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Your search keyword '"Manhua, Nie"' showing total 4 results
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4 results on '"Manhua, Nie"'

1. Drug-induced Fanconi syndrome in patients with kidney allograft transplantation

Author

Zhouqi Tang, Tengfang Li, Helong Dai, Chen Feng, Xubiao Xie, Fenghua Peng, Gongbin Lan, Shaojie Yu, Yu Wang, Chunhua Fang, Manhua Nie, Xiaoqiong Yuan, Xiaotian Tang, Xin Jiang, Xuejing Zhu, Yuxi Fan, Jiawei Peng, Siyu Sun, Mingda Zhong, Hedong Zhang, and Longkai Peng

Subjects
Fanconi syndrome, kidney transplantation, adefovir dipivoxil, tacrolimus, renal tubular injury, osteoporosis, Immunologic diseases. Allergy, RC581-607
Abstract

BackgroundPatients after kidney transplantation need to take long-term immunosuppressive and other drugs. Some of these drug side effects are easily confused with the symptoms of Fanconi syndrome, resulting in misdiagnosis and missed diagnosis, and causing serious consequences to patients. Therefore, improving awareness, early diagnosis and treatment of Fanconi syndrome after kidney transplantation is critical.MethodsThis retrospective study analyzed 1728 cases of allogeneic kidney transplant patients admitted to the Second Xiangya Hospital of Central South University from July 2016 to January 2021. Two patients with Fanconi syndrome secondary to drugs, adefovir dipivoxil (ADV) and tacrolimus, were screened. We summarized the diagnostic process, clinical data, and prognosis.ResultsThe onset of Fanconi syndrome secondary to ADV after renal transplantation was insidious, and the condition developed after long-term medication (>10 years). It mainly manifested as bone pain, osteomalacia, and scoliosis in the late stage and was accompanied by obvious proximal renal tubular damage (severe hypophosphatemia, hypokalemia, hypocalcemia, hypouricemia, glycosuria, protein urine, acidosis, etc.) and renal function damage (increased creatinine and azotemia). The pathological findings included mitochondrial swelling and deformity in renal tubular epithelial cells. The above symptoms and signs were relieved after drug withdrawal, but the scoliosis was difficult to rectify. Fanconi syndrome secondary to tacrolimus has a single manifestation, increased creatinine, which can be easily confused with tacrolimus nephrotoxicity. However, it is often ineffective to reduce the dose of tacrolomus, and proximal renal failure can be found in the later stage of disease development. There was no abnormality in the bone metabolism index and imageological examination findings. The creatinine level decreased rapidly, the proximal renal tubule function returned to normal, and no severe electrolyte imbalance or urinary component loss occurred when the immunosuppression was changed from tacrolimus to cyclosporine A.ConclusionsFor the first time, drug-induced Fanconi syndrome after kidney transplantation was reported. These results confirmed that the long-term use of ADV or tacrolimus after kidney transplantation may have serious consequences, some of which are irreversible. Greater understanding of Fanconi syndrome after kidney transplantation is necessary in order to avoid incorrect and missed diagnosis.

Published
2022
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2. The role of B cells in cancer development

Author

Rongying Tan, Manhua Nie, and Wang Long

Subjects
B cell, tumor, tumor immunity, cancer, immunotherapy, tumor microenvironment, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

B cells play a critical role in adaptive immune responses mainly due to antigen presentation and antibody production. Studies about the tumor-infiltrating immune cells so far demonstrated that the function of B cells in tumor immunity is quite different among various tumor types. The antigen presentation of B cells is mainly anti-tumoral, while the role of antibody production is controversial. Moreover, the immunosuppressive regulatory B cells are detrimental to anti-tumor immunity via the secretion of various anti-inflammatory cytokines. This review briefly summarizes the different roles of B cells classified by the primary function of B cells, antigen presentation, antibody production, and immunity regulation. Further, it discusses the potential therapeutic target of B cells in tumor immunity.

Published
2022
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3. MiR-133b regulates the proliferation, colony formation, and invasion of bladder cancer cells via inhibiting SOX4

Author

Mingda, Zhong, Fen, Jiang, Lei, Song, Manhua, Nie, and Gongbin, Lan

Subjects
Gene Expression Regulation, Neoplastic, MicroRNAs, Urinary Bladder Neoplasms, Carcinogenesis, Cell Movement, Cell Line, Tumor, Urinary Bladder, Humans, Epithelial Cells, Cell Proliferation, SOXC Transcription Factors
Abstract

Bladder cancer is one of the most common urothelial tumors with high incidence and mortality rates. Although it has been reported that microRNA (miR)-133b can regulate tumorigenesis of bladder cancer, the mechanism remains unclear. Sex-determining region Y-box transcription factor 4 (SOX4) exhibits an important role in tumorigenesis, but it is unclear whether SOX4 and miR-133b are associated with regulation of pathogenesis of bladder cancer. This study aims to determine the expressions of SOX4 and miR-133b in bladder cancer tissues and cells, investigate their effects on the proliferation, colony formation, and invasion of bladder cancer cells, and to explore the association between miR-133b and SOX4 in regulating biological featurss of bladder cancer cells.The bladder cancer and adjacent tissue samples of 10 patients who underwent surgical resection in the Second Xiangya Hospital of Central South Universty from Januray to June 2015 were obtained. The levels of miR-133b were tested by real-time PCR, and the protein levels of SOX4 were evaluated using Western blotting in bladder cancer tissues, matched adjacent tissues, and cell lines. The correlation between miR-133b expression and SOX4 expression in bladder cancer tissues was analyzed. Using the online database TargetScan, the relationship between SOX4 and miR-133b was predicted. MiR-133b mimics, miR-133b inhibitor, and short hairpin RNA (shRNA)-SOX4 were transfected into T24 cells by Lipofectamine 2000. The relationship between miR-133b and SOX4 was also verified by a dual-luciferase reporter assay. The proliferation of T24 cells cultured for 0, 12, 48, 72, and 96 h was evaluated by cell counting kit-8 (CCK-8) assay. The colony formation capacity of bladder cancer cells was tested after 14-day culture, and cell invasion capacity was evaluated with Transwell invasion assay.Bladder cancer tissue and bladder cancer cells had low level of miR-133b but high level of SOX4, compared with matched adjacent tissues and normal bladder epithelial cells. A negative correlation betweenThe up-regulation of SOX4 contributes to the progression of bladder cancer, and miR-133b can regulate the proliferation, colony formation, and invasion of bladder cancer cells via inhibiting SOX4.

Published
2022

4. Utilization of HCV Viremic Kidneys with Genotyping/Subtyping-Free Sofosbuvir/Velpatasvir Treatment Strategy: Experience from China

Author

Hedong Zhang, Qiuhao Liu, Shanbiao Hu, Mingda Zhong, Fenghua Peng, Yong Guo, Chunhua Fang, Manhua Nie, Liang Tan, Helong Dai, Xubiao Xie, Longkai Peng, and Gongbin Lan

Subjects
Adult, Male, Article Subject, General Immunology and Microbiology, Genotype, General Medicine, Hepacivirus, Hepatitis C, Chronic, Middle Aged, Kidney, Antiviral Agents, Hepatitis C, Heterocyclic Compounds, 4 or More Rings, General Biochemistry, Genetics and Molecular Biology, Humans, Female, Carbamates, Viremia, Sofosbuvir, Retrospective Studies
Abstract

Background. Owing to the advent of pangenotypic direct-acting antiviral agents (DAAs) for hepatitis C virus (HCV) treatment, utilization of HCV-infected deceased donor kidneys with simplified genotyping/subtyping-free sofosbuvir/velpatasvir (SOF/VEL) treatment strategy is now becoming a promising strategy for expanding the organ donor pool. Methods. This retrospective, comparative, single-center study included HCV viremic donor kidneys that were transplanted to 9 HCV-positive (HCV Ab-positive) recipients (D+/R+ group) and 14 HCV-negative recipients (D+/R- group) from May 2018 to January 2021. Both groups received prophylaxis with SOF/VEL treatment within 1-week posttransplant devoid of HCV genotyping/subtyping. The primary outcomes were sustained virologic response 12 weeks after completion of therapy (SVR12) and graft survival at 1-year posttransplant. Results. Baseline characteristics were similar between the HCV D+/R- and D+/R+ groups. The mean age of all recipients was 39.09 ± 9.65 (SD) years, and 73.9% were male. A total of 92.9% (13 out of 14) recipients had pretreatment HCV viremia in the D+/R- group. The pretreatment HCV viral load in the D+/R+ group (5.98, log 10 IU/mL; IQR, 5.28-6.53) was significantly higher than that in the D+/R- group (3.61, log 10 IU/mL; IQR, 2.57-4.57). After SOF/VEL treatment, SVR12 was achieved in all recipients, with a 100% 1-year patient and graft survival rates. The D+/R+ group had a higher incidence of abnormal liver function (44.4% vs. 7.1%). No significant difference was observed between the two groups in terms of DGF, acute rejection, ALT, serum creatinine, and eGFR within 1-year posttransplant. No severe adverse events associated with either HCV viremia or SOF/VEL were observed. Conclusions. Using a simplified genotyping/subtyping-free SOF/VEL treatment strategy, kidneys from hepatitis C viremic donors for both infected and uninfected recipients presented with safe, excellent, and comparable 1-year outcomes, which can safely expand the donor pool. HCV-positive donor kidneys should be utilized regularly, regardless of the recipient’s HCV status.

Published
2022

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