Development of a greenhouse gas - air pollution interactions and synergies model for Korea (GAINS-Korea).

This study aimed to create Greenhouse Gas - Air Pollution Interactions and Synergies (GAINS)-Korea, an integrated model for evaluating climate and air quality policies in Korea, modeled after the international GAINS model. GAINS-Korea incorporates specific Korean data and enhances granularity for enabling local government-level analysis. The model includes source-receptor matrices used to simulate pollutant dispersion in Korea, generated through CAMx air quality modeling. GAINS-Korea's performance was evaluated by examining different scenarios for South Korea. The business as usual scenario projected emissions from 2010 to 2030, while the air quality scenario included policies to reduce air pollutants in line with air quality and greenhouse gas control plans. The maximum feasible reduction scenario incorporated more aggressive reduction technologies along with air quality measures. The developed model enabled the assessment of emission reduction effects by both greenhouse gas and air pollutant emission reduction policies across 17 local governments in Korea, including changes in PM2.5 (particulate matter less than 2.5 µm) concentration and associated benefits, such as reduced premature deaths. The model also provides a range of visualization tools for comparative analysis among different scenarios, making it a valuable resource for policy planning and evaluation, and supporting decision-making processes.

Increased renal expression of nitric oxide synthase and atrial natriuretic peptide in rats with glycyrrhizic-acid-induced hypertension.

The present study aimed to examine whether there is an altered regulation of local hormonal systems in the kidney following the treatment of glycyrrhizic acid (GA), the active ingredient in licorice. Male Sprague-Dawley rats were treated with GA for 3 weeks. The expression of mineralocorticoid receptor (MR) was determined in the kidney by immunoblotting and real-time polymerase chain reaction (PCR). The protein expression of endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) was determined. The expression of atrial natriuretic peptide (ANP), natriuretic peptide receptor (NPR)-A and NPR-C was determined by real-time PCR. The activity of guanylyl cyclase was determined by the amount of cGMP generated in responses to sodium nitroprusside (SNP) or ANP. Following the GA treatment, systolic blood pressure was increased. The mRNA and protein expressions of MR were increased in the kidney. The protein expression of eNOS and iNOS was also increased. The expression of ANP mRNA was increased although that of NPR-A and NPR-C mRNA was not changed. The cGMP production provoked by either SNP or ANP was not changed. The increased expression of MR may contribute to GA-induced hypertension. The enhanced expression of NOS and ANP may play a compensatory role in GA-induced hypertension.

Continuous renal replacement therapy for the treatment of acute kidney injury.

BACKGROUND/AIMS: Continuous renal replacement therapy (CRRT) has been widely used for treating critically ill patients with acute kidney injury (AKI). Whether CRRT is better than intermittent hemodialysis for the treatment of AKI remains controversial. We sought to identify the clinical features that can predict survival for the patients who are treated with CRRT. METHODS: We analyzed the data of 125 patients who received CRRT between 2005 and 2007. We identified the demographic variables, the underlying diagnoses, the duration of CRRT, the mean arterial blood pressure (ABP) and the Simplified Acute Physiology Score (SAPS) II. The classification/staging system for acute kidney injury (AKI) was applied to all the patients, who were then divided into stage 1-3 subgroups. RESULTS: The average age of the patients was 61.414.3 years and the mortality rate was 60% (75 of 125 patients). The survivors had a significantly higher mean ABP and a higher mean serum bicarbonate level, which were measured the day after CRRT, than the nonsurvivors (86.723.7 vs. 69.224.6 mm Hg, respectively, 21.43.5 vs. 16.45.4 mmol/L, respectively,; p<0.05 for each). The stage 3 AKI patients showed the worst parameters for the SAPS II score and the serum levels of creatinine and blood urea nitrogen. The mortality rate was higher for the stage 3 subgroup than the other groups (70.5%, p<0.05). CONCLUSIONS: The patients with AKI and who require CRRT continue to have a high mortality rate. A higher mean ABP and a higher serum bicarbonate level measured the day after CRRT may predict a more favorable prognosis. The staging system for AKI can improve the ability to predict the outcomes of CRRT patients.

Effects of volume depletion and NaHCO3 loading on the expression of Na+/H+ exchanger isoform 3, Na+: HCO3- cotransporter type 1 and nitric oxide synthase in rat kidney.

1. The effects of volume depletion and NaHCO(3) loading on the expression of Na(+)/H(+) exchanger isoform 3 (NHE3), Na(+) : HCO(3)(-) cotransporter type 1 (NBC1) and neuronal (n) and inducible (i) isoforms of nitric oxide synthase (NOS) were determined in rat kidney. 2. Adult male Sprague-Dawley rats were used. Rats were divided into four groups: (i) euvolaemic (EC); (ii) hypovolaemic (HC); (iii) euvolaemia with NaHCO(3) loading (EB); and (iv) hypovolaemia with NaHCO(3) loading (HB). The expression of NHE3, NBC1, nNOS and iNOS proteins was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Tissue content of nitric oxide (NO) metabolites (NO(x)) were also determined in the cortex using a colourimetric assay. 3. Compared with the EC group, the expression of NHE3 and NBC1 was increased in the HC group and decreased in the EB group. Comparing the EB and HB groups, the expression of NHE3 and NBC1 was higher in the latter group. The expression of NHE3 was decreased and that of NBC1 was increased in the HB group compared with the HC group. The NO(x) content and nNOS expression were decreased in the hypovolaemic (HC) and NaHCO(3)-loaded (EB and HB) rats. Moreover, the expression of iNOS was decreased in the HB group compared with the other groups. 4. An altered volume status and NaHCO(3) loading may affect the regulation of NHE3 and NBC1 in the kidney and the endogenous NO system may play a role in the observed effects.

Effects of alpha-lipoic acid on ischemia-reperfusion-induced renal dysfunction in rats.

We investigated whether alpha-lipoic acid (alpha-LA), an antioxidant, attenuates the ischemia-reperfusion (I/R)-induced dysregulation of these transporters. Both renal pedicles of male Sprague-Dawley rats were clamped for 40 min. alpha-LA (80 mg/kg) was administered intraperitoneally before and immediately after induction of ischemia. After 2 days, the expression of aquaporins (AQPs), sodium transporters, and nitric oxide synthases (NOS) was determined in the kidney by immunoblotting and immunohistochemistry. The expression of endothelin-1 (ET-1) mRNA was determined by real-time PCR. Activities of adenylyl cyclase and guanylyl cyclase were measured by stimulated generation of cAMP and cGMP, respectively. The expression of AQP1-3 as well as that of the alpha(1)-subunit of Na-K-ATPase, type 3 Na/H exchanger, Na-K-2Cl cotransporter, and Na-Cl cotransporter was markedly decreased in response to I/R. The expression of type VI adenylyl cyclase was decreased in I/R-injured rats, which was counteracted by the treatment of alpha-LA. AVP-stimulated cAMP generation was blunted in I/R rats and was then ameliorated by alpha-LA treatment. alpha-LA treatment attenuated the downregulation of AQPs and sodium transporters. The expression of endothelial NOS was decreased in I/R rats, which was prevented by alpha-LA. The cGMP generation in response to sodium nitroprusside was blunted in I/R rats, which was also significantly prevented by alpha-LA. The mRNA expression of ET-1 was increased, which was recovered to the control level by alpha-LA treatment. In conclusion, alpha-LA treatment prevents I/R-induced dysregulation of AQPs and sodium transporters in the kidney, possibly through preserving normal activities of local AVP/cAMP, nitric oxide/cGMP, and ET systems.

Effects of rosiglitazone on heat shock protein and the endothelin system in deoxycorticosterone acetate-salt hypertensive rats.

The deoxycorticosterone acetate (DOCA)-salt rat is known as a model of volume dependent hypertension and characterized by increased cardiac endothelin-1 (ET-1) content. Recently, it has been reported that rosiglitazone (RGT), a peroxisome proliferator-activated subtype gamma receptor agonist, shows blood pressure lowering effect. We investigated whether DOCA-salt hypertension is associated with altered expression of heat shock proteins (HSP) and ET-1 in the heart, aorta, and kidney, and whether RGT changes HSP expression and ET-1 in association with its blood pressure lowering effect. Two weeks after the silastic DOCA (200 mg/kg) strips implantation, DOCA-salt rats were randomly divided to receive control diet with or without RGT (10 mg/kg/day) for another 2 weeks. The mRNA expression of ET-1 was determined by real time polymerase chain reaction. The expression of HSP was determined by semiquantitative immunoblotting. In DOCA-salt rats, systolic blood pressure was markedly increased, while creatinine clearance decreased. RGT treatment attenuated high blood pressure and decreased creatinine clearance in DOCA-salt rats. The mRNA expression of ET-1 was increased in DOCA-salt rats compared to controls, which was counteracted by RGT treatment. The protein expression of HSP70, HSP32, and HSP25 was increased in the kidney and heart in DOCA-salt rats, which was attenuated by RGT treatment in the kidney, but not in the heart. In conclusion, increased expression of ET-1 may play a role in the pathogenesis of hypertension in DOCA-salt rats, which was counteracted by the treatment of RGT. Up-regulation of HSP70, HSP32, and HSP25 in the kidney and heart may play a role in organ protection against a variety of stresses.

Altered regulation of renin-angiotensin, endothelin and natriuretic peptide systems in rat kidney with chronic unilateral ureteral obstruction.

BACKGROUND: The present study was designed to investigate the role of the local renin-angiotensin-aldosterone system (RAAS), endothelin (ET) and the natriuretic peptide system (NPS) for the development of renal fibrosis and progressive renal disease in experimental unilateral ureteral obstructed (UUO) rats. METHODS: Male Sprague-Dawley rats (180-200 g) were unilaterally obstructed by ligation of the proximal ureters for 14 days. Control rats were treated in the same way, except that no ligature was made. The mRNA expressions of local renin-angiotensin system, aldosterone synthase (CYP11B2), ET-1 and NPS was determined in the cortex by real-time polymerase chain reaction. RESULTS: Following the unilateral ureteral obstruction, the mRNA expressions of angiotensin-converting enzyme 1, ET-1 and transforming growth factor-beta1 (TGF-beta1) were increased, while angiotensin-converting enzyme 2 was decreased in the obstructed kidney compared with the controls. Angiotensin II type 1 receptor was decreased and TGF-beta1 was not changed in contralateral kidney compared with the controls. Atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide expressions were increased in UUO kidneys compared with the controls, while natriuretic peptide receptor-A was decreased in UUO kidneys. CONCLUSION: The local RAAS and ET-1 was upregulated which may play a role in the progressive renal fibrosis in obstructed kidneys in rats with UUO. The enhanced activity of NPS in UUO kidney may play a role to compensate against progressive renal fibrosis in chronic obstructive uropathy.

A case of malignant otitis externa caused by Candida glabrata in a patient receiving haemodialysis.

A 74-y-old male receiving haemodialysis presented with right-sided otalgia, otorrhoea and diffuse swelling on the right external auditory canal. Following an initial successful treatment with prolonged intravenous antibiotics, the patient relapsed with a secondary infection in the same site due to Candida glabrata. We report an unusual case of malignant otitis externa caused by the fungus C. glabrata.

Gentamicin decreases guanylyl cyclase activity in rat glomerulus.

BACKGROUND: Effects of gentamicin (GM) on the local natriuretic peptide (NP) and nitric oxide (NO) systems in the kidney were investigated. METHODS: Male Sprague-Dawley rats (180-200 g) were intramuscularly injected with GM (100 mg/kg/day) for 5 days. The expression of NO synthase (NOS) isoforms was determined by Western blot analysis, and that of NPs by real-time polymerase chain reaction. The activity of guanylyl cyclase was also determined by the amount of guanosine 3',5'-cyclic monophosphate (cGMP) generated in responses to atrial natriuretic peptide (ANP) or sodium nitroprusside (SNP). RESULTS: GM treatment resulted in renal failure in association with increases in urinary flow and the fractional excretion of sodium. Accordingly, the expression of inducible NOS was increased in the cortex, while that of endothelial NOS remained unchanged. The urinary excretion of NO metabolites was increased. The expression of ANP, brain natriuretic peptide and C-type natriuretic peptide mRNA was increased in the kidney. The cGMP production provoked by either ANP or SNP was decreased in the glomerulus, but not in the papilla. CONCLUSION: GM-induced nephropathy may be causally related with decreased guanylyl cyclase activities in the glomerulus.

Increased renal expression of aquaporin-3 in rats inhibited type 2 11beta-hydroxysteroid dehydrogenase.

AIMS: To investigate whether the regulation of aquaporin (AQP) channels is altered by inhibition of type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2). METHODS: Male Sprague-Dawley rats were treated with glycyrrhizic acid (GA, 2 g/l drinking water) for 7 days. The expression of AQP2 and AQP3 was determined in the kidney by immunoblotting and immunohistochemistry. The expression of Gsalpha and type VI adenylyl cyclase, and the activity of adenylyl cyclase were also determined. RESULTS: Following the GA treatment, the expression of 11betaHSD2 was significantly decreased in the kidney. The expression of AQP3 was increased, while that of AQP2 remained unchanged. Plasma renin activity and serum aldosterone levels were decreased. Plasma arginine vasopressin (AVP) levels were comparable between the groups. Neither the forskolin-stimulated cAMP generation nor the expression of Gsalpha and type VI adenylyl cyclase was altered significantly. CONCLUSION: A decreased expression of 11betaHSD2 may result in an upregulation of AQP3, in which AVP/cAMP-dependent mechanisms are unlikely to be involved.

SIADH associated with prostate cancer.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common disease leading to hyponatremia, and it is characterized by an inappropriately elevated serum ADH level relative to serum osmolality. This syndrome may occur in a variety of clinical settings including malignancies. However, it is rarely observed in association with prostate cancer. Moreover, its pathogenesis and clinical characteristics have not been completely understood. We report a case of SIADH associated with prostate cancer in a 64-year-old male patient with a literature review.

Altered Regulation of type 3 Na(+)/H(+) exchanger, type 1 Na(+)/HCO3 (-) cotransporter, and Na(+),K(+)-ATPase in the Kidney of Rats with Experimental Rhabdomyolysis.

Metabolic acidosis was shown to correlate with deterioration of renal function in patients with rhabdomyolysis. The present study was aimed to investigate whether the changes of type 3 Na(+)/H(+) exchanger (NHE3), type 1 Na(+)/HCO3 (-) cotransporter (NBC1), and Na(+),K(+)-ATPase α1 subunit may play a role in the pathogenesis of metabolic acidosis in glycerol-induced experimental rhabdomyolysis. Male Sprague-Dawley rats were deprived of fluid intake for 24 hours, and then were injected with 50% glycerol in normal saline (10 mL/kg, intramuscularly). At 24 hours after the glycerol injection, rats were sacrificed by decapitation. Control rats were injected with normal saline. The protein expression of NHE3, NBC1 and Na(+),K(+)-ATPase α1 subunit was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Following the treatment of glycerol, creatinine clearance was significantly decreased, and high anion gap metabolic acidosis developed. In the experimental group, the expression of Na(+),K(+)-ATPase α1 subunit was significantly decreased in the cortex of the kidney. On the contrary, the expression of NHE3 and NBC1 was significantly increased. Immunohistochemical analyses confirmed the immunoblotting data. In conclusion, the coordinate up-regulation of NHE3 and NBC1 may play an adaptive role against the metabolic acidosis in glycerol-induced rhabdomyolysis.

A case of hemolytic uremic syndrome caused by Escherichia coli O104:H4.

A 29-year-old woman presented with bloody diarrhea, abdominal pain, hemolytic anemia, thrombocytopenia, and acute renal failure. She was diagnosed with Escherichia coli O104:H4-associated hemolytic-uremic syndrome (HUS) and treated with plasmapheresis and hemodialysis for 3 weeks. She recovered without sequelae. To the best of our knowledge, this is the first report of Escherichia coli O104:H4-associated HUS in Korea. We recommend that Escherichia coli O104:H4, as well as the more common O157:H7, be considered in the diagnosis of bloody diarrhea-associated HUS.

Decreased expression of aquaporin water channels in denervated rat kidney.

AIMS: A neural mechanism regulating aquaporin (AQP) water channels in the kidney was investigated. METHODS: Male Sprague-Dawley rats were used. Renal denervation was induced by painting the renal vessels with 10% phenol. The expression of AQP1-4 proteins was determined in the denervated and contralateral kidneys. The expression was also examined in rats which were renally denervated and subjected to water restriction or deoxycorticosterone acetate (DOCA)-salt treatment. RESULTS: Following the unilateral denervation, tissue contents of norepinephrine were significantly decreased in the denervated kidney, while increased in the contralateral kidney. Accordingly, the expression of AQP1-4 proteins was decreased by 15-40% in the denervated kidney, and increased by 30-50% in the contralateral kidney. Immunohistochemistry of AQP2 confirmed its decreases in the denervated kidney and increases in the contralateral kidney. In bilaterally denervated rats, the urine flow increased along with decreased osmolarity. The water restriction increased the expression of AQP channels, however, the magnitude of which was lower in the denervated than in the contralateral kidney. Renal denervation decreased the degree of DOCA-salt hypertension, along with lower expression of AQP channels. CONCLUSION: It is suggested that the sympathetic nerve should play a specific excitatory role in the regulation of AQP channels in the kidney.

Increased expression of renal aquaporin water channels in spontaneously hypertensive rats.

AIMS: The present study was aimed to determine whether there exists an altered regulation of aquaporin (AQP) water channels in hypertension. METHODS: Male spontaneously hypertensive rats (SHR) aged 10-12 weeks were used. Age-matched Wistar-Kyoto (WKY) rats served as control. The abundance of AQP1-4 proteins in the kidney was determined by Western blot analysis. The protein expression and activity of adenylyl cyclase were also determined. RESULTS: The medullary expression of AQP2 and AQP3 proteins was increased in SHR compared with that in WKY rats. The expression of AQP1 protein was also significantly increased in the inner medulla, while that of AQP4 was not. Immunohistochemistry of AQP2 revealed that principal cells of the collecting duct have strong immunoreactivity, the degree of which was augmented with prominent apical labeling in SHR. The plasma level of arginine vasopressin (AVP) was higher in SHR; the adenylyl cyclase activity stimulated by AVP was augmented, along with increased expression of type VI adenylyl cyclase. The urine was more concentrated with its volume decreased in SHR. CONCLUSION: The expression of AQP1-3 channels is increased in the kidney, in association with enhanced activity of the AVP/cAMP pathway, in SHR.

Increased expression of sodium transporters in rats chronically inhibited of nitric oxide synthesis.

The present study was done to determine whether endogenous nitric oxide (NO) plays a role in the regulation of sodium transporters in the kidney. Male Sprague-Dawley rats were treated with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 4 weeks. Control rats were supplied with tap water without drugs. Expression of Na, K-ATPase, type 3 Na/H exchanger (NHE3), Na/K/2Cl cotransporter (BSC1), and thiazide-sensitive Na/Cl cotransporter (TSC) proteins was determined in the kidney by Western blot analysis. Catalytic activity of Na,K-ATPase was also determined. The treatment with L-NAME significantly and steadily increased the systemic blood pressure. Total and fractional excretion of urinary sodium decreased significantly, while creatinine clearance remained unaltered. Neither plasma renin activity nor aldosterone concentration was significantly altered. The alpha1 subunit expression and the catalytic activity of Na, K-ATPase were increased in the kidney. The expression of NHE3, BSC1 and TSC was also increased significantly. These results suggest that endogenously-derived NO exerts a tonic inhibitory effect on the expression of sodium transporters, including Na, K-ATPase, NHE3, BSC1, and TSC, in the kidney.

Splenic abscess associated with endocarditis in a patient on hemodialysis: a case report.

Splenic abscess is an unusual condition usually seen in immunocompromised patients or associated with intravenous drug abuses. Several conditions including trauma, immunodeficiency, corticosteroid and/or immunosuppressive therapy and diabetes mellitus have been listed under the predisposing factors for a splenic abscess. Splenic abscess in a patient on hemodialysis is a rare but life-threatening condition if not corrected. We describe a case of splenic abscess with bacterial endocarditis on maintenance hemodialysis. He had staphylococcal septicemia secondary to bacterial endocarditis at the mitral valve from the dialysis access-site infection. Although hematologic seeding from endocarditis has been the predisposing factor for splenic abscess, we postulate that access-site infections may predispose hemodialysis patients to splenic abscess. Splenic abscess may be considered as one of the causes when patients on hemodialysis develop unexplained fever.

Indomethacin enhances shuttling of aquaporin-2 despite decreased abundance in rat kidney.

The effect of nonsteroidal antiinflammatory drugs on the regulation of aquaporin-2 (AQP2) water channels in the kidney was determined. Male Sprague-Dawley rats were injected with indomethacin (5 mg/kg twice a day intraperitoneally) for 2 d. The control group was injected with vehicle. The expression of AQP2 proteins was determined in the kidney by immunoblotting and immunohistochemistry. The expression of G(salpha) and type VI adenylyl cyclase was determined by immunoblotting. The activity of adenylyl cyclase complexes was determined by stimulated accumulation of cAMP. Immunoblotting revealed that indomethacin markedly decreased the expression of AQP2. Accordingly, however, the ratio of AQP2 expression in the membrane fraction versus that in the cytoplasmic fraction was increased. The urinary excretion of AQP2 proteins also increased. Immunohistochemistry demonstrated almost exclusive apical labeling of AQP2 with scanty cytoplasmic localization along the collecting duct. The expression of G(salpha) and adenylyl cyclase VI proteins was decreased. The generation of cAMP provoked by arginine vasopressin, sodium fluoride, or forskolin was blunted. These results suggest that indomethacin increases the shuttling of AQP2 while it decreases its abundance in the collecting duct.

Diminished expression of sodium transporters in the ureteral obstructed kidney in rats.

BACKGROUND/AIMS: Whether the postobstructive natriuresis and diuresis is related with an altered regulation of sodium transporters in the kidney was examined. METHODS: Male Sprague-Dawley rats underwent either bilateral (BUO) or unilateral obstruction (UUO) of the proximal ureters for 24 h. The expression of Na,K-ATPase, type-3 sodium-hydrogen exchanger (NHE3), type-1 bumetanide-sensitive sodium cotransporter (BSC1), and thiazide-sensitive sodium cotransporter (TSC) proteins was determined in the obstructed kidney by Western blot analysis and immunohistochemistry. Catalytic activity of Na,K-ATPase was also determined. RESULTS: The expression of alpha1 and beta1 subunit proteins and the catalytic activity of Na,K-ATPase were significantly decreased in the obstructed kidney in BUO. The expressions of NHE3, BSC1 and TSC proteins were also significantly decreased. Immunohistochemistry confirmed the downregulation of these sodium transporters in the obstructed kidney. In UUO, the expression of sodium transporters was similarly decreased in the obstructed kidney. CONCLUSION: The postobstructive natriuresis and diuresis may in part be accounted for by a reduced abundance of sodium transporters in the kidney.