Modern optical systems increasingly rely on DSP techniques for data transmission at 40Gbs and recently at 100Gbs and above. A significant challenge towards CMOS TX DSP SoC integration is due to requirements for four 6b DACs (Fig. 10.8.1) to operate at 56Gs/s with low power and small footprint. To date, the highest sampling rate of 43Gs/s 6b DAC is reported in SiGe BiCMOS process [1]. CMOS DAC implementations are constraint to 12Gs/s with the output signal frequency limited to 1.5GHz [2][3][4]. This paper demonstrates more than one order of magnitude improvement in 6b CMOS DAC design with a test circuit operating at 56Gs/s, achieving SFDR >30dBc and ENOB>4.3b up to the output frequency of 26.9GHz. Total power dissipation is less than 750mW and the core DAC die area is less than 0.6×0.4 mm 2 .A critical element in CMOS DAC design at sampling rates Fs = 56Gs/s is a small footprint, so that the clock distribution and data path delays are minimized. In addition, short interconnect guarantees low load capacitance for the driver circuitry and further facilitates die size reduction with speed performance improvement. There are two key obstacles in circuit size reduction: circuit topology with relatively large devices (for an example, poly resistors in CML -style logic) and interconnect metal width. Minimum width is limited by electro-migration (EM) reliability rules. A CMOS logic topology with a minimum DC current in interconnects helps to reduce the EM factor. As a result, 56Gs/s 16:1 MUX circuitry is implemented using a combination of CMOS, pseudo-differential CMOS and transmission gate style of logic. Compactness of the 16:1 MUX design then requires clock phase alignment solution to provide the MUX with precise timing, similar to the phase calibration described in [4].DAC architecture ( Fig. 10.8.2) contains a 256×6b data memory with control register, 16:1 MUX, DAC current-steering matrix, DAC current sources, and finally clock generation and phase alignment block. The memory size provides DAC output data pattern length programmability up to 256b at 56Gs/s; sufficient for time domain 256b PRBS, or frequency domain 256-points FFT testing, such as SFDR and ENOB. The DAC current-steering structure combines two segments: 15 thermometer-encoded MSBs and 2 binary LSBs; there are 17 current sources and current-steering switches in total. Thermometer encoding improves DAC linearity and minimizes output glitch energy [5]. The 4b to 2b split in segmentation provides a balance between circuit complexity and DAC overall performance. There are different techniques to generate the remaining binaryweighted LSBs currents across the on-chip 50Ω load [4,6,7]. Two last solutions prevent the use of series inductive peaking (L1 in Fig. 10.8.2) with 50Ω load at the output. This is why the DAC uses binary-weighted currents of Io/2 and Io/4, where Io is the unary current value. The DAC full scale single-ended output current, FS= 15.75·Io. All 17 currents are generated in the DAC current sources block with 2.5V thick oxide devices. Currents...

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A major proportion of urinary dopamine derives from the renal decarboxylation of circulating dopa. This study evaluates the effects of aging on renal production of dopamine using 3- and 12-mo-old male Wistar rats. Urinary excretion of Na+, norepinephrine (NE), 3,4-dihydroxyphenylglycol, and dopa were similar in the two groups. Urinary dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) were lower in older animals (dopamine, 20 +/- 6 vs. 47 +/- 7 nmol/24 h, P < 0.001; DOPAC, 142 +/- 36 vs. 304 +/- 56 nmol/24 h, P < 0.03). Urinary 3-O-methyldopa (OM-dopa) was higher in 12-mo-old rats (6.2 +/- 2.0 vs. 3.3 +/- 0.20 nmol/24 h, P < 0.03). Levels of dopa and NE in renal cortex from 12-mo-old rats were higher (P < 0.001) than in younger animals. Dopamine content in renal cortex from 3-mo-old rats was 295 +/- 64 pmol/g, whereas it was undetectable in 12-mo-old animals. Aromatic-L-amino-acid decarboxylase and monoamine oxidase activities were higher (P < 0.001) in renal cortex from 12-mo-old animals. Catechol-O-methyltransferase activity was similar in both groups. The uptake of dopa by the luminal membrane was explored using brush-border membrane vesicles. The Na(+)-gradient-driven (100 mM) uptake of dopa into vesicles from 3-mo-old animals showed at 10 s an overshoot threefold greater than the equilibrium uptake. The overshoot was blunted in 12-mo-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

SummaryThe twenty-first century arrived in the middle of a global epidemic of metabolic syndrome (MS) and type 2 diabetes mellitus (DM2). It is generally accepted that an excess of nutrients linked to a low physical activity triggers the problem. However, the molecular features that interact to develop the MS are not clear. In an effort to understand and control them, they have been extensively studied, but this goal has not been achieved yet. Nonhuman animal models have been used to explore diet and genetic factors in which experimental conditions are controlled. For example, only one factor in the diet, such as fats or carbohydrates can be modified to better understand a single change that would be impossible in humans. Most of the studies have been done in rodents. However, it is difficult to directly compare them, because experiments are different in more than one variable; genetic strains, amount, and the type of fat used in the diet and sex. Thus, the only possible criteria of comparison are the relevance of the observed changes. We review different animal models and add some original observations on short-term changes in metabolism and beta cells in our own model of adult Wistar rats that are not especially prone to get fat or develop DM2, treated with 20% sucrose in drinking water. One early change observed in pancreatic beta cells is the increase in GLUT2 expression that is located to the membrane of the cells. This change could partially explain the presence of insulin hypersecretion and hyperinsulinemia in these rats. Understanding early changes that lead to MS and in time to pancreatic islet exhaustion is an important biomedical problem that may contribute to learn how to prevent or even reverse MS, before developing DM2.

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