• The Journal of Korean Physical Therapy
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• v.30 no.5
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• pp.181-186
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• 2018

Purpose: This study investigated the effects of home-based exercise intensity on the aerobic capacity and 1 year re-hospitalization rate in patients with chronic heart failure (CHF). Methods: Forty seven patients with CHF (males 33, females 14, age $61.3{\pm}9.8years$) participated in this study. The patients were allocated randomly to 3 groups in accordance with home-based exercise intensity: no home based exercise (NHE, 40%, n=19), moderate intensity home-based exercise (MIHE, 43%, n=20), and high intensity home based exercise (HIHE, 17%, n=8). All patients completed the symptom-limited cardiopulmonary exercise (CPX) test safely at the cardiac rehabilitation hospital. Results: The NHE group significantly showed lower peak $VO_2$ and a higher $VE/VCO_2$ slope than the MIHE (p<0.05) and HIHE (p<0.01) groups. On the other hand, the NHE group did not show significant differences in the other hemodynamic responses, such as heart rate (HR) max, HR reserve, maximal systolic blood pressure (SBP), and SBP reserve. Nine out of 19 NHE patients (47%) were re-hospitalized related to heart disease and two out of 20 MIHE (10%) patients were re-hospitalized, but nobody in the HIHE group were re-hospitalized within 1 year from the CPX test. Conclusion: In patients with CHF, home-based self-exercise is one of the important factors for reducing the re-hospitalization rate. In addition, improved aerobic capacity is strongly associated with a lower re-hospitalization rate. In particular, re-hospitalized CHF patients showed significant differences in respiratory parameters and hemodynamic parameters compared to the non-re-hospitalized patients.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.6
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• pp.331-336
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• 2008

The present study was aimed to determine whether there is an altered regulation of tubular transporters in gentamicin-induced nephropathy. Sprague-Dawley male rats ($200{\sim}250\;g$) were subcutaneously injected with gentamicin (100 mg/kg per day) for 7 days, and the expression of tubular transporters was determined by immunoblotting and immunohistochemistry. The mRNA and protein expression of OAT was also determined. Gentamicin-treated rats exhibited significantly decreased creatinine clearance along with increased plasma creatinine levels. Accordingly, the fractional excretion of sodium increased. Urine volume was increased, while urine osmolality and free water reabsorption were decreased. Immunoblotting and immunohistochemistry revealed decreased expression of $Na^+/K^+$-ATPase, NHE3, NBC1, and AQP1 in the kidney of gentamicin-treated rats. The expression of OAT1 and OAT3 was also decreased. Gentamicin-induced nephropathy may at least in part be causally related with a decreased expression of $Na^+/K^+$-ATPase, NHE3, NBC1, AQP1 and OAT.

• Biomolecules & Therapeutics
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• v.19 no.4
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• pp.445-450
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• 2011

Preciously, we demonstrated that a novel NHE-1 inhibitor, KR-33028 attenuated cortical neuronal apoptosis induced by glutamate. In the present study, we investigated the signaling mechanism of neuroprotective effect of KR-33028 against glutamate-induced neuronal apoptosis, especially focusing on mitochondrial death pathway. Our data showed that glutamate induces a biphasic rise in mitochondrial $Ca^{2+}$ and that KR-33028 significantly prevents the second phase increase, but not the first phase increase in mitochondrial $Ca^{2+}$. Furthermore, KR-33028 restored the ${\Delta}{\Psi}_m$ dissipation and cytochrome c release into cytoplasm induced by glutamate in a concentration-dependent manner. The inhibition of mitochondrial $Ca^{2+}$ overload by ruthenium red also inhibited glutamate-induced apoptotic cell death, mitochondrial membrane potential, ${\Delta}{\Psi}_m$ dissipation and cytochrome c release. These data suggest that inhibition of mitochondrial $Ca^{2+}$ overload is likely to be attributable to anti-apoptotic effect of KR-33028. Taken together, our results suggest that anti-apoptotic effects of NHE-1 inhibitor, KR-33028 may be mediated through maintenance of mitochondrial function.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.53 no.6
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• pp.870-877
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• 2020

Twenty-three Bacillus cereus strain isolated from commercial jeotgal were investigated for 11 toxin genes and susceptibility to 25 different antimicrobials. The hemolytic enterotoxins hblA, hblC, and hblD were detected in 13.0%, and non-hemolytic enterotoxins nheA, nheB, and nheC were detected in 26.1%, 100%, and 100% of the isolates, respectively. The positive rates of cytK, entFM, becT, hlyII, and ces were 73.9%, 60.9%, 26.1%, 8.7%, and 0.0%, respectively. According to the disk diffusion susceptibility test, all of the strains studied were resistant to cefuroxime, followed by cefoxitin (78.3%), oxacillin (78.3%), ampicillin (69.6%), penicillin G (69.6%), and amoxicillin (65.2%). However, all the strains were susceptible to 11 other antimicrobials, including amikacin, chloramphenicol, and ciprofloxacin. The average minimum inhibitory concentrations of amoxicillin, ampicillin, and cefuroxime against B. cereus were 462.9, 235.0, and 135.0 ㎍/mL, respectively. These results highlight the need for sanitizing commercial jeotgal, and provide evidence to help reduce the risk of jeotgal contamination by antimicrobial-resistant bacteria.

• Applied Biological Chemistry
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• v.51 no.4
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• pp.263-268
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• 2008

Seventy-one Bacillus cereus strains (12 references and 59 food isolates) were analyzed for the occurrence of five different enterotoxin genes (nheABC, hblCDA, entFM, cytK, and bceT) and one emetic toxin cereulide synthetase gene (ces) by PCR (polymerase chain reaction). PCR analysis revealed eight toxigenic patterns in all B. cereus strains tested; they all carried both entFM and nheABC. The presence of hblCDA, cytK, and bceT varied according to the enterotoxin-producing strains, among which hblCDA was the least frequently detected in the food-isolated strains. Only five B. cereus strains harbored ces, associated with the emetic type of food poisoning; however, these strains were devoid of hblCDA, cytK, and bceT.

• Proceedings of the Korean Biophysical Society Conference
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• 2001.06a
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• pp.56-56
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• 2001

Increasing evidence suggests that protein-protein interaction is essential in many biological processes including epithelial transport. In this report, we present the significance of protein interactions to HCO$_3$$^{-10}$ secretion in pancreatic duct cells. In pancreatic ducts HCO$_3$$^{-10}$ secretion is mediated by CFTR-activated luminal CUHCO$_3$$^{-10}$ exchange activity and HCO$_3$$^{-10}$ absorption is achieved by Na$^{＋}$-dependent mechanism including NHE3.(omitted)

• Journal of Microbiology and Biotechnology
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• v.25 no.6
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• pp.872-879
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• 2015

Many strains of Bacillus cereus cause gastrointestinal diseases, and the closely related insect pathogen Bacillus thuringiensis has also been involved in outbreaks of diarrhea. The diarrheal diseases are attributed to enterotoxins. Sixteen reference strains of B. cereus and nine commercial and 12 reference strains of B. thuringiensis were screened by PCR for the presence of 10 enterotoxigenic genes (hblA, hblC, hblD, nheA, nheB, nheC, cytK, bceT, entFM, and entS), one emetogenic gene (ces), seven hemolytic genes (hlyA, hlyII, hlyIII, plcA, cerA, cerB, and cerO), and a pleiotropic transcriptional activator gene (plcR). These genes encode various enterotoxins and other virulence factors thought to play a role in infections of mammals. Amplicons were successfully generated from the strains of B. cereus and B. thuringiensis for each of these sequences, except the ces gene. Intriguingly, the majority of these B. cereus enterotoxin genes and other virulence factor genes appeared to be widespread among B. thuringiensis strains as well as B. cereus strains.

• BMB Reports
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• v.49 no.4
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• pp.208-213
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• 2016

Prolonged ER stress (ERS) can be associated with the induction of apoptotic cell death in various heart diseases. In this study, we searched for microRNAs affecting ERS in the heart using in silico and in vitro methods. We found that miR-185 directly targets the 3′-untranslated region of Na⁺/H⁺ exchanger-1 (NHE-1), a protein involved in ERS. Cardiomyocyte ERS-triggered apoptosis induced by 100 ng/ml tunicamycin (TM) or 1 μM thapsigargin (TG), ERS inducers, was significantly reduced by miR-185 overexpression. Protein expression of pro-apoptotic markers such as CCAAT/enhancer-binding protein homologous protein (CHOP) and cleaved-caspase-3 was also markedly reduced by miR-185 in a dose-dependent manner. Cariporide (20 μM), a pharmacological inhibitor of NHE-1, also attenuated ERS-induced apoptosis in cardiomyocytes and CHOP protein expression, suggesting that NHE-1 plays an important role in ERS-associated apoptosis in cardiomyocytes. Collectively, the present results demonstrate that miR-185 is involved in cardio-protection against ERS-mediated apoptotic cell death.

• Journal of the Korean Electrochemical Society
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• v.11 no.3
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• pp.165-169
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• 2008

The effect of reduction of carbon dioxide by CODH(Carbon Monoxide Dehydrogenase) was compared on glassy carbon and gold working electrodes. In case of gold electrode, the choice of the optimum applied potential is very important since $H_2$ evolution can be mixed with $CO_2$ reduction. On the other hand, efficient $CO_2$ reduction was observed up to -650 mV vs. NHE on glassy carbon in neutral solution due to the larger overpotential for $H_2$ evolution on glassy carbon surface than that on gold surface. The optimum potential for $CO_2$ reduction was found to be $-570{\sim}600\;mV$ vs. NHE. The current efficiency of $CO_2$ to CO decreased dramatically at more negative potential according to the activity of enzyme decrease and the hydrogen evolution.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.2
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• pp.91-95
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• 2012

The role of the kidney in combating metabolic acidosis has been a subject of considerable interest for many years. The present study was aimed to determine whether there is an altered regulation of renal acid base transporters in acute and chronic acid loading. Male Sprague-Dawley rats were used. Metabolic acidosis was induced by administration of $NH_4Cl$ for 2 days (acute) and for 7days (chronic). The serum and urinary pH and bicarbonate were measured. The protein expression of renal acid base transporters [type 3 $Na^+/H^+$ exchanger (NHE3), type 1 $Na^+/{HCO_3}^-$ cotransporter (NBC1), Na-$K^+$ ATPase, $H^+$-ATPase, anion exchanger-1 (AE-1)] was measured by semiquantitative immunoblotting. Serum bicarbonate and pH were decreased in acute acid loading rats compared with controls. Accordingly, urinary pH decreased. The protein expression of NHE3, $H^+$-ATPase, AE-1 and NBC1 was not changed. In chronic acid loading rats, serum bicarbonate and pH were not changed, while urinary pH was decreased compared with controls. The protein expression of NHE3, $H^+$-ATPase was increased in the renal cortex of chronic acid loading rats. These results suggest that unaltered expression of acid transporters combined with acute acid loading may contribute to the development of acidosis. The subsequent increased expression of NHE3, $H^+$-ATPase in the kidney may play a role in promoting acid excretion in the later stage of acid loading, which counteract the development of metabolic acidosis.