48 research outputs found
A Study on Development of a Core competencies tool of University Students According to Specialized University
λ³Έ μ°κ΅¬λ ν΅μ¬μλμ λν κ΄μ¬κ³Ό λν νΉμ±νμ μΌνμΌλ‘ λνμμ ν΅μ¬μλμ§λ¨ λꡬλ₯Ό κ°λ°νκ³ μ μ€μν μ°κ΅¬μ΄λ€. κ΅κ°μμ€μμ κ°λ°λ K-CESAμ κ΅λ΄ Hλνμ μΈμ¬μμ μ΅ν©νμ¬ μλ‘μ΄ ν΅μ¬μλ μ§λ¨λꡬλ₯Ό κ°λ°, νλΉν νκ³ μ νμλ€. μ΄λ₯Ό μν΄ λ¨Όμ λ¬Ένκ³ μ°°μ ν΅ν΄ K-CESAμ Hλνμ μΈμ¬μμμ νμν ν΅μ¬μλμ κ²°ν©νμκ³ , μ΄λ₯Ό λ°νμΌλ‘ λ¬Ένμ κ°λ°νμλ€. κ°λ°ν μλΉμ‘°μ¬ λ¬Ένμ μ΄ 74κ°μ λ¬ΈνμΌλ‘ κ³ μ κ²μ¬μ΄λ‘ κ³Ό λ¬Ένλ°μμ΄λ‘ μ κΈ°λ°μΌλ‘ νμ¬ λ¬ΈνλΆμμ μ€μνμμΌλ©°, ꡬμΈνλΉλμ μ λ’°λλ₯Ό κ²μ¦νμλ€. κ·Έ κ²°κ³Ό, μ΅μ’
κ²μ¬λ 48κ°μ λ¬ΈνμΌλ‘ ꡬμ±νμκ³ κ²μ¬μ μ λ’°λμ νλΉλ κ²μ¦μ ν΅ν΄ κ²μ¬μ μ ν©μ±μ κ²μ¦νμλ€. λ³Έ μ°κ΅¬λ₯Ό λ°νμΌλ‘ κ°λ°ν κ²μ¬ λꡬλ λν νΉμ±νμ μΌνμΌλ‘ νμλ€μ ν΅μ¬μλ μμ€μ μ§λ¨ν λΏλ§ μλλΌ κ°λ³ ν΅μ¬μλ μμ€μ μ§λ¨νμ¬ νλ‘κ·Έλ¨μ μ°κ³ν μ μμΌλ©°, κΆκ·Ήμ μΌλ‘ λν μΈμ¬μμ λ§λ μΈμ¬λ₯Ό κΈ°λ₯΄κΈ° μν κΈ°μ΄μλ£λ‘ μ¬μ©μ΄ κ°λ₯ν κ²μ΄λ€This study aims to develop diagnostic tool as a way of interesting in the core competencies and the specialized university that will be able to measure the core competencies of university students. This study focused on developing new diagnostic tool combining K-CESA of national level with right people of H university and validating the new diagnostic tool. For this study, K-CESA and core competencies in right people of H university are combined through the literature review, and test items are developed based on the preceding research. Our process included not only analysis of the test items that consist of 74 developed preliminary study items based on classical test theory and item response theory but also verification of construct validity and reliability. According to the above study result, final test items are made up of 48 items and the test was verified to suitability of the examination after verification of the test validity and reliability. Developed diagnostic tool based on the study can diagnose university students' core competencies as the part of the specialized university and make a connection the program after evaluating the individual level of core competencies. Ultimately, this diagnostic tool is available as a basic data for promising talent based on the University Vision
Congenital Nephrogenic Diabetes Insipidus Presented with Bilateral Hydronephrosis: Genetic Analysis of V2R Gene Mutations
Most cases of hydronephrosis are caused by urinary tract obstruction. However, excessive polyuric syndrome rarely gives rise to non-obstructive hydronephrosis, megaureter, and a distended bladder. The authors report here on two cases of congenital nephrogenic diabetes insipidus (NDI) with severe bilateral hydronephrosis and megaureter. It is Interesting that the patients were symptomless except for their polyuria, and they both presented with bilateral hydronephrosis. Fluid deprivation testing revealed the presence of AVP resistant NDI. Gene analysis for these patients showed the AVP receptor 2 (V2R) missense mutations (Q225X and S126F), which have previously been reported on in other studies. We made the diagnosis of NDI by using a physiologic test, and we confirmed it by mutation analysis of the V2R gene.ope
Prognostic factor for adult focal segmental glomerulosclerosis
μκ³Όνκ³Ό/μμ¬[νκΈ]
μλ°μ± μ΄μ μ± λΆμ ν μ¬κ΅¬μ²΄ κ²½νμ¦μ μ μ¦νκ΅°μ νν μμΈμΌλ‘ νλ¨, κ³ νμ, μ κΈ°λ₯μ μ§νμ± μμ€μ νΉμ§μΌλ‘ νλ€. μλ°μ± μ΄μ μ± λΆμ ν μ¬κ΅¬μ²΄ κ²½νμ¦μ μΉλ£ λ°μμ΄ λμ κ²μΌλ‘ μκ°λμ΄μ Έ μμΌλ μ΅κ·Ό μΉλ£μ λμ κ΄ν΄μ¨κ³Ό ν₯μλ μνκ° λ³΄κ³ λκ³ μμΌλ©° μ¬ν λ¨λ°±λ¨μ κ°μ§μ± μ¬μ νλ± μΌλΆ μμ λ° λ³λ¦¬μ μΈ μ§νλ€μ μν μΈ‘λ©΄μμ μλ―Έλ₯Ό κ°μ§λ€κ³ μλ €μ‘λ€. κ·Έλ¬λ, νμ¬κΉμ§ μΌκ΄λκ² λ³΄κ³ λλ μν μΈμλ μλ μ€μ μ΄λ€. μ΄μ μ μλ μ±μΈ μλ°μ± μ΄μ μ± λΆμ ν μ¬κ΅¬μ²΄ κ²½νμ¦ νμλ€μ λμμΌλ‘ μΉλ£ λ°μμ λν μνμΈμμ μ λΆμ μΌλ‘μ μ§νμ μν₯μ μ£Όλ μνμΈμλ₯Ό μμλ³΄κ³ μ νμλ€. 1991λ
λΆν° 2002λ
κΉμ§ μΈλΈλμ€ λ³μμ μ
μνμ¬ μ μ‘°μ§κ²μ¬μμ μΌμ°¨μ± μ΄μ μ± λΆμ ν μ¬κ΅¬μ²΄ κ²½νμ¦μΌλ‘ μ§λ¨λ°μ μ±μΈ νμλ€μ λμμΌλ‘ μ§λ¨μ μμμ μ§νμ λ³λ¦¬ μ‘°μ§νμ μ§νλ₯Ό νν₯μ μΌλ‘ λΆμνμ¬ λ€μμ κ²°κ³Όλ₯Ό μ»μλ€.
1. λμ νμ 40λͺ
μ μ±λ³μ λ¨λ
κ°κ° 24λͺ
κ³Ό 16λͺ
, νκ· μ°λ Ήμ 42Β±16(νκ· Β±νμ€νΈμ°¨)μΈμλ€.
2. μ μ‘°μ§κ²μ¬μ νμ 26λͺ
(65%)μμ μ μ¦νμμ λ¨λ°±λ¨κ° μμμΌλ©°, 14λͺ
(35%)μμ λΉμ μ¦νμμ λ¨λ°±λ¨κ° μμλ€. μ μ¦νμμ λ¨λ°±λ¨ νμκ΅°μμ λΉμ μ¦νμμ λ¨λ°±λ¨ νμκ΅°λ³΄λ€ νμ² ν¬λ μν°λμΉκ° λμμΌλ©°(P<0.05), λμ΄, μ±λ³, κ³ νμ μ 무, νλ―Έκ²½μ νλ¨ μ 무, μΆμ κ΄μ°°κΈ°κ° λ±μ μλ―Έμλ μ°¨μ΄λ₯Ό 보μ΄μ§ μμλ€.
3. λμ νμμ€ 27λͺ
μμ λ©΄μ μ΅μ μΉλ£λ₯Ό νμμΌλ©° 15λͺ
(55.6%)μμ μΉλ£ λ°μμ΄ μμμΌλ©° μΉλ£ λ°μκ΅°κ³Ό 무λ°μκ΅° μ¬μ΄μ μλ―Έμλ μμ λ° λ³λ¦¬ μ‘°μ§νμ μ§νλ κ΄μ°°λμ§ μμλ€.
4. λμ νμ 40λͺ
μ€ μΆμ κ΄μ°°κΈ°κ° λμ μ μ μ κΈ°λ₯μ μ μ§ν κ΅°κ³Ό λ§μ± μ λΆμ μΌλ‘ μ§νν κ΅° μ¬μ΄μ μ§λ¨μ νμ² ν¬λ μν°λμΉμ μ¦κ°μ μΉλ£μ λν λ°μ μ λ¬΄κ° μλ―Έμλ κ²μΌλ‘ λΆμλμλ€(P<0.05).
5. μ μμ‘΄λΆμμ μΉλ£λ₯Ό ν κ΅°μμ μΉλ£λ₯Ό μν κ΅°λ³΄λ€ μ°μν μμ‘΄κΈ°κ°μ λ³Ό μ μμμΌλ ν΅κ³μ μΌλ‘ μλ―Έλ μμλ€. μΉλ£ λ°μκ΅°μμ μΉλ£ 무λ°μκ΅°λ³΄λ€ μ μνκ² λμ μ μμ‘΄μ¨μ κ΄μ°°ν μ μμλ€(P<0.05).
κ²°λ‘ μ μΌλ‘, μ§λ¨μ μ λΆμ μκ²¬μ΄ μκ±°λ μΉλ£ λ°μμ΄ μλ νμκ΅°μ λΆλν μνλ₯Ό κ°μ§ μ μμΌλ―λ‘ μ΄λ¬ν νμκ΅°μμ λ³΄λ€ μ§μ€μ μΈ μΉλ£μ μ£ΌκΈ°μ μΈ μ κΈ°λ₯μ κ΄μ°°μ΄ νμν κ²μΌλ‘ 보μΈλ€. λν, ν₯ν μ΄μ μ± λΆμ ν μ¬κ΅¬μ²΄ κ²½νμ¦μ μΉλ£μ κ΄ν 무μμ, μ ν₯μ μΈ μ°κ΅¬λ νμν κ²μΌλ‘ 보μΈλ€.
[μλ¬Έ]
Primary focal segmental glomerulosclerosis(FSGS) is common cause of nephrotic syndrome and is characterized by hematuria, hypertension, and progressive loss of renal function to renal failure. Although primary FSGS has been known to be refractory to treatment, recent studies reveal higher remission rate and better prognosis. And it has been reported that some clinical and histopathologic parameters such as heavy proteinuria and interstitial fibrosis were significant to prognosis. But, confirmative prognostic indices remain to be defined. In order to further clarify the prognostic factors to therapeutic response and risk factors for progression to CRF, we reviewed the medical records of adult patients diagnosed as FSGS by renal biopsy from 1991 to 2002 in Severance hospital. Following results were obtained.
1. The patients consisted of 24 male and 16 female, aged of 42Β±16(meanΒ±SD) years.
2. At the time of renal biopsy, 26 patients(65%) had proteinuria of the nephrotic range and 14 patients(35%) had proteinuria of the non-nephrotic range. The serum creatinine level was higher in nephrotic-ranged patients than that in non nephrotic-ranged patients(P<0.05). Age, sex, hypertension, microscopic hematuria, follow-up duration were not significantly different between two groups.
3. Twenty-seven patients were treated with immunosupressant and 15 patients(55.6%) responded to the treatment. There was no significant difference in clinical or histopathological variables between the patients with therapeutic response and the patients without response.
4. In the analysis of risk factors for progression to CRF, high serum creatinine level at diagnosis and responsiveness to treatment were identified as significant.
5. The patients treated with immunosuppressants had longer survival period compared to the patients without treatment, though the differences was not statistically significant. And, treatment responsive group had longer survival period compared to the non-responsive group significantly(P<0.05).
In conclusion, the patient with initial impairment of renal function or poor response to therapy may have worse prognosis, and the intense treatment with regular follow-up of renal function should be recommended for these patients. Furthermore the prospective controlled study for the treatment of FSGS is required.ope
p38 Mitogen-Activated Protein Kinase μ΅μ μ μΈ FR167653μ΄ λΉλ¨ λ°±μ μ¬κ΅¬μ²΄ λ΄ fibronectin λ° μ 4ν collagenμ λ°νμ λ―ΈμΉλ μν₯
Dept. of Medicine/λ°μ¬[νκΈ]
λ°° κ²½: λΉλ¨λ³μ± μ λ³μ¦μ λ³λ¦¬νμ μΌλ‘ μ¬κ΅¬μ²΄ λΉνμ μΈν¬μΈ κΈ°μ§μ μΆμ μ΄ νΉμ§μ μΈ μ견μΌλ‘, λΉλ¨ 쑰건 νμμ p38 mitogen-activated protein kinase (MAPK) κ²½λ‘μ νμ±νλ₯Ό ν΅νμ¬ fibronectinκ³Ό μ 4ν collagenμ λ°νμ΄ μ¦κ°νλ κ²μΌλ‘ λ³΄κ³ λκ³ μλ€. FR167653 {1-[7-(4-fluorophenyl)-1,2,3,4-tetrahydro-8(4- pyridylpyrazolo(5,1-c)(1,2,4)triazin-2-yl]-2-phenylethanedion sulfate monohydrate}μ interleukin-1κ³Ό tumor necrosis factor- μμ±μ μ΅μ μν€λ ν¨κ³Όλ₯Ό κ°μ§ μ½μ λ‘, p38 MAPK κ²½λ‘μ μ΅μ λ₯Ό ν΅ν νμΌμ¦ μμ©μΌλ‘ μΈνμ¬ λ§μ± μ΄μ μ λ³μ¦, λ°μμ μ¬κ΅¬μ²΄μ μΌ, κ·Έλ¦¬κ³ μκ°λ©΄μ μ μ§ν λ±μμ μ μμμ κ°μμμΌ°λ€λ λ³΄κ³ λ μμΌλ, λΉλ¨λ³μ± μ λ³μ¦μμμ ν¨κ³Όμ λν μ°κ΅¬λ νμ¬κΉμ§ μ 무ν μ€μ μ΄λ€. μ΄μ λ³Έ μ°κ΅¬μμλ λΉλ¨ λ°±μλ₯Ό λμμΌλ‘ p38 MAPK μ΅μ μ μΈ FR167653κ° 24μκ° λ¨μλΆλ―Ό λ°°μ€λκ³Ό μ¬κ΅¬μ²΄ λ΄ fibronectinκ³Ό μ 4ν collagenμ λ°νμ λ―ΈμΉλ μν₯μ μμλ³΄κ³ μ νμλ€.λ°© λ²: 32λ§λ¦¬μ Sprague-Dawley λ°±μλ₯Ό λμ‘°κ΅° (16λ§λ¦¬)κ³Ό streptozotocinμ 볡κ°λ΄λ‘ ν¬μ¬νμ¬ λΉλ¨λ₯Ό μ λ°μν¨ λΉλ¨κ΅° (16λ§λ¦¬)μΌλ‘ λλμ΄, κ° κ΅°μμ 8λ§λ¦¬μ©μ p38 MAPK μ΅μ μ μΈ FR167653μ 1μΌ 10 mg/kg μ©λμΌλ‘ 3κ°μκ° λ§€μΌ κ²½κ΅¬ ν¬μ¬νμμΌλ©° (C+FR, DM+FR), λλ¨Έμ§ 8λ§λ¦¬μ©μ μμ½μ ν¬μ¬νμλ€ (C, DM). λΉλ¨ μ λ° 3κ°μ ν 24μκ° μλ³μ μ±μ·¨νμ¬ μλΆλ―Ό λ°°μ€λμ ELISAλ‘ μΈ‘μ νμμΌλ©°, ν¬μμν¨ ν sieveλ₯Ό μ΄μ©νμ¬ λΆλ¦¬ν μ¬κ΅¬μ²΄λ₯Ό μ€νμ μ¬μ©νμλ€. μ¬κ΅¬μ²΄ λ΄ p38 MAPKμ p38 MAPKμ μνμ¬ μ‘°μ λλ μ μ¬μΈμμΈ c-AMP-responsive element binding protein (CREB)μ λ¨λ°± λ°ν λ° νμ±λλ Western blotμΌλ‘, fibronectinκ³Ό μ 4ν collagen mRNAμ λ¨λ°± λ°νμ κ°κ° real time-PCRκ³Ό Western blotμΌλ‘ λΆμνμλ€. λν μ μ₯ μ‘°μ§μ μ΄μ©νμ¬ fibronectinμ λν λ©΄μμ‘°μ§νν μΌμκ³Ό μ 4ν collagenμ λν λ©΄μνκ΄ μΌμλ μννμλ€.κ²° κ³Ό: λΉλ¨ μ λ° 3κ°μ ν 체μ€μ λν μ μ₯ 무κ²λΉλ DMκ΅°μμ 1.54 0.13%λ‘, Cκ΅°μ 0.53 0.04%μ C+FRκ΅°μ 0.59 0.06%μ λΉνμ¬ μ μνκ² μ¦κ°λμμΌλ©°, μ΄λ¬ν μ¦κ°λ FR167653ν¬μ¬λ‘ μλ―Έμκ² μ΅μ λμλ€ (p<0.01). λν, FR167653μ DMκ΅°μμ μμμκ² μ¦κ°λ 24μκ° λ¨μλΆλ―Ό λ°°μ€λμ μ μνκ² κ°μμμΌ°λ€ (C, 0.40 0.06 mg/day; DM, 1.99 0.22 mg/day; DM+FR, 1.04Β±0.19 mg/day; p<0.05). Phospho-specific p38 MAPKμ phospho-specific CREBμ μ΄μ©ν Western blot λΆμμ p38 MAPKμ CREBμ νμ±λλ Cκ΅°μ λΉνμ¬ DMκ΅°μμ κ°κ° 1.8λ°° (p<0.05), 2.3λ°° μ¦κ°λμμΌλ©° (p<0.01), μ΄λ¬ν μ¦κ°λ FR167653 ν¬μ¬λ‘ κ°κ° 77.8% (P<0.05), 63.4% (p<0.01) μ΅μ λμλ€. λ°λ©΄μ μ΄ p38 MAPKμ μ΄ CREBμ λ¨λ°± λ°νμ λ€ κ΅° μ¬μ΄μ μλ―Έμλ μ°¨μ΄κ° μμλ€. Fibronectinκ³Ό μ 4ν collagenμ mRNA λ°νμ Cκ΅°μ λΉνμ¬ DMκ΅°μμ κ°κ° 2.1λ°°, 1.9λ°° μ¦κ°λμμΌλ©°, FR167653μ DMκ΅°μμ μ¦κ°λ fibronectinκ³Ό μ 4ν collagenμ mRNA λ°νμ μμμκ² μ΅μ μμΌ°λ€. Western blotμ μ μ‘°μ§ μΌμμΌλ‘ λΆμν fibronectinκ³Ό μ 4ν collagenμ λ¨λ°± λ°νλ mRNA λ°ν μμκ³Ό μ μ¬νμλ€.κ²° λ‘ : μ΄μμ κ²°κ³Όλ‘, p38 MAPK μ΅μ μ κ° λΉλ¨λ³μ± μ λ³μ¦μ λ°μ μλ°©μ λμμ΄ λ μ μμ κ²μΌλ‘ μκ°λλ€.
[μλ¬Έ]Background. Diabetic nephropathy is characterized by glomerular hypertrophy and ECM accumulation, and the p38 MAPK pathway is known to be activated in diabetic glomeruli, leading to an increase in fibronectin and type IV collagen expression. This study was undertaken to investigate the effect of a p38 MAPK inhibitor, FR167653, on urinary albumin excretion and on glomerular fibronectin and type IV collagen expression in diabetic rats.Methods. Thirty-two Sprague-Dawley rats were injected with diluent (C, N=16) or streptozotocin intraperitoneally (DM, N=16). Eight rats from each group were treated with 10 mg/kg/day FR167653 (C+FR, DM+FR) for 3 months. At the time of sacrifice, 24-hour urinary albumin excretion was determined by ELISA. Glomerular p38 MAPK and c-AMP-responsive element binding protein (CREB) activities were determined by Western blot with phospho-specific antibodies, and glomerular fibronectin and type IV collagen mRNA and protein expression were determined by real-time PCR and Western blot, respectively, with sieved glomeruli.Results. The ratio of kidney weight to body weight (KW/BW) in DM (1.54Β±0.13%) was significantly higher than that in C rats (0.53Β±0.04%; p<0.01), and the increase in KW/BW was ameliorated by FR167653 administration (0.84Β±0.07%; p<0.01). FR167653 also significantly inhibited the increase in albuminuria in DM rats (C, 0.40Β±0.06 mg/day; C+FR, 0.41Β±0.07; DM, 1.99Β±0.22 mg/day; DM+FR, 1.04Β±0.19 mg/day; p<0.05). Glomerular p38 MAPK and CREB activities were significantly increased in 3-month DM rats compared to C rats, and FR167653 significantly abrogated the increase in p38 MAPK and CREB activities in DM glomeruli (p<0.05). Fibronectin and type IV collagen mRNA expression were significantly increased in DM glomeruli and these increases were inhibited by 86.8% and 79.9%, respectively, with FR167653 treatment (p<0.05). FR167653 also ameliorated the increases in fibronectin and type IV collagen protein expression in DM glomeruli (p<0.05).Conclusions. These findings suggest that p38 MAPK could be a potential target for preventing nephropathy in diabetes.ope
Prognostic Factor for Adult Primary Focal Segmental Glomerulosclerosis
Background : Primary focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome in adult. Although primary FSGS has been known to be refractory to treatment, recent studies reveal higher remission rate and better prognosis. And it has been reported that some clinical and histopathologic paramenters are significant to prognosis. But, confirmative prognostic indices remain to be defined. In order to further clarify the prognostic factors for therapeutic response and risk factors for progression to chronic renal failure (CRF), we reviewed the medical records of primary adult FSGS patients. Methods : Forty-adult patients diagnosed as primary FSGS between 1991 to 2002 were enrolled. We retrospectively analyzed the clinical and histopathological parameters of all patinents at the time of renal biopsy. In addition, the therapeutic responses to immunosuppressants and the renal survival were analyzed. Results : At the time of renal biopsy, 26 patients (65%) had proteinuria of the nephrotic range and 14 patients (35%) had proteinuria of the non-nephrotic range. The serum creatinine level was higher in nephrotic-ranged patients than that in non nephroticranged patients (pοΌ0.05). The other parameters were not significantly different between two groups. Twenty-seven patients were treated with immunosuppressants and 15 patients (55.6%) responded to the treatment. There was no significant difference in clinical or histopathological variables between the responders and the non-responders. High serum creatinine level at diagnosis and responsiveness to treatment appeared to be significant as risk factors for progression to CRF (pοΌ0.05). The paticnts treated with immunosuppressants had longer survival period, compared with those without treatment. And the responders had significantly longer survival period compared with the non-responders (pοΌ0.05). Conclusion : The patients with initial impairment of renal function or poor response to therapy may have worse prognosis, and the intense treatment with regular follow-up of renal function should be recommended for these patients.ope