Layers of Uranium Phosphate Nanorods and Nanoplates Encrusted on Fungus Cladosporium sp. Strain F1 Hyphae.

The hyphae of Cladosporium sp. strain F1 (CFGR 2020-301-00084) were heavily encrusted with pre-synthesized uranium phosphate minerals under a wide range of pH conditions. SEM and TEM images showed that nanorods and nanoplates of uranium phosphate minerals at pH 4 and 5 and at pH 6, 7, and 8, respectively, were tightly adsorbed along the hyphae of Cladosporium sp. strain F1, while only a few uranium phosphate minerals were observed on the hyphae of Aspergillus niger VKMF 1119. Based on the physical mobility and chemical stability of uranium phosphate minerals under in situ oxidizing environmental conditions, the application of Cladosporium sp. strain F1 has potential as a novel strategy for the remediation of uranium contamination in sediments and aquifers under a wide range of pH conditions where larger amounts of phosphate are present in the environment.

What Is the Ideal Entry Point for Transforaminal Endoscopic Lumbar Discectomy?

OBJECTIVE: The method of approach during transforaminal endoscopic lumbar discectomy (TELD) has been the subject of repeated study. However, the ideal entry point during TELD has not been studied in detail. Therefore, this study investigated the ideal entry point for avoiding complications using computed tomography (CT) scans obtained from patients in the prone position. METHODS: Using CT scans obtained from patients in the prone position, we checked for retroperitoneal or visceral violations and measured the angles of approach with five conventional approach lines drawn on axial CT scans at each disc space level (L2-3, L3-4, and L4-5). We also determined the ideal entry point distance and approach angles for avoiding retroperitoneal or visceral violations. Correlation analysis was performed to identify the patient characteristics related to the ideal entry point properties. RESULTS: We found that the far lateral approach at the L2-3 level resulted in high rates of visceral violation. However, rates of visceral violation at the L3-4 and L4-5 levels were remarkably low or absent. The ideal angles of approach decreased moving caudally along the spine, and the ideal entry point distances increased moving caudally along the spine. Weight, body mass index (BMI), and the depth of the posterior vertebral line from the skin were positively associated with the distance of the ideal entry point from the midline. CONCLUSION: We reviewed the risk of the extreme lateral approach by analyzing rates of retroperitoneal and visceral violations during well-known methods of approach. We suggested an ideal entry point at each level of the lumbar spine and found a positive correlation between the distance of the entry point to the midline and patient characteristics such as BMI, weight, and the depth of the posterior vertebral line from the skin.

Comparison of five extraction methods for evaluating cadmium and zinc immobilization in soil.

The remediation of soil contaminated with heavy metals is an ongoing environmental concern. Paddy soils contaminated with Cd and Zn were collected from around abandoned metals mines in Korea. Limestone and steel slag were mixed with the collected soil, as amendments for Cd and Zn immobilization. Sequential extraction, lettuce cultivation and five single extraction methods were carried out to assess the effects on Cd and Zn immobilization using amendments. The exchangeable fraction of Cd and Zn was decreased and Fe-Mn oxides fraction increased by stabilization using amendments. In addition, the accumulation of Cd and Zn in lettuce decreased in treated soil and indicated the Cd and Zn immobilization effect in soil by the amendments. The extractable Cd and Zn by CaCl2 and Mehlich-3 in the untreated soils were higher than that of treated soils, whereas Cd and Zn extraction by ethylenediaminetetraacetic acid (EDTA), diethylene tetramine penta-acetic acid (DTPA) and toxicity characteristic leaching procedure (TCLP) has a small or no difference between the untreated and treated soils. The extraction results by CaCl2 and Mehlich-3 methods present reasonable results for Cd and Zn immobilization in soil than EDTA, DTPA and TCLP methods. Therefore, the choice of appropriate extraction method is very important when there is the assessment of Cd and Zn immobilization efficiency.

Alpha-lipoic acid attenuates lipopolysaccharide-induced kidney injury.

BACKGROUND: Kidney is one of the major target organs in sepsis, while effective prevention of septic acute kidney injury has not yet been established. α-Lipoic acid (LA) has been known to exert beneficial effects against lipopolysaccharide (LPS)-induced damages in various organs such as heart, lung, and liver. We investigated the protective effect of LA on LPS-induced kidney injury. METHODS: Two groups of rats were treated with LPS (20 mg/kg, i.p.), one of which being co-treated with LA (50 mg/kg), while the control group was treated with vehicle alone. Human renal proximal tubular epithelial cells (HK-2 cells) were cultured with or without LPS (10 µg/ml) in the presence or absence of LA (100 µg/ml) for 3 h prior to LPS treatment. RESULTS: Serum creatinine level was increased in LPS-treated rats, which was attenuated by LA co-treatment. LPS treatment induced cleaved caspase-3 expression in the kidney, which was counteracted by LA. Terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells increased in the kidneys of LPS-treated rats compared with controls, which was counteracted by LA treatment. Protein expression of inducible nitric oxide synthase and cyclooxygenase-2 detected by immunoblotting and/or immunohistochemical staining, along with mRNA levels of pro-inflammatory cytokines detected by real-time polymerase chain reaction, was increased in the kidney with LPS administration, which was ameliorated with LA treatment. LA also protected LPS-induced tubular dysfunction, preserving type 3 Na(+)/H(+) exchanger and aquaporin 2 expressions in the kidney. Suppression of LPS-induced expression of cleaved caspase-3 by LA was also observed in HK-2 cells. Increased protein expression of phospho-extracellular signal-regulated kinases 1/2 and c-Jun N-terminal kinases by LPS treatment was attenuated by LA pretreatment, while p38 was not affected by either LPS or LA treatment. MitoTracker Red demonstrated LA prevented LPS-induced increment of mitochondrial oxidative stress, where concurrent 4',6-diamidino-2-phenylindole staining also revealed marked fragmentation and condensation of nuclei in HK-2 cells treated with LPS, which was prevented by LA. CONCLUSION: LA treatment attenuates LPS-induced kidney injury, such as renal tubular dysfunction, by suppression of apoptosis, and inflammation.

Antiapoptotic Effect of Paricalcitol in Gentamicin-induced Kidney Injury.

While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 µg/kg/day) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.

Macrophage-stimulating protein attenuates hydrogen peroxide-induced apoptosis in human renal HK-2 cells.

Macrophage-stimulating protein (MSP) and its receptor, recepteur d'origine nantais (RON), play an important role in cell proliferation and migration. We have investigated the role of MSP in hydrogen peroxide (H2O2)-induced renal tubular apoptosis. Human renal proximal tubular (HK-2) cells were incubated with H2O2 for 24h in the presence of different concentrations of MSP, and cell viability was measured by MTT assay. The protein expression of Bax, Bcl-2, caspase-3, mitogen-activated protein kinases (MAPKs), phosphatidylinositol-3-kinase (PI3K)/Akt, and nuclear factor-kappa B (NF-κB) was determined by semiquantitative immunoblotting. Apoptosis was assessed by flow cytometry analysis after HK-2 cells were stained with fluorescein isothiocyanate-conjugated annexin V protein and propidium iodide. H2O2 treatment decreased cell viability in HK-2 cells; this was counteracted by MSP pretreatment. H2O2 treatment induced an increased ratio of Bax/Bcl-2, cleaved caspase-3, and the number of condensed nuclei, which was also counteracted by MSP. Flow cytometry analysis showed H2O2-induced apoptosis, and its prevention by MSP treatment. Increased protein expression of phospho-p38 MAPK was attenuated by MSP, while phospho-extracellular signal-regulated kinase and c-Jun-N-terminal kinase were not affected. H2O2 induced NF-κB activation and IκB-α degradation, but the increased nuclear NF-κB activation was counteracted by MSP or by a p38 MAPK inhibitor. H2O2 treatment decreased expression of phospho-PI3K and phospho-Akt, which was reversed by MSP pretreatment. These findings suggest that MSP attenuates H2O2-induced apoptosis in HK-2 cells by modulating the p38 and NF-κB, as well as PI3K/Akt, signaling pathways.

The role of Acidithiobacillus ferrooxidans and Acidithiobacillus thiooxidans in arsenic bioleaching from soil.

Bioleaching of As from the soil in an abandoned Ag-Au mine was carried out using Acidithiobacillus ferrooxidans and Acidithiobacillus thiooxidans. A. ferrooxidans is an iron oxidizer and A. thiooxidans is a sulfur oxidizer. These two microbes are acidophilic and chemoautotrophic microbes. Soil samples were collected from the Myoungbong and Songcheon mines. The main contaminant of the soil was As, with an average concentration of 4,624 mg/kg at Myoungbong and 5,590 mg/kg at Songcheon. A. ferrooxidans and A. thiooxidans generated lower pH conditions during their metabolism process. The bioleaching of As from soil has a higher removal efficiency than chemical leaching. A. ferrooxidans could remove 70 % of the As from the Myoungbong and Songcheon soils; however, A. thiooxidans extracted only 40 % of the As from the Myoungbong soil. This study shows that bioleaching is an effective process for As removal from soil.

Macrophage-stimulating protein attenuates gentamicin-induced inflammation and apoptosis in human renal proximal tubular epithelial cells.

The present study aimed to investigate whether macrophage-stimulating protein (MSP) treatment attenuates renal apoptosis and inflammation in gentamicin (GM)-induced tubule injury and its underlying molecular mechanisms. To examine changes in MSP and its receptor, recepteur d'origine nantais (RON) in GM-induced nephropathy, rats were injected with GM for 7 days. Human renal proximal tubular epithelial (HK-2) cells were incubated with GM for 24h in the presence of different concentrations of MSP and cell viability was measured by MTT assay. Apoptosis was determined by flow cytometry of cells stained with fluorescein isothiocyanate-conjugated annexin V protein and propidium iodide. Expression of Bcl-2, Bax, caspase-3, cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB), IκB-α, and mitogen-activated protein kinases (MAPKs) was analyzed by semiquantitative immunoblotting. MSP and RON expression was significantly greater in GM-treated rats, than in untreated controls. GM-treatment reduced HK-2 cell viability, an effect that was counteracted by MSP. Flow cytometry and DAPI staining revealed GM-induced apoptosis was prevented by MSP. GM reduced expression of anti-apoptotic protein Bcl-2 and induced expression of Bax and cleaved caspase 3; these effects and GM-induced expression of COX-2 and iNOS were also attenuated by MSP. GM caused MSP-reversible induction of phospho-ERK, phospho-JNK, and phospho-p38. GM induced NF-κB activation and degradation of IκB-α; the increase in nuclear NF-κB was blocked by inhibitors of ERK, JNK, p-38, or MSP pretreatment. These findings suggest that MSP attenuates GM-induced inflammation and apoptosis by inhibition of the MAPKs/NF-κB signaling pathways.

Renoprotective effects of sildenafil in DOCA-salt hypertensive rats.

BACKGROUND/AIMS: Sildenafil, the first selective phosphodiesterase-5 (PDE5) inhibitor to be widely used for treating erectile dysfunction, has been investigated with regard to its cardioand renoprotective effects in animal models. This study further investigated the renoprotective effects of sildenafil and their molecular mechanisms in deoxycorticosterone acetate (DOCA)-salt hypertensive (DSH) rats. METHODS: DOCA strips (200 mg/kg) were implanted in rats 1 week after unilateral nephrectomy. These rats were fed on a control diet, with or without sildenafil (50 mg·kg(-1)day(-1)), for 2 weeks. Systolic blood pressure (SBP) was measured by the tail cuff method, and the urinary albumin-to-creatinine ratio (ACR) was calculated. The extent of glomerulosclerosis and tubulointerstitial fibrosis was determined by Masson's trichrome stain. Renal expression of ED-1, transforming growth factor-ß1 (TGF-ß1), Bax, and Bcl-2 were determined by semiquantitative immunoblotting, polymerase chain reaction (PCR), and immunohistochemistry. TUNEL staining was used for detecting apoptotic cells. RESULTS: The increased SBP in DSH rats was not attenuated by sildenafil treatment. The decreased creatinine clearance and increased ACR in DSH rats, compared with control animals, were attenuated by sildenafil treatment. Further, sildenafil treatment attenuated glomerulosclerosis and tubulointerstitial fibrosis in DSH rats and counteracted the increased expression of ED-1, TGF-ß1, and Bax and the decreased expression of Bcl-2 in the kidneys of these rats. The increase in the number of apoptotic cells in DSH rats was attenuated by sildenafil treatment. CONCLUSION: Sildenafil effectively prevented the progression of renal injury in DSH rats via its anti-inflammatory, antifibrotic, and antiapoptotic effects.

Altered regulation of renal Acid base transporters in response to ammonium chloride loading in rats.

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(4)Cl 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.

Ex-situ field application of electrokinetics for remediation of shooting-range soil.

Electrokinetic process for remediation of a shooting-range site was evaluated in this study. By field operation for 100 days, the newly designed electrokinetic system was evaluated for process stability, performance, and efficiency. The field site of this study was an abandoned military shooting range located in the Civilian Control Line of South Korea. The target area, only, was heavily contaminated by Pb and Cu to a depth of 0.5 m. After dry-sieving of the field soil to separate particulate Pb, two cells in a hexagonal (two-dimensional) arrangement, including ten anodes outside the cell and two cathodes in the middle, were prepared. The pH of each electrolyte was adjusted by use of concentrated HNO(3), resulting in acid-enhanced electrokinetics. The monitoring results indicated that overall removal of heavy metals (Pb, Cu) was achieved, and that both heavy metals were removed from outside the cell. The average final efficiency of removal of Pb and Cu was 39.5 ± 35 and 63.8 ± 12%, respectively. Although the feasibility of this system was confirmed, for commercialization of the process confirmed drawbacks must be improved by further study.

Activation of the Renal PI3K/Akt/mTOR Signaling Pathway in a DOCA-Salt Model of Hypertension.

The present study investigated the changes that occurred in the mammalian target of rapamycin (mTOR) signaling pathway in the kidney as a result of deoxycorticosterone acetate (DOCA)-salt hypertension. Rats were implanted with DOCA strips (200 mg/kg) 1 week after unilateral nephrectomy and were then supplied with 0.9% saline to drink. Four weeks after DOCA implantation, systolic blood pressure (SBP) was measured by use of the tail-cuff method. The expression levels of phosphorylated phosphatidylinositol-3-kinase (PI3K), Akt, and mTOR, as well as the protein expression levels of ED-1 and cyclooxygenase-2 (COX-2), transforming growth factor-ß1 (TGF-ß1), α-smooth muscle actin (SMA), caspase-3, Bax, and Bcl-2, were then examined in the kidney by semiquantitative immunoblotting. DOCA-salt hypertensive rats were found to have significantly increased SBP as well as an increased kidney weight-to-body weight ratio. Moreover, the phosphorylation of PI3K, Akt, and mTOR was increased in the kidney of DOCA-salt hypertensive rats compared with the control, as was the protein expression of ED-1, COX-2, TGF-ß1, and α-SMA. The expression levels of caspase-3 and Bax were increased significantly, whereas Bcl-2 expression was decreased. In conclusion, the phosphorylation of PI3K/Akt/mTOR was increased in the kidney of DOCA-salt hypertensive rats.

Altered Regulation of Renal Nitric Oxide and Atrial Natriuretic Peptide Systems in Lipopolysaccharide-induced Kidney Injury.

Nitric oxide (NO) and atrial natriuretic peptide (ANP) may induce vascular relaxation by increasing the production of cyclic guanosine monophosphate (cGMP), an important mediator of vascular tone during sepsis. This study aimed to determine whether regulation of NO and the ANP system is altered in lipopolysaccharide (LPS)-induced kidney injury. LPS (10 mg.kg(-1)) was injected in the tail veins of male Sprague-Dawley rats; 12 hours later, the kidneys were removed. Protein expression of NO synthase (NOS) and neutral endopeptidase (NEP) was determined by semiquantitative immunoblotting. As an index of synthesis of NO, its stable metabolites (nitrite/nitrate, NOx) were measured using colorimetric assays. mRNA expression of the ANP system was determined by real-time polymerase chain reaction. To determine the activity of guanylyl cyclase (GC), the amount of cGMP generated in response to sodium nitroprusside (SNP) and ANP was calculated. Creatinine clearance decreased and fractional excretion of sodium increased in LPS-treated rats compared with the controls. Inducible NOS protein expression increased in LPS-treated rats, while that of endothelial NOS, neuronal NOS, and NEP remained unchanged. Additionally, urinary and plasma NOx levels increased in LPS-treated rats. SNP-stimulated GC activity remained unchanged in the glomerulus and papilla in the LPS-treated rats. mRNA expression of natriuretic peptide receptor (NPR)-C decreased in LPS-treated rats, while that of ANP and NPR-A did not change. ANP-stimulated GC activity reduced in the glomerulus and papilla. In conclusion, enhancement of the NO/cGMP pathway and decrease in ANP clearance were found play a role in the pathogenesis of LPS-induced kidney injury.

Rho kinase inhibition by fasudil attenuates cyclosporine-induced kidney injury.

It has been shown that the inhibition of the Rho/Rho kinase (ROCK) pathway prevents tubulointerstitial fibrosis and ameliorates renal function in various progressive renal disorders. The present study was to determine whether fasudil, a ROCK inhibitor, has a protective effect on cyclosporine A (CsA)-induced nephropathy. Male Sprague-Dawley rats were treated with CsA (n = 10, 20 mg · kg(-1) day(-1) s.c.), CsA + fasudil (n = 10, 3 mg · kg(-1) day(-1) i.p.), or vehicle alone (n = 10) for 28 days. Fasudil cotreatment ameliorated CsA-induced changes and restored renal function. CsA decreased the expression of endothelial nitric-oxide synthase and increased inducible nitric-oxide synthase/3-nitrotyrosine in the kidney. Accordingly, there was infiltration of inflammatory cells and up-regulation of inflammatory cytokines. Fasudil also significantly suppressed the expression of transforming growth factor-ß1, Smad signaling, and subsequent epithelial-to-mesenchymal processes. In addition, fasudil augmented p27(kip1) expression and decreased the number of proliferating cell nuclear antigen-positive cells. In another series of experiments using HK-2 cells in culture, fasudil also suppressed CsA-induced increases in mitogen-activated protein kinase phosphorylation. CsA induced expression of p53, the degree of which was attenuated by fasudil in association with decreases of proapoptotic markers such as Bad, Bax, and total/cleaved caspase-3. These results suggest that inhibition of the Rho/ROCK pathway attenuates CsA-induced nephropathy through the suppression of the induction of inflammatory, apoptotic, and fibrogenic factors, along with inhibition of Smad, mitogen-activated protein kinases, and nitric oxide signaling pathways.

Remifentanil decreases sevoflurane requirements to block autonomic hyperreflexia during transurethral litholapaxy in patients with high complete spinal cord injury.

BACKGROUND: An inhaled anesthetic concentration required to block autonomic hyperreflexia (AHR) is high enough to cause severe hypotension in patients with high spinal cord injury (SCI). We determined the effects of remifentanil on the sevoflurane requirement to block AHR in SCI. METHODS: The study involved 96 patients with chronic, complete SCI scheduled to undergo transurethral litholapaxy during general anesthesia. Anesthesia was induced with thiopental, and sevoflurane concentrations in 50% nitrous oxide were adjusted to maintain a bispectral index of 40 to 50. Whether the patient develops an AHR [an increase of systolic blood pressure (SBP) >20 to 40 mm Hg] was first examined by distending the bladder with glycine solution (the first trial). Patients who developed AHR were then allocated to receive no remifentanil infusion (control, n = 31), a target-controlled plasma concentration of 1 ng/mL (n = 25), or 3 ng/mL remifentanil (n = 24). After baseline hemodynamics had recovered, the target sevoflurane and remifentanil concentrations were maintained for at least 20 minutes and the procedure was resumed (the second trial). Each target sevoflurane concentration was determined by the up-and-down method based on changes (15% increase or more) of SBP in response to the bladder distension. SBP, heart rate, and bispectral index were measured before and during the bladder distension during the trials, and plasma concentrations of catecholamines during the first trial. RESULTS: Eighty-two (85.4%) of 96 patients developed AHR during the first trial, in which 2 were excluded because of hypotension (mean arterial blood pressure <50 mm Hg) developed during target-controlled drug administration. During the second trial, the end-tidal concentrations of sevoflurane to prevent AHR were reduced to 2.6% (95% confidence interval 2.5% to 2.8%, P < 0.01) and 2.2% (2.1% to 2.4%, P < 0.0001) in the groups receiving 1 and 3 ng/mL remifentanil, respectively, in comparison with 3.1% (2.9% to 3.3%) in the control. When considering minimum anesthetic concentration (MAC) values and the contribution of 50% nitrous oxide (0.48 MAC), the combined MAC values, expressed as multiples of MAC, were 2.27, 1.98, and 1.75 in the control, 1 ng/mL remifentanil, and 3 ng/mL remifentanil groups, respectively. CONCLUSIONS: Target-controlled concentrations of 1 and 3 ng/mL remifentanil would reduce the requirement of sevoflurane combined with 50% nitrous oxide to block AHR by 16% and 29%, respectively, in SCI patients undergoing transurethral litholapaxy.

Renoprotective effect of rosuvastatin in DOCA-salt hypertensive rats.

BACKGROUND: Pleiotropic effects of statins represent potential mechanisms for the treatment of end organ damage in hypertension. This study has investigated the effects of rosuvastatin (10 mg/kg/day) on renal function impairment, glomerulosclerosis and tubulointerstitial fibrosis in deoxycorticosterone acetate (DOCA)-salt hypertensive (DSH) rat. METHODS: Rats were implanted with DOCA strips (200 mg/kg) on 1 week after unilateral nephrectomy. Rats received a controlled diet with or without rosuvastatin. Three weeks after DOCA implantation, systolic blood pressure (SBP) was measured by tail-cuff method. The glomerulosclerosis and tubulointerstitial fibrosis was determined by Masson's trichrome stain. The tumour necrosis factor (TNF-alpha), interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma), monocyte chemoattractant protein1 (MCP1), intercellular adhesion molecule-1 (ICAM-1) and endothelin-1 (ET-1) were determined by real-time polymerase chain reaction. The expression of ED-1, transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) was determined in the kidney by immunoblotting and immunohistochemistry. RESULTS: In DSH rats, SBP was increased, which was not affected by rosuvastatin treatment. Creatinine clearance was decreased while urinary albumin excretion ratio was increased in DSH rats compared with controls, which were attenuated by rosuvastatin treatment. Glomerulosclerosis and tubulointerstitial fibrosis in DSH rats were attenuated by rosuvastatin treatment. The messenger RNA expression of TNF-alpha, IL-1beta, IFN-gamma, MCP1, ICAM-1 and ET-1 was increased in DSH, which was attenuated by rosuvastatin treatment. The expression of ED-1, TGF-beta and CTGF was increased in the kidney of DSH, which was counteracted by rosuvastatin treatment. CONCLUSION: Rosuvastatin is effective in preventing progression of renal injury in DSH, the mechanism of which is associated with anti-inflammatory and anti-fibrotic effects.

Recurrent attacks of post-intubation right upper lobe atelectasis.

A 22-year-old woman with no history of asthma developed an acute recurrent attack of severe bronchoconstriction and right upper lobe atelectasis immediately after laryngoscopy and endotracheal intubation. The first attack had taken place 2 months earlier under identical circumstances. Induction of anesthesia for tracheal intubation was achieved using propofol, fentanyl, and rocuronium. Bronchial obstruction and bronchial intubation were excluded by bronchoscopy. The atelectasis was quickly resolved with mechanical ventilation and spasmolytic treatment on both occasions. The surgical procedure could proceed soon after resolution of the atelectasis.

Enhancement of arsenic mobility by indigenous bacteria from mine tailings as response to organic supply.

Arsenic leaching by indigenous bacteria in abandoned Au-Ag mine tailings which contained approximately 3200 mg/kg of As was investigated after supply of various organic substrates. Sequential extraction analysis designed to determine the mode of As occurrence in the tailings revealed that most As (90%) was closely associated with the Fe fraction. When glucose was supplied as a C source, indigenous bacteria significantly enhanced the extent of As release from the tailings into solution under both aerobic and anaerobic conditions. Anaerobic indigenous bacteria leached more amount of As from the tailings than aerobes. Highly positive correlation between the extracted amounts of As and Fe implied that microbial dissolution of Fe(III)-oxides, whether it was ligand- and proton-promoted dissolution or reductive dissolution, might be dominantly responsible for the As release. Bacterial strains which were resistant to up to 100 mM As(V) was aerobically isolated from the tailings. One of the isolates appeared to reduce some aqueous As(V) to likely As(III) in a batch type experiment, which indicated that indigenous bacteria can mediate the electrochemical speciation and thus the mobility of As in the tailings. The results suggest that indigenous bacteria in As-contaminated tailings can increase As mobility from the solid media when microbially available organic substrates are supplied, and thus enhance the risk of As dispersion to nearby soil, sediment and groundwater.

Microbiological reduction of hexavalent chromium by indigenous chromium-resistant bacteria in sand column experiments.

Indigenous bacteria that are resistant to high concentrations of Cr(VI) were isolated from a Cr-contaminated sediment. Sand column experiments were conducted using the isolated bacteria to investigate microbial effects on Cr(VI) reduction in open systems that simulated subsurface conditions. The indigenous Cr-resistant bacteria appeared to reduce Cr(VI) in the column experiments. When 12 mg/L of Cr(VI) was injected into the columns, the removal efficiencies of Cr(VI) by the isolated bacteria were 39.1%, 62.5%, and 63.6% at 24, 48, and 72 h retention times of Cr(VI) solution, respectively. These results imply that the linear velocity of groundwater or pore water should be less than 0.63 cm/h for effective removal of Cr(VI) in subsurface conditions. In comparison, the noninoculated control column did not show a significant variation in dissolved Cr(VI) concentration. The results indicated that reduction of Cr(VI) was occurring in the column due to the activity of the indigenous bacteria.