Application Of SITS Research Articles

The effects of system and information quality on acceptance of digital public service transportations

The application of ICT in central and regional governments to cities in Indonesia seems to be the new face of the National bureaucracy, not least with digital public transportation services, Surabaya is a pilot application of smart cities because one of them implementing the Surabaya Smart Transportation System (SITS), this condition further strengthens that policy Public digital services are taken to make it easier for the public to monitor the crowd or the density of the highway, unfortunately, if you review the SITS comment column on Google Play, the negative sentiment is far big more than the positive sentiment. So, this study aims to capture the phenomenon of resistance by exploring the quality of information and system quality as predictors of public acceptance of the application of SITS. A result, empirically the quality of information and the quality of the system indirectly affect public acceptance of the application of SITS, as among the findings served that system quality is more dominant in influencing acceptance. So, it is highly recommended that the city government pays attention to the development of SITS applications based on system reliability.

EFFECT OF DIFFERENT PLANTING GEOMETRY AND SULPHUR FERTILIZATION ON GROWTH AND YIELD OF SUNFLOWER IN SUNFLOWER + GREENGRAM INTERCROPPING SYSTEM

A field experiment was carried out during Mar-May, 2019 at the Experimental Farm, Department of Agronomy, Faculty of Agriculture, Annamalai University, Annamalai nagar-608002, to study the effect of different planting geometry and sulphur levels in sunflower + greengram intercropping system on the growth and yield attributes and yield of sunflower. The experiment consisted of twenty treatments and were laid out in factorial randomized block design with two replications. The treatment consisted of Factor A(different plant geometry levels): M1 - sole sunflower (60 x 30 cm),M2 - sunflower (60 x 30 cm) + 1 row of greengram, M3 - sunflower (90 x 30 cm) + 2 rows of greengram, M4 - sunflower (120 x 30 cm) + 3 rows of greengram, M5 -sole greengram and Factor B (sulphur levels): S0 - 0 kg S ha-1, S1 - 20kgS ha-1,S2 - 40kg S ha-1 and S3 - 60kg S ha-1.The results revealedthat growth, yield attributes and yieldwere significantly influenced by different plant geometry and various sulphur levels. Among the different planting geometry levels tried, sole sunflower (60 x 30 cm) (M1 ) significantly recorded maximum growth and yield attributes and yield of sunflower. With regard to various sulphur levels tried, application of sulphur at 40 kg ha-1 (S2 ) significantly recorded maximum growth and yield attributes and yield of sunflower. Interaction between planting geometry and sulphur levels were significant.Among the treatment combinations tried, sole cropping of sunflower (60 x 30 cm) along with application of S at40 kg ha-1 (M1 S2 )had a spectacular effect on growth and yield attributes, ultimately leading to maximum seed yield(2152 kg ha-1). The minimum growth attributes were recorded in sunflower(120 x 30 cm) intercropped with three rows of greengram along with application ofSat 0 kg ha-1 (M4 S0 ).

신제품 콘셉트 발상을 위한 SIT&BCC 활용에 관한 연구

신제품 콘셉트 발상을 위한 SIT&BCC 활용에 관한 연구

Effects of chloride ion channel and its blockers on myocardial ischemia reperfusion arrhythmias in rabbits

To explore the impact of chloride ion channel and its blockers 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS), cyanato-stilbene-2, 2'-disulfonic acid (SITS) and 5-nitro-2-(3-phenyl-propylamino) benzoic acid (NPPB) on arrhythmias caused by myocardial ischemia reperfusion. A total of 40 rabbits were divided into control, ischemia reperfusion, DIDS low-dose, DIDS high-dose, SITS low-dose, SITS high-dose, NPPB low-dose and NPPB high-dose groups. Myocardial ischemia reperfusion model was established by ligation of anterior descending coronary artery. And standard limb lead II of electrocardiogram (ECG) was continuously monitored during the experimental process. Then comparisons of heart rate, ECG P wave, R wave, T wave, ST segment changes and arrhythmias score were made between the above groups. During 30-minute ischemia, compared with the control group, all other groups showed significantly decreased heart rate ((199.8 ± 4.0) - (253.6 ± 2.1) vs (267.0 ± 3.4), all P < 0.01), elevated ECG P wave ((0.216 ± 0.019) - (0.356 ± 0.024) vs (0.186 ± 0.019), all P < 0.01), R wave ((0.564 ± 0.017) - (1.138 ± 0.048) vs (0.506 ± 0.018), all P < 0.01), T wave ((0.542 ± 0.013) - (0.856 ± 0.045) vs (0.278 ± 0.015), all P < 0.01) and ST segment ((0.326 ± 0.027) - (0.668 ± 0.054) vs (0.024 ± 0.023), all P < 0.01) and increased arrhythmia score ((1.4 ± 0.5) - (4.6 ± 0.5) vs (0.4 ± 0.5), all P < 0.01). Compared with the ischemia reperfusion group, the above indices significantly improved in the intervention groups (heart rate: (214.8 ± 3.4) - (246.8 ± 4.0) vs (199.8 ± 4.0), all P < 0.01; P wave: (0.216 ± 0.019) - (0.316 ± 0.011) vs (0.356 ± 0.024), all P < 0.01; R wave: (0.564 ± 0.017) - (0.980 ± 0.035) vs (1.138 ± 0.048), all P < 0.01; T wave: (0.542 ± 0.013) - (0.792 ± 0.026) vs (0.856 ± 0.045), all P < 0.01; ST segment: (0.326 ± 0.027) - (0.596 ± 0.018) vs (0.668 ± 0.054), all P < 0.01; arrhythmia score: (1.4 ± 0.5) - (3.8 ± 0.4) vs (4.6 ± 0.5), all P < 0.01). Among which, the DIDS group was the best, followed by the SITS group and then the NPPB group. And the high-dose subgroups were better than those of the low-dose subgroups. During 60-minute reperfusion, the decreased heart rate upswing significantly in each group and the elevated P wave, R wave, T wave and ST segment fell back gradually. The DIDS group showed the most obvious amplitude change, followed by the SITS group and then the NPPB group. And the high-dose subgroups were better than those of the low-dose subgroups. The arrhythmia score during reperfusion showed the same trend. Chloride ion channel is involved in the generation of myocardial ischemia reperfusion arrhythmia.Early application of chloride ion channel blockers DIDS, SITS and NPPB may improve the ECG manifestations and reduce the degree of reperfusion arrhythmia.

Corrigendum

William C. WohlforthUnipolarity, Status Competition, and Great Power Wardoi:10.1017/S0043887109000021World Politics 61, no. 1 (January 2009)Pages 28–57The author neglected to acknowledge the following unpublished manuscript in footnote 71 (page 54) of the original article: Deborah Welch Larson and Alexei Shevchenko, “United States' Grand Strategy and Rising Powers: Russia and China.” This paper by Larson and Shevchenko is the most comprehensive application of SIT to post-cold war Russian and Chinese strategy.

Advances in the clinical application of allergen specific-immunotherapy

Besides allergen avoidance,allergen-specific immunotherapy(SIT)is the only treatment that may alter the natural course of allergic diseases.which ale traditionally managed by subcutaneous immunization with natural allergen extracts.With the development in clinical medicine.molecular biology and molecular immunology,great progress has been made in SIT.Recently,various novel vaccines and adjuvants have been exploited and developed,and clinicians have attempted to use sublingual immunotherapy in clinical settings.Also.SIT has been introduced into the prevention and therapy of allergic rhinoconjunctiVitjs,allergic asthma and venom allergy.HoweveL the application of SIT in atopic dermatitis is still in experimental stage. Key words: Allergens; Adjuvants,immunologic; Vaccines

Who Is Blameworthy? : Social Identity and Inter-Group Bullying

Using social identity theory (SIT; Tajfel and Turner, 1979) and social identity development theory (SIDT; Nesdale, 1999) as a framework, this study investigated attitudes towards inter-group bullying at school. Preadolescent boys and girls ( n = 314) participated in a study, utilizing the short story technique, in which they were induced to identify with their own school-class, whose social status was manipulated to be high or low. A story was told in which the group engaged in an episode of physical bullying as either the bully group or the victim group. The designed out-group was another class of the same school. Attribution of blame to both the in-group and the out-group was assessed. Results showed a higher preference for the in-group when it was the victimized group. Moreover, participants blamed the high status out-group more than any other group. The results are discussed in relation to the literature about bullying and the application of SIT and SIDT to this domain.

The enhancing effect of nasal absorption of FITC-dextran 4,400 by β-sitosterol β- d-glucoside in rabbits

The effect and mechanism of action of β-sitosterol β- d-glucoside (Sit-G) on the in vitro and in vivo nasal absorption of FITC-dextran (molecular weight, 4400; FD-4) in rabbits were studied in comparison with β-sitosterol (Sit). The FD-4 permeation in the powder dosage form was increased by Sit-G and Sit and related to the uptake of Sit-G and Sit with no changes in the amount of cholesterol in the excised nasal mucosa. The application of Sit and Sit-G increased FD-4 permeation with and without a decrease in transepithelial resistance (TEER), respectively. These results suggested that the mechanism of the enhancement by Sit-G was different from those of Sit and sodium caprate; Sit-G may exert its effects mainly via the transcellular pathway due to perturbation of the mucosal membrane.

Role of endolymphatic anion transport in forskolin-induced Cl − activity increase of scala media

To determine the role of anion transport in the forskolin-induced Cl − increase of scala media (SM), effects of forskolin on the EP (endocochlear potential) and Cl − activity (A Cl) in SM were examined with double-barrelled Cl −-selective microelectrodes. The experiments were carried out on guinea pig cochleae, using a few anion transport inhibitors: IAA-94 for a Cl − channel blocker, bumetanide (BU) for an Na +/K +/2Cl − cotransport blocker, and SITS and DIDS for Cl − HCO 3 − exchange blockers. The application of forskolin (200 μM) into scala vestibuli (SV) caused a 20 mEq increase of endolymphatic A Cl and a 15 mV elevation of EP, and IAA-94 with forskolin completely abolished these responses. Although each application of BU, SITS or DIDS did not completely suppress EP elevation, the concurrent application of these inhibitors completely suppressed EP with endolymphatic A Cl increase. The results indicate the involvement of Cl − channels, Na +/K +/2Cl − cotransport and Cl − HCO 3 − exchange in forskolin-induced increase of A Cl and EP. The role of adenylate cyclase activation and Cl − transport in endolymph homeostasis was discussed.

Mechanism of pHi regulation by locust neurones in isolated ganglia: a microelectrode study.

1. We have measured membrane potential (Em) and intracellular pH (pHi), and sodium and chloride activities (aNai and aCli) in exposed dorsal unpaired median neurones in isolated metathoracic ganglia from the desert locust, Schistocerca gregaria using eccentric double-barrelled ion-sensitive microelectrodes. 2. In the absence of added HCO3- the steady-state pHi was 7.21 +/- 0.13 (mean +/- S.D.) at a mean membrane potential of -37 +/- 7.0 mV (S.D.) (n = 44 cells). The pHi was always more alkaline than predicted for passive H+ distribution. 3. The pHi recovery from acid loads, induced by weak acid application or weak base removal, was pHi dependent and associated, in both the presence and absence of added CO2-HCO3-, with a transient increase in aNai. 4. In the absence of added HCO3-, application of the Na(+)-H+ exchange blocker amiloride or external Na+ removal caused intracellular acidification. Also in the absence of added HCO3- the inhibitor SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid) caused an acidification of about 0.2 pH units which was not additive to the effects of the removal of external Na+. 5. We found that the application of a CO2-HCO3(-)-containing solution increased the rate of pHi recovery from acidification. 6. Intracellular chloride was decreased by intracellular acidification in the presence of added CO2-HCO3-. In the presence of amiloride, intracellular Cl- depletion inhibited pHi regulation. 7. Simultaneous application of SITS (160 microM) and removal of CO2-HCO3- revealed a continuous underlying acid load of 0.03-0.05 pH unit min-1. 8. We conclude that locust neurones possess at least two pHi-regulating mechanisms which operate against a continuous acid load. One is a Na(+)-H+ exchanger which can be blocked by amiloride, while the second is a Na(+)-dependent Cl(-)-HCO3- exchanger. The latter mechanism appears to be able to operate in the absence of added HCO3- and can recover pHi to around pH 7.4; it is probably the main pHi regulating mechanism. The Na(+)-H+ exchanger appears to activate at more acid pHi and being less energy efficient may serve a protective role.

Studies on Stability Constants of Europium(III) Carbonate Complexes and Application of SIT and Ion-Pairing Models

Studies on Stability Constants of Europium(III) Carbonate Complexes and Application of SIT and Ion-Pairing Models

Characterization of a 25-pS nonselective cation channel in a cultured secretory epithelial cell line

We have studied a 25-pS nonselective cation channel from the apical membranes of cell line ST885, derived from neonatal mouse mandibular glands. Its Cl- permeability was not significantly different from zero. The permeabilities (relative to Na+) for inorganic cations were NH4+ (1.87) greater than K+ (1.12) greater than Li+ (1.02) greater than Na+ (1) greater than Rb+ (0.81) greater than Mg2+ (0.07) greater than Ca2+ (0.002), and for organic cations, guanidinium (1.61) greater than ethanolamine (0.70) greater than 4-aminopyridine (0.66) greater than diethylamine (0.54) greater than piperazine (0.25) greater than Tris (0.18) greater than N-methylglucamine (0.12). The Tris and N-methylglucamine permeabilities differed significantly from zero. Fitting the Renkin equation indicated that the channel had an equivalent pore radius of 0.49 nm. The channel was activated by Ca2+ on the cytosolic surface (greater than 0.1 mmol/liter) with a Hill coefficient of 1.2; it was also activated by depolarization. Open- and closed-time histograms indicated that it had at least two open and two closed states. The channel was blocked by cytosolic AMP or ATP (0.1 mmol/liter). It was also blocked by the Cl- channel blocker, diphenylamine-2-carboxylate (DPC; 0.1 mmol/liter), applied to the extracellular but not the cytosolic surface. 4-Amino-pyridine, which permeated the channel when applied to the extracellular surface, blocked it when applied in low concentrations (5 mmol/liter) to the cytosolic surface. Quinine (0.1 mmol/liter) blocked from both the extracellular and cytosolic surfaces, blockade from either side being enhanced by depolarization. The channel was held open by application of SITS (0.1 mmol/liter) to the cytosolic surface. The channel shows striking similarities to the nicotinic acetylcholine receptor channel, viz., both channel types are abnormally permeable to 4-aminopyridine applied externally, and their selectivity sequences for inorganic ions are similar and for organic cations are identical.

Evidence of chloride/bicarbonate exchange mediating bicarbonate efflux from S3 segments of rabbit renal proximal tubule

The mechanism of HCO3- exit from rabbit renal proximal tubule S3 segments was investigated. Isolated tubules were perfused luminally and peritubularly with test solutions and cell pH (pHi), cell Cl- activity ([Cl-]i) and cell Na+ activity ([Na+]i) were measured with ion-selective microelectrodes. From the response of pHi and [Cl-]i to changes in bath Cl- or HCO3- concentrations a Cl-/HCO3- exchanger was identified in the basolateral cell membrane. It was reversibly inhibited by millimolar concentrations of the disulfonic stilbene SITS (4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid). Cell potential measurements and preliminary determinations of initial ion flux rates suggested a stoichiometry of Cl- to HCO3- flux near 1.0. The transport rate appeared to saturate already at low bath Cl- concentrations (approximately 30 mmol/l), but it was independent of bath pH in the range of 7.4-6.4. Cl-/HCO3- exchange was not directly coupled to Na+ flux although in approximately half of the experiments long-term incubation in Na(+)-free solutions indirectly inhibited the exchanger. Sudden application of SITS under control conditions revealed that the exchanger normally facilitates the exit of HCO3- from cell to interstitium at the expense of Cl- uptake into the cell. How Cl- ions recirculate towards the peritubular surface is presently not known.

Intracellular pH regulation in cultured mouse oligodendrocytes.

1. Intracellular pH (pHi) and the mechanism of pHi regulation have been investigated in cultured oligodendrocytes from mouse spinal cord using double-barrelled neutral-carrier H+-selective microelectrodes. The distribution of H+ was not in electrochemical equilibrium. The pHi was more alkaline than the pH of the bathing medium (pHo), namely 7.5 at pHo 7.2 at 7.6 at pHo 7.4. 2. Removal of HCO3- from the bathing medium reduced the steady-state pHi by 0.4 units. An increase in extracellular K+ caused, with a delay, an increase in pHi. A decrease in pHo to 6.2 caused an acidification of pHi by 0.5 units. 3. The pHi regulation was studied by applying and subsequently removing NH4+ which resulted in an acidification of the cell. The subsequent recovery of pHi could then be analysed. The recovery from an acidification by 1 pH unit lasted 3-10 min. In HCO3- -free solution pHi recovery was slowed. 4. In HCO3- -free solution pHi recovery was completely blocked when either Na+ was removed or when amiloride was applied indicating an exclusive activation of the Na+-H+ exchanger. 5. In the presence of HCO3-, removal of Na+ also completely blocked pHi recovery. When Na+ was readded, pHi recovered. In HCO3- -containing solution amiloride slightly slowed, but did not block pHi recovery. 6. Removal of Cl- or application of SITS, DIDS or furosemide, blockers of Cl- -coupled transport mechanisms, did not affect the pHi recovery in the presence of HCO3-. 7. In conclusion, oligodendrocytes possess two mechanisms regulating pHi, a Na+-H+ exchanger and a Na+-HCO3- co-transporter while the latter is clearly more potent. It follows that pHi regulation of oligodendrocytes is dependent on the transmembrane Na+ gradient and is strictly separated from regulation of internal Cl-.

Intracellular chloride activity of rabbit proximal straight tubule perfused in vitro.

To examine the cellular mechanism of Cl- transport in the proximal tubule, cell Cl- activity (aiCl) was measured with double-barreled Cl(-)-selective microelectrodes in the rabbit proximal straight tubules (PST) perfused in vitro. When tubules were perfused and bathed with ultrafiltrate-like solution, aiCl (corrected for the interference from undetermined intracellular anions, 4.2 mM) was 17.8 +/- 0.5 mM (n = 90), and this value was 1.3 times higher than that predicted from passive distribution (basolateral membrane potential, Vbl = -51.9 +/- 0.8 mV). Reducing either luminal or bath Cl- indicated that the basolateral membrane plays a more important role as a determinant of aiCl. aiCl reduction rates induced by luminal Cl- removal was inhibited by 75% by 1 mM SITS added to the lumen but was not inhibited by furosemide (0.1 mM). Application of SITS in the lumen in the control condition, however, did not change aiCl appreciably. Reducing the luminal HCO3- from 25 to 5 mM did not significantly change aiCl or Vbl. Replacing luminal Na+ with choline decreased aiCl but these effects were still present when luminal Cl- was absent. We conclude that in the rabbit PST: 1) Cl- is taken up into the cell against the electrochemical gradient, 2) the basolateral membrane plays a more important role in the regulation of aiCl, and 3) luminal Cl- transport is SITS sensitive and Na+ independent.

Evidence for coupled transport of bicarbonate and sodium in cultured bovine corneal endothelial cells.

Using intracellular microelectrode technique, the response of the voltage V across the plasma membrane of cultured bovine corneal endothelial cells to changes in sodium and bicarbonate concentrations was investigated. (1) The electrical response to changes in [HCO3-]o (depolarization upon lowering and hyperpolarization upon raising [HCO3-]o) was dependent on sodium. Lithium could fairly well be substituted for sodium, whereas potassium or choline were much less effective. (2) Removal of external sodium caused a depolarization, while a readdition led to a hyperpolarization, which increased with time of preincubation in the sodium-depleted medium. (3) The response to changes in [Na+]o was dependent on bicarbonate. In a nominally bicarbonate-free medium, its amplitude was decreased or even reversed in sign. (4) Application of SITS or DIDS (10(-3) M) had a similar effect on the response to sodium as bicarbonate-depleted medium. (5) At [Na+]o = 151 mM and [HCO3-]o = 46 mM, the transients of V depended, with 39.0 +/- 9.0 (SD) mV/decade, on bicarbonate and, with 15.3 +/- 5.8 (SD) mV/decade, on sodium. (6) After the preincubation of cells with lithium, replacement of Li by choline led to similar effects as the replacement of sodium by choline, though the response of V was smaller with Li. This response could be reduced or reversed by the removal of bicarbonate or by the application of SITS. (7) Amiloride (10(-3) M) caused a reversible hyperpolarization of the steady-state potential by 8.5 +/- 2.6 mV (SD). It did not affect the immediate response to changes in [Na+]o or [HCO3-]o, but reduced the speed of regaining the steady-state potential after a change in [HCO3-]o. (8) Ouabain (10(-4) M) caused a fast depolarization of -6.8 +/- 1.1 (SD) mV, which was followed by a continuing slower depolarization. The effect was almost identical at 10(-5) M. (9) It is suggested, that corneal endothelial cells possess a cotransport for sodium and bicarbonate, which transports net negative charge with these ions. It is inhibitable by stilbenes, but not directly affected by amiloride or ouabain. Lithium is a good substitute for sodium with respect to bicarbonate transport and is transported itself. In addition, the effect of amiloride provides indirect evidence for the existence of a Na+/H+-antiport. A model for the transepithelial transport of bicarbonate across the corneal endothelium is proposed.

Acid influx into snail neurones caused by reversal of the normal pHi-regulating system.

Intracellular pH (pHi), and Na+ and Cl- activities were measured with ion-sensitive micro-electrodes in Helix aspersa neurones, and the effects of reducing external pH (pHo) were investigated. When pHo was changed from 7.5 to 6.5 keeping CO2 constant, there was a slow fall in pHi, a rise in internal Cl and a fall in internal Na. These ionic changes are opposite to those caused by normal operation of the pHi-regulating system. These effects of external acidification were inhibited by the application of SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid) or by the removal of external Cl. Raising intracellular Na activity by inhibiting the Na pump increased the rate of fall of pHi in acid solutions. In acid solutions the average rate of acid uptake attributable to reversed pHi-regulation was about three times the rate of loss of internal Na, and about twice the rate of Cl uptake. We conclude that these intracellular ion changes in acid solutions were largely due to a reversal of the pHi-regulating mechanism, so that it carried acid into, rather than out of, the cell interior.

An investigation of the ionic mechanism of intracellular pH regulation in mouse soleus muscle fibres.

1. Intracellular pH (pH(i)) of surface fibres of the mouse soleus muscle was measured in vitro by recessed-tip pH-sensitive micro-electrodes. pH(i) was displaced in an acid direction by removal of external (NH(4))(2)SO(4) after a short exposure, and the mechanism of recovery from this acidification was investigated.2. Removal of external K caused a very slow acidification (probably due to the decreasing Na gradient) but had no effect on the rate of pH(i) recovery following acidification. This indicates that K(+)-H(+) exchange is not involved in the pH(i) regulating system.3. Short applications of 10(-4)M ouabain had no obvious effect on pH(i) and did not alter the rate of pH(i) recovery following acidification. This suggests that there is no direct connexion between the regulation of pH(i) and the Na pump.4. Reduction of external Ca from 10 to 1 mM caused a transient fall in pH(i), but the rate of pH(i) recovery following acidification was unaffected. This suggests that Ca(2+)-H(+) exchange is not involved in the pH(i) regulating system.5. An 11% reduction in external Na caused a significant slowing of pH(i) recovery following acidification. 90% or complete removal of external Na almost stopped pH(i) recovery. This suggests that Na(+)-H(+) exchange is involved in pH(i) regulation.6. Amiloride (10(-4)M) reversibly reduced the rate of pH(i) recovery to much the same extent as removal of external Na. Its effect was not additive to that of removal of external Na.7. Internal Na ion concentration ([Na(+)](i)), measured using Na(+)-sensitive micro-electrodes, fell on application of (NH(4))(2)SO(4) and increased on its removal. The increase transiently raised [Na(+)](i) above the level recorded before (NH(4))(2)SO(4) application. This overshoot of [Na(+)](i) was almost completely inhibited by amiloride. This is consistent with the involvement of Na(+)-H(+) exchange in the pH(i) regulating system.8. Removal of external CO(2) or application of SITS (10(-4)M) caused some slowing of the rate of pH(i) recovery following acidification by removal of (NH(4))(2)SO(4). The effect of SITS was additive to that of Na-free Ringer or amiloride. These results suggest that Cl(-)-HCO(3) (-) exchange is also involved in the pH(i) regulating system and that it is a separate mechanism. Under the conditions used, Cl(-)-HCO(3) (-) exchange formed about 20% of the pH(i) regulating system.9. Decreasing the temperature from 37 to 28 degrees C not only caused an increase in pH(i), but also considerably slowed the rate of pH(i) recovery following acidification. We have calculated a Q(10) for Na(+)-H(+) exchange of 1.4 and for Cl(-)-HCO(3) (-) exchange, 6.9.10. We conclude that the pH(i) regulating system is comprised of two separate ionic exchange mechanisms. The major mechanism is Na(+)-H(+) exchange, which is probably driven by the transmembrane Na gradient. The other mechanism is Cl(-)-HCO(3) (-) exchange, which probably requires metabolic energy.