Delay Compensation in a Feeder-Conveyor System Using the Smith Predictor: A Case Study in an Iron Ore Processing Plant.

Conveyor belts serve as the primary mode of ore transportation in mineral processing plants. Feeders, comprised of shorter conveyors, regulate the material flow from silos to longer conveyor belts by adjusting their velocity. This velocity manipulation is facilitated by automatic controllers that gauge the material weight on the conveyor using scales. However, due to positioning constraints of these scales, a notable delay ensues between measurement and the adjustment of the feeder speed. This dead time poses a significant challenge in control design, aiming to prevent oscillations in material levels on the conveyor belt. This paper contributes in two key areas: firstly, through a simulation-based comparison of various control techniques addressing this issue across diverse scenarios; secondly, by implementing the Smith predictor solution in an operational plant and contrasting its performance with that of a single PID controller. Evaluation spans both the transient flow rate during step change setpoints and a month-long assessment. The experimental results reveal a notable increase in production by 355 t/h and a substantial reduction in flow rate oscillations on the conveyor belt, evidenced by a 55% decrease in the standard deviation.

DNA barcode for the identification of the sand fly Lutzomyia longipalpis plant feeding preferences in a tropical urban environment.

Little is known about the feeding behavior of hematophagous insects that require plant sugar to complete their life cycles. We studied plant feeding of Lutzomyia longipalpis sand flies, known vectors of Leishmania infantum/chagasi parasites, in a Brazilian city endemic with visceral leishmaniasis. The DNA barcode technique was applied to identify plant food source of wild-caught L. longipalpis using specific primers for a locus from the chloroplast genome, ribulose diphosphate carboxylase. DNA from all trees or shrubs within a 100-meter radius from the trap were collected to build a barcode reference library. While plants from the Anacardiaceae and Meliaceae families were the most abundant at the sampling site (25.4% and 12.7% of the local plant population, respectively), DNA from these plant families was found in few flies; in contrast, despite its low abundance (2.9%), DNA from the Fabaceae family was detected in 94.7% of the sand flies. The proportion of sand flies testing positive for DNA from a given plant family was not significantly associated with abundance, distance from the trap, or average crown expansion of plants from that family. The data suggest that there may indeed be a feeding preference of L. longipalpis for plants in the Fabaceae family.

Sodium bicarbonate treatment prevents gastric emptying delay caused by acute exercise in awake rats.

Physical exercise, mainly after vigorous activity, may induce gastrointestinal dysmotility whose mechanisms are still unknown. We hypothesized that physical exercise and ensuing lactate-related acidemia alter gastrointestinal motor behavior. In the present study, we evaluated the effects of short-term exercise on gastric emptying rate in awake rats subjected to 15-min swimming sessions against a load equivalent to 5% of their body weight. After 0, 10, or 20 min of exercise testing, the rats were gavage fed with 1.5 ml of a liquid test meal (0.5 mg/ml of phenol red in 5% glucose solution) and euthanized 10 min postprandially to measure fractional gastric dye recovery. In addition to inducing acidemia and increasing blood lactate levels, acute exercise increased (P < 0.05) gastric retention. Such a phenomenon presented a positive correlation (P < 0.001) between blood lactate levels and fractional gastric dye recovery. Gastric retention and other acidbase-related changes were all prevented by NaHCO3 pretreatment. Additionally, exercise enhanced (P < 0.05) the marker's progression through the small intestine. In anesthetized rats, exercise increased (P < 0.05) gastric volume, measured by a balloon catheter in a barostat system. Compared with sedentary control rats, acute exercise also inhibited (P < 0.05) the contractility of gastric fundus strips in vitro. In conclusion, acute exercise delayed the gastric emptying of a liquid test meal by interfering with the acid-base balance.

Safety and pharmacokinetics of a recombinant fusion protein linking coagulation factor VIIa with albumin in healthy volunteers.

BACKGROUND: Development of neutralizing antibodies remains the most problematic complication in treating congenital hemophilia. Control and prevention of bleeding events in such patients with recombinant factor VIIa (rFVIIa) is limited by the short half-life of the available product. Here, we report on the pharmacokinetics and safety of a novel, recombinant fusion protein linking coagulation FVIIa with albumin (rVIIa-FP) in a first-in-human study in healthy male subjects. METHODS: Forty healthy male subjects between 18 and 35 years of age were included and dosed in five consecutive cohorts. In each cohort, six subjects were randomized to a single dose of rVIIa-FP (140, 300, 500, 750, or 1000 µg kg(-1) ) and two to placebo. All subjects received anticoagulation with an oral vitamin K antagonist to reach an international normalized ratio between 2 and 3 prior to dosing with rVIIa-FP/placebo. Dosing with oral vitamin K antagonist was continued at a fixed dose for 6 days after injection of rFVIIa. RESULTS AND CONCLUSIONS: Tolerance of rVIIa-FP was good at all dose levels. No serious adverse events were observed. None of the subjects developed anti-drug antibodies. The maximum baseline-corrected mean (SD) FVIIa plasma activity increased in a dose-proportional manner. Across the dose range, the median half-life was consistent, ranging from 6.1 to 9.7 h. At the highest dose of 1000 µg kg(-1) , the median FVIIa activity-based half-life was 8.5 h. Clearance ranged from 7.62 to 12.74 mL h(-1) kg(-1) . Compared with the commercially available rFVIIa product, rVIIa-FP had a reduced clearance resulting in an approximately 3- to 4-fold increase in half-life.

Aortocaval fistula delays gastric emptying of liquid test meal in awake rats.

Arteriovenous anastomoses disrupt cardiovascular and renal homeostasis, eliciting hemodynamic adjustments, resetting the humoral pattern, and inducing cardiac hypertrophy. Because acute circulatory imbalance alters gut motor behavior, we studied the effects of arteriovenous fistula placement on the gastric emptying (GE) of a liquid meal in awake rats. After laparotomy, we created an aortocaval fistula (ACF) by aorta and cava wall puncture with a 21-, 23-, or 26-gauge needle. The ACF was not created in the control group, which underwent sham operation. After 12, 24, or 48 h, mean arterial pressure, heart rate, and central venous pressure were continuously recorded, and cardiac output was estimated by thermal dilution. The rats were then gavage fed a test meal (i.e., phenol red in glucose solution), and fractional dye retention was determined 10, 20, or 30 min later. The effect of prior bleeding on ACF-induced GE delay, the role of neuroautonomic pathways, and changes in plasma hormone levels (i.e., angiotensin II, arginine vasopressin, atrial natriuretic peptide, corticosterone, and oxytocin) were evaluated. When compared with the sham-operated group, ACF rats exhibited arterial hypotension, higher (P < 0.05) heart rate, central venous pressure, and cardiac output values and increased (P < 0.05) gastric dye retention, a phenomenon prevented by bilateral subdiaphragmatic vagotomy and hexamethonium treatment. Pirenzepine also impaired the occurrence of gastric delay in subjects with ACF. In addition to causing hyperkinetic circulation, ACF placement delayed the GE of liquid in awake rats, an effect that likely involves a parasympathetic pathway.

Proteasomal inhibition alters the trafficking of the neurotrophin receptor TrkA.

Neurotrophin receptors of the Trk family promote neuronal survival. The signal transduction of Trk receptors is regulated by endosomal trafficking. Monoubiquitination of receptor tyrosine kinases is an established signal for sorting of internalized receptors to late endosomes. The NGF receptor TrkA is sorted to late endosomes and undergoes ubiquitination, indicating a so far undefined regulatory role of proteasomal activity in the trafficking of TrkA. Surprisingly, we found that proteasomal inhibition alters the trafficking of TrkA from the late endosomal sorting pathway to the recycling pathway. Many neurodegenerative diseases are associated with impaired proteasomal activity. Thus, our study suggests that missorting of neurotrophic receptors might contribute to neuronal death in those neurodegenerative diseases that are known to be associated with impaired proteasomal function.

Tracking TrkA's trafficking: NGF receptor trafficking controls NGF receptor signaling.

Growth factors such as the neurotrophins promote neuronal survival and shape neuronal morphology. Neurotrophin receptors are located on the surface of axons and dendrites and must convey their signal retrogradely to the nucleus to influence transcription of target genes. The distance between the site of receptor activation and the nucleus is tremendous. How is the retrograde transmission of survival signals being achieved? Recent work showed that signaling endosomes containing neurotrophin receptors and associated downstream kinases undergo retrograde vesicular transport along microtubules, propelled by the molecular motor dynein. The next objective in the "neurotrophin receptor trafficking meets signal transduction field" will be to elucidate the traffic control mechanisms governing the directed movement of signaling endosomes. Much is already known on the trafficking of the receptor for epidermal growth factor, EGFR. We will summarize the known traffic control mechanisms for EGFR and hypothesize whether EGFR-relevant traffic control mechanisms might also be relevant for neurotrophin receptor traffic control. Moreover, we speculate about potential implications of neurotrophin receptor traffic jams for neurodegenerative diseases.