JongUn Lee

Acute Respiratory Distress Syndrome Associated With Pulmonary Cement Embolism Following Percutaneous Vertebroplasty With Polymethylmethacrylate

Study Design. A case of acute respiratory distress syndrome following percutaneous vertebroplasty is described. Objective. To alert clinicians to the potential occurrence of acute respiratory distress syndrome following use of polymethylmethacrylate bone cement. Summary of Background Data. Noncardiogenic pulmonary edema has not been reported following intravertebral injection of polymethylmethacrylate. Methods. A 68-year-old woman underwent percutaneous vertebroplasty for a painful L5 compression fracture under local anesthesia. A contralateral transpedicular approach was made to inject polymethylmethacrylate. Results. On the third postoperative day, she developed arthralgia, myalgia, fever, and frequent coughing. Chest radiography revealed bilateral, multifocal, patchy consolidations, suggestive of acute respiratory distress syndrome, and a 5-cm-long tubular radiopacity in the right pulmonary artery. She died 20 days after the vertebroplasty. Conclusion. This case illustrates that clinicians must be aware of the potential occurrence of acute respiratory distress syndrome in patients who received percutaneous vertebroplasty.

Studies on adsorptive removal of Co(II), Cr(III) and Ni(II) by IRN77 cation-exchange resin

The adsorption of cobalt, chromium and nickel from aqueous solutions on IRN77 cation-exchange resin has been studied comparatively. The percentage removal of cobalt, chromium and nickel was examined by varying experimental conditions, viz. dosage of adsorbent, pH of the solution and contact time. It was found that more than 95% removal was achieved under optimal conditions. The adsorption capacity (k) for cobalt, chromium and nickel were calculated from the Freundlich adsorption isotherm. The adsorption of cobalt, chromium and nickel on this cation-exchange resin followed the Lagergren kinetic model. Also the competitive adsorption of multi-metals onto the IRN77 resin was studied. The studies showed that this cation-exchange resin can be used as an efficient adsorbent material for the removal of cobalt, chromium and nickel from water and nuclear power plant coolant water.

ASSESSMENT OF As AND HEAVY METAL CONTAMINATION IN THE VICINITY OF DUCKUM Au-Ag MINE, KOREA

In order to assess the potential of As and heavy metal contamination derived from past mining activity and to estimate the human bioavailability quotients for As and heavy metals. Tailings, soils and crop samples were collected and analysed for As, Cd, Cu, Pb and Zn. The mean concentrations of As, Cd, Cu, Pb and Zn in the tailings were 68.5, 7.8, 99, 3,754 and 733 µg g−1, respectively. Maximum Pb concentration in tailings was up to 90 times higher than its tolerable level. The concentrations of these metals were highest in the soils from the dressing plant area, and decreased in the order: farmland soil to paddy soil. In particular, some of the soils from the dressing plant area contained more than 1% of Pb and Zn. The pollution index ranged from 0.19 to 1.93 in paddy soils, and from 1.47 to 3.60 in farmland soils. The average concentrations of heavy metals in crops collected from farmland were higher than those in rice stalks or rice grains, and higher than the internationally accepted limits for vegetables. Element concentrations extracted from farmland soils within the simulated human stomach for 1 h are 9.4 mg kg−1 As, 3.8 mg kg−1 Cd, 37 mg kg−1 Cu, 250 mg kg−1 Pb and 301 mg kg−1 Zn. In particular, the extracted concentrations of Cd, Pb and Zn are in excess of the tolerable levels. The results of the simple bioavailability extraction test (SBET) indicate that regular ingestion (by inhalation and from dirty hands) of soils by the local population could pose a potential health threat due to long-term toxic element exposure.

The effects of volatile anesthetics on spontaneous contractility of isolated human pregnant uterine muscle : A comparison among sevoflurane, desflurane, isoflurane, and halothane

We examined the effects of equianesthetic concentrations of sevoflurane, desflurane, isoflurane, and halothane on the spontaneous contractility of isolated human pregnant uterine muscles. We also determined if their action was related to potassium channels. Uterine specimens were obtained from normal full-term pregnant women undergoing elective lower-segment cesarean delivery. Longitudinal muscle strips were mounted vertically in tissue chambers. Their isometric tension was recorded while they were exposed to 0.5–3 minimum alveolar concentration (MAC) of volatile anesthetics in the absence and presence of the high conductance calcium-activated potassium channel blocker, tetraethylammonium, or the adenosine triphosphate-sensitive potassium channel (KATP)-blocker, glibenclamide. The anesthetics examined produced a dose-dependent depression of contractility. The inhibitory potency of sevoflurane and desflurane was comparable to, whereas that of isoflurane was smaller than, that of halothane: concentrations causing 50% inhibition of the contractile amplitude (ED50) were 1.72, 1.44, 2.35, and 1.66 MAC (P < 0.05), respectively. Tetraethylammonium and glibenclamide did not affect the uterine response to the anesthetics, except for glibenclamide, which attenuated the response to isoflurane. These results indicate that the volatile anesthetics have inhibitory effects on the contractility of the human uterus. The inhibitory effect of isoflurane may in part be mediated through activation of KATP channels.

Paricalcitol attenuates cyclosporine-induced kidney injury in rats

Despite its benefits, the clinical use of cyclosporine A (CsA) is limited by its nephrotoxic properties. Because paricalcitol (19-nor-1,25-hydroxyvitamin D(2)) has renoprotective effects, we tested whether it can blunt renal dysfunction and fibrosis in a rat model of CsA-induced nephropathy. Treatment with CsA decreased creatinine clearance, increased monocyte/macrophage infiltration, and increased the expression of inflammatory cytokines within the kidney. Paricalcitol reduced the decline in kidney function and pro-fibrotic changes and also blunted the increased transforming growth factor (TGF)-beta1 expression and Smad signaling. Using an in vitro model, we treated HK-2 cells with CsA and found that paricalcitol attenuated the CsA-induced increases in phosphorylated extracellular signal-regulated and c-Jun N-terminal kinases, and also prevented the activation of nuclear factor-kappaB. Paricalcitol effectively prevented TGF-beta1-induced epithelial-to-mesenchymal transitions and extracellular matrix accumulation as evidenced by attenuated collagen deposition and fibrosis in CsA-treated rats. In addition, paricalcitol decreased the number of TUNEL-positive nuclei and reduced the expression of pro-apoptotic markers in CsA-treated HK-2 cells. Thus, paricalcitol appears to attenuate CsA-induced nephropathy by suppression of inflammatory, pro-fibrotic, and apoptotic factors through inhibition of the nuclear factor-kappaB, Smad, and mitogen-activated protein kinase signaling pathways.

Cerebral Oxygen Saturation Measured by Near-infrared Spectroscopy and Jugular Venous Bulb Oxygen Saturation during Arthroscopic Shoulder Surgery in Beach Chair Position under Sevoflurane-Nitrous Oxide or Propofol-Remifentanil Anesthesia

Background: We examined the effects of different anesthetics on cerebral oxygenation and systemic hemodynamics in patients undergoing surgery in beach chair position (BCP). Jugular venous bulb oxygen saturation (SjvO2) and regional cerebral tissue oxygen saturation (SctO2) were determined while patients were placed from the supine to BCP. Whether SctO2 and SjvO2 are interchangeable in assessing the cerebral oxygenation was also examined. Methods: Forty patients undergoing shoulder surgery in BCP were randomly assigned to receive sevoflurane-nitrous oxide (S/N) or propofol-remifentanil (P/R) anesthesia. Four patients taking angiotensin II receptor antagonists were excluded post hoc. Mean arterial pressure and heart rate, as well as SjvO2 and SctO2, were measured before (postinduction baseline in supine position) and after BCP. Results: Mean arterial pressure decreased by BCP in both groups. It was, however, significantly higher in S/N (n = 19) than in P/R group (n = 17) at 7 to 8 min after the positioning. SjvO2 also significantly decreased after BCP in both groups, the magnitude of which was lower in S/N than in P/R group (11 ± 10% vs. 23 ± 9%, P = 0.0006). The incidences of SjvO2 <50% and mean arterial pressure less than 50 mmHg were lower in S/N group, but SctO2and the incidence of cerebral desaturation (more than 20% decrease from baseline) did not significantly differ between the groups. SctO2 and SjvO2 were only weakly correlated (&bgr; = 0.218, r2 = 0.133). Bland-Altman analysis showed a mean difference of −7.2% with 95% limit of agreement between −38.2% and 23.8%. Conclusions: The margin of safety against impaired cerebral oxygenation is greater and SjvO2 is more preserved with S/N than with P/R anesthesia. SctO2 may not be reliable in detecting a low SjvO2 during the surgery in BCP.

Renoprotective effects of paricalcitol on gentamicin-induced kidney injury in rats.

Vitamin D is thought to exert a protective effect on renal disease progression, but the underlying molecular mechanism remains unclear. We investigated whether paricalcitol ameliorates tubular dysfunction and fibrosis in gentamicin (GM)-induced renal injury. Two groups of rats were treated with GM (100 mg x kg(-1) x day(-1)), one of which was cotreated with paricalcitol (0.3 microg x kg(-1) x day(-1)) for 14 days and the other was not. The control group was treated with vehicle only. HK-2 cells were cultured with GM in the absence or presence of paricalcitol. Paricalcitol restored impaired renal function and the downregulated renal sodium transporters and aquaporin-1 expression caused by GM. ED-1-expressing monocyte/macrophage accumulation induced by GM was attenuated by paricalcitol treatment. Paricalcitol prevented upregulated inflammatory cytokines (TNF-alpha, IL-1beta, INF-gamma) and adhesion molecules (monocyte chemoattractant protein-1, ICAM-1, VCAM-1) induced by GM. In addition, paricalcitol effectively reversed TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) process and extracellular matrix accumulation in GM-induced nephropathy. Increased collagen deposition and fibrosis in GM-treated kidney were ameliorated by paricalcitol. Paricalcitol also attenuated the upregulated NF-kappaB and phosphorylated ERK1/2 expression in HK-2 cells cultured with GM. In conclusion, paricalcitol prevents GM-induced renal injury by inhibiting renal inflammation and fibrosis, the mechanism of which is the interruption of NF-kappaB/ERK signaling pathway and preservation of tubular epithelial integrity via inhibiting EMT process.

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal, inducible, and endothelial NOS (n/i/eNOS). NO-mediated effects can be beneficial or harmful depending on the specific risk factors affecting the disease. In hypertension, the vascular relaxation response to acetylcholine is blunted, and that to direct NO donors is maintained. A reduction in the activity of eNOS is mainly responsible for the elevation of blood pressure, and an abnormal expression of iNOS is likely to be related to the progression of vascular dysfunction. While eNOS/nNOS-derived NO is protective against the development of atherosclerosis, iNOS-derived NO may be proatherogenic. eNOS-derived NO may prevent the progression of myocardial infarction. Myocardial ischemia/reperfusion injury is significantly enhanced in eNOS-deficient animals. An important component of heart failure is the loss of coronary vascular eNOS activity. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2 abundance. In chronic kidney disease model of subtotal-nephrectomized rats, treatment with NOS inhibitors decreased systemic NO production and induced left ventricular systolic dysfunction (renocardiac syndrome).

α-Lipoic acid prevents cisplatin-induced acute kidney injury in rats

BACKGROUND Cisplatin-induced nephropathy has been related to increased lipid peroxide formation and decreased activity of antioxidant enzymes in the kidney. The present study aimed to examine whether treatment with alpha-lipoic acid (alpha-LA) prevents the cisplatin-induced nephrotoxicity. METHODS Two groups of rats were treated with cisplatin, one of which being cotreated with alpha-LA. The control group was treated with vehicle only. Four days later, the expression of aquaporins and sodium transporters was determined in the kidney by immunoblotting and immunohistochemistry. The arginine vasopressin-stimulated generation of cAMP was measured by radioimmunoassay. The expression of nitric oxide synthases (NOS) was determined by immunoblotting. The mRNA expression of endothelin-1 (ET-1) and tumour necrosis factor (TNF)-alpha was measured by real-time PCR. Apoptosis was examined by TUNEL staining. RESULTS Following the treatment with cisplatin, urinary volume and fractional excretion of sodium increased. Accordingly, the expression of aquaporins 1-3, Na,K-ATPase, NHE3 and NKCC2 was decreased. The expression of adenylyl cyclase VI and vasopressin-stimulated cAMP generation was decreased. The expression of inducible NOS was increased, while that of endothelial NOS decreased. The ET-1 expression was increased. TUNEL-positive cells were increased, in association with an increased expression of TNF-alpha. alpha-LA treatment prevented dysregulation of these parameters and resumed the renal function. CONCLUSION alpha-LA may prevent the cisplatin-induced nephrotoxicity, possibly through preserving the activities of NO and ET systems and inhibiting the development of apoptosis.

Renoprotective effects of the direct renin inhibitor aliskiren on gentamicin-induced nephrotoxicity in rats

This study aimed to examine the protective effects of aliskiren on gentamicin-induced nephropathy. Rats were injected with gentamicin (100 mg/kg per day) for 14 days. Aliskiren was infused for two weeks. Human proximal tubular epithelial cell lines (HK-2) were cultured with gentamicin in the absence or presence of aliskiren. Inflammatory profibrotic and apoptotic markers were evaluated in vivo and in vitro. Aliskiren treatment attenuated the decreased creatinine clearance, increased fractional sodium excretion, glomerulosclerosis and tubulointerstitial fibrosis and counteracted the increased ED-1 expression in gentamicin-treated rats. The levels of inflammatory cytokines (TNF-α, IL-1β and IFN-γ) and adhesion molecules (MCP-1, ICAM-1 and VCAM-1) increased in the gentamicin-treated kidneys. These changes were restored by aliskiren co-treatment. Aliskiren effectively reversed transforming growth factor-β-induced fibrotic responses such as induction of α-smooth muscle actin in gentamicin-treated rat kidneys. Along with these changes, aliskiren also attenuated the increase in nuclear factor κB and phosphorylated extracellular signal-regulated kinase (pERK 1/2) levels in HK-2 cells cultured with gentamicin. In addition, aliskiren decreased the number of TUNEL-positive nuclei and reduced the expression of proapoptotic markers in gentamicin-treated HK-2 cells. These findings suggest that aliskiren attenuates gentamicin-induced nephropathy by suppression of inflammatory, profibrotic and apoptotic factors through inhibition of the nuclear factor κB, Smads and mitogen-activated protein kinase signaling pathways.