University of Texas at Dallas

About: University of Texas at Dallas is a education organization based out in Richardson, Texas, United States. It is known for research contribution in the topics: Population & Computer science. The organization has 14986 authors who have published 35589 publications receiving 1293714 citations. The organization is also known as: UT-Dallas & UT Dallas.

Commensal bacteria regulate toll-like receptor 3-dependent inflammation after skin injury

Abstract: The normal microflora of the skin includes staphylococcal species that will induce inflammation when present below the dermis but are tolerated on the epidermal surface without initiating inflammation Here we reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation This inhibition is mediated by staphylococcal lipoteichoic acid (LTA) and acts selectively on keratinocytes triggered through Toll-like receptor 3(TLR3) We show that TLR3 activation is required for normal inflammation after injury and that keratinocytes require TLR3 to respond to RNA from damaged cells with the release of inflammatory cytokines Staphylococcal LTA inhibits both inflammatory cytokine release from keratinocytes and inflammation triggered by injury through a TLR2-dependent mechanism To our knowledge, these findings show for the first time that the skin epithelium requires TLR3 for normal inflammation after wounding and that the microflora can modulate specific cutaneous inflammatory responses

All-digital TX frequency synthesizer and discrete-time receiver for Bluetooth radio in 130-nm CMOS

Abstract: We present a single-chip fully compliant Bluetooth radio fabricated in a digital 130-nm CMOS process. The transceiver is architectured from the ground up to be compatible with digital deep-submicron CMOS processes and be readily integrated with a digital baseband and application processor. The conventional RF frequency synthesizer architecture, based on the voltage-controlled oscillator and the phase/frequency detector and charge-pump combination, has been replaced with a digitally controlled oscillator and a time-to-digital converter, respectively. The transmitter architecture takes advantage of the wideband frequency modulation capability of the all-digital phase-locked loop with built-in automatic compensation to ensure modulation accuracy. The receiver employs a discrete-time architecture in which the RF signal is directly sampled and processed using analog and digital signal processing techniques. The complete chip also integrates power management functions and a digital baseband processor. Application of the presented ideas has resulted in significant area and power savings while producing structures that are amenable to migration to more advanced deep-submicron processes, as they become available. The entire IC occupies 10 mm/sup 2/ and consumes 28 mA during transmit and 41 mA during receive at 1.5-V supply.

Functional requirement of p23 and Hsp90 in telomerase complexes

Abstract: Most normal human diploid cells have no detectable telomerase; however, expression of the catalytic subunit of telomerase is sufficient to induce telomerase activity and, in many cases, will bypass normal senescence. We and others have previously demonstrated in vitro assembly of active telomerase by combining the purified RNA component with the reverse transcriptase catalytic component synthesized in rabbit reticulocyte extract. Here we show that assembly of active telomerase from in vitro-synthesized components requires the contribution of proteins present in reticulocyte extracts. We have identified the molecular chaperones p23 and Hsp90 as proteins that bind to the catalytic subunit of telomerase. Blockade of this interaction inhibits assembly of active telomerase in vitro. Also, a significant fraction of active telomerase from cell extracts is associated with p23 and Hsp90. Consistent with in vitro results, inhibition of Hsp90 function in cells blocks assembly of active telomerase. To our knowledge, p23 and Hsp90 are the first telomerase-associated proteins demonstrated to contribute to telomerase activity.

Cocaine-induced coronary-artery vasoconstriction.

Abstract: Intranasal cocaine is used frequently as a local anesthetic during many rhinolaryngologic procedures. Although its "recreational" use in high doses has been associated with chest pain and myocardial infarction, this association has not been established when cocaine is used in low doses as a topical anesthetic, and its effect on the coronary vasculature of humans is unknown. We studied the effects of intranasal cocaine (10 percent cocaine hydrochloride; 2 mg per kilogram of body weight) on the blood flow in and dimensions of the coronary arteries and on myocardial oxygen demand in 45 patients (34 men and 11 women, 36 to 67 years of age) who were undergoing cardiac catheterization for the evaluation of chest pain. Heart rate, arterial pressure, blood flow in the coronary sinus (measured by thermodilution), and the dimensions of the epicardial left coronary artery (measured by quantitative arteriography) were measured before and 15 minutes after the intranasal administration of saline (in 16 patients) or cocaine (in 29). No variables changed after the administration of saline. After cocaine was administered, the heart rate and arterial pressure rose, the coronary-sinus blood flow fell (from a mean [+/- SD] of 149 +/- 59 ml per minute to 124 +/- 53 ml per minute), and the diameter of the left coronary artery decreased by 8 to 12 percent (P less than 0.01 for all comparisons). No patient had chest pain or electrocardiographic evidence of myocardial ischemia after the administration of cocaine. Subsequently, the administration of the alpha-adrenergic blocking agent phentolamine caused all these values to return to base-line levels. There was no difference in response between the patients found to have disease of the left coronary artery (n = 28) and those without such disease (n = 17). We conclude that the intranasal administration of cocaine near the dose used for topical anesthesia causes vasoconstriction of the coronary arteries, with a decrease in the coronary blood flow, despite an increase in myocardial oxygen demand, and that these effects are mediated by alpha-adrenergic stimulation. It is reasonable to assume that these effects would be more pronounced at the much higher doses associated with the recreational use of cocaine.