“…It has been shown that glucokinase can initiate phosphorylation of glucose after it has diffused into liver cells. Glucose is temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back through the cell membrane [17]. These observations suggest that lowering of serum glucose by exendin-4 in the present study may have been achieved by a similar mechanism.Figure 1.Treatment with exendin-4 in NMRI mice decreased serum glucose (a), insulin and HOMA-IR (b), and increased insulin secretion by pancreatic islets cultured in medium containing different concentrations of glucose (c).…”
Investigations into pharmaceutical intervention of pancreatic and hepatic dysfunction associated with metabolic disturbances have received relatively little attention. The aim of this study was to investigate the protective effects of exendin-4 in mice receiving D-galactose, a reducing sugar that triggers ROS production and inflammatory mediators affecting the pancreas and liver. Exendin-4 is an United States Food and Drug Administration (FDA) approved glucagon-like peptide that increases insulin dependent glycogen synthesis and glucose uptake. Male NMRI mice (20–25 g), 3 months of age, were randomly divided into 6 groups of 12 mice each: control, exendin-4 (1 nmol/kg), exendin-4 (10 nmol/kg), D-galactose, D-galactose + exendin-4 (1 nmol/kg) and D-galactose + exendin-4 (10 nmol/kg). D-galactose (500 mg/kg) was given daily by oral gavage for 6 weeks. During the last 10 days, exendin-4 (1 and 10 nmol/kg) was injected intraperitoneally daily. Glucose, insulin, insulin resistance, lipid profiles, and hepatic enzyme levels significantly increased in the D-galactose group (p < 0.05), along with a significant decrease in superoxide dismutase activity and pancreatic islet insulin secretion (p < 0.05). Exendin-4 decreased D-galactose-induced increases in serum glucose and insulin, insulin resistance, lipid profiles, and hepatic enzymes, and improved pancreatic islet insulin secretion and antioxidant defense status. The results show that exendin-4 can prevent complications in mice with compromised pancreatic and hepatic function. Long term administration of D-galactose in mice may be a useful model to study insulin resistance, metabolic syndrome, and aging.
“…It has been shown that glucokinase can initiate phosphorylation of glucose after it has diffused into liver cells. Glucose is temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back through the cell membrane [17]. These observations suggest that lowering of serum glucose by exendin-4 in the present study may have been achieved by a similar mechanism.Figure 1.Treatment with exendin-4 in NMRI mice decreased serum glucose (a), insulin and HOMA-IR (b), and increased insulin secretion by pancreatic islets cultured in medium containing different concentrations of glucose (c).…”
Investigations into pharmaceutical intervention of pancreatic and hepatic dysfunction associated with metabolic disturbances have received relatively little attention. The aim of this study was to investigate the protective effects of exendin-4 in mice receiving D-galactose, a reducing sugar that triggers ROS production and inflammatory mediators affecting the pancreas and liver. Exendin-4 is an United States Food and Drug Administration (FDA) approved glucagon-like peptide that increases insulin dependent glycogen synthesis and glucose uptake. Male NMRI mice (20–25 g), 3 months of age, were randomly divided into 6 groups of 12 mice each: control, exendin-4 (1 nmol/kg), exendin-4 (10 nmol/kg), D-galactose, D-galactose + exendin-4 (1 nmol/kg) and D-galactose + exendin-4 (10 nmol/kg). D-galactose (500 mg/kg) was given daily by oral gavage for 6 weeks. During the last 10 days, exendin-4 (1 and 10 nmol/kg) was injected intraperitoneally daily. Glucose, insulin, insulin resistance, lipid profiles, and hepatic enzyme levels significantly increased in the D-galactose group (p < 0.05), along with a significant decrease in superoxide dismutase activity and pancreatic islet insulin secretion (p < 0.05). Exendin-4 decreased D-galactose-induced increases in serum glucose and insulin, insulin resistance, lipid profiles, and hepatic enzymes, and improved pancreatic islet insulin secretion and antioxidant defense status. The results show that exendin-4 can prevent complications in mice with compromised pancreatic and hepatic function. Long term administration of D-galactose in mice may be a useful model to study insulin resistance, metabolic syndrome, and aging.
“…yðt − t′ÞSðt′Þ dt′, [7] whereRðtÞ = RðtÞ − E½RðtÞ andSðtÞ = SðtÞ − E½SðtÞ , in which E½ · means the expectation of the corresponding random variable. Two remarks are of importance here.…”
The probabilistic nature of neurotransmitter release in synapses is believed to be one of the most significant sources of noise in the central nervous system. We show how p 0 , the probability of release per docked vesicle when an action potential arrives, affects the dynamics of the rate of vesicle release in response to changes in the rate of arrival of action potentials. Furthermore, we examine the theoretical capability of a synapse in the estimation of desired signals using information from the stochastic vesicle release events under the framework of optimal linear filter theory. We find that a small p 0 , such as 0.1, reduces the error in the reconstruction of the input, or in the reconstruction of the time derivative of the input, from the time series of vesicle release events. Our results imply that the probabilistic nature of synaptic vesicle release plays a direct functional role in synaptic transmission.synaptic transmission | stochastic vesicle release | release probability | optimal filter R andomness is present in almost all levels of all nervous systems, such as in ionic channels of individual neurons, in synapses between neurons, and in environmental stimuli. The probabilistic nature of the synaptic vesicle release process is believed to be one of the most significant sources of randomness. Stochastic vesicle release affects information transfer from a presynaptic neuron to a postsynaptic neuron, and hence may play not only an important role in synaptic plasticity (1, 2) but also a significant role in determining the functionality of certain synapses, a point we will argue in this article. The functional role of stochastic vesicle release in synaptic transmission is likely to be more significant in those synapses in the central nervous system, where the size of the readily releasable vesicle pool is usually smaller than those in the periphery.Synaptic vesicle release has only recently been studied in a probabilistic or information-theoretic manner (3-5). A systematic perspective on how stochastic vesicle release affects neural code processing at synapses is still lacking. On the experimental front, a comprehensive, quantitative knowledge about the nature of vesicle docking, priming, fusing, undocking, replenishing, and recycling is far from complete, and hence a biophysically detailed model of the entire vesicle release process is not yet possible.Despite current limited understanding of the synaptic vesicle release process, a probabilistic model that captures the essential elements of that process can still be built to study the effect of various sources of randomness on synaptic transmission. Rosenbaum et al. (3) recently constructed such a model to study how variability in vesicle dynamics affects information transfer from one neuron to another. They found that the depletion of docked vesicles at higher rates of arrival of action potentials makes the synapse act as a highpass filter from a signal processing point of view. Motivated by Rosenbaum et al.'s (3) model of the presynaptic vesicle r...
“…The ventilation/perfusion ratio also plays a factor in human alveolar gas exchange. A large surface area in pulmonary gas exchange (70-100 m 2 ) is facilitated by the numerous branches of the respiratory tree and large number of terminal alveoli [8].…”
Section: B Lung Anatomy and Physiologymentioning
confidence: 99%
“…Much of the lung is composed of thin-walled alveoli, which and their vascular supply [8] are made up of a monolayer of squamous epithelium. A thin layer of connective tissue may be found between the alveoli.…”
Section: B Lung Anatomy and Physiologymentioning
confidence: 99%
“…These cell types include alveolar macrophages, neutrophils, and leukocytes that continuously mitigate the threat of bacterial and fungal contamination at the alveolar interface [10]. [11] Vital functions of the lungs include serving as the site of gas exchange, regulating blood pressure and pH, and removing foreign bodies [8]. Grossly, the right and left human lungs consist of three and two lobes, respectively.…”
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