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Background Renal infarction (RI) is an uncommon disease that is difficult to diagnose. As little is known about clinical characteristics of this disease, we investigated its underlying risk factors and outcomes. Methods We performed a retrospective single-center study of 89 patients newly diagnosed with acute RI between January 2002 and March 2015 using imaging modalities. Clinical features, possible etiologies, and long-term renal outcome data were reviewed. Results The patients' mean age was 63.5 ± 15.42 years; 23.6% had diabetes and 56.2% had hypertension. Unilateral and bilateral involvements were shown in 80.9% and 19.1% of patients, respectively; proteinuria and hematuria were reported in 40.4% and 41.6%, respectively. Cardiovascular disease was the most common underlying disease, followed by renal vascular injury and hypercoagulability disorder. Fourteen patients had no specific underlying disease. At the time of diagnosis, acute kidney injury (AKI) was found in 34.8% of patients. Univariate analysis revealed diabetes mellitus (DM), leukocytosis, and high C-reactive protein (CRP) as significant risk factors for the development of AKI. On multivariate analysis, DM and high CRP levels were independent predictors for AKI. During follow-up, chronic kidney disease developed in 27.4% of patients. Univariate and multivariate Cox regression analyses showed old age to be an independent risk factor for this disease, whereas AKI history was a negative risk factor. Conclusion DM patients or those with high CRP levels should be observed for renal function deterioration. Clinicians should also monitor for RI in elderly patients.

Lymphedema is a condition characterized by tissue swelling caused by localized fluid retention. Advanced lymphedema is characterized by irreversible skin fibrosis (stage IIIb) and nonpitting edema, with leather-like skin, skin crypts, and ulcers with or without involvement of the toes (stage IVa and IVb, respectively). Recently, surgical treatment of advanced lymphedema has been a challenging reconstructive modality. Microvascular techniques such as lymphaticovenous anastomosis and vascularized lymph node flap transfer are effective for early stage lymphedema. In this study, we performed a two-stage operation in an advanced lymphedema patient. First, a debulking procedure was performed using liposuction. A vascularized free lymph node flap transfer was then conducted 10 weeks after the first operation. In this case, good results were obtained, with reduced circumferences in various parts of the upper extremity noted immediately postoperation.

Solar energy will be an increasingly important part of power generation because of its ubiquity abundance, and sustainability. To manage effectively solar energy to power system, it is essential part In this paper, we develop the PV power prediction algorithm using adaptive neuro-fuzzy model considering various input factors such as temperature, solar irradiance, sunshine hours, and cloudiness. To evaluate performance of the proposed model according to input factors, we performed various experiments by using real data.

BackgroundAlthough lung cancer screening using low-dose computed tomography (LDCT) is now widely used in clinical practice, the characteristics and outcomes of diagnostic procedures related to screen-detected nodules in never-smokers remain unclear. We aimed to determine the incidence of nodules considered for invasive biopsy and evaluate the final diagnoses and procedure-related complications in never-smokers in comparison to ever-smokers who underwent LDCT screening.MethodsWe evaluated 37 436 asymptomatic adults (17 968 never-smokers and 19 468 ever-smokers) who underwent LDCT screening for lung cancer between January 2009 and December 2018 at a tertiary centre in South Korea. The rates of invasive diagnostic procedures for detected nodules and related complications, and the diagnostic outcomes were determined in the never-smoker and ever-smoker groups.ResultsAmong the never-smokers, 2908 (16.2%) out of 17 968 had positive nodules. Overall, 139 (0.77%) out of 17 968 never-smokers and 194 (1.00%) out of 19 468 ever-smokers underwent invasive biopsy (p=0.022). Lung cancer was diagnosed in 84 (0.47%) out of 17 968 never-smokers and 123 (0.63%) out of 19 468 ever-smokers (p=0.032). The proportions of participants diagnosed with benign disease after invasive biopsy (false-positive) were 50 (0.28%) out of 17 968 and 69 (0.35%) out of 19 468 in the never-smoker and ever-smoker groups, respectively (p=0.191). Multivariate analyses revealed no significant associations of smoking with the risk of a false-positive diagnosis (OR 0.98, 95% CI 0.62–1.57) and complications (OR 1.33, 95% CI 0.65–3.73) after biopsy. Of the 84 never-smokers with lung cancer, 82 (97.6%) had adenocarcinoma, and 75 (89.3%) were in stage I with a favourable prognosis.ConclusionsLDCT screening in never-smokers resulted in a notable detection rate of lung nodules, which warranted invasive biopsy. The lung cancer detection rate was lower in never-smokers than in ever-smokers. However, no significant differences in the false-positive and complication rates were observed between the two groups. Accordingly, a more specifically tailored management strategy is needed for screen-detected nodules in Asian never-smokers.

Lobectomy is considered the standard strategy for early-stage non-small cell lung cancer (NSCLC). However, sublobar resection for NSCLC has recently received increased attention. The objective of this study was to compare 5-year survival, recurrence-free survival, postoperative mortality, and postoperative morbidities in patients who received segmentectomy versus those who received lobectomy through a meta-analysis. Sixteen studies were included and the combined hazard ratios or odds ratios were calculated. The results revealed that the 5-year survival rate after segmentectomy was comparable to that of lobectomy for stage IA NSCLC. However, segmentectomy for stage I NSCLC had lower rates of postoperative mortality and morbidities than lobectomy.

Background Whether perioperative hyperchloremia can induce postoperative acute kidney injury (AKI) is controversial. We investigated the association between perioperative hyperchloremia and postoperative AKI in patients admitted to the intensive care unit (ICU) after surgery. Methods We performed a retrospective observational study of patients admitted to the surgical ICU at a single tertiary care hospital between January 2011 and June 2016. Our primary objective was to determine whether hyperchloremia or an increase in serum chloride levels was associated with postoperative AKI. Perioperative hyperchloremia was defined as serum chloride levels ≥ 110 mmol·L− 1 during postoperative days (PODs) 0–3. The increase in serum chloride levels was defined as the difference between preoperative and maximum postoperative serum chloride levels during the first 3 days after surgery. Results Of the 7991 patients included in the final analysis, 1876 (23.5%) developed hyperchloremia during PODs 0–3, and 1187 (14.9%) developed postoperative AKI. Exposure to hyperchloremia during the first 3 days after surgery was not associated with postoperative AKI (odds ratio, 1.09; 95% confidence interval, 0.80–1.49; P = 0.571). However, among patients with preoperative chronic kidney disease stage ≥ 3 (estimated glomerular filtration rate 6 mmol·L− 1 in serum chloride levels than in patients with an increase ≤ 1 mmol·L− 1 (odds ratio, 1.42; 95% confidence interval, 1.09–1.84; P = 0.009). In addition, the incidence of postoperative AKI stage ≥ 2 was not associated with exposure to hyperchloremia or with the increase in serum chloride levels during PODs 0–3, regardless of preoperative kidney function. Conclusions Exposure to perioperative hyperchloremia is not associated with postoperative AKI in surgical ICU patients. However, in patients with moderate-to-severe chronic kidney disease (stage ≥ 3), a substantial perioperative increase in serum chloride levels may reflect a higher risk of AKI. Electronic supplementary material The online version of this article (10.1186/s13054-018-2216-5) contains supplementary material, which is available to authorized users.

The increase in the elderly population increases the incidence of geriatric diseases such as cancer, stroke, heart disease, and dementia. Cognitive impairment and a debilitated memory ability decreases the quality of life of patients owing to the associated economical and physical problems, and increases the burden on their family. The impairment of cognitive function due to dementia can be reduced through repeated and systematic training; however, this process can lead to disinterest and loss of concentration. Toys can stimulate various parts of the brain by inducing patient’s finger exercise, and various rehabilitative techniques based on toys are being studied by researchers. In this study, we develop a smart cognitive rehabilitation block(LED blocks, 8x8 dot matrix blocks, speaker blocks, signage blocks, PWM switch blocks, 7-segment blocks), and establish a cognitive rehabilitation platform for patient management and develop cognitive rehabilitation contents.

Background: Previous cross-sectional studies have shown that low muscle mass is associated with albuminuria in the general population. However, the longitudinal association of low muscle mass with the development of albuminuria is not well known at this time. Methods: We evaluated 48,101 individuals without chronic kidney disease (CKD) who underwent 2 health check-ups in 2012 and 2016. Participants’ skeletal muscle masses were measured using a bioelectrical impedance analyzer and compared via a skeletal muscle mass index (SMI; SMI [%] = total skeletal muscle mass [kg]/body weight [kg] × 100). Urine albumin was determined by dipstick semi-quantitative analysis and incident albuminuria was defined as ≥1+ dipstick albumin at the time of the second check-up. We used logistic regression analysis to determine the relationship between skeletal muscle mass and incident albuminuria. Results: The study participants were divided into quartiles according to baseline SMI. After 4 years, 305 cases of incident albuminuria were observed. The cumulative incidences of albuminuria were 0.78, 0.66, 0.62, and 0.47% for the first through fourth quartiles of SMI respectively. Multivariable logistic analysis revealed that the ORs (95% CIs) for incident albuminuria were 1.63 (1.05–2.55) in the first quartile compared with those in the fourth quartile and 1.40 (1.05–1.88) in the participants with sarcopenia versus those without sarcopenia. Conclusions: Low skeletal muscle mass was independently associated with the development of dipstick albuminuria after 4 years in Korean adults without CKD. Further research is needed to verify the role of low muscle mass in the development of albuminuria and renal injury.

Background /Objective: The conventional models currently used to evaluate various anti-tumor therapeutic agents are not sufficient for representing human pancreatic ductal adenocarcinoma (PDA), which has a unique tumor microenvironment. We aimed to produce an organotypic slice culture model from human PDA that resembles the in vivo situation and to evaluate the responses of PDA slices to established cytotoxic drugs. Methods PDA tissues were obtained from 10 patients who underwent pancreatic resection. The tissues were sliced by a vibratome, and the tumor slices were then cultured. The viability of tumor slices during slice culture was evaluated using H&E and immunohistochemical staining, and stromal cells were demonstrated. The effects of cytotoxic drugs on PDA cell lines and slices were analyzed. Results Tumor slices maintained their surface areas and tissue viability for at least five days during culture. Preserved proliferation and apoptosis in tumor slices were observed by the expression of Ki-67 and cleaved caspase-3. Stromal cells including macrophages (CD68+ and CD163+), T cells (CD3+, CD8+, and FOXP3+), and myeloid cells (CD11b+) were present throughout the culture period. Staurosporine, gemcitabine, and cisplatin treatment of PDA cell lines and tumor slices exerted proportional cytotoxic effects in terms of MTT viability, tumor cell number, and Ki-67 and cleaved caspase-3 expression. Conclusions Organotypic human PDA slice cultures preserved their viability and tumor microenvironment for at least five days during slice culture. PDA slice culture appears to be a feasible preclinical test model to assess the response to anti-tumor agents.

Although low serum bicarbonate level is known to be associated with adverse outcomes in patients with chronic kidney injury, it is unclear whether low serum bicarbonate level is associated with the development of acute kidney injury (AKI). The purpose of our study was to determine whether serum bicarbonate levels at admission could be a risk factor for AKI development and mortality in hospitalised patients. We retrospectively enrolled 17,320 adult patients who were admitted to the academic teaching hospital from January 2013 to December 2013. Patients were divided into 2 groups based on the first measurement of serum bicarbonate level at admission. The incidence of AKI was higher in patients with low serum bicarbonate level than in those with normal serum bicarbonate level (8.0% vs. 4.1%). Low serum bicarbonate levels at admission were significantly associated with the development of AKI. In addition, low serum bicarbonate levels also independently predicted the 90-day mortality. Pre-existing low bicarbonate levels and subsequent development of AKI increased in-hospital mortality by 15 times compared with that in patients with normal bicarbonate levels and no AKI. Low serum bicarbonate levels may be associated with the development of AKI and high mortality in hospitalised patients.

We prepared an implantable device of small volume (SID) that is enabled with on-demand, pulsatile drug release. The device was designed to be actuated via a magnetic field; hence, there was no need for a battery. The device was actuated when the magnet was applied from the outside and infused the drug solution outward via the outlet ports in the device. When there was no external magnetic field, no drug was released. In this work, we varied the amount of delivered drug by varying the number of outlet ports. Thus, as the number of outlet ports increased from one to three, the average amount of drug release per actuation increased from 60.7 ± 1.79 μg to 122.6 ± 1.27 μg. In addition, when the SID with three outlet ports (SID3) was actuated once and thrice, the amount of drug release increased from 123.0 ± 6.99 μg to 357.3 ± 9.70 μg, respectively, which was reproducible over 30 days. When the SID3 was implanted in living animals for 30 days, plasma drug concentration was measured to be 92–146 ng ml−1 or 210–363 ng ml−1 when the device was actuated once or three consecutive times, respectively.

Background Emerging evidence suggests that intestinal dysbiosis is associated with diverse pathological processes. In this study we demonstrated intestinal barrier disruption and aberrant mucosal immunity in 5/6 nephrectomized mice and the effect of probiotics on chronic kidney disease (CKD). Methods CKD was induced in 6-week-old mice by 5/6 nephrectomy. They were fed a lactobacilli mixture for 8 weeks. Serum, urine and stool samples were collected for renal function assessments and gut microbiome analyses. Gut permeability, colon heat shock protein 70 (HSP70) and colon epithelial integrity were evaluated and cytokine levels in colon and kidney were measured. Colon leukocytes were analyzed by flow cytometry and bone marrow-derived cells were cocultured with lactobacilli mixture. Results In CKD mice, 'leaky gut' was accompanied by decreased colon HSP70 and claudin-1 expression, whereas it increased pore-forming claudin-2 expression and apoptosis. Although the percentage of regulatory T cells did not differ between CKD and control mice, cytokine expression and the ratio of CX3CR1intermediate:CX3CR1high pro-inflammatory/resident macrophages increased in the colon of CKD mice. Orally administered lactobacilli partially mitigated the CKD-induced 'leaky gut'; restored colon epithelial HSP70, claudin-1 and claudin-2 expression and decreased apoptosis. Probiotic treatment also restored the CX3CR1intermediate:CX3CR1high macrophage ratio and increased circular dichroism (CD)103+CD11c+ regulatory dendritic cells in the colon. These changes suppressed systemic inflammation and kidney fibrosis. Conclusions Our results suggest that intestinal dysbiosis-associated gut barrier disruption and aberrant mucosal immunity are important for the systemic inflammation and progressive fibrosis of CKD. Targeting the intestine might provide novel therapeutic opportunities for CKD.

Background Percutaneous tracheostomy (PT) is a common procedure in critical care medicine. No definite clinical practice guidelines recommended on the choice of the direction of skin incision, vertical or transverse for tracheostomy in critically ill patients. The objective of this retrospective study was to compare the outcomes associated with vertical and transverse skin incisions in patients undergoing PT. Methods Patients who underwent PT between March 2011 and December 2015 in the intensive care unit (ICU) of a tertiary hospital were retrospectively included. PTs were performed by pulmonary intensivists at the ICU bedside using the single tapered dilator technique assisted by flexible bronchoscopy. The primary outcome was the incidence of tracheostomy site ulcers at 7 days after PT. Results Of the 458 patients who underwent PT, a vertical incision was made in 27.1% and a transverse incision was made in 72.9%. There were no tracheostomy-related mortalities, and no significant difference in the incidence of immediate postoperative complications, including bleeding, tracheal ring fracture, and subcutaneous emphysema. Thirty-five patients (7.6%) developed complications within 7 days after PT, in which tracheostomy-related pressure ulcers were the most frequent. Compared with vertical incisions, transverse incisions were associated with significantly lower incidence of complications (14.1% vs. 5.4%, P = 0.001). Conclusions This retrospective study showed that transverse skin incisions in PTs for critically ill patients, resulted in a significant decrease in overall complications, particularly ulcers in the tracheostomy site.

When BDNF binds to its receptors, TrkB and p75NTR, the BDNF-receptor complex is endocytosed and trafficked to the cell body for downstream signal transduction, which plays a critical role in neuronal functions. Huntingtin-associated protein 1 (HAP1) is involved in trafficking of vesicles intracellularly and also interacts with several membrane proteins including TrkB. Although it has been known that HAP1 has functions in vesicular trafficking and receptor stabilisation, it is not yet established whether HAP1 has a role in BDNF and its receptor endocytosis. In the present study, we found that HAP1 is in an interacting complex with p75NTR,TrkB and BDNF, especially newly endocytosed BDNF.BDNF and TrkB internalisation is abolished in HAP1 knock-out (KO) cortical neurons. TrkB downstream signalling pathways such as ERK, Akt and PLCγ-1 are also impaired in HAP1 KO cortical neurons upon BDNF stimulation. Proliferation of cerebellar granule cells is also impaired in cell culture and cerebellum of HAP1 KO mice. Our findings suggest that HAP1 may play a key role in BDNF and its receptor endocytosis and may promote neuronal survival and proliferation. Refereed/Peer-reviewed

This paper presents overall procedure by experimental study in order to deriving design factors of snow removal machine on roof of multi-span greenhouse. For the purpose of the testing, the scale model of the machine was made in the form to drive above the monorail. The test was performed in order to calculating friction coefficient of the machine and shear coefficient between sliced horizontal section of snow at constant temperature and humidity room in National Academic of Agricultural Science. As a result of the laboratory test, shear coefficient between sliced horizontal section of snow were calculated 1.60~2.37. Further investigation, we will study to derive the relationship between the real and scaled model through the field test.

Reconstruction of complex upper extremity defects requires a need for multiple tissue components. The supercharged latissimus dorsi (LD)-groin compound flap is an option that can provide a large skin paddle with simultaneous functional muscle transfer. It is necessary to supercharge the flap with the superficial circumflex iliac pedicle to ensure the viability of its groin extension. In this report, we present a case of a supercharged LD-groin flap in combination with vascularized inguinal lymph nodes, which was used for upper limb reconstruction in a young male patient, following excision of high-grade liposarcoma. Resection resulted in a 28 cm × 15 cm skin defect extending from the upper arm to the proximal forearm, also involving the triceps muscle, a segment of the ulnar nerve and the axillary lymph nodes. Restoration of triceps function was achieved with transfer of the innervated LD muscle. Part of the ulnar nerve was resected and repaired with sural nerve grafts. Post-operatively, the flap survived fully with no partial necrosis, and no complications at both the recipient and donor sites. At 1-year follow up, the patient had a well-healed wound with good elbow extension (against resistance), no tumor recurrence, and no signs of lymphedema. We believe this comprehensive approach may represent a valuable technique, for not only the oncological reconstruction of upper extremity, but also for the prevention of lymphedema. © 2015 Wiley Periodicals, Inc. Microsurgery 36:689-694, 2016.

With the improvement of living standards and economic development, electricity consumption continues to grow. The electricity is a special energy which is hard to store, so its supply must be consistent with the demand. The objective of electricity demand forecasting is to make best use of electricity energy and provide balance between supply and demand. Hence, it is very important work to forecast electricity demand with higher precision. So, various forecasting methods have been developed. They can be divided into five broad categories such as time series models, regression based model, artificial intelligence techniques and fuzzy logic method without considering special-day effects. Electricity demand patterns on holidays can be often idiosyncratic and cause significant forecasting errors. Such effects are known as special-day effects and are recognized as an important issue in determining electricity demand data. In this research, we developed the power demand forecasting method using ELM(Extreme Learning Machine) for special day, particularly, lunar new year and Chuseok holiday.Key Words : ELM, Forecasting model, Power demand, Special-day *Dept. of Electrical Engineering, Korea National University of Transportation, Korea†Corresponding Author : Dept. of Electrical Engineering Daeduk College, Korea E-mail : jylim@ddc.ac.kr접수일자 : 2015년 5월 3일최종완료 : 2015년 5월 20일

Although perforator-to-perforator anastomosis in supermicrosurgery may be used in transferring free flaps with small vessels, it is still difficult in certain situations that include potentially infected wounds. Moreover, it is limited to smaller flaps. Anastomosis of large vessels is still safer for transfer of a large flap for most surgeons. The harvesting of a patch of the parent artery together with the perforator supplying the flap allows the surgeon to perform an anastomosis between the vessel ends of larger caliber, and possibly with greater anastomotic success.When the vascular pedicle of a free flap is0.8 mm, an option is to take a cuff of the major artery for an end-to-patch anastomosis. From 1983 to 2013, this method was applied to the anteromedial thigh (AMT) flap (seven cases), the groin flap (81 cases), and the free Becker's flap (five cases). When a patch was taken from the femoral artery, direct anastomosis for the major artery was performed using 5/0 Prolene sutures, followed by coverage with local soft tissue. When a patch was taken from the ulnar artery, a patch of vein graft was used for repair of the ulnar artery. In one case, a segment of the femoral artery was harvested with an AMT flap and a segment of a sartorius muscle flap; the compound tissue was transferred to the neck with the femoral artery to replace the left carotid artery. In the donor site, the defect of the femoral artery was reconstructed with an artificial graft.The flaps had no failure or partial necrosis, but one patient developed bleeding from the femoral artery 2 days postoperatively. It was treated by adding one more suture for the femoral artery and coverage with the sartorius muscle. In the ulnar artery, the patients did not complain of cold intolerance and the postoperative angiogram showed good patency of the ulnar artery after an average follow-up of 1 year.For the majority of plastic surgeons, this method provides a reliable and comfortable anastomosis when transferring a flap with small vessels. The only concern is to repair the donor artery carefully and ensure coverage of the repair site with local tissue.

Due to the increasing of power consumption, it is difficult to construct accurate prediction model for daily peak power demand. It is very important work to know power demand in next day for manager and control power system. In this research, we develop a daily peak power demand prediction method considering of characteristics of day of week. The proposed method is composed of liner model based on AR model and nonlinear model based on ELM to resolve the limitation of a single model. Using data sets between 2006 and 2010 in Korea, the proposed method has been intensively tested. As the prediction results, we confirm that the proposed method makes it possible to effective estimate daily peak power demand than conventional methods.Key Words : Power demand, AR, ELM, Linear model, Nonlinear model†교신저자 : 대덕대학교 전자공학과 교수․공박E-mail : jylim@ddc.ac.kr*한국교통대 전기공학과 교수․공박 접수일자 : 2014년 11월 12일수정일자 : 2014년 11월 25일 최종완료 : 2014년 11월 26일 1. 서 론 전력 수요 예측은 전력의 안정적인 공급 및 운용을 위해 필수적이다. 이러한 전력의 수요를 예측하기 위하여 시계열 분석방법에 기반을 알고리즘이 사용된다. 전력 수요 예측 모델은 회귀모델과 신경회로망 등으로 대표되는 지능형 예측 모델로 분류된다. 회귀 모델을 이용한 연구동향을 살펴보면, 다중회귀분석법을 이용하여 지역전력의 수요를 예측한 방법[1], 지수평활법 모델[2]과 이중계절 지수평활법[3], 삼중 계절 지수평활법[4], ARIMA 모형[5]을 이용한 전력수요 예측 방법이 있다. 또한 다양한 시계열 모형에 따른 일별 최대 수요전력의 예측 성능을 분석한 연구[6]도 진행되었다. 지능형 모델을 이용한 연구동향을 살펴보면, SVR(Support Vector Regression)을 이용하여 월별 전력수요예측을 적용한 방법[7], 뉴로-퍼지 모델을 이용하여 시간, 일간, 주간 단위 전력을 예측한 방법[8] 등이 있다. 최근에는 두 가지 알고리즘을 융합한 하이브리드 형태의 예측모델이 개발되고 있다. 대표적인 하이브리드 모델로는 웨이블렛과 신경회로망을 결합한 모델[9, 10]과 웨이블렛과 뉴로퍼지모델을 결합한 모델[11] 등이 있다. 웨이블렛과 신경회로망을 결합한 모델[10]에서는 지능형 하이브리드 웨이블렛 모델을 이용하여 단기 부하 예측모델을 개발하고, 그 유용성을 평가하였다. 특히, 시계열 데이터를 웨이블렛에 의해 고주파 신호를 제거한 후, 저주파 신호가 강조된 시계열 데이터와 신경회로망을 접목한 모델을 개발한 것이 특징으로서, 입력인자로는 과거 수요데이터와 온도 특성을 고려하였다. 전력 수요예측을 위해 널리 사용되는 지능형 알고리즘은 학습 데이터와 검증 데이터 간의 상관성이 높은 경우 효과적이지만, 상관성이 떨어지는 경우 학습 데이터를 기준으로 학습이 이루어짐으로 과적합(over-fitting)의 문제점을 지니고 있다. 본 논문에서는 이러한 문제점을 해결하기 위하여 상관성이 높은 요일에 대해서는 학습 알고리즘인 ELM(Extreme Learning Machine)을 이용하여 예측하고, 상관성이 적은 요일에 대해서는 선형 모델인 자기회귀(AR:Auto-Regressive)모델을 이용하여 예측하는 모델을 제안하며, 기존에 널리 사용되는 자기회귀모델, ELM 기법들과 비교함으로서 제안방법의 타당성을 입증하고자 한다.

We investigated the influence of simvastatin, a statin, on the secretion of catecholamines (CA) in rat adrenal glands, and clarified its action mechanism. Simvastatin suppressed acetylcholine (ACh)-evoked CA release in a dose- and time-dependent fashion. In the presence of simvastatin, CA secretion evoked by 1.1-dimethyl-4-phenyl piperazinium iodide (DMPP), angiotensin II, high K

Background Euglycaemic ketoacidosis has been reported after sodium–glucose cotransporter 2 (SGLT2) inhibitor treatment. However, the degree of ketonaemia and its metabolic effects have not been well investigated. Our study examined the degree of ketonaemia induced by SGLT2 inhibition and its association with metabolic profiles in type 2 diabetes mellitus (T2DM). Methods Biochemical parameters, including insulin, glucagon, free fatty acid (FFA), β-hydroxybutyrate (BHB) and acetoacetate (ACA) levels, were measured in 119 T2DM patients after dapagliflozin treatment for>3 months, and compared with a matched control group. Results Levels of total ketones, BHB and ACA were significantly higher in the dapagliflozin group than in the control group: 283.7±311.0 vs 119.8±143.8μmol/L; 188.3±226.6 vs 78.0±106.7μmol/L; and 94.1±91.3 vs 41.8±39.1μmol/L, respectively (all P 440μmol/L) in 13 (10.9%) patients who had no relevant symptoms. BHB level after dapagliflozin treatment correlated positively with HbA 1c ( r =0.280), FFA levels ( r =0.596) and QUICKI ( r =0.238), and negatively with BMI ( r =−0.222), insulin-to-glucagon ratio ( r =−0.199) and HOMA-IR ( r =−0.205; all P Conclusion Ketone levels were higher in T2DM patients treated with dapagliflozin than in controls, but with no clinical symptoms or signs of ketonaemia. Low-grade ketonaemia after dapagliflozin treatment may also be associated with improved insulin sensitivity.

Power transformers are an important factor for power transmission and cause fatal losses if faults occur. Various diagnostic methods have been applied to predict the failure and to identify the cause of the failure. Typical diagnostic methods include the IEC diagnostic method, the Duval diagnostic method, the Rogers diagnostic method, and the Doernenburg diagnostic method using the ratio of the main gas. However, each diagnostic method has a disadvantage in that it can't diagnose the state of the power transformer unless the gas ratio is within the defined range. In order to solve these problems, we propose a fault diagnosis scheme for power transformer using confidence weight based fusion method. The final diagnosis is performed by multiplying the result of diagnosis in the four diagnostic methods (IEC, Duval, Rogers, and Doernenburg) by the confidence weight. To show its effectiveness, the proposed fault diagnostic system has been intensively tested with the dissolved gases acquired from various power transformers.

Background: Recent observational studies have shown that in chronic kidney disease (CKD) patients, a significantly smaller percentage of patients with an episode of acute kidney injury (AKI) have full recovery of renal function compared to those without CKD. However, precise mechanisms involved in the incomplete repair after AKI with preexisting CKD have not been completely ascertained. Here, we assessed the impact of preexisting CKD on the severity and recovery of AKI in a mouse model of 5/6 nephrectomy. Methods: Male CD-1 mice underwent 5/6 nephrectomy (Nx). Six weeks post surgery, ischemia reperfusion injury (IRI) or a sham operation was performed and functional, histological, and various molecular parameters were compared between them. Results: Serum creatinine level on day 1 after IRI was comparable between control and Nx mice. However, serum creatinine remained significantly higher throughout the recovery phase in Nx mice compared to control mice. mRNA and protein expression of the cell cycle regulatory proteins were persistently elevated in Nx mice and this was associated with significantly increased levels of the G1 cell cycle arrest markers. Treatment with a p53 inhibitor following IRI resulted in not only decreased expression of G1 arrest markers but also decreased fibrosis, suggesting that prolonged epithelial G1 cell cycle arrest might be partially responsible for impaired recovery from superimposed AKI on CKD. Conclusion: Taken together, reduced nephron mass have a negative effect on the repair process that is partially mediated by the disruption of the cell cycle regulation.

Maxillary sinus mucocele can occur due to many medical factors such as chronic infection, allergic sinonasal disease, trauma, and previous surgery. However, it occurs mainly after Caldwell-Luc operation, usually more than 10 years after surgery. There are a few cases of maxillary sinus mucocele with ocular symptoms. Also, a case causing ocular symptoms because of invasion to the orbital floor is rare. Therefore, we report a case of a 55-year-old male patient who underwent Caldwell-Luc operation about 30 years ago. Then, symptoms such as exophthalmos, diplopia, and visual disturbance developed suddenly 3 months prior to admission. Computed tomography showed a cyst invading the orbital floor which resulted in eyeball deviation. The orbital floor defect measured approximately 2.5×3.3 cm. Maxillary sinus mucocele was removed through an endoscopic approach. After this, we reconstructed the orbital floor through a subciliary incision. Observation was carried out after three years, and ocular symptoms such as diplopia and exophthalmos did not recur.

Background Recently, urinary tissue inhibitor of metalloproteinase–2 (TIMP-2) and insulin-like growth factor–7 (IGFBP-7), markers for G1 cell cycle arrest, have been identified and validated in predicting the development of acute kidney injury in critically ill patients. It is unknown, however, whether these two biomarkers could predict the development of delayed graft function (DGF) after kidney transplantation (KT). Methods This is a single-center, prospective, observational study. We enrolled 74 patients who underwent KT between August 2013 and December 2016. Urine sample were collected immediately after the operation. The primary outcome was development of DGF as defined by need for dialysis of more than 1 session within 7 days of KT. Results Twenty-three patients (31%) were diagnosed with DGF. In univariate analysis, kidneys from expanded criteria donors, higher donor serum creatinine, lower donor estimated glomerular filtration rate, antithymoglobulin exposure, neutrophil gelatinase associated lipocalin, and urinary [TIMP-2]·[IGFBP7] were significantly different between early graft function and DGF. However, in multivariate analysis adjusting other factors, deceased donor and urinary [TIMP-2]·[IGFBP7] at 0 hours post-transplantation could predict the development of DGF. The receiver operating characteristic curve for prediction of DGF showed an area under the curve of 0.867 (sensitivity 0.86, specificity 0.71) for a cutoff value of 1.39. Conclusions Our results indicate that urine [TIMP-2]·[IGFBP7] immediately after transplantation could be an early, predictive biomarker of DGF in kidney transplantation.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a progressive deposition of amyloid beta (Aβ) and dysregulation of neurotrophic signaling, causing synaptic dysfunction, loss of memory, and cell death. The expression of p75 neurotrophin receptor is elevated in the brain of AD patients, suggesting its involvement in this disease. However, the exact mechanism of its action is not yet clear. Here, we show that p75 interacts with beta-site amyloid precursor protein cleaving enzyme-1 (BACE1), and this interaction is enhanced in the presence of Aβ. Our results suggest that the colocalization of BACE1 and amyloid precursor protein (APP) is increased in the presence of both Aβ and p75 in cortical neurons. In addition, the localization of APP and BACE1 in early endosomes is increased in the presence of Aβ and p75. An increased phosphorylation of APP-Thr668 and BACE1-Ser498 by c-Jun N-terminal kinase (JNK) in the presence of Aβ and p75 could be responsible for this localization. In conclusion, our study proposes a potential involvement in amyloidogenesis for p75, which may represent a future therapeutic target for AD. (Figure presented.). Cover Image for this Issue: doi. 10.1111/jnc.14163. Refereed/Peer-reviewed

Huntingtin-associated protein 1 (HAP1) was initially identified as a binding partner of huntingtin, mutations in which underlie Huntington's disease. Subcellular localization and protein interaction data indicate that HAP1 may be important in vesicle trafficking, cell signalling and receptor internalization. In this study, a proteomics approach was used for the identification of novel HAP1-interacting partners to attempt to shed light on the physiological function of HAP1. Using affinity chromatography with HAP1-GST protein fragments bound to Sepharose columns, this study identified a number of trafficking-related proteins that bind to HAP1. Interestingly, many of the proteins that were identified by mass spectrometry have trafficking-related functions and include the clathrin light chain B and Sec23A, an ER to Golgi trafficking vesicle coat component. Using co-immunoprecipitation and GST-binding assays the association between HAP1 and clathrin light chain B has been validated in vitro. This study also finds that HAP1 co-localizes with clathrin light chain B. In line with a physiological function of the HAP1-clathrin interaction this study detected a dramatic reduction in vesicle retrieval and endocytosis in adrenal chromaffin cells. Furthermore, through examination of transferrin endocytosis in HAP1−/− cortical neurons, this study has determined that HAP1 regulates neuronal endocytosis. In this study, the interaction between HAP1 and Sec23A was also validated through endogenous co-immunoprecipitation in rat brain homogenate. Through the identification of novel HAP1 binding partners, many of which have putative trafficking roles, this study provides us with new insights into the mechanisms underlying the important physiological function of HAP1 as an intracellular trafficking protein through its protein-protein interactions. Refereed/Peer-reviewed

Lymphedema is a chronic disorder characterized by lymph stasis in the subcutaneous tissue. Lymphatic fluid contains several components including hyaluronic acid and has many important properties. Over the past few years, significant research has been performed to identify an ideal tissue to implant as a filler. Because of its unique composition, fat harvested from the lymphedema tissue is an interesting topic for investigation and has significant potential for application as a filler, particularly in facial rejuvenation. Over a 36-month period, we treated and assessed 8 patients with lymphedematous limbs who concurrently underwent facial rejuvenation with lymphedema fat (LF). We conducted a pre- and post-operative satisfaction questionnaire survey and a histological assessment of the harvested LF fat. The overall mean general appearance score at an average of 6 months after the procedure was 7.2±0.5, demonstrating great improvement. Patients reported significant improvement in their skin texture with a reading of 8.5±0.7 and an improvement in their self-esteem. This study demonstrates that LF as an ideal autologous injectable filler is clinically applicable and easily available in patients with lymphedema. We recommend the further study and clinical use of this tissue as it exhibits important properties and qualities for future applications and research.

Introduction: Treatment of advanced lymphedema remains a challenge in reconstructive surgery. Microsurgical techniques seem to be effective in early stage lymphedema, however in advanced stages their role is not well established. In this study, we present a novel approach for advanced lymphedema combining excisional procedure (Charles) with transferring lymph node flap. Patients and method: From 2010 to 2013, 24 patients (18 women, six men, mean age 53 years old) presented with late stage of lower extremity lymphedema. The modification of Charles procedure consisted of preserving the superficial venous system of the dorsum of the foot and the lesser saphenous vein, which were used for the venous anastomosis of the transferred lymph node flap. In 11 patients we transferred the inguinal lymph node flaps from the contralateral site, meanwhile in 13 patients supraclavicular lymph node flaps were used. Results: Maximum reduction of the lymphedema was achieved. No major complication was detected postoperatively. There were two patients with partial loss of the skin graft necessitated re-grafting. All the lymph node flaps survived well. The patients resumed normal daily activities within a period of 2 months. The mean follow-up was 14 months (3‐26 months). During this period, no recurrence of the lymphedema was observed. Conclusion: The combination of the modified Charles procedure with vascularized transferring of lymph node flap is an effective method for treatment of advanced stage lymphedema. V C 2014 Wiley Periodicals, Inc. Microsurgery 00:000‐000, 2014. Lower extremity lymphedema is a major source of morbidity. It can be either congenital or secondary following trauma or surgery for the treatment of cancer that includes removal of lymph nodes and/or radiotherapy. Congenital lymphedema may be caused by congenital aplasia or hypoplasia of peripheral lymphatics, congenital abnormalities of the abdominal or thoracic lymphatic trunk, and congenital valvular incompetence, usually associated with mega-lymphatics. 1 Primary or secondary lymphedema is characterized by the accumulation of the protein-rich lymph fluid in the subcutaneous tissue, which results in tissue hypertrophy, fibrosis, and lymphostatic elephantiasis. 2 In the medical literature have been described several staging systems of lymphedema. The International Society of Lymphology divides the severity of lymphedema in three stages. 3 Karri et al. 4 reported a modified staging system, dividing the severity of lymphedema in four stages. According to their system, the advanced lymphedema is characterized by irreversible skin fibrosis (stage IIIb) and nonpitting edema, with leather-like skin, skin crypts, and ulcers with or without involvement of the toes (stage IVa and IVb, respectively). The surgical treatment of advanced lymphedema is a challenge reconstructive procedure. Microvascular techniques such as lymphaticovenous anastomosis and vascularized lymph node flap transfer seems to be effective at early stage lymphedema, with the last one to gain popularity among the plastic surgeons. 5‐13 However, the role of these techniques in advanced lymphedema is not well established.

Background/Objective: The oragnotypic tumor slice culture model resembles the in vivo situation of tumor. It may serve as a proper ex vivo platform for response to anti-tumor therapies. We aimed to evaluate the response of pancreatic ductal adenocarcinoma (PDA) cells and helper, cytotoxic, and regulatory T cells to gemcitabine using human PDA slice culture model. Methods: PDA tissues were obtained from patients who were operated on for pancreatic resection. The tumors were sliced by a vibratome, and the tumor slices were then cultured until 5 days with 0.1 μM, 1 μM, and 10 μM gemcitabine for 1 or 2 days. Tumor responses were evaluated by number of tumor cells and proportion of Ki-67 or caspase-3 positively expressed cells in the tumor. CD4+, CD8+, and FOXP3+ cells were analyzed by immunohistochemistry staining. Results: Gemcitabine treatment to PDA slices exerted proportional cytotoxic effects in terms of tumor cell number, and Ki-67 and cleaved caspase-3 expression. Mean Ki-67 positive cells in PDA cells tended to decrease according to increase of gemcitabine concentration (case 1, 48 hr treatment; 65.7% in control vs. 27.9% in 0.1 μM, p=0.025). Mean caspase-3 positive cells in PDA cells tended to increase according to increase of gemcitabine concentration (case 1, 48 hr treatment; 8.6% in control vs. 18.6% in 0.1 μM, p=0.042). Mean PDA cells per x200 tended to decrease according to increase of gemcitabine concentration (case 2, 48 hr treatment; 78.3 in 1.0 μM vs. 27.3 in 10 μM, p=0.042). Mean CD4+, CD8+, and FOXP3+ cells/total cells tended to decrease according to increase of gemcitabine concentration; in case 3 (24hr treatment), mean CD4+ cells/total cells decreased as 2.6%, 1.6%, 1.5%, and 0.5%, mean CD8+ cells/total cells decreased as 2.6%, 1.5%, 1.4%, and 1.1%, and mean FOXP3+ cells/total cells were 0.2%, 0.3%, 0.2%, and 0.1% in control, 0.1 μM, 1 μM, and 10 μM gemcitabine, respectively. However, mean CD8+/FOXP3+ cell ratio did not significantly decrease, and even increase from 4.4 in 0.1 μM to 8.6 in 1 μM (p=0.039). Conclusions: Tumoricidal effect of gemcitabine could be demonstrated using organotypic slice culture model. T cells in the tumor decreased according to increase of gemcitabine concentration; however CD8+/FOXP3+ cell ratio relatively maintained. Citation Format: Jae Hyuck Chang, Chae Yoon Lim, Weon Sun Lee, Guk Jin Lee. Response of pancreatic ductal adenocarcinoma to gemcitabine using human organotypic slice cultures [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1096.

Background: The present study was the first attempt to explore the characteristics of ginsenoside-Rg3 (Rg3) on release of catecholamines (CA) in the perfused rat adrenal medullae and also to verify the underlying action mechanism. Materials and Methods: The adrenal medulla was separated by some modification of the previous method and perfused with Krebs solution. CA was assayed directly by the fluorometry. Results: Rg3 reduced acetylcholine (ACh)-produced CA release in a dose- and time-dependent manner. Rg3 time-dependently depressed CA release produced by 3-(m-chloro-phenyl-carbamoyl-oxy)-2-butynyltrimethyl ammonium chloride (McN-A-343), 1,1-dimethyl-4-phenyl piperazinium iodide, and angiotensin II. In the presence of Rg3, the CA release produced by high K+, veratridine, cyclopiazonic acid, and methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4- (2-trifluoromethyl-phenyl)-pyridine-5-carboxylate (Bay-K-8644) was also markedly suppressed. However, during the simultaneous perfusion of Rg3 and Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME), the release of CA produced by ACh, angiotensin II, Bay-K-8644, and veratridine was restored closely to the level of each control, in contrast to that of Rg3-treatment alone. The nitric oxide (NO) release was significantly elevated by Rg3-treatment. Furthermore, in the coexistence of Rg3 and fimasartan, ACh-produced CA release was more significantly reduced as compared to that of fimasartan-treatment alone. Conclusions: We present the first evidence that Rg3 markedly depresses the CA secretion produced by activation of neuronal cholinergic and angiotensinergic receptors. Rg3-produced inhibition appears to be evoked not only by blocking the inflow of Na+ and Ca2+ into adrenomedullary cells but also by preventing the Ca2+ release from intracellular storage, partly through enhancement of NO release by NO synthase activation. Coadministration of Rg3 and fimasartan may be clinically beneficial for the treatment of cardiovascular diseases. Abbreviations used: Rg3: Ginsenoside-Rg3; VDCC: L-type voltage-dependent Ca2+ channels; Bay–K-8644: Methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethyl-phenyl)-pyridine-5-carboxylate; ACh: Acetylcholine; McN-A-343: 3-(m-chloro-phenyl-carbamoyl-oxy)-2-butynyltrimethyl ammonium; DMPP: 1.1-dimethyl-4-phenyl piperazinium; NO: Nitric oxide; L-NAME: Nω-nitro-l-arginine methyl ester; nNOS: Neuronal NO synthase.

목적: 국가 결핵 관리 프로그램을 통해 국내 결핵 발병률과 사망률은 감소하고 있지만, 결핵은 여전히 중요한 감염병이다. 저자들은 국내 소아청소년을 대상으로 한 결핵 관련 논문의 동향과 연구 분야를 분석하여 향후 연구가 필요한 분야를 확인하기 위해 연구를 시행하였다. 방법: 국내외 6개의 데이터베이스에서 ‘tuberculo*’ 또는 ‘TB’, ‘child*’ 또는 ‘adolescen*’ 또는 ‘neonat*’ 또는 ‘infant*’ 또는 ‘pediatric*’ 그리고 ‘korea*’를 포함하여 제목과 초록을 검색하였다. 국내 소아와 청소년을 대상으로 한 결핵 관련 문헌의 논문 종류, 발행 연도, 연구 영역, 투고된 학술지명, 연구 대상을 분석했다. 결과: 검색된 257편의 문헌 중 120편의 논문이 분석에 포함되었다. 이 중 82편(68.3%)은 원저였고, 증례 33편(27.5%), 종설 4편(3.3%), 지침 1편(0.8%)이었다. 원저의 연구 영역을 분류했을 때, 가장 흔한 주제는 임상적 특징(36.6%)이었고 진단(29.3%), 접촉자 조사(9.8%), 역학(6.1%), 치료(4.9%), 백신(3.6%), 잠복결핵감염(3.6%), 합병증(3.6%) 그리고 결핵에 대한 인식(2.4%)에 대한 연구가 뒤를 이었다. 1962년에 출판된 논문을 시작으로 1960년대 4편, 1970년대 10편, 1980년대 11편, 1990년대 22편, 2000년대 26편, 2010년 이후 47편의 문헌이 발표되었다. 결론: 국내 소아를 대상으로 한 결핵 관련 연구는 지난 50년 간 증가해 왔지만, 연구 영역이 임상적 기술과 진단에 치우쳐 있었다. 치료나 백신과 같은 또 다른 영역에 대한 연구가 다양하게 수행되어야 할 필요가 있겠다.

Due to the increase of power consumption, it is difficult to construct an accurate prediction model for daily peak power demand. It is very important work to know power demand in next day to manage and control power system. In this research, we develop a daily peak power demand prediction method based on Extreme Learning Machine(ELM) with fast learning procedure. Using data sets between 2006 and 2010 in Korea, the proposed method has been intensively tested. As the prediction results, we confirm that the proposed method makes it possible to effective estimate daily peak power demand than conventional methods.

Earth equipments are essential to protect ITS facilities from abnormal situation. In this research, an estimation algorithm of earth parameters and equivalent resistivity is introduced. Traditional estimation methods can be divided into graphic method and numerical method. The result of graphic method is varied by the ability of expert or repeated calculation and it is hard to estimate the parameters precisely. The numerical method requires special techniques such as optimizing theory, and numerous calculations, whose results can be varied with initial values. The proposed algorithm is based on the relationship between apparent resistances and earth parameters and approximates the nonlinear characteristics of earth using ANN(artificial neural networks). The effectiveness of proposed method is verified in case studies.

Background: In recent decades, the role of brain-derived neurotrophic factor (BDNF) in depression has received intensive attention. However, the relationship between proBDNF and depression has not been clearly elucidated. Conclusion: The balance between the proBDNF/p75NTR/sortilin and mBDNF/TrkB signaling pathways appears dysregulated in major depression and both pathways should be considered as biomarkers for the major depression Limitations: More cases on both genders should be enrolled in our study. And further works on the mechanisms of how BDNF and its receptors are regulated in depression should also be carried out. Methods: Forty drug-free women patients diagnosed with major depression and 50 healthy female controls were enrolled in our study. Peripheral blood was sampled from all the subjects. With the blood samples, we assessed the relationship between BDNF and major depression from following aspects: the levels of BDNF, proBDNF and their receptors in the sera and lymphocytes. The mRNA levels of these factors in lymphocytes were also examined. Furthermore, the correlations between each factor and the severity of major depression were tested. Results: It was found that: (a) the protein and serum levels of proBDNF, sortilin and p75NTR were higher in major depressive patients than in healthy controls while mature BDNF and TrkB levels were lower; (b) the BDNF, TrkB, sortilin and p75NTR mRNA levels changed in line with their protein levels; (c) The levels of mature BDNF and TrkB had negative correlations with the major depression severity, and the levels of proBDNF, p75NTR and sortilin were positively correlated with the scores of HRSD-21; (d) the ratio of proBDNF and mBDNF was imbalanced in major depressive patients. Refereed/Peer-reviewed

Sortilin, a Golgi sorting protein and a member of the VPS10P family, is the co-receptor for proneurotrophins, regulates protein trafficking, targets proteins to lysosomes, and regulates low density lipoprotein metabolism. The aim of this study was to investigate the expression and regulation of sortilin in Alzheimer's disease (AD). A significantly increased level of sortilin was found in human AD brain and in the brains of 6-month-old swedish-amyloid precursor protein/PS1dE9 transgenic mice. Aβ42 enhanced the protein and mRNA expression levels of sortilin in a dose- and time-dependent manner in SH-SY5Y cells, but had no effect on sorLA. In addition, proBDNF also significantly increased the protein and mRNA expression of sortilin in these cells. The recombinant extracellular domain of p75NTR (P75ECD-FC), or the antibody against the extracellular domain of p75NTR, blocked the up-regulation of sortilin induced by Amyloid-β protein (Aβ), suggesting that Aβ42 increased the expression level of sortilin and mRNA in SH-SY5Y via the p75NTR receptor. Inhibition of ROCK, but not Jun N-terminal kinase, suppressed constitutive and Aβ42-induced expression of sortilin. In conclusion, this study shows that sortilin expression is increased in the AD brain in human and mice and that Aβ42 oligomer increases sortilin gene and protein expression through p75NTR and RhoA signaling pathways, suggesting a potential physiological interaction of Aβ42 and sortilin in Alzheimer's disease. Sortilin is the co-receptor of p75NTR which signals the cell death induced by Aβ and proneurotrophins. We found that sortilin is increased in the AD brain and up-regulated by Aβ and pro-brain-derived neurotrophic factor (proBDNF). Aβ-induced upregulation of sortilin is mediated by p75NTR and the down-streaming RhoA-ROCK signaling pathway. The Aβ/Sortilinp/75NTR signaling may play a role in the pathogenesis of AD. Refereed/Peer-reviewed

The aim of this study was to determine whether fimasartan, a newly developed AT(1) receptor blocker, can affect the CA release in the isolated perfused model of the adrenal medulla of spontaneously hypertensive rats (SHRs). Fimasartan (5~50 µM) perfused into an adrenal vein for 90 min produced dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high K(+) (56 mM, a direct membrane depolarizer), DMPP (100 µM) and McN-A-343 (100 µM). Fimasartan failed to affect basal CA output. Furthermore, in adrenal glands loaded with fimasartan (15 µM), the CA secretory responses evoked by Bay-K-8644 (10 µM, an activator of L-type Ca(2+) channels), cyclopiazonic acid (10 µM, an inhibitor of cytoplasmic Ca(2+)-ATPase), and veratridine (100 µM, an activator of Na(+) channels) as well as by angiotensin II (Ang II, 100 nM), were markedly inhibited. In simultaneous presence of fimasartan (15 µM) and L-NAME (30 µM, an inhibitor of NO synthase), the CA secretory responses evoked by ACh, high K(+), DMPP, Ang II, Bay-K-8644, and veratridine was not affected in comparison of data obtained from treatment with fimasartan (15 µM) alone. Also there was no difference in NO release between before and after treatment with fimasartan (15 µM). Collectively, these experimental results suggest that fimasartan inhibits the CA secretion evoked by Ang II, and cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization from the rat adrenal medulla. It seems that this inhibitory effect of fimasartan may be mediated by blocking the influx of both Na(+) and Ca(2+) through their ion channels into the rat adrenomedullary chromaffin cells as well as by inhibiting the Ca(2+) release from the cytoplasmic calcium store, which is relevant to AT(1) receptor blockade without NO release.

In power system, substation facilities have become too complex and larger according to an extended power system. Also, customers require the high quality of electrical power system. However, some facilities become old and often break down unexpectedly. The unexpected failure may cause a break in power system and loss of profits. Therefore it is important to prevent abrupt faults by monitoring the condition of power systems. Among the various power facilities, power transformers play an important role in the transmission and distribution systems. In this research, we develop intelligent diagnosis technique for monitoring of power transformer by FCM(Fuzzy c-means) and ELM(Extreme Learning Machine). The proposed technique make it possible to diagnosis the faults occurred in transformer. To demonstrate the validity of proposed method, various experiments are performed and their results are presented.

Between 2010 and 2016, 110 patients with extremity lymphedema underwent vascularized lymph node (VLN) transfer: groin (G-VLN = 20), supraclavicular (SC-VLN = 54), and right gastroepiploic (RGE-VLN = 36) open and laparoscopic approach. Herein, we discuss the pearls and pitfalls for VLN harvest and compare donor site morbidity and complications. Lymphatic leakage: G-VLN (n = 1) and SC-VLN (n = 1) and one hematoma: SC-VLN were found. Laparoscopic harvest of the RGE-VLN reduces donor site morbidity. However, surgeons experience is imperative to minimize donor site morbidity and complications. J. Surg. Oncol. 2017;115:37-42. © 2016 Wiley Periodicals, Inc.

The ADAMTS13-von Willebrand factor (vWF) axis has been suggested to play a critical role in the pathophysiology of ischaemia-reperfusion injury (IRI) in the heart or brain. Therefore, we aimed to investigate whether this axis was involved in the pathophysiology of IRI-induced acute kidney injury.We performed renal IRI in ADAMTS13 knockout (KO) or wild type (WT) mice. Functional and histological kidney damage, and inflammation were compared and the effect of anti-vWF antibodies in ADAMTS13 KO mice was assessed.Following IRI, the blood and kidney ADAMTS13 levels were significantly decreased. vWF expression was significantly upregulated in both the medulla and cortex of injured kidneys as shown by immunohistochemistry and western blot analyses. There was also an increased level of vWF dimers after IRI. In ADAMTS13 KO mice, kidney vWF levels were further increased and this was associated with greater endothelial and epithelial injury compared to WT mice, suggesting an important role of vWF in renal IRI. In addition, the number of Gr-1Our data show that the ADAMTS13-vWF axis is partially involved in the pathophysiology of kidney IRI, suggesting that regulating ADAMTS13- and vWF-dependent mechanisms could have therapeutic potential to limit renal IRI.

Huntingtin-associated protein-1 (HAP1) is involved in intracellular trafficking, vesicle transport, and membrane receptor endocytosis. However, despite such diverse functions, the role of HAP1 in the synaptic vesicle (SV) cycle in nerve terminals remains unclear. Here, we report that HAP1 functions in SV exocytosis, controls total SV turnover and the speed of vesicle fusion in nerve terminals and regulates glutamate release in cortical brain slices. We found that HAP1 interacts with synapsin I, an abundant neuronal phosphoprotein that associates with SVs during neurotransmitter release and regulates synaptic plasticity and neuronal development. The interaction between HAP1 with synapsin I was confirmed by reciprocal co-immunoprecipitation of the endogenous proteins. Furthermore, HAP1 co-localizes with synapsin I in cortical neurons as discrete puncta. Interestingly, we find that synapsin I localization is specifically altered in Hap1−/− cortical neurons without an effect on the localization of other SV proteins. This effect on synapsin I localization was not because of changes in the levels of synapsin I or its phosphorylation status in Hap1−/− brains. Furthermore, fluorescence recovery after photobleaching in transfected neurons expressing enhanced green fluorescent protein-synapsin Ia demonstrates that loss of HAP1 protein inhibits synapsin I transport. Thus, we demonstrate that HAP1 regulates SV exocytosis and may do so through binding to synapsin I. (Figure presented.) The Proposed mechanism of synapsin I transport mediated by HAP1 in neurons. HAP1 interacts with synapsin I, regulating the trafficking of synapsin I containing vesicles and/or transport packets, possibly through its engagement of microtubule motors. The absence of HAP1 reduces synapsin I transport and neuronal exocytosis. These findings provide insights into the processes of neuronal trafficking and synaptic signaling. Refereed/Peer-reviewed

Although it is possible to generate neural stem cells (NSC) from somatic cells by reprogramming technologies with transcription factors, clinical utilization of patient-specific NSC for the treatment of human diseases remains elusive. The risk hurdles are associated with viral transduction vectors induced mutagenesis, tumor formation from undifferentiated stem cells, and transcription factors-induced genomic instability. Here we describe a viral vector-free and more efficient method to induce mouse fibroblasts into NSC using small molecules. The small molecule-induced neural stem (SMINS) cells closely resemble NSC in morphology, gene expression patterns, self-renewal, excitability, and multipotency. Furthermore, the SMINS cells are able to differentiate into astrocytes, functional neurons, and oligodendrocytesin vitroandin vivo. Thus, we have established a novel way to efficiently induce neural stem cells (iNSC) from fibroblasts using only small molecules without altering the genome. Such chemical induction removes the risks associated with current techniques such as the use of viral vectors or the induction of oncogenic factors. This technique may, therefore, enable NSC to be utilized in various applications within clinical medicine.

Oxidative stress and endothelial dysfunction are closely associated with hypertension and insulin resistance (IR) in metabolic syndrome (MetS). It is still controversial whether green tea extract (GTE) may have blood pressure (BP) lowering effect. Decaffeinated GTE might be presumed to have strong antioxidative effect and BP-lowering effect as compared with catechins. Thus we investigated whether decaffeinated-GTE could attenuate hypertension and IR by improving endothelial dysfunction and reducing oxidative stress in a rat model of MetS.20 Otsuka Long-Evans Tokushima Fatty (OLETF) rats at 13 weeks old, MetS rats, were randomized into a saline treated group (OLETF; n = 10) and a group treated with decaffeinated-GTE (25 mg/kg/day) (GTE-OLETF; n = 10). Intraperitoneal glucose tolerance tests and BP measurements were performed at 13 and 25 weeks. Decaffeinated-GTE significantly reduced BP (OLETF vs. GTE-OLETF; 130 ± 7 vs. 121 ± 3 mmHg, p = 0.01), fasting/postprandial 2 h glucose (141 ± 18/159 ± 13 vs. 115 ± 7/132 ± 16 mg/dL, p = 0.009/0.002) and insulin levels (4.8 ± 2.3 vs. 2.4 ± 1.3 ng/mL, p0.001). Decaffeinated-GTE significantly reduced vascular reactive oxygen species (ROS) formation and NADPH oxidase activity, and improved endothelium dependent relaxation in the thoracic aorta of OLETF rats. Decaffeinated-GTE also suppressed the expression of p47 and p22phox (NADPH oxidase subunits) in the immunohistochemical staining, and stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) and Akt in the immunoblotting of aortas.Decaffeinated-GTE reduced the formation of ROS and NADPH oxidase activity and stimulated phosphorylation of eNOS and Akt in the aorta of a rat model of MetS, which resulted in improved endothelial dysfunction and IR, and eventually lowered BP.

Amyloid precursor protein (APP) is involved in the pathogenesis of Alzheimer's disease. It is axonally transported, endocytosed and sorted to different cellular compartments where amyloid beta (Aβ) is produced. However, the mechanism of APP trafficking remains unclear. We present evidence that huntingtin associated protein 1 (HAP1) may reduce Aβ production by regulating APP trafficking to the non-amyloidogenic pathway. HAP1 and APP are highly colocalized in a number of brain regions, with similar distribution patterns in both mouse and human brains. They are associated with each other, the interacting site is the 371-599 of HAP1. APP is more retained in cis-Golgi, trans-Golgi complex, early endosome and ER-Golgi intermediate compartment in HAP1-/- neurons. HAP1 deletion significantly alters APP endocytosis and reduces the re-insertion of APP into the cytoplasmic membrane. Amyloid precursor protein-YFP(APP-YFP) vesicles in HAP1-/- neurons reveal a decreased trafficking rate and an increased number of motionless vesicles. Knock-down of HAP1 protein in cultured cortical neurons of Alzheimer's disease mouse model increases Aβ levels. Our data suggest that HAP1 regulates APP subcellular trafficking to the non-amyloidogenic pathway and may negatively regulate Aβ production in neurons.