http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Reviews : Renal Dysfunction in Patients with Chronic Liver Disease
Jay Wook Lee 대한전해질·혈압학회 2009 Electrolytes & Blood Pressure Vol.7 No.2
Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
Review : Fluid and Electrolyte Disturbances in Critically Ill Patients
( Jay Wook Lee ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2
Disturbances in fluid and electrolytes are among the most common clinical problems encountered in the intensive care unit (ICU). Recent studies have reported that fluid and electrolyte imbalances are associated with increased morbidity and mortality among critically ill patients. To provide optimal care, health care providers should be familiar with the principles and practice of fluid and electrolyte physiology and pathophysiology. Fluid resuscitation should be aimed at restoration of normal hemodynamics and tissue perfusion. Early goaldirected therapy has been shown to be effective in patients with severe sepsis or septic shock. On the other hand, liberal fluid administration is associated with adverse outcomes such as prolonged stay in the ICU, higher cost of care, and increased mortality. Development of hyponatremia in critically ill patients is associated with disturbances in the renal mechanism of urinary dilution. Removal of nonosmotic stimuli for vasopressin secretion, judicious use of hypertonic saline, and close monitoring of plasma and urine electrolytes are essential components of therapy. Hypernatremia is associated with cellular dehydration and central nervous system damage. Water deficit should be corrected with hypotonic fluid, and ongoing water loss should be taken into account. Cardiac manifestations should be identified and treated before initiating stepwise diagnostic evaluation of dyskalemias. Divalent ion deficiencies such as hypocalcemia, hypomagnesemia and hypophosphatemia should be identified and corrected, since they are associated with increased adverse events among critically ill patients.
Role of IL-1α in Cisplatin-Induced Acute Renal Failure in Mice
( Jay Wook Lee ),( Woo Jin Nam ),( Min Jee Han ),( Jung Ho Shin ),( Jin Gun Kim ),( Su Hyun Kim ),( Hye Ryoun Kim ),( Dong Jin Oh ) 대한내과학회 2011 The Korean Journal of Internal Medicine Vol.26 No.2
Background/Aims: For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1α. We thus asked whether IL-1α deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice. Methods: Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1α was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1α -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1α -/- mice. Results: Compared with vehicle-treated mice, renal IL-1α increased in cisplatin-treated wild-type mice beginning on day 1. IL-1α -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1α -/- mice. Conclusions: Mice deficient in IL-1α are protected against cisplatin-induced ARF. The lack of IL-1α may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1α -/- mice in cisplatin-induced ARF merits further study. (Korean J Intern Med 2011;26:187-194)
증례 : 광방기에 의해 발생한 Chinese Herb Nephropathy 1예
이재욱 ( Jay Wook Lee ),손민정 ( Min Jung Sohn ),허남주 ( Nam Joo Heo ),주권욱 ( Kwon Wook Joo ),정윤철 ( Yoon Chul Jung ),이정상 ( Jung Sang Lee ),한진석 ( Jin Suk Han ) 대한내과학회 2006 대한내과학회지 Vol.71 No.2
본 증례의 환자는 근위부 신세뇨관 산증, 진행성 만성 신부전증, 세뇨관 위축 및 간질 섬유화 등 CHN에 잘 맞는 임상 증상 및 조직 소견을 보였고, 복용하던 한약재에서 AA가 검출되어 AA에 의한 CHN 또는 AAN으로 진단할 수 있었다. 이러한 환자의 신조직에서 AA-DNA adduct를 추가로 검출할 수 있다면 진단의 정확성을 더욱 높일 수 있을 것으로 보인다. Chinese herb nephropathy (CHN) is characterized by progressive tubulointerstitial nephritis and development of renal failure in a couple of years after diagnosis. Aristolochic acid (AA) is believed to be associated with the development of CHN. The authors report a case of CHN in which AA in the herb regimen was identified by high-performance liquid chromatography (HPLC). A 32-year-old female presented with nausea, vomiting and generalized weakness. She had been taking Chinese herbs for symptomatic care. Clinical and laboratory examinations revealed Fanconi syndrome, renal failure, and severe anemia. Renal biopsy showed severe tubulointerstitial nephritis with moderate tubular atrophy and interstitial fibrosis. She developed end-stage renal failure 4 months after diagnosis. The herb she had been taking was Aristolochia fangchi. HPLC technique was used to identify AA and to measure its concentration in the herb. From the clinical and laboratory data, the patient was diagnosed with CHN caused by aristolochic acid.(Korean J Med 71:224-228, 2006)
Lee, Suk-Woo,Bak, Seong-Min,Lee, Chang-Wook,Jaye, Cherno,Fischer, Daniel A.,Kim, Bae-Kyun,Yang, Xiao-Qing,Nam, Kyung-Wan,Kim, Kwang-Bum American Chemical Society 2014 JOURNAL OF PHYSICAL CHEMISTRY C - Vol.118 No.5
<P>We explore structural changes of the carbon in MnO<SUB>2</SUB>/reduced graphene oxide (RGO) hybrid materials prepared by the direct redox reaction between carbon and permanganate ions (MnO<SUB>4</SUB><SUP>–</SUP>) to reach better understanding for the effects of carbon corrosion on carbon loss and its bonding nature during the hybrid material synthesis. In particular, we carried out near-edge X-ray absorption fine structure spectroscopy at the C K-edge (284.2 eV) to show the changes in the electronic structure of RGO. Significantly, the redox reaction between carbon and MnO<SUB>4</SUB><SUP>–</SUP> causes both quantitative carbon loss and electronic structural changes upon MnO<SUB>2</SUB> deposition. Such disruptions of carbon bonding have a detrimental effect on the initial electrical properties of the RGO and thus lead to a significant decrease in electrical conductivity. Electrochemical measurements of the MnO<SUB>2</SUB>/reduced graphene oxide hybrid materials using a cavity microelectrode revealed unfavorable electrochemical properties that were mainly due to the poor electrical conductivity of the hybrid materials. The results of this study should serve as a useful guide to rationally approaching the syntheses of metal/RGO and metal oxide/RGO hybrid materials.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jpccck/2014/jpccck.2014.118.issue-5/jp411176b/production/images/medium/jp-2013-11176b_0008.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/jp411176b'>ACS Electronic Supporting Info</A></P>