bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the Health‐Promoting School Supporting Network in Taiwan
Authors: Liao Li‐Ling , Liu Chieh‐Hsing , Chang Fong‐Ching , Cheng Chi‐Chia J. , Niu Yu‐Zhen , Chang Tzu‐Chau 
Published: June 2015

ABSTRACTBACKGROUNDTaiwan has advocated health‐promoting schools (HPS) since 2001 and established the Health‐Promoting School Supporting Network (HPSSN) in 2005 to offer administrative support and consultation. Respondents' opinions about HPSSN and the relationship between these perceptions and HPS implementation were examined.METHODSIn 2011, 800 primary and middle schools were selected through stratified random sampling. School staff members (N = 656) in charge of HPS programs reported their impressions of the HPSSN's support.RESULTSRespondents were most satisfied with consultants and schools' recognition of responsibilities and rules and their interactions with HPSSN administrators. They were least satisfied with the extent of their HPSSN consultant interaction and believed HPSSN provided insufficient resources to establish HPS. Respondents' consultant partnerships and satisfaction with HPSSN administration significantly predicted HPS implementation. Additionally, the predictive values of healthy policies and school‐community relationships were greater than the other 6 HPS components.CONCLUSIONSHPSSN positively influenced HPS implementation; however, consultant/school partnerships and school resource allocations must be improved.
Influence of Simulated Double‐crested Cormorant, Phalacrocorax auritus, Predation on Multiple‐batch Production of Channel Catfish, Ictalurus punctatus
Authors: Dorr Brian S. , Engle Carole R. 
Published: June 2015

AbstractThe double‐crested cormorant, Phalacrocorax auritus, is considered the primary depredating bird species on commercially produced channel catfish, Ictalurus punctatus, in the southeastern USA. We simulated different levels of cormorant predation on losses at harvest and economic effects on channel catfish production in a multiple‐batch cropping system. We observed significant (P < 0.05) declines in catfish production at increasing levels of cormorant predation in this study. This decline was mitigated by increased individual growth of catfish at higher predation rates (i.e., lower catfish densities). This mitigating effect produced a non‐linear relationship with total kg of catfish harvested per pond resulting in a non‐linear incremental increase in breakeven price related to predation. Costs of production ($/kg) increased with increasing predation levels up to very high levels of predation with a cumulative maximum increase in breakeven price of $0.143/kg. These results indicate that losses at harvest due to cormorant predation occur immediately but are mitigated in part by compensatory growth of individual catfish. Losses due to cormorant predation in multi‐batch systems can be considerable, but there is not a 1:1 relationship between losses and kg of catfish harvested due to compensatory factors.
Growth, Survivorship, Air‐bubble Disease, and Attachment of Feeble Juvenile Seahorses, Hippocampus kuda (Bleeker, 1852)
Authors: Zhang Yanhong , Qin Geng , Lin Junda , Lin Qiang 
Published: June 2015

AbstractSeahorse aquaculture has been a focus for meeting the demand of traditional medicine and aquarium. Feeble (poor quality) juveniles are commonly found in the commercial seahorse culture. In this study, we compared the growth and survival performances of the feeble and healthy common seahorses Hippocampus kuda. The results show that the feeble juveniles had high growth and survival at the temperature of 27–29 C and salinity of 26–28‰ with frequent feeding (≥three times a day) during first 5 wk. Through a 12‐wk investigation, we found that the air‐bubble disease could significantly affect the specific growth rate and survival of the feeble juveniles. There was a positive and significant correlation between the substrate‐attachment rate and survival rate in the feeble juveniles, and substrate‐attachment rate may be used to assess the quality of the feeble populations in the seahorse H. kuda.
A refractory case of subclinical antibody‐mediated rejection due to anti‐HLA‐DQ antibody in a kidney transplant patient
Authors: Fujimoto Toshinari , Nakada Yasuyuki , Yamamoto Izumi , Kobayashi Akimitsu , Tanno Yudo , Yamada Hiroki , Miki Jun , Ohkido Ichiro , Tsuboi Nobuo , Yamamoto Hiroyasu , Yokoo Takashi 
Published: June 2015

AbstractWe herein report a refractory case of subclinical antibody‐mediated rejection (AMR) due to anti‐HLA‐DQ antibody in a kidney transplant patient. A 45‐year‐old man was admitted for a protocol biopsy; he had a serum creatinine (S‐Cr) level of 1.8 mg/dL 3 years following primary kidney transplantation. Histological examination revealed moderate to severe inflammatory cell infiltration in the peritubular capillaries. Thorough laboratory examination showed that the patient had donor‐specific antibodies (DSAbs) to DR9 and DQ9. Considering both the histological and laboratory findings, we diagnosed acute antibody‐mediated rejection. The patient underwent 3 days of consecutive steroid pulse therapy, intravenous immunoglobulin (IVIG), and plasma exchange. We also administered rituximab (200 mg/body). Six months after the treatment, a second allograft biopsy revealed the progression of interstitial fibrosis and tubular atrophy and persistence of mild peritubular capillaritis. Further analysis showed that the anti‐DR9 antibodies had disappeared, but that the mean fluorescence intensity value of the anti‐DQ9 antibodies had increased. Therefore, we repeated the plasma exchange and IVIG. Allograft function was stable throughout the course of treatment, and the S‐Cr level remained at 1.8 mg/dL. This case report demonstrates the difficulty of treating AMR due to the presence of anti‐DQ DSAbs and the necessity for subsequent therapies in refractory cases.
Recurrence of diabetic kidney disease in a type 1 diabetic patient after kidney transplantation
Authors: Nyumura Izumi , Honda Kazuho , Babazono Tetsuya , Horita Shigeru , Murakami Toru , Fuchinoue Shohei , Uchigata Yasuko 
Published: June 2015

AbstractPost‐transplant hyperglycaemia of diabetic patients may cause recurrent diabetic kidney disease (DKD) in kidney allografts. We report a patient with slowly progressive DKD with calcineurin inhibitor toxicity (CNI) toxicity after the kidney transplantation. A 28‐year‐old female with type 1 diabetes mellitus underwent successful kidney transplantation from her mother in April 2003, and the kidney graft survived for more than 10 years. She was treated with combined immunosuppressive therapy consisting of cyclosporine and mycophenolate mofetil. After transplantation, she continued to take insulin injection four times per day, but her glycosylated haemoglobin (HbA1c) was above 10%. Protocol allograft kidney biopsies performed 5 and 10 years after transplantation revealed the recurrence of slowly progressive diabetic kidney disease. In addition, arteriolar hyalinosis partly associated with calcineurin inhibitor toxicity (CNI) was detected with progression. Post‐transplant hyperglycaemia causes recurrent diabetic kidney disease (DKD) in kidney allografts, but its progression is usually slow. For long‐term management, it is important to prevent the progression of the calcineurin inhibitor arteriolopathy, as well as maintain favourable glycaemic control.
A case of recurrent focal segmental glomerulosclerosis after kidney transplantation associated with variant conversion in the Columbia classification
Authors: Unagami Kohei , Kawanishi Kunio , Shimizu Tomokazu , Kanzawa Taichi , Toki Daisuke , Okumi Masayoshi , Omoto Kazuya , Horita Shigeru , Koike Junki , Honda Kazuho , Nagashima Yoji , Ishida Hideki , Tanabe Kazunari , Nitta Kosaku 
Published: June 2015

AbstractFocal segmental glomerulosclerosis commonly recurs following kidney transplantation. A 33‐year‐old man underwent living donor kidney transplantation. Proteinuria appeared two months after transplantation, and an episode biopsy on postoperative day 66 revealed recurrent focal segmental glomerulosclerosis lesions of the cellular variant by Columbia classification. We reviewed the native kidney biopsy and confirmed collapsing variant focal segmental glomerulosclerosis. Plasma exchange therapy was performed, and his proteinuria temporarily resolved. A second allograft biopsy performed on postoperative day 200 showed no evidence of focal segmental glomerurosclerosis. He experienced incomplete remission with a proteinuria of 0.5 g/day during the subsequent three years until his urinary protein level rose to 1.3 g/day. A third biopsy performed on postoperative day 1248 showed focal segmental glomerulosclerosis cellular variant lesions. Plasma exchange was resumed in combination with additional rituximab, but his proteinuria persisted. Intermittent plasma exchange was performed 42 times in total. However, his proteinuria continued, and his renal function gradually worsened. A fourth biopsy performed on postoperative day 2540 showed focal segmental glomerulosclerosis collapsing variant lesions with severe interstitial fibrosis and tubular atrophy. He ultimately required hemodialysis seven years after transplantation. Intensive therapy with long‐term intermittent plasma exchange and rituximab suppressed proteinuria and preserved graft function for seven years, at which time graft failure occurred. We here present the clinical course and histological findings from consecutive allograft biopsies.
Phospholipase A2 receptor positive membranous nephropathy long after living donor kidney transplantation between identical twins
Authors: Saito Hisako , Hamasaki Yoshifumi , Tojo Akihiro , Shintani Yukako , Shimizu Akira , Nangaku Masaomi 
Published: June 2015

AbstractAlthough membranous nephropathy (MN) is a commonly observed cause of post‐transplant glomerulonephritis, distinguishing de novo from recurrent MN in kidney allograft is often difficult. Phospholipase A2 receptor (PLA2R) staining is useful for diagnosing recurrent MN in allografts similarly to idiopathic MN in native kidney. No specific treatment strategy has been established for MN, especially when accompanied with HCV infection in kidney transplant recipients. This report describes a 66‐year‐old man who was diagnosed as having PLA2R positive membranous nephropathy accompanied with already‐known IgA nephropathy and HCV infection 26 years after kidney transplantation conducted between identical twins. PLA2R was detected along capillary loops, implying that this patient is affected by the same pathogenic mechanism as idiopathic MN, not secondary MN associated with other disorders such as HCV infection. The patient successfully achieved clinical remission after steroid therapy.
Treatment of acute antibody‐mediated rejection using bortezomib: a case report
Authors: Sin Yong‐Hun , Kim Yong‐Jin , Oh Joon Seok , Lee Jin Ho , Kim Seong Min , Kim Joong Kyung 
Published: June 2015

AbstractHere we report the successful treatment of acute antibody‐mediated rejection (AMR) with bortezomib. Bortezomib rescue treatment was administered after a 42‐year‐old woman failed to respond to steroid pulse and plasmapheresis with intravenous immunoglobulin (IVIG). The patient underwent a second renal transplantation with a deceased donor kidney. She was treated pre‐operatively with rituximab (200 mg/body) and underwent plasmapheresis twice (day‐1 and operation day) because ELISA screening revealed that her pre‐operative peak panel reactive antibody (PRA) composition was 100% class I and 100% class II and 15 times of cross‐match positive history during the waiting period for transplantation. The patients received induction therapy with Simulect (an IL‐2‐blocking agent). A 1‐hour protocol biopsy revealed C4d‐positivity and mild peritubular capillary inflammation. This was suggestive of early AMR‐associated changes. After transplantation, the patient underwent plasmaphereses (nine times) with low‐dose IVIG (2 mg/kg). Despite this treatment regimen, serum creatinine levels increased to 3.4 mg/dL on post‐transplant day 15. A second graft biopsy was performed, which showed overt AMR with glomerulitis, peritubular capillary inflammation and no C4d deposition. On post‐operative day (POD) 22, treatment with four doses of bortezomib (1.3 mg/m2) was initiated with the patient's consent. On POD 55, renal function had recovered and serum creatinine was 1.5 mg/dL. In summary, bortezomib was administered as a rescue treatment for a patient who developed AMR that was refractory to a combination of plasmaphereses with low‐dose IVIG and preemptive administration of rituximab.
Arteriosclerosis in zero‐time biopsy is a risk factor for tacrolimus‐induced chronic nephrotoxicity
Authors: Yagisawa Takafumi , Omoto Kazuya , Shimizu Tomokazu , Ishida Hideki , Tanabe Kazunari 
Published: June 2015

AbstractAimCalcineurin inhibitors reduce the acute rejection rate and greatly improve renal allograft survival. However, they are associated with some adverse events, including nephrotoxicity, a risk factor for allograft failure. Chronic calcineurin inhibitor‐induced nephrotoxicity causes irreversible damage to renal components, such as arteriolar hyaline thickening. The aim of this study is to investigate the risk factors for tacrolimus‐induced chronic nephrotoxicity using zero‐time biopsy specimens.MethodsBetween January 2001 and December 2010, 483 patients who underwent living‐related kidney transplantation and had also been placed on a tacrolimus‐based regimen were enrolled in this study. There were 1859 specimens evaluated comprising 483 zero‐time biopsy specimens and 1376 protocol and for‐cause biopsy specimens. De novo arteriolar hyaline thickening due to tacrolimus‐induced chronic nephrotoxicity was scored according to the Banff classification aah score. In this study, tacrolimus‐induced nephrotoxicity was defined as a positive aah score.ResultsOf the 483 patients, 108 patients (22.4%) had biopsy‐proven tacrolimus‐induced chronic nephrotoxicity. Multivariate analysis showed that interlobular arteriosclerosis proven by zero‐time biopsy (OR: 2.23, 95%CI: 1.38–3.58, P < 0.01) and acute rejection episodes (OR: 1.58, 95%CI: 1.00–2.47, P = 0.04) were independent risk factors for tacrolimus‐induced chronic nephrotoxicity. However, tacrolimus‐induced chronic nephrotoxicity did not affect long‐term graft survival.ConclusionThis is the first report showing that arteriosclerosis in zero‐time biopsy specimens is a risk factor for histological tacrolimus‐induced chronic nephrotoxicity.
Atypical hemolytic uremic syndrome diagnosed four years after ABO‐incompatible kidney transplantation
Authors: Kawaguchi Keiko , Kawanishi Kunio , Sato Masayo , Itabashi Mitsuyo , Fujii Akiko , Kanetsuna Yukiko , Huchinoue Shouhei , Ohashi Ryuji , Koike Junki , Honda Kazuho , Nagashima Yoji , Nitta Kosaku 
Published: June 2015

AbstractAtypical hemolytic uremic syndrome (aHUS) in allograft kidney transplantation is caused by various factors including rejection, infection, and immunosuppressive drugs. We present a case of a 32 year old woman with aHUS four years after an ABO‐incompatible kidney transplantation from a living relative. The primary cause of end‐stage renal disease was unknown; however, IgA nephropathy (IgAN) was suspected from her clinical course. She underwent pre‐emptive kidney transplantation from her 60 year old mother. The allograft preserved good renal function [serum creatinine (sCr) level 110–130 μmol/L] until a sudden attack of abdominal pain four years after transplant, with acute renal failure (sCr level, 385.3 μmol/L), decreasing platelet count, and hemolytic anemia with schizocytes. On allograft biopsy, there was thrombotic microangiopathy in the glomeruli, with a cellular crescent formation and mesangial IgA and C3 deposition. Microvascular inflammation, such as glomerulitis, peritubular capillaritis, and arteriole endarteritis were also detected. A disintegrin‐like and metalloproteinase with thrombospondin type 1 motifs 13 (ADAMTS13) did not decrease and Shiga toxin was not detected. Donor‐specific antibodies or autoantibodies, including anti‐neutrophil cytoplasmic antibody and anti‐glomerular basement membrane (anti‐GBM) antibody, were negative. The patient was diagnosed with aHUS and received three sessions of plasmapheresis and methylprednisolone pulse therapy, followed by oral methylprednisolone (0.25–0.5 mg/kg) instead of tacrolimus. She temporarily required hemodialysis (sCr level, 658.3 μmol/L). Thereafter, her sCr level improved to 284.5 μmol/L without dialysis therapy. This case is clinically considered as aHUS after kidney transplantation, associated with various factors, including rejection, glomerulonephritis, and toxicity from drugs such as tacrolimus.
Acute T cell‐mediated rejection accompanied by C4d‐negative acute antibody‐mediated rejection and cell debris in tubulus: A case report
Authors: Takamura Tsuyoshi , Yamamoto Izumi , Nakada Yasuyuki , Katsumata Haruki , Yamakawa Takafumi , Furuya Maiko , Mafune Aki , Kobayashi Akimitsu , Tanno Yudo , Miki Jun , Ohkido Ichiro , Tsuboi Nobuo , Yamamoto Hiroyasu , Yokoo Takashi 
Published: June 2015

AbstractHerein, we report a complicated case of acute T‐cell‐mediated rejection (ACR) accompanied by C4d‐negative acute antibody‐mediated rejection (AMR) and cell debris in tubulus. A 32 year‐old male was admitted for an episode biopsy with a serum creatinine (S‐Cr) level of 1.83 mg/dL and pyuria (20–29 white blood cells per high power field) 49 days following kidney transplantation. Histological features included three distinct entities, mainly, in one of the three specimens: 1) focal aggressive tubulointerstitial inflammatory cell infiltration with moderate tubulitis, 2) inflammatory cell infiltration in peritubular capillaries (including neutrophils) and glomerular capillaries, and 3) cell debris consisting mainly of neutrophils in tubulus. Laboratory examination revealed evidence of non‐human leukocyte antigen donor‐specific antibodies. However, urinary culture and gram staining were negative. Considering both the histological and laboratory findings, the patient was diagnosed with ACR accompanied by C4d‐negative AMR and suspicion of a urinary tract infection (UTI). The patient was treated for three consecutive days with steroid pulse therapy. The patient's S‐Cr level decreased to ∼1.5 mg/dL following treatment and did not increase thereafter. A second biopsy 133 days following kidney transplantation showed an excellent response to treatment and revealed no evidence of rejection. This case report demonstrates the difficulty in the diagnosis of, and therapy for, the complicated pathological findings of ACR, AMR and suspicion of a UTI.
Banff 2013 update: Pearls and pitfalls in transplant renal pathology
Authors: Hara Shigeo 
Published: June 2015

AbstractThe pathological classification of rejection in renal allografts (Banff classification) has undergone substantial evolution for more than 20 years, and has been the diagnostic gold standard in clinical practice. The 2013 updated Banff classification encompasses a revised scheme of antibody‐mediated rejection (ABMR) that consists of donor‐specific antibody (DSA) positivity, characteristic histological manifestations for both acute and chronic ABMR, and DSA‐induced endothelial cell injury which is represented by either C4d positivity, microvascular inflammation or expression of activated endothelial gene transcripts. Other modified criteria include a C4d positivity threshold, and histological definition of transplant glomerulitis and transplant glomerulopathy. Morphologically, glomerulonephritis, either recurrent or de novo, can be challenging to differentiate from ABMR‐mediated transplant glomerulitis. Endothelial arteritis by itself does not warrant the diagnosis of acute T‐cell mediated rejection; ABMR should also be considered based on the DSA test results. With regard to polyomavirus BK‐associated nephropathy, immunohistochemical examination using anti‐simian virus (SV) 40 antibody can be a promising method to assess the quantitative viral load of polyomavirus BK and graft survival. In summary, the 2013 updated Banff classification strictly defines ABMR with histopathological and serological criteria irrespective of C4d positivity. Inclusion of gene expression data relevant to ABMR highlights that the Banff criteria have entered the era of ‘Seeing the Unseen’ schemes, reflecting recent advances in understanding the molecular events in allograft injury.
Validation of chronic kidney disease risk categorization system in Chinese patients with kidney disease: A cohort study
Authors: Liu Qingyan , Lv Jicheng , Li Haixia , Jiao Lili , Yang Hongyun , Song Yinan , Xu Guobin 
Published: June 2015

AbstractAimTo validate the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines risk stratification system based on the combination of estimated glomerular filtration rate (eGFR) and proteinuria.MethodsThis was a cohort study. A total of 1219 study population were recruited. Estimated GFR and proteinuria measured by using 24 h urine protein excretion rate (PER) were predictors. Adverse outcomes included all‐cause mortality (ACM) and end‐stage renal disease (ESRD). Follow‐up was done by regular visit, telephone interview and electronic medical records.ResultsOver a median follow‐up of 4.6 years, 153 (12.6%) and 43 (3.5%) patients experienced ESRD and ACM, respectively. On multivariable analysis, the adjusted hazard ratio for ESRD and ACM (compared with patients with eGFR > 60 mL/min per 1.73 m2) was of 29.8 and 3.6 for those with eGFR of 15–29 mL/min per 1.73 m2, respectively. The adjusted hazard ratio for ESRD and ACM (compared with patients with PER < 150 mg/24h) was of 15.9 and 3.9 for those with PER > 500 mg/24h. Higher KDIGO guidelines risk categories (indicating lower eGFR or higher proteinuria) were associated with a graded increase in the risk for the ESRD (P < 0.001) and ACM (P < 0.001). Reclassification of KDIGO guidelines risk categories yielded net reclassification improvements for those with ESRD or ACM event (NRIevents) of 33.3% or 30.2%.ConclusionLower eGFR and higher proteinuria are risk factors for ESRD and ACM in Chinese patients. The KDIGO guidelines risk categorization system assigned patients who went on to have the event to more appropriate CKD risk categories.