CEN Case Reports最新文献

{"title":"Case of successful treatment with glucocorticoid for isolated anti-centromere antibody-positive acute interstitial nephritis.","authors":"Chisa Takata, Akihiro Kuma, Atsuko Suwabe, Takahide Iwasaki, Takahiro Kuragano","doi":"10.1007/s13730-024-00937-4","DOIUrl":"10.1007/s13730-024-00937-4","url":null,"abstract":"<p><p>Acute interstitial nephritis (AIN) is known to cause acute kidney injury and is characterized by immunocyte infiltration and interstitial fibrosis. Primary etiologies include drugs, infections, and autoimmune disorders. Herein, we presented the case of a 78-year-old woman patient with AIN with anti-centromere antibody (ACA) positivity, secondary to an idiopathic immune system disorder. Her serum creatinine (sCr) was 0.67 mg/dL 2 months prior to consulting us, which increased to 2.79 mg/dL. The renal biopsy revealed an AIN comprising interstitial infiltration with immunocytes and CD138 + cells. Furthermore, all other antibodies tested negative using immunofluorescence on both glomeruli and tubulointerstitial lesions. The ACA was elevated to a level of ≥ 500 U/mL. The ACA positive has been known to be accompanied by worsening kidney function in patients with systemic sclerosis and primary biliary cholangitis. However, any autoimmune disease were not diagnosed. Successful treatment with an initial dose of 30 mg/day of glucocorticoids tapered to 25 mg/day resulted in a decrease in the sCr to 1.53 mg/dL 4 weeks later. Nine months later, glucocorticoids was tapered, based on the threshold of a sCr of 1.03 mg/dL and the titer of ACA of 291 U/mL. In this case, glucocorticoid treatment remarkably improved renal function in AIN containing CD138 + cells accompanied by a reduction of ACA titer. The etiology of ACA-positive AIN was unknown; however, the incidence of ACA-positive AIN should always be deliberated.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"230-235"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unusual late presentation of cryptococcal meningitis with simultaneous CMV antigenemia in a kidney transplant recipient.","authors":"Tsz Hing Mok, Li Man Maggie Lam, Chi Yuen Cheung","doi":"10.1007/s13730-024-00939-2","DOIUrl":"10.1007/s13730-024-00939-2","url":null,"abstract":"<p><p>Cryptococcosis is the third most common invasive fungal infection in solid-organ transplant (SOT) recipients after candidiasis and aspergillosis. These patients are at risk of disseminated cryptococcosis because of immuosuppressive therapy. The median time to disease onset after kidney transplantation is approximately 35 months and it rarely occurs more than 10 years after transplantation. Herein, we report a case of 64-year-old kidney transplant recipient suffering from coexisting disseminated cryptococcosis with brain and skin involvement, together with cytomegalovirus (CMV) antigenemia more than 20 years after transplant. She presented with frontal headache and bilateral hand tremor, in addition to multiple nodular lesions over bilateral lower limbs. The diagnosis was made after lumbar puncture and skin biopsy. She was successfully treated with a course of anti-fungal and anti-CMV regimen without any relapse of central nervous system infection. Our case illustrates that disseminated cryptococcosis can occur very late after organ transplant. It is thus important to watch out for late-onset opportunistic infections and strike the balance between risks of infections and rejections in SOT patients.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"242-245"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tubulointerstitial nephritis with IgM-positive plasma cells complicated by liver failure.","authors":"Takashi Kudo, Daigo Nakazawa, Saori Nishio, Fumihiko Hattanda, Yusho Ueda, Junpei Yoshikawa, Satoka Shiratori-Aso, Sari Iwasaki, Takahiro Tsuji, Yasuni Nakanuma, Goki Suda, Koji Ogawa, Naoya Sakamoto, Tatsuya Atsumi","doi":"10.1007/s13730-024-00932-9","DOIUrl":"10.1007/s13730-024-00932-9","url":null,"abstract":"<p><p>Tubulointerstitial nephritis (TIN) is characterized by inflammation of the renal interstitium with the infiltration of immune cells, mainly consisting of T cells. Recently, patients with TIN with the predominant infiltration of immunoglobulin M (IgM)-positive plasma cells were reported, coined IgMPC-TIN. Here we report the case of a 70-year-old woman diagnosed with Fanconi syndrome and renal tubular acidosis. Renal biopsy revealed IgMPC-TIN. Her renal dysfunction and clinical findings improved after corticosteroid therapy. However, the patient died of progressive liver failure and spontaneous bacterial peritonitis. In laboratory tests, viral hepatitis was excluded, and autoantibodies associated with liver diseases were negative. Generally, IgMPC-TIN is often complicated by primary biliary cholangitis (PBC), whereas her autopsy revealed the local infiltration of IgM-positive plasma cells, obliterative portal venopathy, and nodular regenerative hyperplasia in liver. This case is the first demonstration that IgMPC-TIN is also seen in liver disease with nodular regenerative hyperplasia, although IgMPC-TIN is more common in anti-M2 antibody-positive disease.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"253-260"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autosomal-dominant tubulointerstitial kidney disease with a novel UMOD mutation, overlapping with Sjogren's syndrome: a case report.","authors":"Hiroki Nobayashi, Tomomichi Iida, Takuya Fujimaru, Takayasu Mori, Yumi Ito, Hiroyuki Ueda, Eisei Sohara, Shinichi Uchida, Ryuji Aoyagi, Takashi Yokoo","doi":"10.1007/s13730-024-00915-w","DOIUrl":"10.1007/s13730-024-00915-w","url":null,"abstract":"<p><p>Autosomal-dominant tubulointerstitial kidney disease caused by UMOD (encoding uromodulin) mutation (ADTKD-UMOD) is a rare hereditary disease. A strong family history of hyperuricemia or gout and inherited kidney disease raises the suspicion of ADTKD-UMOD. Genetic testing can confirm the diagnosis without a kidney biopsy. However, when complicated by other diseases that can cause tubulointerstitial disease, renal biopsy is indispensable for the diagnosis and decisions on treatment strategy. We report the case of a 44-year-old woman referred for evaluation of kidney dysfunction. She had an attack of gout 1 month before referral and a family history of hyperuricemia. She was diagnosed with primary Sjogren's syndrome through an immune workup and ophthalmological examination. However, a kidney biopsy revealed histological features suggesting ADTKD rather than gouty kidney or tubulointerstitial nephritis associated with Sjogren's syndrome, and immunostaining revealed a characteristic staining pattern with UMOD. Comprehensive genetic testing of 93 genes responsible for polycystic kidney disease revealed a novel heterozygous missense variant (c.649 T > A:p. Cys217Ser) in UMOD, and the patient was diagnosed with ADTKD-UMOD. In this case, kidney biopsy contributed to the correct diagnosis of tubulointerstitial kidney disease. This case emphasizes the importance of suspecting ADTKD-UMOD based on family history and careful evaluation of kidney biopsy findings.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"113-118"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Behcet's disease presenting as malignant hypertension induced by renovascular hypertension.","authors":"Sho Kinguchi, Misumi Tamura, Rika Furuta, Kazuki Toyota, Kohei Ishiga, Tomohiko Kanaoka, Kengo Azushima, Hiromichi Wakui, Nobuhito Hirawa, Kouichi Tamura","doi":"10.1007/s13730-024-00918-7","DOIUrl":"10.1007/s13730-024-00918-7","url":null,"abstract":"<p><p>Hypertension is an uncommon manifestation of Behcet's disease, which is also an uncommon cause of renovascular hypertension. We herein report a case of malignant hypertension associated with unilateral renal artery stenosis due to vascular Behcet's disease. A 19-year-old man, who had no significant medical history, was referred to ophthalmology at our hospital because he was suspected to have uveitis and Vogt-Koyanagi-Harada syndrome. In addition to poor eyesight, he had been aware of a fever, loss of appetite, and weight loss for a month. He was admitted with markedly elevated blood pressure (222/140 mmHg), hypertensive retinopathy, and acute kidney injury, who was diagnosed with malignant hypertension. Laboratory findings showed high plasma renin activity and plasma aldosterone concentration, hypokalemia, and elevated inflammatory response. Computed tomography showed an atrophic right kidney and a compensatorily enlarged left kidney. Renal computed tomography angiography revealed severe and diffuse stenosis of the right renal artery, and stenosis of the ostium of celiac artery. Since he was suspected to have uveitis and his inflammatory responses were elevated on admission, we listed Behcet's disease as a differential diagnosis. Medical interview and examination focusing on Behcet's disease revealed that the patient had recurrent oral aphthous lesions and folliculitis, and a positive pathergy test, which led to the patient being diagnosed with vascular Behcet's disease. After admission, his blood pressure was well controlled with multiple antihypertensive drugs including an angiotensin receptor/neprilysin inhibitor, and his oral aphthous lesions and skin lesion were improved with colchicine. When young men who are at a higher risk for vascular Behcet's disease show renovascular hypertension with an elevated inflammatory reaction, vascular Behcet's disease should be considered as a differential diagnosis.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"135-140"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Managing malignant hypertension with renal TMA: a case for caution in blood-pressure reduction.","authors":"Narumichi Iwamura, Yuta Matsukuma, Eisuke Katafuchi, Yoshiko Nakano, Kanako Tsutsumi, Yuki Ueno, Yasuhisa Tamura, Toshiaki Nakano","doi":"10.1007/s13730-024-00933-8","DOIUrl":"10.1007/s13730-024-00933-8","url":null,"abstract":"<p><p>Malignant hypertension with renal thrombotic microangiopathy is a rare yet serious cause of acute kidney injury (AKI). Patients are often treated with antihypertensive therapy; however, managing their blood pressure is complex, with targets for initial treatment unclear. We report on a 55-year-old male with severe hypertension (blood pressure 210/140 mmHg), AKI (serum creatinine 9.27 mg/dL), anemia (hemoglobin 7.6 g/dL), thrombocytopenia (platelets 113 k/μL), and renal biopsy confirming malignant arteriolar nephrosclerosis and thrombotic microangiopathy. Previously prescribed 20-mg azilsartan daily, he lost consciousness the next day and was urgently admitted with a blood pressure of 118 mmHg and increased serum creatinine from 1.28 to 9.27 mg/dL over 6 months. Azilsartan was stopped; blood pressure managed with 12.5 mg of losartan daily, targeting systolic pressure between 150 and 160 mmHg. His creatinine peaked on day 14; however, treatment with 12.5 - 50 mg/day of losartan and 5 - 10 mg/day of amlodipine gradually improved renal function to 4.48 mg/dL by month ten without hemodialysis or further syncope. Our case suggests a gradual approach to blood-pressure management to avoid ischemic risks.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"271-279"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parathyroid carcinoma in a dialysis patient definitively diagnosed after parathyroidectomy for uncontrolled secondary hyperparathyroidism.","authors":"Ryoko Tatsumi, Yusuke Tomita, Shinya Takiguchi, Saeko Uehara, Michio Nakamura","doi":"10.1007/s13730-024-00924-9","DOIUrl":"10.1007/s13730-024-00924-9","url":null,"abstract":"<p><p>Secondary hyperparathyroidism (SHPT) is a well-known complication in chronic kidney disease patients undergoing maintenance dialysis. In 2006, the Japanese Society for Dialysis Therapy recommended parathyroidectomy (PTx) for medically resistant SHPT cases, resulting in an increase in the performance of PTx. However, after calcimimetics were added to the treatment options in 2008, the number of cases requiring PTx has decreased. Presented here is the case of a dialysis patient with SHPT under medical treatment with calcimimetics, who was normocalcemic but showed persistently high levels of parathyroid hormone (PTH), suggesting the possibility of parathyroid carcinoma. Parathyroid carcinoma is a very rare endocrine malignancy characterized by hypercalcemia and increased PTH level. With appropriately performed PTx at the proper time, the definitive diagnosis was made and the patient has not developed any recurrences or metastases to date. In cases of SHPT refractory to medical therapy, the possibility of parathyroid carcinoma should be considered as an alternative. We report a case in which parathyroid carcinoma was diagnosed after appropriate conversion from medical therapy to PTx with reference to ultrasonographic images.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"167-170"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141999447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute tubulointerstitial nephritis associated with infliximab therapy in a patient with Crohn's disease: a case report.","authors":"Naif Alghamdi, Fahad Alshehri, Sultan Alhazza, Fahad Bhutto, Azhari Alhassan, Mohammed Kechrid, Dhafer Alshehri, Kadi Alshammari, Talal Assiri, Ohoud Assiri, Emad Darewsh, Mohammed Ali, Ruba Qadri, Yasser Alahmadi","doi":"10.1007/s13730-024-00943-6","DOIUrl":"10.1007/s13730-024-00943-6","url":null,"abstract":"<p><p>We report the case of a 39-year-old man who presented with a history of generalized fatigue, nausea, subjective fever with rigors, and renal dysfunction after receiving infliximab (IFX) therapy for Crohn's disease. A renal biopsy revealed acute tubulointerstitial nephritis (ATIN). After other causes of acute kidney injury were excluded, steroid therapy was initiated, his fever subsided, and kidney function improved. From this case report, infliximab could be a rare cause of elevated kidney function and that it should be not considered a completely safe treatment or disregarded as potential cause of ATIN.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"266-270"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoglobulin A-dominant membranoproliferative glomerulonephritis-like pattern of injury as a possible paraneoplastic nephropathy in a breast cancer patient.","authors":"Shuntaro Taira, Mika Kawagoe, Hitoshi Anzai, Minoru Yasukawa, Shinichiro Asakawa, Shigeyuki Arai, Osamu Yamazaki, Yoshifuru Tamura, Yasutoshi Oshima, Satoe Numakura, Ryuji Ohashi, Shigeru Shibata, Yoshihide Fujigaki","doi":"10.1007/s13730-024-00936-5","DOIUrl":"10.1007/s13730-024-00936-5","url":null,"abstract":"<p><p>A middle-aged woman was found to have proteinuria during a health check-up. About sixteen months later, she was diagnosed with stage IIA invasive ductal carcinoma of the right breast. Her proteinuria progressed to nephrotic syndrome with significant hematuria. Hormone therapy was initiated for her estrogen and progesterone receptor-positive breast cancer. A kidney biopsy performed 47 days after starting the therapy revealed an IgA-dominant membranoproliferative glomerulonephritis-like pattern of injury. Electron microscopy showed subendothelial-dominant electron-dense deposits (EDD), with small amounts of mesangial EDD and a single occurrence of subepithelial hump-like EDD, along with occasional mesangial interpositions. Similar pathology can be caused by IgA vasculitis with nephritis, IgA-dominant infection-associated glomerulonephritis, and liver disease-associated glomerulopathy, but all of these were ruled out. The deposited IgA was found to be galactose-deficient IgA1. Thus, IgA nephropathy with glomerular capillary IgA deposition was considered. She underwent a right partial mastectomy and sentinel lymph node biopsy in the right axilla 75 days after starting hormone therapy, followed by adjuvant radiation. Proteinuria and hematuria tended to decrease after the treatment, and this trend continued even after corticosteroid therapy for glomerulonephritis, which was administered 156 days after starting hormone therapy. Approximately 15 months after starting hormone therapy, her proteinuria had reduced to around 1.0 g/g of creatinine, and her hematuria was negative. IgA nephropathy with glomerular capillary IgA deposition is known to be resistant to corticosteroid therapy. The favorable clinical course of the rare glomerulopathy following breast cancer treatment suggested a diagnosis of paraneoplastic glomerulopathy secondary to breast cancer in our patient.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"217-223"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unusual course of glyphosate-induced acute kidney injury: a case report of tubulointerstitial nephritis treated with steroids.","authors":"Daichi Omote, Shin-Ichi Makino, Issei Okunaga, Masayoshi Ishii, Narihito Tatsumoto, Masashi Aizawa, Katsuhiko Asanuma","doi":"10.1007/s13730-024-00914-x","DOIUrl":"10.1007/s13730-024-00914-x","url":null,"abstract":"<p><p>Glyphosate is a widely used herbicide that is generally considered safe; however, acute kidney injury (AKI) caused by glyphosate ingestion can be severe and require hemodialysis. We present a unique case of a 68-year-old Japanese man who developed AKI after accidental ingestion of glyphosate and required hemodialysis. Based on the clinical presentation and findings, the patient was diagnosed with renal AKI with severe tubulointerstitial damage. However, the precise pathogenesis of the tubulointerstitial damage remained unclear. An elevated beta-2 microglobulin level discovered by the urinalysis during admission raised the suspicion of tubulointerstitial nephritis caused by glyphosate. Gallium scintigraphy revealed accumulation in both kidneys. A renal biopsy revealed acute tubulointerstitial nephritis rather than acute tubular necrosis, which is commonly observed with glyphosate-induced renal injury. After initiating steroid therapy, his kidney function gradually improved and he was weaned from hemodialysis. This report is the first to describe glyphosate-induced acute tubulointerstitial nephritis that was successfully treated with immunosuppressive therapy. Furthermore, this report highlights the importance of steroid therapy for cases of persistent kidney injury after the discontinuation of agents associated with acute tubulointerstitial nephritis.</p>","PeriodicalId":9697,"journal":{"name":"CEN Case Reports","volume":" ","pages":"128-134"},"PeriodicalIF":1.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}