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To estimate fermentative capacity among lemur species, four fiber substrates were tested across three species, Eulemur fulvus, Hapalemur griseus and Varecia variegata. The substrates, cellulose, beet pulp, citrus pulp and citrus pectin, ranged in composition from completely insoluble fiber (IF) to completely soluble fiber (SF), respectively. The lemurs consumed a nutritionally complete biscuit formulated for primates [85 g/100 g diet dry matter (DM)] and locally available produce (15 g/100 g diet DM). Feces were then collected and used to inoculate fermentation tubes prefilled with fiber substrates and an anaerobic growth medium. Dry matter disappearance (DMD), and acetate, propionate, butyrate, and total short-chain fatty acid (SCFA) production were measured in tubes subjected to 6, 12, 24 or 48 h of fermentation. Results were fitted to a logistic growth model. The maximal production (MP) time at which production or disappearance is at one-half maximum (t(50)) and the fermentation rate at 3 h were calculated. The maximal disappearance of DM differed among substrates (citrus pectin > citrus pulp > beet pulp; P < 0.0001) and species (E. fulvus > H. griseus > V. variegata; P < 0.001). V. variegata reached t(50) for acetate and total SCFA production faster than H. griseus or E. fulvus (P < 0.02). Three-hour production rates of acetate and total SCFA were also greater for V. variegata for citrus pulp and citrus pectin (P < 0.01). Few species differences were observed for beet pulp. Results provide evidence for differences in fermentative capacity and suggest that fiber solubility and fermentability should be considered when assessing the nutritional management of lemurs. [ABSTRACT FROM AUTHOR]

Our objective was to determine whether the beta-adrenergic agonist ractopamine altered sensitivity or responsiveness to insulin. We used the hyperinsulinemic, euglycemic clamp approach in five multicatheterized beef steers to evaluate insulin sensitivity (ED50) and responsiveness (Rmax or Rmin) during control or ractopamine feeding (80 mg/kg feed). Steers had blood vessel catheters and ultrasound flow probes that allowed measurement of net uptake and release of glucose and insulin by portal-drained viscera (PDV), liver and hindlimb. Steers ate meals of equal size every 2 h. Steers were fed at 1.8 times calculated maintenance energy. The design was a single reversal. Two rates of insulin infusion followed a base-line period on each of three sample days. Insulin was infused into a mesenteric vein at 10, 20, 40, 80, 160 and 320 mU/(h.kg body weight). During the base-line period, arterial concentrations of glucose, oxygen, nonesterified fatty acids and insulin were not different between control and ractopamine feeding. Arterial urea was lower during ractopamine than during control feeding (5.02 vs. 6.20 mmol/L, respectively, P < 0.01). Net release of glucose by liver and net uptake of glucose by the hindlimb were not affected by treatment. Similarly, net release of insulin by PDV and net uptake of insulin by liver were not affected by treatment. The Rmax and ED50 for steady-state glucose infusion rate, total glucose entry, hepatic glucose production and hindlimb glucose uptake did not differ between treatments. There was a trend for a lower ED50 in hindlimb with ractopamine treatment (P < 0.13). These data do not support a change in sensitivity or responsiveness of tissues to insulin as a major component of the mechanism of action of ractopamine. [ABSTRACT FROM AUTHOR]

We report a case of an immunosuppressed 67-year-old woman who presented with fever of unknown origin. Further investigation revealed multiple left renal and perinephric abscesses. These were managed with percutaneous drainage and broad-spectrum antibiotics; however, no clinical improvement resulted. No organism was identifiable on standard microscopy and culture of all drain, blood and urine samples taken. Left nephrectomy with right urinary diversion was performed for sepsis management and to protect the patient's right kidney. Eventually, Ureaplasma species' RNA was detected in the patient's drain fluid using PCR and 16S ribosomal RNA gene sequencing. The patient was treated successfully with targeted antibiotic therapy and underwent extensive rehabilitation following this. Histopathology of the nephrectomy specimen suggested xanthogranulomatous pyelonephritis., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: The lectin DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) augments Ebola virus (EBOV) infection. However, it its unclear whether DC-SIGN promotes only EBOV attachment (attachment factor function, nonessential) or actively facilitates EBOV entry (receptor function, essential)., Methods: We investigated whether DC-SIGN on B cell lines and dendritic cells acts as an EBOV attachment factor or receptor., Results: Engineered DC-SIGN expression rendered some B cell lines susceptible to EBOV glycoprotein (EBOV GP)-driven infection, whereas others remained refractory, suggesting that cellular factors other than DC-SIGN are also required for susceptibility to EBOV infection. Augmentation of entry was independent of efficient DC-SIGN internalization and might not involve lectin-mediated endocytic uptake of virions. Therefore, DC-SIGN is unlikely to function as an EBOV receptor on B cell lines; instead, it might concentrate virions onto cells, thereby allowing entry into cell lines expressing low levels of endogenous receptor(s). Indeed, artificial concentration of virions onto cells mirrored DC-SIGN expression, confirming that optimization of viral attachment is sufficient for EBOV GP-driven entry into some B cell lines. Finally, EBOV infection of dendritic cells was only partially dependent on mannose-specific lectins, such as DC-SIGN, suggesting an important contribution of other factors., Conclusions: Our results indicate that DC-SIGN is not an EBOV receptor but, rather, is an attachment-promoting factor that boosts entry into B cell lines susceptible to low levels of EBOV GP-mediated infection.

Platelets can engulf human immunodeficiency virus type 1 (HIV-1), and a significant amount of HIV-1 in the blood of infected individuals is associated with these cells. However, it is unclear how platelets capture HIV-1 and whether platelet-associated virus remains infectious. DC-SIGN and other lectins contribute to capture of HIV-1 by dendritic cells (DCs) and facilitate HIV-1 spread in DC/T-cell cocultures. Here, we show that platelets express both the C-type lectin-like receptor 2 (CLEC-2) and low levels of DC-SIGN. CLEC-2 bound to HIV-1, irrespective of the presence of the viral envelope protein, and facilitated HIV-1 capture by platelets. However, a substantial fraction of the HIV-1 binding activity of platelets was dependent on DC-SIGN. A combination of DC-SIGN and CLEC-2 inhibitors strongly reduced HIV-1 association with platelets, indicating that these lectins are required for efficient HIV-1 binding to platelets. Captured HIV-1 was maintained in an infectious state over several days, suggesting that HIV-1 can escape degradation by platelets and might use these cells to promote its spread. Our results identify CLEC-2 as a novel HIV-1 attachment factor and provide evidence that platelets capture and transfer infectious HIV-1 via DC-SIGN and CLEC-2, thereby possibly facilitating HIV-1 dissemination in infected patients.

The lectins DC-SIGN and DC-SIGNR can augment viral infection; however, the range of pathogens interacting with these attachment factors is incompletely defined. Here we show that DC-SIGN and DC-SIGNR enhance infection mediated by the glycoprotein (GP) of Marburg virus (MARV) and the S protein of severe acute respiratory syndrome coronavirus and might promote viral dissemination. SIGNR1, a murine DC-SIGN homologue, also enhanced infection driven by MARV and Ebola virus GP and could be targeted to assess the role of attachment factors in filovirus infection in vivo.

We analyzed human immunodeficiency virus type 1 (HIV-1) Nef variants to further evaluate the functional relevance of the R71T substitution previously proposed to attenuate viral replication (Fackler et al., Curr. Biol. 11:1294-1299, 2001). Our results demonstrate that this variation in the proline-rich region does not significantly affect the functional activity of Nef or HIV-1 infectivity or replication., (Copyright 2004 American Society for Microbiology)

Twenty-four Holstein bull calves were fed a milk replacer diet to assess the effects of Cr on calf performance and metabolism of glucose. Treatments consisted of no supplemental Cr (control) or 0.4 mg/kg of dry matter of supplemental Cr from CrCl3 or from a Cr-nicotinic acid complex. Supplementation with the Crt-nicotinic acid complex increased the average daily gain and feed efficiency from d 28 to 42, but not over the entire 63-d performance phase. Calves that were fed diets supplemented with CrCl3 or the Cr-nicotinic acid complex had lower plasma glucose concentrations at 45 to 180 min after an i.v. infusion of insulin than did controls. Calves fed diets supplemented with the Cr-nicotinic acid complex also had lower plasma glucose concentrations from 90 to 180 min after insulin challenge than did calves that were fed diets supplemented with CrCl3. After an i.v. infusion of glucose, calves that were fed diets supplemented with CrCl3 had lower serum insulin concentrations at 10 to 25 min after challenge than did controls or calves that were fed diets supplemented with the Cr-nicotinic acid complex. However, the glucose clearance rate after glucose infusion was not affected by Cr supplementation. Chromium supplementation did not markedly affect the performance of calves, but the Cr-nicotinic acid complex and CrCl3 did intensify the response to insulin administered i.v.

Planar PCB congeners are embryotoxic and teratogenic to birds including American kestrels. The developmental toxicity of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) was studied in the posthatching kestrel as a model for the eagle. Nestlings were dosed orally for 10 days with 5 microl/g body weight of corn oil (controls) or the planar PCB 126 at concentrations of 50, 250, or 1000 ng/g body weight. Dosing with 50 ng/g of PCB 126 resulted in a hepatic concentration of 156 ng/g wet weight, liver enlargement and mild coagulative necrosis, over 10-fold increases in hepatic microsomal ethoxyresorufin-O-dealkylase and benzyloxyresorufin-O-dealkylase, and approximately a 5-fold increase in methoxyresorufin-O-dealkylase. At this dose, mild to moderate lymphoid depletion of the spleen was apparent, as were decreased follicle size and content of the thyroid. At 250 ng/g, concentration of PCB 126 in the liver was 380 ng/g with increasing multifocal coagulative necrosis, decreased bone growth, decreased spleen weight with lymphocyte depletion of the spleen and bursa, and degenerative lesions of the thyroid. At 1000 ng/g, the liver concentration was 1098 ng/g, accompanied by decreased bursa weight, decreased hepatic thiol concentration, and increased plasma enzyme activities (ALT, AST, and LDH-L) in addition to the previous effects. Highly significant positive correlations were noted between liver concentrations of PCB 126 and the ratio of oxidized to reduced glutathone. These findings indicate that nestling kestrels are more susceptible to PCB 126 toxicity than adults, but less sensitive than embryos, and that planar PCBs are of potential hazard to nestling birds.

The objective was to determine the effect of daily s.c. injection of bovine growth hormone (bGH) on nitrogen and energy balance in six Hereford heifers. In addition, effects on urinary excretion of 3-methylhistidine and hydroxyproline and on serum mineral concentrations were monitored. A single reversal design was used with two 14-d injection periods of placebo or bGH (29.2 IU/d). Measurements were made on d 8-14 of each period. Injection of bGH did not alter apparent digestibility of dry matter, energy or nitrogen, nor urinary excretion of 3-methylhistidine or hydroxyproline. Serum concentrations of calcium, phosphorus and magnesium were normal with bGH treatment. Nitrogen retention was higher and urinary nitrogen excretion was lower when the heifers were injected with bGH than with the placebo demonstrating an effect of bGH on postabsorptive metabolism of nitrogen. Total energy balance was not altered by treatment. Energy retained as protein was higher after bGH treatment than after the placebo, implying decreased energy retained as fat and demonstrating a role for GH in altering energy partition in growing animals. Total heat production was not altered by treatment indicating no change in the gross efficiency of metabolizable energy use with bGH treatment.

The objective was to compare blood flow to the hindquarters of steers measured by transit time ultrasound with blood flow determined by indicator (p-aminohippurate) dilution. Five Hereford steers had ultrasonic flow probes on the abdominal aorta and catheters in the abdominal aorta and inferior vena cava inserted through both sets of circumflex iliac vessels. Indicator was infused continuously into the abdominal aorta through both arterial catheters simultaneously, then through each of the arterial catheters in succession. Samples of blood from the inferior vena cava and jugular vein were taken during infusion for measurement of p-aminohippurate. Blood flow determined by the ultrasonic flow probe was averaged over each blood sampling interval. Compared with the ultrasonic flow probe there was no difference in mean blood flow measured by p-aminohippurate, regardless of method of infusion. Correlation of individual values between ultrasound and p-aminohippurate was .87 when p-aminohippurate was infused into both arterial catheters, .44 when p-aminohippurate was infused into the left arterial catheter, and .78 when p-aminohippurate was infused into the right arterial catheter. The respective ranges for ultrasonic measurements and p-aminohippurate were 3.62 to 10.99 L/min and 2.25 to 30.43 L/min. Although means by the two methods do not differ, there is a greater range and incidence of occasional high values with p-aminohippurate dilution.

The objectives were to determine the effects of daily injection of bovine growth hormone (bGH) on the metabolism of [1-14C]leucine and [1-14C]palmitate and on hormone and metabolite concentrations in growing Hereford heifers. The experimental design was a 28-d single reversal with two 14-d injection periods of placebo or bGH. Energy intake was restricted to a level slightly above maintenance. Injection of bGH did not affect circulating concentrations of glucose, beta-hydroxybutyrate, urea nitrogen, prolactin, triiodothyronine or thyroxine. Plasma concentrations of insulin and nonesterified fatty acids (NEFA) were chronically elevated whereas leucine concentration was chronically decreased after 1 wk of bGH injection compared to placebo injection. Leucine oxidation was lower and whole-body protein synthesis was higher during bGH injection than during placebo injection. There were increases in both total irreversible loss and oxidation of NEFA during bGH injection compared to placebo injection. These results suggest mobilization of stored fatty acids and increased reliance on NEFA to provide energy for cellular processes. The dual and reciprocal effects of bGH on nitrogen and NEFA metabolism demonstrate its role as a homeorhetic regulator, affecting metabolism of several body tissues to support lean body accretion in Hereford heifers at near-maintenance intake of metabolizable energy.