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Article: Steroid-resistant nephrotic syndrome associated with certain

Yang, Siying / He, Yonghua / Zhou, Jianhua / Yuan, Huiqing / Qiu, Liru

2023 Volume 11, Page(s) 1079758

Abstract: Objectives: Steroid-resistant nephrotic syndrome (SRNS) is a clinical syndrome characterized by the lack of response to standard steroid therapy, usually progressing to end-stage renal disease. We reported two cases of female identical twins with SRNS ... ...

Abstract	Objectives: Steroid-resistant nephrotic syndrome (SRNS) is a clinical syndrome characterized by the lack of response to standard steroid therapy, usually progressing to end-stage renal disease. We reported two cases of female identical twins with SRNS caused by Methods: Two cases of nephrotic syndrome caused by Results: We described two Chinese identical twin girls with isolated SRNS due to compound heterozygous variants in the Conclusions: These two female identical twins were the first reported cases of isolated SRNS caused by
Language	English
Publishing date	2023-02-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2023.1079758
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Article ; Online: Mutations in the NUP93, NUP107 and NUP160 genes cause steroid-resistant nephrotic syndrome in Chinese children.

Han, Yanxinli / Sha, Hongyu / Yang, Yuan / Yu, Zhuowei / Zhou, Lanqi / Wang, Yi / Yang, Fengjie / Qiu, Liru / Zhang, Yu / Zhou, Jianhua

Italian journal of pediatrics

2024 Volume 50, Issue 1, Page(s) 81

Abstract: Background: The variants of nucleoporins are extremely rare in hereditary steroid-resistant nephrotic syndrome (SRNS). Most of the patients carrying such variants progress to end stage kidney disease (ESKD) in their childhood. More clinical and genetic ... ...

Abstract	Background: The variants of nucleoporins are extremely rare in hereditary steroid-resistant nephrotic syndrome (SRNS). Most of the patients carrying such variants progress to end stage kidney disease (ESKD) in their childhood. More clinical and genetic data from these patients are needed to characterize their genotype-phenotype relationships and elucidate the role of nucleoporins in SRNS. Methods: Four patients of SRNS carrying biallelic variants in the NUP93, NUP107 and NUP160 genes were presented. The clinical and molecular genetic characteristics of these patients were summarized, and relevant literature was reviewed. Results: All four patients in this study were female and initially presented with SRNS. The median age at the onset of the disease was 5.08 years, ranging from 1 to 10.5 years. Among the four patients, three progressed to ESKD at a median age of 7 years, ranging from 1.5 to 10.5 years, while one patient reached stage 3 chronic kidney disease (CKD3). Kidney biopsies revealed focal segmental glomerulosclerosis in three patients. Biallelic variants were detected in NUP93 in one patient, NUP107 in two patients, as well as NUP160 in one patient respectively. Among these variants, five yielded single amino acid substitutions, one led to nonsense mutation causing premature termination of NUP107 translation, one caused a single nucleotide deletion resulting in frameshift and truncation of NUP107. Furthermore, one splicing donor mutation was observed in NUP160. None of these variants had been reported previously. Conclusion: This report indicates that biallelic variants in NUP93, NUP107 and NUP160 can cause severe early-onset SRNS, which rapidly progresses to ESKD. Moreover, these findings expand the spectrum of phenotypes and genotypes and highlight the importance of next-generation sequencing in elucidating the molecular basis of SRNS and allowing rational treatment for affected individuals.
MeSH term(s)	Humans ; Female ; Nuclear Pore Complex Proteins/genetics ; Child ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/congenital ; Child, Preschool ; China ; Mutation ; Infant ; East Asian People
Chemical Substances	Nuclear Pore Complex Proteins ; Nup93 protein, human
Language	English
Publishing date	2024-04-22
Publishing country	England
Document type	Journal Article ; Case Reports
ZDB-ID	2088556-8
ISSN	1824-7288 ; 1720-8424
ISSN (online)	1824-7288
ISSN	1720-8424
DOI	10.1186/s13052-024-01656-3
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Article ; Online: Zero-contrast PTRA and stenting for child with TRAS: A case report.

Xie, Yang / He, Xingwei / Qiu, Liru / Zeng, Hesong

Pediatric transplantation

2021 Volume 26, Issue 2, Page(s) e14183

Abstract: Background: Kidney transplantation is often complicated by TRAS, and PTRA can effectively treat it. However, PTRA is not appropriate for patients with CKD because iodinated contrast agent may induce nephropathy.: Methods: This article reports about a ...

Abstract	Background: Kidney transplantation is often complicated by TRAS, and PTRA can effectively treat it. However, PTRA is not appropriate for patients with CKD because iodinated contrast agent may induce nephropathy. Methods: This article reports about a 14-year-old boy with a history of kidney transplantation complicated by RAS. He initially underwent percutaneous balloon dilation to relieve the stenosis. One and half a year after dilation, he received zero-contrast PTRA and stenting under the guidance of external and IVUS with reference to previous PAG image. Results: After successful stent implantation, the cross-sectional area of the renal artery lumen was significantly increased.The blood pressure and level of creatinine also decreased and kept stable during follow-up. Conclusion: This report suggests the feasibility of external ultrasound and IVUS guided, zero-contrast PTRA in patients with poor renal function or iodinated contrast allergy.
MeSH term(s)	Adolescent ; Angioplasty, Balloon/methods ; Computed Tomography Angiography ; Humans ; Kidney Failure, Chronic/surgery ; Kidney Transplantation ; Male ; Postoperative Complications/diagnostic imaging ; Postoperative Complications/surgery ; Renal Artery Obstruction/diagnostic imaging ; Renal Artery Obstruction/surgery ; Stents ; Ultrasonography, Doppler
Language	English
Publishing date	2021-11-01
Publishing country	Denmark
Document type	Case Reports
ZDB-ID	1390284-2
ISSN	1399-3046 ; 1397-3142
ISSN (online)	1399-3046
ISSN	1397-3142
DOI	10.1111/petr.14183
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Zs.A 4947: Show issues

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Article ; Online: Perfusion heterogeneity of cerebral small vessel disease revealed via arterial spin labeling MRI and machine learning.

Lu, Weizhao / Yu, Chunyan / Wang, Liru / Wang, Feng / Qiu, Jianfeng

NeuroImage. Clinical

2022 Volume 36, Page(s) 103165

Abstract: Cerebral small vessel disease (CSVD) is associated with altered cerebral perfusion. However, global and regional cerebral blood flow (CBF) are highly heterogeneous across CSVD patients. The aim of this study was to identify subtypes of CSVD with ... ...

Abstract	Cerebral small vessel disease (CSVD) is associated with altered cerebral perfusion. However, global and regional cerebral blood flow (CBF) are highly heterogeneous across CSVD patients. The aim of this study was to identify subtypes of CSVD with different CBF patterns using an advanced machine learning approach. 121 CSVD patients and 53 healthy controls received arterial spin label MRI, T1 structural MRI and clinical measurements. Regional CBF were used to identify distinct perfusion subtypes of CSVD via a semi-supervised machine learning algorithm. Statistical analyses were used to explore alterations in CBF, clinical measures, gray and white matter volume between healthy controls and different subtypes of CSVD. Correlation analysis was used to assess the association between clinical measures and altered CBF in each CSVD subtype. Three subtypes of CSVD with distinct CBF patterns were found. Subtype 1 showed decreased CBF in the temporal lobe and increased CBF in the parietal and occipital lobe. Subtype 2 exhibited decreased CBF in the right hemisphere of the brain, and increased CBF in the left cerebrum. Subtype 3 demonstrated decreased CBF in the posterior part of the brain, and increased CBF in anterior part of the brain. The three subtypes also differed significantly in gender (p = 0.005), the proportion of subjects with lacune (p = 0.002), with periventricular white matter hyperintensity (p = 0.043), and CSVD burden score (p = 0.048). In subtype 3, it was found that widespread decreased CBF was correlated with total CSVD burden score (r = -0.324, p = 0.029). Compared with healthy controls, the three CSVD subtypes also showed distinct volumetric patterns of white matter. The current results associate different subtypes with different clinical and imaging phenotypes, which can improve the understanding of brain perfusion alterations of CSVD and can facilitate precision diagnosis of CSVD.
Language	English
Publishing date	2022-08-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701571-3
ISSN	2213-1582 ; 2213-1582
ISSN (online)	2213-1582
ISSN	2213-1582
DOI	10.1016/j.nicl.2022.103165
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Article ; Online: CUBN gene mutations may cause focal segmental glomerulosclerosis (FSGS) in children.

Yang, Jing / Xu, Yongli / Deng, Linxia / Zhou, Luowen / Qiu, Liru / Zhang, Yu / Zhou, Jianhua

BMC nephrology

2022 Volume 23, Issue 1, Page(s) 15

Abstract: Background: Imerslund-Gräsbeck Syndrome (IGS) is mainly caused by CUBN gene biallelic mutations. Proteinuria accompanies IGS specific symptoms in about half of the patients, isolated proteinuria is rarely reported. Here we present 3 patients with ... ...

Abstract	Background: Imerslund-Gräsbeck Syndrome (IGS) is mainly caused by CUBN gene biallelic mutations. Proteinuria accompanies IGS specific symptoms in about half of the patients, isolated proteinuria is rarely reported. Here we present 3 patients with isolated proteinuria and focal segmental glomerulosclerosis (FSGS) caused by CUBN gene biallelic pathogenic variants. Method: Whole exome sequencing was performed on three children with isolated proteinuria. CUBN gene biallelic pathogenic variants were found and then verified by sanger sequencing. Their clinical, pathological and molecular genetic characteristics were analyzed and correlated accordingly. Results: All three children presented with isolated proteinuria, no megaloblastic anemia. Their urine levels of β2 microglobulin were normal or slightly higher. Renal biopsies showed focal segmental glomerulosclerosis with mild glomerular mesangial hypercellularity, partial effacement of foot processes and podocyte microvillation. Two of them were found to carry compound heterozygous mutations and one homozygous mutation of CUBN gene. Totally four CUBN gene biallelic pathogenic variants were identified, including c.9287 T > C (p.L3096P), c.122 + 1G > A, c.7906C > T (p.R2636), c.10233G > A (p.W3411). Except for intron splice-site mutation, all other variants are located in highly conserved sites of CUB domain for binding to albumin. Conclusion: The results demonstrate that CUBN gene mutations may cause isolated proteinuria pathologically presented as FSGS. Our cases extend the spectrum of renal manifestation and genotype of CUBN gene mutations.
MeSH term(s)	Child ; Female ; Glomerulosclerosis, Focal Segmental/genetics ; Glomerulosclerosis, Focal Segmental/pathology ; Glomerulosclerosis, Focal Segmental/urine ; Heterozygote ; Homozygote ; Humans ; Male ; Mutation ; Proteinuria/genetics ; Receptors, Cell Surface/genetics ; Whole Genome Sequencing ; beta 2-Microglobulin/urine
Chemical Substances	Receptors, Cell Surface ; beta 2-Microglobulin ; intrinsic factor-cobalamin receptor
Language	English
Publishing date	2022-01-03
Publishing country	England
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-021-02654-x
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Article ; Online: Long noncoding RNA MEG3 inhibits oral squamous cell carcinoma progression via GATA3

Hu, Yan / Lv, Feifei / Li, Na / Yuan, Xuewei / Zhang, Liru / Zhao, Shuangling / Jin, Linyu / Qiu, Yongle

FEBS Open Bio. 2023 Jan., v. 13, no. 1, p. 195-208

2023 , Page(s) 195–208

Abstract: Oral squamous cell carcinoma (OSCC) accounts for about 90% of oral cancers. Expression of the long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has previously been reported to be downregulated in OSCC, and its overexpression can inhibit ... ...

Abstract	Oral squamous cell carcinoma (OSCC) accounts for about 90% of oral cancers. Expression of the long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has previously been reported to be downregulated in OSCC, and its overexpression can inhibit proliferation, migration, and invasion and promote apoptosis of OSCC cells. However, the mechanism underlying MEG3 downregulation in OSCC has not been well characterized. Here we report that low expression of MEG3 is caused by H3K27me3 modification of the MEG3 gene locus, and this is associated with the poor prognosis of OSCC. Overexpression of MEG3 inhibited the proliferation and invasion of OSCC cells. We observed that MEG3 was modified by m6A and bound to YTHDC1. Enhancer‐controlled genes positively regulated by MEG3 were functionally enriched for the ‘negative regulation of Wnt signaling pathway’ term, as determined using metascape. GATA3 was predicted to be a transcription factor for these genes, and was demonstrated to bind to MEG3. Knockdown of GATA3 countered the effects on proliferation, invasion, and increased transcription of HIC1 and PRICKLE1 induced by MEG3 overexpression. In conclusion, our data suggest that MEG3 is downregulated in OSCC due to trimethylation of H3K27 at the MEG3 gene locus. The inhibitory effect of MEG3 on proliferation and invasion of OSCC cells was dependent on the binding of GATA3.
Keywords	GATA transcription factors ; apoptosis ; genes ; loci ; non-coding RNA ; prognosis ; squamous cell carcinoma
Language	English
Dates of publication	2023-01
Size	p. 195-208
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	2651702-4
ISSN	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13532
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Article ; Online: Clinical, histological and molecular characteristics of Alport syndrome in Chinese children.

Zhou, Lanqi / Xi, Bijun / Xu, Yongli / Han, Yanxinli / Yang, Yuan / Yang, Jing / Wang, Yi / Qiu, Liru / Zhang, Yu / Zhou, Jianhua

Journal of nephrology

2023 Volume 36, Issue 5, Page(s) 1415–1423

Abstract: Background: Alport syndrome is caused by COL4A3, COL4A4, or COL4A5 gene mutations. The present study aims to compare the clinicopathological features, gene mutations, and outcome of Chinese children with different forms of Alport syndrome.: Methods: ... ...

Abstract	Background: Alport syndrome is caused by COL4A3, COL4A4, or COL4A5 gene mutations. The present study aims to compare the clinicopathological features, gene mutations, and outcome of Chinese children with different forms of Alport syndrome. Methods: One hundred twenty-eight children from 126 families diagnosed with Alport syndrome through pathological and genetic examination between 2003 and 2021 were included in this single-center retrospective study. The laboratory and clinicopathological features of the patients with different inheritance patterns were analyzed. The patients were followed-up for disease progression and phenotype-genotype correlation. Results: Of the 126 Alport syndrome families, X-linked forms accounted for 77.0%, autosomal recessive for 11.9%, autosomal dominant for 7.1%, and digenic for 4.0%. Among the patients, 59.4% were males and 40.6% were females. Altogether, 114 different mutations were identified in 101 patients from 99 families by whole-exome sequencing, of which 68 have not been previously reported. The most prevalent type of mutation was glycine substitution, which was identified in 52.1%, 36.7%, and 60% of the patients with X-linked Alport syndrome, autosomal recessive and autosomal dominant Alport syndrome, respectively. At the end of a median follow up of 3.3 (1.8-6.3) years, Kaplan-Meier curves showed kidney survival was significantly lower in autosomal recessive compared to X-linked Alport syndrome (P = 0.004). Pediatric patients with Alport syndrome seldom presented extrarenal involvement. Conclusions: X-linked Alport syndrome is the most frequent form found in this cohort. Progression was more rapid in autosmal recessive than in X-linked Alport syndrome.
MeSH term(s)	Humans ; Male ; Female ; Nephritis, Hereditary/diagnosis ; Nephritis, Hereditary/genetics ; Retrospective Studies ; East Asian People ; Collagen Type IV/genetics ; Pedigree ; Mutation ; Autoantigens/genetics
Chemical Substances	Collagen Type IV ; Autoantigens
Language	English
Publishing date	2023-04-25
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1093991-x
ISSN	1724-6059 ; 1120-3625 ; 1121-8428
ISSN (online)	1724-6059
ISSN	1120-3625 ; 1121-8428
DOI	10.1007/s40620-023-01570-7
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Zs.A 3369: Show issues

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Article ; Online: Screening and cellular validation of prognostic genes regulated by super enhancers in oral squamous cell carcinoma.

Zhang, Liru / Li, Huanju / Qiu, Yongle / Liu, Yuanhang / Liu, Xin / Wang, Wenjing

Bioengineered

2021 Volume 12, Issue 2, Page(s) 10073–10088

Abstract: Oral squamous cell carcinoma (OSCC) is the leading cause of death in patients with head and neck cancer. Reliable biomarkers to guide treatment decisions for OSCC remain scarce. The purpose of this study was to identify novel prognostic markers regulated ...

Abstract	Oral squamous cell carcinoma (OSCC) is the leading cause of death in patients with head and neck cancer. Reliable biomarkers to guide treatment decisions for OSCC remain scarce. The purpose of this study was to identify novel prognostic markers regulated by super enhancers in OSCC. Eight modules were obtained by weighted gene co-expression network analysis (WGCNA), among which MEblue module had the highest correlation with tumor stage, alcohol consumption and smoking. There were 41 genes regulated by super enhancers in MEblue module. Functional analysis showed that 41 super enhancer-regulated genes were involved in cancer progression. A total of twenty transcription factors of the 41 genes were predicted. Prognostic analysis of the 41 genes and the top 5 transcription factors showed that patients with high expression of AHCY, KCMF1, MANBAL and TFDP1 had a poor prognosis. Immunohistochemical analysis showed that AHCY, KCMF1 and MANBAL were highly expressed in OSCC tissue. Cellular experiment demonstrated that TFDP1 promoted AHCY, KCMF1 and MANBAL expression by binding to the super enhancers of these genes. Knockdown of TFDP1, AHCY, KCMF1 and MANBAL inhibited the proliferation of OSCC cells. In conclusion, AHCY, KCMF1 and MANBAL were recognized as super enhancer-regulated prognostic biomarkers regulated by TFDP1 in OSCC.
MeSH term(s)	Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; Cell Proliferation/genetics ; Early Detection of Cancer ; Enhancer Elements, Genetic/genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Gene Regulatory Networks ; Genes, Neoplasm ; Humans ; Mouth Neoplasms/genetics ; Mouth Neoplasms/pathology ; Prognosis ; Reproducibility of Results ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors
Language	English
Publishing date	2021-10-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2737830-5
ISSN	2165-5987 ; 2165-5979
ISSN (online)	2165-5987
ISSN	2165-5979
DOI	10.1080/21655979.2021.1997089
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Article ; Online: Reliability and validity of the East Asian children's version of mini-MACS in children with cerebral palsy.

Hou, Xiaohui / Qiu, Huiying / Liu, Liru / Li, Yinhua / He, Lu / Li, Jinling / Tang, Hongmei / Xu, Kaishou

Frontiers in rehabilitation sciences

2022 Volume 3, Page(s) 997221

Abstract: Background: Mini-Manual Ability Classification System (Mini-MACS) was developed for children with cerebral palsy aged 1-4 years, but its validity and reliability in different cultures are unavailable yet. This study was to determine the reliability and ... ...

Abstract	Background: Mini-Manual Ability Classification System (Mini-MACS) was developed for children with cerebral palsy aged 1-4 years, but its validity and reliability in different cultures are unavailable yet. This study was to determine the reliability and validity of Mini-MACS in East Asian children with cerebral palsy and investigate the correlation between Mini-MACS and Gross Motor Function Classification System. Methods: One hundred and four East Asian children with cerebral palsy aged 12-48 months were classiﬁed by one of their parents, an occupational therapist, and a physical therapist with Mini-MACS. The results were analyzed for inter-rater reliability by using intraclass correlation coefficient (ICC). The Nine-hole Peg Test was used for the criterion-related validity analysis, and parents retested their children after 2 weeks to evaluate test-retest reliability. Gross Motor Function Classification System levels were also collected to investigate the correlation with Mini-MACS. Results: Good inter-rater reliability among the occupational therapist, physical therapist, and parents was found [ICC = 0.984 (95% confidence interval, CI, 0.976-0.989), 0.973 (95% CI 0.960-0.982), and 0.966 (95% CI 0.950-0.977), respectively; Conclusion: The Mini-MACS demonstrates evidence that it is a valid and reliable tool to classify manual ability in East Asian children with cerebral palsy and is also positively related to the Gross Motor Function Classification System.
Language	English
Publishing date	2022-11-21
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-6861
ISSN (online)	2673-6861
DOI	10.3389/fresc.2022.997221
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Article ; Online: Long noncoding RNA MEG3 inhibits oral squamous cell carcinoma progression via GATA3.

Hu, Yan / Lv, Feifei / Li, Na / Yuan, Xuewei / Zhang, Liru / Zhao, Shuangling / Jin, Linyu / Qiu, Yongle

FEBS open bio

2022 Volume 13, Issue 1, Page(s) 195–208

Abstract	Oral squamous cell carcinoma (OSCC) accounts for about 90% of oral cancers. Expression of the long noncoding RNA (lncRNA) maternally expressed 3 (MEG3) has previously been reported to be downregulated in OSCC, and its overexpression can inhibit proliferation, migration, and invasion and promote apoptosis of OSCC cells. However, the mechanism underlying MEG3 downregulation in OSCC has not been well characterized. Here we report that low expression of MEG3 is caused by H3K27me3 modification of the MEG3 gene locus, and this is associated with the poor prognosis of OSCC. Overexpression of MEG3 inhibited the proliferation and invasion of OSCC cells. We observed that MEG3 was modified by m6A and bound to YTHDC1. Enhancer-controlled genes positively regulated by MEG3 were functionally enriched for the 'negative regulation of Wnt signaling pathway' term, as determined using metascape. GATA3 was predicted to be a transcription factor for these genes, and was demonstrated to bind to MEG3. Knockdown of GATA3 countered the effects on proliferation, invasion, and increased transcription of HIC1 and PRICKLE1 induced by MEG3 overexpression. In conclusion, our data suggest that MEG3 is downregulated in OSCC due to trimethylation of H3K27 at the MEG3 gene locus. The inhibitory effect of MEG3 on proliferation and invasion of OSCC cells was dependent on the binding of GATA3.
MeSH term(s)	Humans ; Carcinoma, Squamous Cell/metabolism ; Squamous Cell Carcinoma of Head and Neck/genetics ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Cell Proliferation/genetics ; Cell Line, Tumor ; Mouth Neoplasms/metabolism ; Head and Neck Neoplasms ; GATA3 Transcription Factor/genetics
Chemical Substances	RNA, Long Noncoding ; GATA3 protein, human ; GATA3 Transcription Factor
Language	English
Publishing date	2022-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2651702-4
ISSN	2211-5463 ; 2211-5463
ISSN (online)	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13532
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