Implications of Implementing HDTV Over Digital Subscriber Line Networks

This thesis addresses the different challenges a telecommunications company would face when trying to implement an HDTV video service over a Digital Subscriber Line (DSL) connection. Each challenge is discussed in detail and a technology, protocol, or method is suggested to overcome that particular challenge. One of the biggest challenges is creating a network architecture that can provide enough bandwidth to support video over a network that was originally designed for voice traffic. The majority of the network connections to a customer premises in a telephony network consists of a copper pair. This type of connection is not optimal for high bandwidth services. This limitation can be overcome using Gigabit Ethernet (GE) over fiber in the core part of the network and VDSL2 in the access part of the network. For the purposes of this document, the core portion of the network is considered to be an area equal to several counties or approximately 50 miles in radius. The core network starts at the primary central office (CO) and spreads out to central offices in suburbs and small towns. The primary central office is a central point in the telecom operator\u27s network. Large trunks are propagated from the primary central office to smaller central offices making up the core network. The access portion of the network is considered to be an area within a suburb or small town from the central office to a subscriber\u27s home. Appendix A, located on page 60, contains a network diagram illustrating the scope of each of the different portions of the network. Considerations must also be given for the internal network to the residence such as category 5 (Cat5) cable or higher grade and network equipment that can provide up to 30 Megabits per second (Mbps) connections or throughput. The equipment in the telecommunications network also plays a part in meeting the challenge of 30 Mbps bandwidth. GE switches should be used with single mode fiber optic cable in the core part of the network. Digital Subscriber Line Access Multiplexers (DSLAM) with the capability to filter Internet Group Management Protocol (IGMP) messages should be used in the access part of the network to facilitate bandwidth utilization. Placement of this equipment and how the data is aggregated is another issue to consider when implementing HDTV service. Another major challenge facing the implementation of HDTV over DSL networks is controlling quality of service (QoS) throughout the network. Class of Service (CoS) and Differentiated Services (DiffServ) is a method of QoS that would enable video packets to have a higher priority and less delay than other data packets. The consumer could have data, video, and voice traffic all over the same DSL connection. Data, video and voice packets would need to have a different priority in order to maintain appropriate QoS levels for each service. The use of advanced technology in video encoding will be essential to the success of the video service. MPEG-2, MPEG-4, and Windows Media 9 are just a few of the video encoding technologies that could be used to reduce the necessary bandwidth for HDTV. The advancement of this technology is essential to allow telecommunications providers to offer HDTV. Another challenge for the telecom operator concerns the security of the network and service after implementation. Theft of service will be another area that the telecomm operator will be forced to resolve. The cable operators currently face this issue and lose millions of dollars in revenue. Authentication, IP filtering and MAC address blocking are a few possible solutions to this problem

Increased FAT/CD36 Cycling and Lipid Accumulation in Myotubes Derived from Obese Type 2 Diabetic Patients

BACKGROUND: Permanent fatty acid translocase (FAT/)CD36 relocation has previously been shown to be related to abnormal lipid accumulation in the skeletal muscle of type 2 diabetic patients, however mechanisms responsible for the regulation of FAT/CD36 expression and localization are not well characterized in human skeletal muscle. METHODOLOGY/PRINCIPAL FINDINGS: Primary muscle cells derived from obese type 2 diabetic patients (OBT2D) and from healthy subjects (Control) were used to examine the regulation of FAT/CD36. We showed that compared to Control myotubes, FAT/CD36 was continuously cycling between intracellular compartments and the cell surface in OBT2D myotubes, independently of lipid raft association, leading to increased cell surface FAT/CD36 localization and lipid accumulation. Moreover, we showed that FAT/CD36 cycling and lipid accumulation were specific to myotubes and were not observed in reserve cells. However, in Control myotubes, the induction of FAT/CD36 membrane translocation by the activation of (AMP)-activated protein kinase (AMPK) pathway did not increase lipid accumulation. This result can be explained by the fact that pharmacological activation of AMPK leads to increased mitochondrial beta-oxidation in Control cells. CONCLUSION/SIGNIFICANCE: Lipid accumulation in myotubes derived from obese type 2 diabetic patients arises from abnormal FAT/CD36 cycling while lipid accumulation in Control cells results from an equilibrium between lipid uptake and oxidation. As such, inhibiting FAT/CD36 cycling in the skeletal muscle of obese type 2 diabetic patients should be sufficient to diminish lipid accumulation

Metformin reduces liver glucose production by inhibition of fructose-1-6-bisphosphatase.

Metformin is a first-line drug for the treatment of individuals with type 2 diabetes, yet its precise mechanism of action remains unclear. Metformin exerts its antihyperglycemic action primarily through lowering hepatic glucose production (HGP). This suppression is thought to be mediated through inhibition of mitochondrial respiratory complex I, and thus elevation of 5'-adenosine monophosphate (AMP) levels and the activation of AMP-activated protein kinase (AMPK), though this proposition has been challenged given results in mice lacking hepatic AMPK. Here we report that the AMP-inhibited enzyme fructose-1,6-bisphosphatase-1 (FBP1), a rate-controlling enzyme in gluconeogenesis, functions as a major contributor to the therapeutic action of metformin. We identified a point mutation in FBP1 that renders it insensitive to AMP while sparing regulation by fructose-2,6-bisphosphate (F-2,6-P2), and knock-in (KI) of this mutant in mice significantly reduces their response to metformin treatment. We observe this during a metformin tolerance test and in a metformin-euglycemic clamp that we have developed. The antihyperglycemic effect of metformin in high-fat diet-fed diabetic FBP1-KI mice was also significantly blunted compared to wild-type controls. Collectively, we show a new mechanism of action for metformin and provide further evidence that molecular targeting of FBP1 can have antihyperglycemic effects

Adiposity-Independent Effects of Aging on Insulin Sensitivity and Clearance in Mice and Humans.

ObjectiveAging is associated with impaired insulin sensitivity and increased prevalence of type 2 diabetes. However, it remains unclear whether aging-associated insulin resistance is due to increased adiposity or other age-related factors. To address this question, the impact of aging on insulin sensitivity was investigated independently of changes in body composition.MethodsCohorts of mice aged 4 to 8 months ("young") and 18 to 27 months ("aged") exhibiting similar body composition were characterized for glucose metabolism on chow and high-fat diets. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp analyses. The relationship between aging and insulin resistance in humans was investigated in 1,250 nondiabetic Mexican Americans who underwent hyperinsulinemic-euglycemic clamps.ResultsIn mice with similar body composition, age had no detrimental effect on plasma glucose and insulin levels. While aging did not diminish glucose tolerance, hyperinsulinemic-euglycemic clamps demonstrated impaired insulin sensitivity and reduced insulin clearance in aged mice on chow and high-fat diets. Consistent with results in the mouse, age remained an independent determinant of insulin resistance after adjustment for body composition in Mexican American males.ConclusionsThis study demonstrates that in addition to altered body composition, adiposity-independent mechanisms also contribute to aging-associated insulin resistance in mice and humans