Omnivory by the Small Cosmopolitan Hydromedusa Aglaura Hemistoma

We investigated the feeding of the small hydromedusa, Aglaura hemistoma (bell diameter \u3c 4 mm), to determine if it occupies a trophic position similar to that of large medusae. Feeding was examined using gut-content analysis of preserved and unpreserved medusae and by analyzing prey-capture events using microvideographic techniques. Analysis of gut contents and prey-capture events revealed that A. hemistoma fed heavily on protistan prey and that it possessed a prey-capture mechanism, specifically a feeding current,that is effective at entraining and capturing protists with low motility. We suggest that many species of small hydromedusae possess prey-capture mechanisms adapted to capture small protistan prey and that many of these small hydromedusae feed omnivorously on microplanktonic prey. The trophic roles of small hydromedusae in different systems are not understood and more studies are needed. However, based on their often high abundances and the cosmopolitan nature, if small hydromedusae are primarily omnivores, they need to be considered when estimating the impact of zooplankton on primary production and, more generally, protistan community dynamics

Peierls transition in the quantum spin-Peierls model

We use the density matrix renormalization group method to investigate the role of longitudinal quantized phonons on the Peierls transition in the spin-Peierls model. For both the XY and Heisenberg spin-Peierls model we show that the staggered phonon order parameter scales as $\sqrt{\lambda}$ (and the dimerized bond order scales as $\lambda$) as $\lambda \to 0$ (where $\lambda$ is the electron-phonon interaction). This result is true for both linear and cyclic chains. Thus, we conclude that the Peierls transition occurs at $\lambda=0$ in these models. Moreover, for the XY spin-Peierls model we show that the quantum predictions for the bond order follow the classical prediction as a function of inverse chain size for small $\lambda$. We therefore conclude that the zero $\lambda$ phase transition is of the mean-field type

1862-07-12 Sergeant William H. Higgins of Company D requests a promotion

https://digitalmaine.com/cw_me_3rd_regiment_corr/1302/thumbnail.jp

1865-07-29 William H. Higgins inquires about deserters

https://digitalmaine.com/cw_me_3rd_regiment_corr/1601/thumbnail.jp

1861-07-10 William H. Higgins requests a Navy revolver from the Arsenal as a present from the Governor

https://digitalmaine.com/cw_me_3rd_regiment_corr/1073/thumbnail.jp

Resistant starch consumption promotes lipid oxidation

BACKGROUND: Although the effects of resistant starch (RS) on postprandial glycemia and insulinemia have been extensively studied, little is known about the impact of RS on fat metabolism. This study examines the relationship between the RS content of a meal and postprandial/post-absorbative fat oxidation. RESULTS: 12 subjects consumed meals containing 0%, 2.7%, 5.4%, and 10.7% RS (as a percentage of total carbohydrate). Blood samples were taken and analyzed for glucose, insulin, triacylglycerol (TAG) and free fatty acid (FFA) concentrations. Respiratory quotient was measured hourly. The 0%, 5.4%, and 10.7% meals contained 50 μCi [1-(14)C]-triolein with breath samples collected hourly following the meal, and gluteal fat biopsies obtained at 0 and 24 h. RS, regardless of dose, had no effect on fasting or postprandial insulin, glucose, FFA or TAG concentration, nor on meal fat storage. However, data from indirect calorimetry and oxidation of [1-(14)C]-triolein to (14)CO(2 )showed that addition of 5.4% RS to the diet significantly increased fat oxidation. In fact, postprandial oxidation of [1-(14)C]-triolein was 23% greater with the 5.4% RS meal than the 0% meal (p = 0.0062). CONCLUSIONS: These data indicate that replacement of 5.4% of total dietary carbohydrate with RS significantly increased post-prandial lipid oxidation and therefore could decrease fat accumulation in the long-term

The TgsGP gene is essential for resistance to human serum in Trypanosoma brucei gambiense

Trypanosoma brucei gambiense causes 97% of all cases of African sleeping sickness, a fatal disease of sub-Saharan Africa. Most species of trypanosome, such as T. b. brucei, are unable to infect humans due to the trypanolytic serum protein apolipoprotein-L1 (APOL1) delivered via two trypanosome lytic factors (TLF-1 and TLF-2). Understanding how T. b. gambiense overcomes these factors and infects humans is of major importance in the fight against this disease. Previous work indicated that a failure to take up TLF-1 in T. b. gambiense contributes to resistance to TLF-1, although another mechanism is required to overcome TLF-2. Here, we have examined a T. b. gambiense specific gene, TgsGP, which had previously been suggested, but not shown, to be involved in serum resistance. We show that TgsGP is essential for resistance to lysis as deletion of TgsGP in T. b. gambiense renders the parasites sensitive to human serum and recombinant APOL1. Deletion of TgsGP in T. b. gambiense modified to uptake TLF-1 showed sensitivity to TLF-1, APOL1 and human serum. Reintroducing TgsGP into knockout parasite lines restored resistance. We conclude that TgsGP is essential for human serum resistance in T. b. gambiense