Complement activation is implicated in the development of obesity and insulin resistance, and loss of signaling by the anaphylatoxin C3a prevents obesity-induced insulin resistance in mice. Here we have identified C1q in the classical pathway as required for activation of complement in response to high fat diets. After 8 weeks of high fat diet, wild-type mice became obese and developed glucose intolerance. This was associated with increased apoptotic cell death and accumulation of complement activation products (C3b/iC3b/C3c) in liver and adipose tissue. Previous studies have shown that high fat diet-induced apoptosis is dependent on Bid; here we report that Bid-mediated apoptosis was required for complement activation in adipose and liver. Although C1qa deficiency had no effect on high fat diet-induced apoptosis, accumulation of complement activation products and the metabolic complications of high fat diet-induced obesity were dependent on C1q. When wild-type mice were fed a high fat diet for only 3 days, hepatic insulin resistance was associated with the accumulation of C3b/iC3b/C3c in the liver. Mice deficient in C3a receptor were protected against this early high fat diet-induced hepatic insulin resistance, whereas mice deficient in the negative complement regulator CD55/DAF were more sensitive to the high fat diet. C1qa^−/− mice were also protected from high fat diet-induced hepatic insulin resistance and complement activation. Evidence of complement activation was also detected in adipose tissue of obese women compared with lean women. Together, these studies reveal an important role for C1q in the classical pathway of complement activation in the development of high fat diet-induced insulin resistance.     

Synthesis and two-dimensional electrophoretic analysis of mixed populations of circular and linear RNAs.

Spontaneous cleavage of the less abundant form of tobacco ringspot virus satellite RNA is readily reversible. Capitalizing on earlier observations by Feldstein and Bruening that small 'mini-monomer' RNAs derived from this molecule and containing little more than covalently attached ribozyme and substrate cleavage products are able to efficiently circularize, we have constructed a series of self-circularizing RNAs of precisely known size. Mixtures of linear and circular RNAs synthesized in vitro and containing 225-1132 nt could be completely resolved using a novel two-dimensional denaturing polyacrylamide gel electrophoresis system. Similar analyses of a complex mixture of coconut cadang-cadang viroid RNAs revealed the presence of relatively large amounts of a previously undescribed 'fast-slow' heterodimeric RNA species in infected palms. Only a single DNA template is required to prepare each pair of circular and linear RNA markers.     

Hepatocyte-specific Bid depletion reduces tumor development by suppressing inflammation-related compensatory proliferation

Liver cancer is a major health-care concern and its oncogenic mechanisms are still largely unclear. Persistent hepatocyte cell death is a common feature among various chronic liver diseases, the blocking of which presents as logical treatment. Therefore, we aimed at investigating tumor development in mice with hepatocyte-specific Bid depletion – a BH3-only Bcl-2 family member that amplifies apoptotic death signals. Hepatocyte-specific conditional Bid-knockout mice (Bid^Δhep) were injected with 25 mg/kg diethylnitrosamine (DEN) at 14 days of age, and liver tumorigenesis was investigated 9 months later. Additionally, different models of acute liver injury were used including: acute high-dose DEN challenge, 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet and carbon tetrachloride (CCL4) injection. Bid^Δhep mice developed significantly fewer tumors, showed smaller maximal and average tumor size and reduced tumor incidence. In the acute DEN model, 48 h post injection we observed a significant reduction in liver injury in Bid^Δhep animals, assessed via serum transaminases and liver histopathology. Furthermore, TNF-α, IL-1ß, cJUN and IL-6 mRNA expression was reduced. These findings were accompanied by reduced compensatory hepatocyte proliferation in Bid^Δhep mice when compared with controls by immunohistochemistry for Ki67 and proliferating cell nuclear antigen 48 h after DEN injection. In the acute CCL4 model, Bid^Δhep mice displayed reductions in liver injury and inflammation when compared with controls. No differences in liver injury and serum bilirubin levels were detected in Bid^Δhep and Bid^flo/flo mice fed with DDC, which induces bile duct injury and a ductular reaction. Our study demonstrates that in DEN-induced hepatocellular carcinoma, the inhibition of hepatocyte death pathways through Bid deletion protects animals from tumorigenesis. These results suggest that reducing hepatocyte cell death, liver inflammation and compensatory proliferation has a stronger beneficial effect than the potential side effect of enhancing tumor cell survival.Liver cancer is a major health-care concern with diverse etiology. Viral hepatitis, alcoholic liver disease, carcinogen exposure and metabolic liver diseases are known major causes.¹ Recent studies indicate that the incidence of hepatocellular carcinoma (HCC) is rising in the westernized world. Since effective and established chemotherapeutic agents for HCC are currently unavailable and its recurrence rate is high, the overall prognosis of HCC remains poor. The development of HCC, accounting for ~75% of primary malignant liver tumors, has also been linked to chronic viral infections, alcoholic and non-alcoholic fatty liver disease, to exposure to toxic chemicals, such as polycystic aromatic hydrocarbons and nitrosamines, and is more frequently found in patients with preexisting liver cirrhosis and liver inflammation.^{2, 3} HCC that closely resembles the human disease can be induced in mice with a single postnatal injection of the tumor initiator diethylnitrosamine (DEN).⁴ Many investigators have employed DEN to induce liver tumors in mice by i.p. injecting 14-day-old pups, giving rise to HCC 8–9 months later.^{5, 6} In the DEN model, carcinogen-induced DNA damage promotes cell death, causing a Kupffer cell-mediated inflammatory response that further stimulates tumor development via hepatocyte compensatory proliferation.⁷Notably, hepatocyte cell death is a common, yet integral, feature in various chronic liver diseases that result in cirrhosis and hepatocarcinogenesis. Apoptotic cell death has evolved as a pivotal event in several liver diseases. In particular, mounting evidence supports a central role for this form of cell death in liver injury associated with non-alcoholic fatty liver disease (NAFLD), currently the most common form of chronic liver disease in both adults and children that has been linked to HCC development even in the absence of liver cirrhosis. NAFLD has been recognized, as one of the key drivers for the increase in the number of cases of HCC.^{8, 9} NAFLD, a spectrum of disorders related to the abnormal accumulation of fat in the liver, affects approximately 20–30% of the adult population in the United States and many other westernized countries and is closely associated with obesity, insulin resistance and type 2 diabetes.¹⁰ Growing epidemiological evidence link NAFLD to the increase in HCC rates. Moreover, several reports suggest that HCC may arise in histologically confirmed NAFLD without cirrhosis.^{11, 12, 13} Improving our understanding of the molecular mechanisms determining HCC development and progression, in particular in the context of NAFLD, is integral to the development of novel therapeutic strategies for this disease. Therefore, the blocking of hepatocyte death pathways, especially apoptotic cell death, presents itself as a logical treatment point of chronic liver disease and, concomitantly, as a preventive measure for liver cancer. However, it is not clear how a general suppression of cell death, especially apoptosis, would affect pre-neoplastic cells, with putative potential to enhance tumorigenesis.Bid is a BH3-only Bcl-2 family member that is cleaved by caspase-8 into its active form, tBID, which links the extrinsic and intrinsic apoptosis pathways. tBid formation is crucial for amplification of apoptotic death signals in cells like hepatocytes (called type 2 cells), where activation of the mitochondrial pathway is essential for cell death to occur. Bid, however, is dispensable for apoptosis in most other cell types (called type 1 cells). We recently demonstrated that hepatocyte-specific BID-deficient mice are resistant to the lethal effects of Fas activation in vivo.¹⁴ Here, we tested the hypothesis that selective ablation of Bid in hepatocytes modulates the development of liver tumors. Using the hepatocyte-specific Bid knockout mouse – Bid^Δhep – model, we show that the inhibition of hepatocyte apoptosis protects from tumorigenesis in two patho-physiologically relevant murine models of HCC. Our data suggest that reducing hepatocyte cell death, liver inflammation and compensatory proliferation has a pronounced beneficial effect vis-a-vis the potential side effect of enhancing tumor cell survival.