4E Assessment of an Organic Rankine Cycle (ORC) Activated with Waste Heat of a Flash-Binary Geothermal Power Plant.

In this paper, the 4E assessment (Energetic, Exergetic, Exergoeconomic and Exergoenvironmental) of a low-temperature ORC activated by two different alternatives is presented. The first alternative (S1) contemplates the activation of the ORC through the recovery of waste heat from a flash-binary geothermal power plant. The second alternative (S2) contemplates the activation of the ORC using direct heat from a geothermal well. For both alternatives, the energetic and exergetic models were established. At the same time, the economic and environmental impact models were developed. Finally, based on the combination of the exergy concepts and the economic and ecological indicators, the exergoeconomic and exergoenvironmental performances of the ORC were obtained. The results show higher economic, exergoeconomic and exergoenvironmental profitability for S1. Besides, for the alternative S1, the ORC cycle has an acceptable economic profitability for a net power of 358.4 kW at a temperature of 110 °C, while for S2, this profitability starts being attractive for a power 2.65 times greater than S1 and with a temperature higher than 135 °C. In conclusion, the above represents an area of opportunity and a considerable advantage for the implementation of the ORC in the recovery of waste heat from flash-binary geothermal power plants.

The impact of lymph node density as a predictive factor for survival and recurrence of tongue squamous cell carcinoma.

The oral tongue is considered the most frequently involved site in cases of oral squamous cell carcinoma (OSCC). Lymph node (LN) density, defined as the number of positive LNs divided by the total number of resected LNs, is considered an important prognostic factor in OSCC; however the cut-off point remains uncertain. A retrospective study was performed involving 104 patients who underwent a glossectomy procedure for oral tongue squamous cell carcinoma (OTSCC) between the years 2008 and 2018. LN density and other related prognostic factors, including pathological N-stage (pN), extranodal extension (ENE), perineural invasion (PNI), and depth of invasion (DOI), were investigated in relation to survival and recurrence rates. pN + stage, the presence of ENE, the presence of PNI, and increased DOI were found to be associated with increased LN density values, as well as lower patient survival and higher recurrence rates. The statistical analysis identified a cut-off point for LN density of 2.5%. In advanced stage disease, LN density values above 2.5% had a significant impact on the survival rate (P = 0.005), as well as the recurrence rate (P = 0.038). In conclusion, in addition to other previously known prognostic factors, LN density may serve as a strong prognostic factor for survival and recurrence in patients with advanced- and early-stage OTSCC.

Eliciting the low-activity aldehyde dehydrogenase Asian phenotype by an antisense mechanism results in an aversion to ethanol.

A mutation in the gene encoding for the liver mitochondrial aldehyde dehydrogenase (ALDH2-2), present in some Asian populations, lowers or abolishes the activity of this enzyme and results in elevations in blood acetaldehyde upon ethanol consumption, a phenotype that greatly protects against alcohol abuse and alcoholism. We have determined whether the administration of antisense phosphorothioate oligonucleotides (ASOs) can mimic the low-activity ALDH2-2 Asian phenotype. Rat hepatoma cells incubated for 24 h with an antisense oligonucleotide (ASO-9) showed reductions in ALDH2 mRNA levels of 85% and ALDH2 (half-life of 22 h) activity of 55% equivalent to a >90% inhibition in ALDH2 synthesis. Glutamate dehydrogenase mRNA and activity remained unchanged. Base mismatches in the oligonucleotide rendered ASO-9 virtually inactive, confirming an antisense effect. Administration of ASO-9 (20 mg/kg/day for 4 d) to rats resulted in a 50% reduction in liver ALDH2 mRNA, a 40% inhibition in ALDH2 activity, and a fourfold (P < 0.001) increase in circulating plasma acetaldehyde levels after ethanol (1 g/kg) administration. Administration of ASO-9 to rats by osmotic pumps led to an aversion (-61%, P < 0.02) to ethanol. These studies provide a proof of principle that specific inhibition of gene expression can be used to mimic the protective effects afforded by the ALDH2-2 phenotype.

Sandwich osteotomy for the reconstruction of deficient alveolar bone.

Alveolar bone deficiency is a very common problem encountered by the practitioner when planning dental implants. The severity of the deficiency is variable. Many practitioners perform augmentation using the method they feel comfortable with and do not necessarily use the most appropriate method. This is a retrospective study on 21 patients between the ages of 25 and 63 years exhibiting moderate vertical alveolar bone deficiency and treated by the sandwich technique. Mean vertical bone gain was 7.5mm. Sixty-one dental implants were inserted showing a survival rate of 96.7% with a median of 3.1 years follow-up. Main advantages of the method include minimal relapse, single operation and preservation of the native cortical bone in the occlusal surface. We believe the surgeon should maintain the capability of using different augmentation techniques and utilize them appropriately for different severities of deficiency. We wish to establish a paradigm for using different augmentation methods We recommend using the sandwich technique in the moderate deficient cases as described in this work, using alveolar distraction osteogenesis for the severe cases as described in our previous work, where lack of soft tissue for proper closure is a major limitation, and using guided bone regeneration for minor deficiencies.

GABA receptor subtype antagonists in the nucleus accumbens shell and ventral tegmental area differentially alter feeding responses induced by deprivation, glucoprivation and lipoprivation in rats.

GABA(A) and GABA(B) receptor agonists stimulate feeding following microinjection into the nucleus accumbens shell and ventral tegmental area, effects blocked selectively and respectively by GABA(A) and GABA(B) receptor antagonists. GABA antagonists also differentially alter opioid-induced feeding responses elicited from these sites. Although GABA agonists and antagonists have been shown to modulate feeding elicited by deprivation or glucoprivation, there has been no systematic examination of feeding elicited by homeostatic challenges following GABA antagonists in these sites. Therefore, the present study examined the dose-dependent ability of GABA(A) (bicuculline, 75-150 ng) and GABA(B) (saclofen, 1.5-3 microg) antagonists administered into the nucleus accumbens shell or ventral tegmental area upon feeding responses elicited by food deprivation (24 h), 2-deoxy-D-glucose-induced glucoprivation (500 mg/kg) or mercaptoacetate-induced lipoprivation (70 mg/kg). A site-specific effect of GABA receptor antagonism was observed for deprivation-induced feeding in that both bicuculline and saclofen administered into the nucleus accumbens shell, but not the ventral tegmental area, produced short-term (1-4 h), but not long-term (24-48 h) effects upon deprivation-induced intake without meaningfully altering body weight recovery. In contrast to the relative inability of GABA receptor antagonism in both sites to alter 2-deoxy-D-glucose-induced intake, mercaptoacetate-induced intake was eliminated by saclofen and significantly reduced by bicuculline in the nucleus accumbens shell and eliminated by both bicuculline and saclofen in the ventral tegmental area. These data reinforce the findings that GABA(A) and GABA(B) receptors in the nucleus accumbens shell and ventral tegmental area are not only important in the modulation of pharmacologically induced feeding responses, but also participate in differentially mediating the short-term feeding response to food deprivation in the nucleus accumbens shell as well strongly modulating lipoprivic, but not glucoprivic feeding responses in both sites.

Changes from high potassium (hk) to low potassium (lk) in bovine red cells.

Red cells of newborn calves contain 105-110 mmole K(+) and 1-5 mmole Na(+) per liter of cells. As the animals age the K(+) content decreases to a value of 25-30 mmole/liter of cells after about 60 days. At approximately the same time, the sodium content reaches a value of 60-70 mmole/liter. The time required for half change (t((1/2))) is 35-37 days for both Na(+) and K(+). The activity of (Na + K)-adenosine triphosphatase (ATPase) and the influx of K(42) and Rb(86) into the red cells are high at birth and are reduced to 5 and 15% of their original values, respectively, in mature animals. t((1/2)) for both is of the order of 30-35 days. The membrane Mg-ATPase activity is also high at birth and is reduced with a t((1/2)) of 28-32 days to a final value of about 20% of its activity at birth. Separation of red cells according to their age showed that, in animals at the age of transition, newly formed red cells contain a higher K/Na ratio and a higher active transport capacity than older red cells of the same animal. It is suggested that the changes observed are a reflection of the average age of the red cell population as the animal grows.

NPY-induced feeding: pharmacological characterization using selective opioid antagonists and antisense probes in rats.

The ability of neuropeptide Y to potently stimulate food intake is dependent in part upon the functioning of mu and kappa opioid receptors. The combined use of selective opioid antagonists directed against mu, delta or kappa receptors and antisense probes directed against specific exons of the MOR-1, DOR-1, KOR-1 and KOR-3/ORL-1 opioid receptor genes has been successful in characterizing the precise receptor subpopulations mediating feeding elicited by opioid peptides and agonists as well as homeostatic challenges. The present study examined the dose-dependent (5-80 nmol) cerebroventricular actions of general and selective mu, delta, and kappa1 opioid receptor antagonists together with antisense probes directed against each of the four exons of the MOR-1 opioid receptor gene and each of the three exons of the DOR-1, KOR-1, and KOR-3/ORL-1 opioid receptor genes upon feeding elicited by cerebroventricular NPY (0.47 nmol, 2 ug). NPY-induced feeding was dose-dependently decreased and sometimes eliminated following pretreatment with general, mu, delta, and kappa1 opioid receptor antagonists. Moreover, NPY-induced feeding was significantly and markedly reduced by antisense probes directed against exons 1, 2, and 3 of the MOR-1 gene, exons 1 and 2 of the DOR-1 gene, exons 1, 2, and 3 of the KOR-1 gene, and exon 3 of the KOR-3/ORL-1 gene. Thus, whereas the opioid peptides, beta-endorphin and dynorphin A(1-17) elicit feeding responses that are respectively more dependent upon mu and kappa opioid receptors and their genes, the opioid mediation of NPY-induced feeding appears to involve all three major opioid receptor subtypes in a manner similar to that observed for feeding responses following glucoprivation or lipoprivation.

Mutations in mitochondrial aldehyde dehydrogenase (ALDH2) change cofactor affinity and segregate with voluntary alcohol consumption in rats.

Genetic factors influence alcohol consumption and alcoholism. A number of groups have bred alcohol drinker and non drinker rat strains, but genetic determinants remain unknown. The University of Chile rat lines UChA (low drinkers) and UChB (high drinkers) display differences in the relative K(m) for NAD+ of mitochondrial aldehyde dehydrogenase (ALDH2) but no V(max) differences. The relative K(m) differences may be due to mitochondrial changes or to genetic differences coding for ALDH2. We investigated whether there are differences in the coding regions of ALDH2 cDNA in these lines and whether the Aldh2 genotype predicts the phenotype of alcohol consumption and the K(m) of ALDH2 for NAD+. Liver cDNA was prepared, and the Aldh2 transcript was amplified, cloned and sequenced. Genotyping was conducted by DNA amplification and restriction enzyme digestion. When compared to Aldh21 of Sprague-Dawley, 94% of the UChA (low drinker) rats (n = 61), presented a mutation that changes Gln67 to Arg in the mature enzyme (allele referred to as Aldh22). In UChB (high drinker) rats (n = 69), 58% presented the Aldh21 allele, while 42% presented the Gln67Arg change plus a second mutation that changed Glu479 to Lys (allele Aldh23). The Aldh22 allele was absent in high drinker rats. Rats of different Aldh2 genotypes displayed marked phenotypic differences in both ethanol consumption (g/kg/day; means +/- SE): (Aldh21/Aldh21) = 5.7 +/- 0.2, (Aldh22/Aldh22) = 0.9 +/- 0.2 and (Aldh23/Aldh23) = 4.6 +/- 0.2; and K(m)s for NAD+ of 43 +/- 3 microm, 132 +/- 13 microm and 41 +/- 2 microm, respectively (Aldh22 versus Aldh21 or Aldh23; P < 0.0001 for both phenotypes). Overall, the data show that alleles of Aldh2 strongly segregate with the phenotype of ethanol consumption and the relative K(m) for NAD+ of ALDH2. Bases mutated suggest that non drinker Aldh22 is ancestral with regard to the coding changes in either Aldh21 or Aldh23, variants which would allow ethanol consumption and may provide an evolutionary advantage by promoting calorie intake from fermented products along with carbohydrates.

Cloning of two additional catecholamine receptors from rat brain.

An approach based on the polymerase chain reaction (PCR) was used to isolate additional members of the G-linked receptor family from a rat striatal lambda gtII cDNA library. Priming with one degenerate probe corresponding to highly conserved consensus sequences in the third transmembrane (TM) domain of 15 G-linked receptors and sequences in the phage vector resulted in one clone (G-13) encoding a dopamine D2 receptor variant with a 29 amino acid insert in the third cytoplasmic loop. In addition, the amino acid sequence encoded by clone G-36 contained conserved sequences characteristic of the G-linked class of receptors and displayed sequence homology in TM domains with the beta 2-adrenergic receptor (48%). Two conserved serine residues in TM5 postulated to be part of a ligand binding site in the adrenergic receptor, suggests that G-36 encodes a catecholaminergic receptor. Northern blot analysis confirmed the expression of G-36 in rat brain, but not in kidney, heart and lung. Several strong hybridizing bands to G-36 were obtained in both human and rat genomic DNA. The general PCR strategy employed here should prove to be extremely useful for the isolation of other members of the G-linked receptor family.

Simple method for the preparation of antigen emulsions for immunization.

We have developed a rapid, safe, and reliable method to prepare emulsions of water-soluble antigens in an adjuvant oil phase for immunization purposes. The method, based on well established emulsification principles, employs a three-way 'T' connector to which three disposable syringes are attached. The system allows the stepwise addition of small volumes of the water phase, into the oil phase. We have compared the time required for emulsification, the rate of antigen release from the emulsion into a physiological phase, and the immunogenic properties of bovine serum albumin and transferrin contained in emulsions made by the new stepwise addition method, with those made by the widely used double-hubbed needle method. We report a significantly shorter (P < 0.001) and a more reproducible emulsification time for the stepwise addition method (6.1 +/- 2.1 min; mean +/- SD) than for the double-hubbed needle method (41.1 +/- 28.0 min). The stepwise addition method always yielded water-in-oil emulsions, while the double-hubbed needle method failed, about 20% of the time, to produce a water-in-oil emulsion after 120 min of mixing. Since the stepwise addition method employs a connector with a larger inner diameter (1.75 mm) than the one required for the double-hubbed needle method (0.84 mm); the pressure required for the former is markedly reduced compared with that required for the latter, thus making the new method safer and less labor-intensive. The rate of antigen release from the emulsions was significantly slower when the stepwise addition method was employed (P < 0.01). There were no differences in viscosity and stability in the emulsions prepared by the two methods. The ability of antigen-containing emulsions to elicit an immune response was found to be identical by the two methods; no significant differences were found in antibody titers as determined by enzyme-linked immunosorbent assays. These characteristics make the stepwise addition system the method of choice.

Inhibitory effect of propylthiouracil on the development of metabolic tolerance to ethanol.

Chronic ethanol administration (4-5 weeks) to female spontaneously hypertensive (SH) rats led to a marked increase in the rate of ethanol metabolism. This was accompanied by an increase in hepatic alcohol dehydrogenase (ADH) and by an increase in the rate of oxygen consumption in perfused livers of these animals. Treatment with the antithyroid drug 6-n-propyl-2-thiouracil (PTU) during the last 9 days (40 mg/kg/day) of the chronic administration of ethanol reduced hepatic oxygen consumption, resulting in a net diminution of the metabolic tolerance to ethanol, despite a further elevation in ADH activity. In these animals, microsomal ethanol-oxidizing system (MEOS) activity was not affected by chronic ethanol administration or by treatment with PTU. Data strongly suggest that in the female SH rat all the metabolic tolerance to ethanol proceeds via the ADH pathway, and that the increase in hepatic oxygen consumption is more important in the development of metabolic tolerance to ethanol than the increased ADH levels.

The swift increase in alcohol metabolism. Inhibition by propylthiouracil.

Administration of a single large dose of ethanol (5 g/kg) to rats elevates the rates of ethanol metabolism and of oxygen consumption in perfused livers in 2-3 hr. Pretreatment with the antithyroid drug propylthiouracil (PTU) for 10 days abolished both of these effects. Under all treatment conditions studied (controls; PTU-pretreatment; acute ethanol treatment; PTU-pretreated + acute ethanol treatment),, a significant correlation between ethanol metabolism and oxygen consumption was observed (r = 0.86). It is concluded that a normal thyroidal state is required to evoKe the swift increase in alcohol metabolism (SIAM) and an elevation of oxygen consumption.

Blood acetaldehyde and the ethanol-induced increase in splanchnic circulation.

Acute oral administration of ethanol significantly increases (50-60%) portal blood flow to the liver. As earlier studies have indicated that this effect is maximal at concentrations of ethanol that saturate the alcohol dehydrogenase (ADH) system and is blocked by the ADH inhibitor 4-methylpyrazol, we investigated the possible role of acetaldehyde, a product in the ADH reaction, as a mediator of this effect. In the first series of experiments it was shown that, contrary to expectations, cyanamide administration prior to alcohol suppressed fully the effect of ethanol on portal blood flow without altering it in the absence of ethanol [ethanol = 69.5 +/- 5.6; ethanol + cyanamide 42.9 +/- 2.4; control = 43.0 +/- 3.0; cyanamide = 55.1 +/- 3.7 ml X min-1 X (kg body wt)-1]. Arterial blood concentrations of acetaldehyde were elevated from 3.6 +/- 0.3 microM in the presence of ethanol to 293 +/- 48 microM in the presence of ethanol + cyanamide. Infusion of acetaldehyde either into the left ventricle, resulting in arterial blood acetaldehyde levels of 227 +/- 77 microM, or into the portal circulation, resulting in arterial blood levels of 198 +/- 40 microM, did not modify portal blood flow or splanchnic hemodynamics, nor the effect of ethanol per se. The combination of cyanamide + ethanol significantly reduced total peripheral resistance (from 28 +/- 3 to 19 +/- 2 dyne X cm X sec-5), while neither ethanol or cyanamide per se, nor acetaldehyde affected total peripheral resistance. Data suggest that acetaldehyde is not involved in the ethanol-mediated increase in portal vein flow. Further studies indicate that the effects of cyanamide in suppressing the ethanol-induced increase in portal blood flow and increasing total peripheral resistance appear to be related to an ethanol-cyanamide interaction which is independent of the acetaldehyde levels in the circulation.

Effect of propylthiouracil treatment on NADPH-cytochrome P450 reductase levels, oxygen consumption and hydroxyl radical formation in liver microsomes from rats fed ethanol or acetone chronically.

The antithyroid drug propylthiouracil (PTU) has been shown previously to reduce hepatic oxygen utilization and to protect the liver from ethanol-induced injury. The present study examined the effect of PTU on hepatic microsomal oxygen consumption and on the activities of NADPH-cytochrome P450 reductase (CYP-reductase) and cytochrome P4502E1 (CYP2E1) in rats receiving ethanol or acetone chronically. Liver microsomes from rats treated with ethanol for 29 days displayed increases in (i) O2 consumption (70%), (ii) hydroxyl radical (.OH) production (49%) and (iii) ethanol oxidation (50%). Microsomal CYP2E1 levels were increased markedly by chronic ethanol administration, while CYP-reductase was affected marginally, but not significantly (P = 0.06). Chronic treatment with acetone for 14 days, produced similar effects, except that .OH production was not enhanced. Administration of PTU (25 mg/kg/day) to ethanol- or acetone-fed rats, for 10 and 14 days, respectively, led to a marked reduction in the levels and activity of CYP-reductase, and to a decrease in the rates of microsomal O2 consumption, .OH production and ethanol oxidation, but did not lower the levels of CYP2E1 or the metabolism of the CYP2E1 substrate N,N-nitrosodimethylamine. These data suggest that the ability of PTU to protect the liver from ethanol-induced injury may be due to a reduction in the levels of CYP-reductase, thereby minimizing the enhancement of microsomal oxygen consumption and free radical generation associated with ethanol-induced CYP2E1 activity.

Reduction of voluntary alcohol consumption in the rat by transplantation of hypothalamic grafts.

Stimulation of the peripheral renin-angiotensin system has been shown previously to decrease the voluntary intake of ethanol in the rat. The existence of a separate brain renin-angiotensin system, independent from that of the periphery, has been widely demonstrated. The brain renin-angiotensin system plays an important role in the regulation of water and electrolyte balance and neuroendocrine function. However, the role played by this system in the regulation of voluntary alcohol consumption has not yet been studied. The goal of the present work was to assess the feasibility of decreasing the voluntary alcohol intake in a strain of rats (Rapp SS/Jr rats) that have a genetic deficiency responsible for a low activity of the renin-angiotensin system and elevated alcohol intake. Adult Rapp SS/Jr rats received intraventricular transplants of fetal hypothalamic grafts (from normal donors), known to contain angiotensin-immunoreactive cell bodies. Our studies revealed that angiotensin-immunoreactivity in the cell bodies and fibres in the paraventricular, supraoptic and suprachiasmatic nuclei of the hypothalamus in Rapp SS/Jr rats was markedly reduced. Animals that had surviving grafts containing angiotensin-immunoreactive cell bodies in the dorsal third ventricle--but not in the ventral third ventricle, in the lateral ventricles, or sham operated animals--had a 40% decrease of their voluntary alcohol intake, when compared to their intake before surgery, or to the control group. However, water consumption was not reduced in both the sham and transplanted animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement of noradrenaline-induced metabolic coronary dilatation by ethanol.

Isolated perfused rat hearts receiving noradrenaline as a cardiostimulatory agent show the characteristic metabolic coronary dilatations which correlate with the inotropic effect elicited by noradrenaline. Addition of ethanol (20-400 mg/dl) to the perfusion fluid produced a concentration-dependent enhancement of the metabolic coronary dilatation. The latter was increased by 50% at about 125 mg ethanol/dl. Since the inotropic responses to noradrenaline were not affected by ethanol it is suggested that alcohol produces an alteration in the system that normally adapts the coronary flow to an increased cardiac performance. The effect of ethanol was fully reversible; removal of alcohol from the perfusion fluid restored the metabolic coronary dilatation in response to noradrenaline to control values. At high concentrations, 200-400 mg/dl, ethanol produced a small but significant reduction in contractility of the myocardium (11.1 +/- 2.4%). At these concentrations ethanol enhanced the noradrenaline induced metabolic coronary dilatation by about 100%. These data indicate that ethanol at concentrations that are commonly found in blood in vivo may be beneficial in facilitating the coronary reactions during cardiac exertion. However cardiodepressant effects, particularly at higher concentrations, must also be considered.

Effect of alpha- and beta-blockers on ethanol metabolism.

The acute administration of propranolol or phentolamine resulted in a small (16-19%) but significant reduction in the rate of ethanol disappearance in vivo in the naive Wistar rat. A reduction of essentially similar magnitude was also observed in ethanol-treated rats and pair-fed (sucrose) control animals, following the administration of these blockers.

On the characteristics of alcohol-induced liver enlargement and its possible hemodynamic consequences.

Chronic consumption of alcohol leads to an increase in liver weight, primarily due to an increase in hepatocyte volume. About 50-60% of such an increase is due to an increase in intracellular water. Accumulation of intracellular K+ osmotically accounts for about one half of the increase in intracellular water, while an increase in soluble proteins plays only a minor role in such an increase in cell volume. The increase in intracellular water is accompanied by a relative reduction in water in the extracellular space, probably due to compression of the extracellular volume by the enlarged hepatocytes. It is suggested that such an increase in hepatocyte size, with an attending reduction of the extracellular volume, results in an increased resistance to blood flow through the liver and thus in an increase in portal pressure. In alcoholics, portal and intrahepatic pressure correlate with cell size both in cirrhotics (r = 0.79) and in non-cirrhotics (r = 0.74), thus suggesting that cell enlargement plays a major role in the production of portal hypertension in the alcoholic.

A simple technique for quantifying intoxication-induced by low doses of ethanol.

A simple technique for the measurement of intoxication induced by low doses of alcohol in the rat was developed. Rats are required to maintained their balance on a rectangular wooden bar that oscillates in a 120 degree angle in an arch-like fashion. A steady baseline can be obtained for each animal with approximately 10 min of training time. Ethanol, in a dose range from 0.5-1.5 g/kg, given orally or by IP route, impairs animal's performance in a dose-related manner. At the same blood ethanol concentration, a higher degree of impairment is observed at higher oscillating frequency. Significant impairment of performance can be detected at ethanol dose of 0.5 g/kg given IP or orally. Pentobarbital and chlordiazepoxide, in doses of comparable potencies to those of ethanol doses also produce a dose-related impairment of performance. The oscillating bar test is a simple but sensitive test that can qualitatively assess intoxication induced by low doses of ethanol or other sedative hypnotic drugs.

The dependence of the dropping mercury electrode potential at constant current on the concentration of an electroactive constituent involved in reversible or irreversible electrode reactions.

A new method is described in which the potential of the d.m.e. is measured as a function of the concentration of an electroactive constituent when a constant current is maintained by adjusting the voltage applied to the polarographic cell. Equations are derived describing the expected potential change caused by changing the concentration of a constituent involved in a reversible or an irreversible electrode reaction. Graphical interpretations of the derived equation are made, indicating the most suitable conditions for performing potential measurements, yielding potential differences that greatly exceed those obtained by conventional potentiometry, especially when the method is applied to irreversible electrode reactions at the d.m.e. Experimental evidence is presented, which not only verifies all expectations, but also indicates that the method offers a new approach to the investigation of some fundamental problems.