[The association of high-sensitivity C-reactive protein with new-onset hypertension in different age groups].

Objective: To investigate the association between high sensitivity C-reactive protein (hsCRP) level and new-onset hypertension in different age groups. Methods: This was a prospective cohort study involving non-hypertensive population in Kailuan Group community who participated in health examination between 2006 and 2007.Follow-up was conducted every 2 years, and the time of new onset of hypertension was used as the endpoint of follow-up. The endtime of follow-up for patients without hypertension was the time of death or the last follow-up (December 31, 2017).According to the baseline hsCRP level, the participants were divided into low-risk group (hsCRP<1.0 mg/L), medium-risk group (hsCRP ≥1.0 and ≤3.0 mg/L), and high-risk group (hsCRP>3.0 mg/L), and further stratified by age. Kaplan-Meier method was used to calculate the cumulative incidence of hypertension in each group. Multivariate Cox regression model was used to analyze the association between hsCRP level and new-onset hypertension. Results: A total of 51 179 participants were included in this study, including 38 606 males (75.43%) with an average age of (48.1±12.2) years. The baseline hsCRP was 0.64 (0.25, 1.60) mg/L. The baseline hsCRP was 0.30 (0.16, 0.59), 1.57 (1.20, 2.10), 5.17 (3.80, 7.10) mg/L respectively in low-, medium- and high-risk groups. During the follow-up of (8.1±2.2) years, a total of 9 523 (18.60%) patients developed hypertension, and the cumulative incidence rates of low-, medium- and high-risk groups were 17.41%, 20.48% and 20.73%, respectively. The cumulative incidence of hypertension in low-, medium- and high-risk groups of<45, 45-54, 55-64, ≥65 years old were 13.53%, 15.82%, 16.76%; 19.27%, 22.84%, 21.62%; 21.55%, 24.19%, 24.88%;20.20%, 22.35%, 19.11%, respectively. Except for people aged ≥65 years, there were significant differences in the cumulative incidence of hypertension in low-, medium- and high-risk groups (all P<0.05).Multivariate Cox regression analysis showed that the risk of new-onset hypertension in the high risk group was 1.11 times higher than that in the low risk group (HR=1.11, 95%CI 1.05-1.18). The risk of new-onset hypertension in the high-risk group was 1.22 times (HR=1.22, 95%CI 1.08-1.38), 1.14 times (HR=1.14, 95%CI 1.04-1.26), 1.16 times (HR=1.16, 95%CI 1.04-1.30), and 1.02 times (HR=1.02, 95%CI 0.86-1.20) of the low-risk group, in the<45, 45-54, 55-64, and ≥65 years old groups, respectively. Conclusion: Higher hsCRP level is a risk factor for new-onset hypertension, and the risk of developing hypertension caused by elevated hsCRP is age-dependent.

C1q/tumor necrosis factor-related protein-3 acts as a target treating hepatic fibrosis.

OBJECTIVE: C1q/tumor necrosis factor-related protein-3 (CTRP3) is demonstrated as a crucial factor that participated in various fibrotic diseases. Activation of hepatic stellate cell in liver takes a critical effect on the pathogenesis of hepatic fibrosis. However, the role of CTRP3 in hepatic fibrosis remains elusive. Our present study aimed to explore the molecular mechanism of CTRP3 in fibroblast activation and the development of hepatic fibrosis. MATERIALS AND METHODS: We carried out overexpression (OE) of CTRP3 or knockout (KO) of CTRP3 in hepatic stellate cells (HSCs), respectively. Then, transforming growth factor-beta (TGF-ß) was used to stimulate HSCs activation. Adult male C57BL/6J mice were treated tetrachloromethane by intraperitoneal injection and mice injected saline were served as control. Recombinant CTRP3 (RC-CTRP3) was employed to treat CCl4-induced liver fibrosis. Then, the expression of fibrotic biomarkers, Notch signaling pathway-associated factors, liver histology and liver function were investigated in vivo, respectively. RESULTS: Our results showed that CTRP3 decreased in fibrotic liver and TGF-ß treated HSCs. In vitro, CTRP3 inhibited the activation of HSCs and impeded extracellular matrix (ECM) including collagen I and fibronectin via inhibiting Notch-1/Jagged-1 signaling pathway. In vivo, the indexes of fibrogenesis in liver fibrotic mice received RC-CTRP3 were mitigated via regulation of Notch-1/Jagged-1 signaling pathway. Moreover, liver histology and liver function were improved through the increase of CTRP3 level. CONCLUSIONS: The results proved that CTRP3 as a distinguished anti-fibrotic target inhibited HSCs activation by TGF-ß inducement and protected the liver tissue in the process of liver fibrosis.

[Rare thalassemia caused by novel nucleotide variants in the globin gene: four case reports and literature review].

Objective: To analyze the DNA sequences and clinical phenotypes of four cases with rare thalassemia to improve its recognition and accurate diagnosis. Methods: The DNA sequence characteristics of four cases with rare thalassemia diagnosed from May 2014 to December 2019 were retrospectively analyzed, and related literature was reviewed. Results: The results of the routine gene test for thalassemia indicated that the common three type of deletion and three point mutations in hemoglobin alpha 1/2 (HBA1/A2) , and 16 point mutations in hemoglobin beta (HBB) gene were unable to be detected in cases 1-3, and case 4 was--SEA. However, the results of HBA1/A2 and HBB whole-genome sequencing revealed that the four cases had a point mutation of HBB:c.347C>A, HBB:c.1A>G, HBB:c.393T>G, and HBA2: c.301-1G>A (IVS II-142 G>A) , respectively. Meanwhile, the father, aunt, and grandfather of case 2 carried the HBB:c.1 A>G heterozygous point mutation. Conclusion: The novel mutations in HBB and HBA2 genes, resulting in a rare thalassemia, were revealed. Among them, the HBB:c.347C>A, HBB:c.1A>G, and HBA2:c.301-1G>A (IVS II-142 G>A) mutations were first reported in Chinese patients with thalassemia. Contrarily, HBB:c.393T>G mutation has not yet been recorded in the databases of human hemoglobin variants and thalassemia. The discovery of these novel nucleotide variants in this study would enrich the DNA mutation gene database of thalassemia.

[Clinical characteristics of "classical" and "non-classical" paraneoplastic neurological syndrome].

Objective: To explore the clinical features of classical and non-classical paraneoplastic neurological syndrome (PNS). Methods: From 2015 to 2020, 48 cases of definite PNS admitted to the First Affiliated Hospital of University of Science and Technology of China were retrospectively collected, and classification, clinical characteristics, onconeural antibodies and primary tumors were analyzed. The included cases were divided into classical and non-classical groups according to Graus criteria, and the differences of clinical characteristics, onconeural antibodies, combined tumors, time of diagnosis and mortality were compared between the two groups. Results: Among the 48 confirmed patients, 21 (43.8%) were positive for well-characterized onconeural antibodies. There were 28 cases (58.3%) and 20 cases (41.7%) in classic and non-classical PNS groups, respectively. No significant differences of age, sex, clinical involvement site, characteristic positive antibody type, tumor diagnosis rate and follow-up mortality were found between the two groups (all P>0.05). The time of diagnosis in the non-classical PNS group was 3.0 (2.0, 6.5) months, which was significantly longer than that in the classical PNS group 1.0(0.6, 3.0) months (P<0.05). Meanwhile, the combination rate of non-characteristic antibodies in the classical PNS group (10 cases, 35.7%) was significantly higher than that in the non-classical PNS group (1 case, 5.0%) (P=0.016). During the follow-up, 39 patients (81.3%) with tumor were confirmed, and 29 patients (60.4%) were diagnosed with PNS before the tumor was found. Conclusions: The"non-classical"PNSs are common in clinical settings. Diagnosis may be delayed due to the nonclassical symptoms of the patients. When patients have clinical symptoms related to PNS, onconeural antibodies should be detected and the relevant tumors should also be screened. Patients have positive antibodies but with no tumors should be closely followed up for more than 5 years.

Research progress on flat epithelium of the inner ear.

Sensorineural hearing loss and vertigo, resulting from lesions in the sensory epithelium of the inner ear, have a high incidence worldwide. The sensory epithelium of the inner ear may exhibit extreme degeneration and is transformed to flat epithelium (FE) in humans and mice with profound sensorineural hearing loss and/or vertigo. Various factors, including ototoxic drugs, noise exposure, aging, and genetic defects, can induce FE. Both hair cells and supporting cells are severely damaged in FE, and the normal cytoarchitecture of the sensory epithelium is replaced by a monolayer of very thin, flat cells of irregular contour. The pathophysiologic mechanism of FE is unclear but involves robust cell division. The cellular origin of flat cells in FE is heterogeneous; they may be transformed from supporting cells that have lost some features of supporting cells (dedifferentiation) or may have migrated from the flanking region. The epithelial-mesenchymal transition may play an important role in this process. The treatment of FE is challenging given the severe degeneration and loss of both hair cells and supporting cells. Cochlear implant or vestibular prosthesis implantation, gene therapy, and stem cell therapy show promise for the treatment of FE, although many challenges remain to be overcome.

MiR-145-5p alleviates hypoxia/reoxygenation- induced cardiac microvascular endothelial cell injury in coronary heart disease by inhibiting Smad4 expression.

OBJECTIVE: To investigate the effects and mechanism of miR-145-5p on hypoxia/reoxygenation (H/R)-induced cardiac microvascular endothelial cell (CMEC) injury in coronary heart disease (CHD). PATIENTS AND METHODS: Patients with CHD (n=96) and healthy volunteers (n=96) were enrolled, and H/R injury model of CMECs was established. The expression of miR-145-5p and mothers against decapentaplegic homolog 4 (Smad4) mRNA in cells was quantified with reverse transcription polymerase chain reaction (RT-PCR). Then, miR-145-5p mimics and Smad4 inhibitor were transfected into CMECs. Cell counting kit-8 (CCK-8) was employed for proliferation detection, flow cytometry for apoptosis detection, and Western Blot for measuring the expression of apoptosis-related proteins and Smad4 protein. RESULTS: The expression of serum miR-145-5p in patients with CHD was significantly lower than that in healthy individuals. The area under the curve (AUC) of miR-145-5p in diagnosing CHD was 0.894, and the expression of miR-145-5p was negatively correlated with that of Smad4 (p<0.05). Over-expression of miR-145-5p promoted the proliferation, inhibited the apoptosis, and reduced inflammatory responses and oxidative stress in H/R-injured CMECs. Moreover, miR-145-5p might negatively regulate the expression of Smad4 in CMECs. Dual-Luciferase reporter assay determined the targeting relation between miR-145-5p and Smad4. CONCLUSIONS: MiR-145-5p is lowly expressed in patients with CHD, and its over-expression effectively alleviates H/R-induced CMEC injury by inhibiting Smad4.

[Consideration of surgeons participating in 2019 coronavirus disease emergency medical rescue].

As a newly epidemic, 2019 coronavirus disease (COVID-19) with a concentrated outbreak poses a great challenge to medical treatment. The severe and critical patients are complex complicatied with the psychological problems, and the medical staff are overworked and under tremendous psychological pressure. The surgeon participated in emergency medical rescue could provide professional treatment for the patients combined with surgical diseases, as well as specialized training for the non-surgeon crew, to reduce surgical-related mortality. With the advantages of good team consciousness, strong aseptic concept and good psychological quality, the surgeons can quickly adapt to and carry out rescue work under the premise of good self-protection. Surgeons need to develop critical care management concepts and focus on the critical care support equipment. Some suggestions are put forward for the standardized training of resident surgeons to cultivate compound talents. It is hoped that this article can lead to the thinking of how to participate in the emergency medical rescue of infectious diseases among surgeons and provide some enlightenment for future surgical education.

High diversity of Diaporthe species associated with pear shoot canker in China.

Species of Diaporthe (syn. Phomopsis) are important endophytes, saprobes and pathogens, infecting a wide range of plants and resulting in important crop diseases. However, the species occurring on pear remain largely unresolved. In this study, a total of 453 Diaporthe isolates were obtained from branches of Pyrus plants (including P. bretschneideri, P. communis, P. pyrifolia and P. ussuriensis collected from 12 provinces in China) showing shoot canker symptoms. Phylogenetic analyses based on five loci (ITS, TEF, CAL, HIS, and TUB) coupled with morphology of 113 representative isolates revealed that 19 Diaporthe species were isolated, representing 13 known species (including D. caryae, D. cercidis, D. citrichinensis, D. eres, D. fusicola, D. ganjae, D. hongkongensis, D. padina, D. pescicola, D. sojae, D. taoicola, D. unshiuensis and D. velutina) and six new species described here as D. acuta, D. chongqingensis, D. fulvicolor, D. parvae, D. spinosa and D. zaobaisu. Although Koch's postulates confirmed all species to be pathogenic, a high degree of variation in aggressiveness was observed. Moreover, these species have a high diversity, plasticity, and prevalence related to the geographical location and pear species involved.

Colletotrichum species associated with anthracnose of Pyrus spp. in China.

Colletotrichum species are plant pathogens, saprobes, and endophytes on a range of economically important hosts. However, the species occurring on pear remain largely unresolved. To determine the morphology, phylogeny and biology of Colletotrichum species associated with Pyrus plants, a total of 295 samples were collected from cultivated pear species (including P. pyrifolia, P. bretschneideri, and P. communis) from seven major pear-cultivation provinces in China. The pear leaves and fruits affected by anthracnose were sampled and subjected to fungus isolation, resulting in a total of 488 Colletotrichum isolates. Phylogenetic analyses based on six loci (ACT, TUB2, CAL, CHS-1, GAPDH, and ITS) coupled with morphology of 90 representative isolates revealed that they belong to 10 known Colletotrichum species, including C. aenigma, C. citricola, C. conoides, C. fioriniae, C. fructicola, C. gloeosporioides, C. karstii, C. plurivorum, C. siamense, C. wuxiense, and two novel species, described here as C. jinshuiense and C. pyrifoliae. Of these, C. fructicola was the most dominant, occurring on P. pyrifolia and P. bretschneideri in all surveyed provinces except in Shandong, where C. siamense was dominant. In contrast, only C. siamense and C. fioriniae were isolated from P. communis, with the former being dominant. In order to prove Koch's postulates, pathogenicity tests on pear leaves and fruits revealed a broad diversity in pathogenicity and aggressiveness among the species and isolates, of which C. citricola, C. jinshuiense, C. pyrifoliae, and C. conoides appeared to be organ-specific on either leaves or fruits. This study also represents the first reports of C. citricola, C. conoides, C. karstii, C. plurivorum, C. siamense, and C. wuxiense causing anthracnose on pear.

[The value of acoustic parameters in the voice therapy for patients with unilateral vocal cord paralysis].

Objective: To investigate the value of acoustic parameters in the voice therapy for patients with unilateral vocal cord paralysis (UVCP). Methods: From May 2015 to April 2018, 51 patients with UVCP and 59 healthy controls in Department of Otorhinolaryngology Head and Neck Surgery, Tianjin First Central Hospital, were involved in this research retrospectively. The UVCP patients were diagnosed with stroboscopic laryngoscopy. The minimum glottal area (MGA) was calculated by KIPS software when the people were pronouncing/i:/. The fundamental frequency (F0), Jitter, Shimmer and NHR were detected by CSL4500 multiple acoustic voice analyzer. Results: MGA of UVCP patients was much higher than that of healthy control (male: 433.68±64.52 vs. 294.41±51.82, t=9.23, P=0.000; female: 498.80±73.42 vs. 302.03±76.54, t=13.21, P=0.000), which meaned vocal cord insufficiency.After voice therapy, MGA reduced significantly (male: 288.48±55.09, female: 258.22±57.17, t=24.41 and 31.22, P=0.000 vs. pre-therapy). MGA of untreated patients decreased in varying degrees. Compared with the voice therapy group, the MGA decreased in a significantly lower extent (24.25±22.91 vs. 188.31±54.37, t=8.97, P=0.000). The F0, Jitter, Shimmer and NHR raised significantly in UVCP patients group (P=0.000 vs. healthy control group), and they were reduced by voice therapy (all P<0.05). Each of the four acoustic parameters was relative with MGA, r=0.551, 0.867, 0.853 and 0.875 in turn, P=0.001, 0.000, 0.000, and 0.000. Conclusion: MGA and acoustic parameters can reflect the acoustic features of UVCP patients, which are useful tools in the UVCP assessment and voice therapy.

LINC01096 knockdown inhibits progression of triple-negative breast cancer by increasing miR-3130-3p.

OBJECTIVE: Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer. Long noncoding RNAs (lncRNAs) have been reported to be involved in the development of TNBC. However, the role and mechanism of LINC01096 in TNBC are largely unclear. This work aims to investigate the effect of LINC01096 on cell viability, apoptosis, migration, and invasion of TNBC cells, as well as explore the interaction between LINC01096 and microRNA (miR)-3130-3p. PATIENTS AND METHODS: Sixty TNBC patients were recruited. T47-D and BT-549 cells were cultured for experiments in vitro. The expression levels of LINC01096 and miR-3130-3p were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability, apoptosis, migration, and invasion were determined by MTT, flow cytometry, and trans-well assays. The target association between LINC01096 and miR-3130-3p was confirmed by the luciferase reporter assay. RESULTS: The expression of LINC01096 was enhanced in TNBC tissues and cells. High expression of LINC01096 predicted poor outcomes of patients with TNBC. Silence of LINC01096 led to the suppression of cell viability, migration, and invasion, as well as the promotion of apoptosis in TNBC cells. MiR-3130-3p was targeted by LINC01096 and lowly expressed in TNBC. Overexpression of miR-3130-3p repressed cell viability, migration, and invasion, while it induced apoptosis. However, the knockdown of miR-3130-3p induced the opposite effect. This was weakened by inhibiting LINC01096. CONCLUSIONS: Knockdown of LINC01096 inhibited cell viability, migration, and invasion; however, it promoted apoptosis in TNBC by up-regulating miR-3130-3p, indicating a novel target for the treatment of TNBC.

[Epidemiological survey of mental disorders in the rural left behind elderly aged 60 years and older in Gansu].

Objective: To investigate the prevalence, demographic characteristics and social life function of mental disorders in the rural left behind elderly aged 60 years and older in Gansu. Methods: Between November 2017 and June 2018, a multi-stage stratified cluster sampling method was used to randomly select the rural left behind elderly aged 60 years and older in Gansu, and totally 6 000 elderly were enrolled. By using the extended general health questionnaire (GHQ-12) and the American Handbook for Diagnosis and Statistics of Mental Disorders (DSM-Ⅳ) Axis Ⅰ Disorders Formal Clinical Examination Patient Edition, all the included subjects were screened and diagnosed. Functional status was assessed by the Global Assessment Function scale (GAF). Statistical analysis of the prevalence of various mental illnesses, as well as the differences in the prevalence of different gender, marital status and age groups was performed. Results: Totally, 6 000 subjects completed the survey. The adjusted current prevalence of any mental disorder was 20.11% (95%CI 17.70%-22.85%). The six most prevalent specific disorders were major depressive disorder (9.20%), pain disorder (2.71%), mood disorder due to the body condition (2.08%), generalized anxiety disorder (1.99%), anxiety disorder not otherwise specified (1.15%) and dysthymic disorder (0.84%). The lifetime prevalence of mental disorders was 20.54% (95%CI 18.40%-23.39%). The overall current prevalence of mental disorders was higher in women (242.89‰) than in men (119.55‰), and the unmarried (248.37‰) was higher than those married (187.53‰). There was no significant difference in the prevalence of mental disorders among different age groups (P>0.05). The GAF score of mental disorders was 56±11, and 71.82% was moderate to severe functional impairment. Conclusions: The prevalence of mental disorders is high in rural left-behind population aged 60 years and over in Gansu Province. Major depression is a condition that deserves special attention.

[Nephrogenic clear cell carcinoma of nasal cavity：a case report].

SummaryRenal clear cell carcinoma（RCCC） is the most common type of renal cell carcinoma, but metastasis to the nasal cavity is extremely rare. A case of RCCC to the nasal cavity and paranasal sinuses was reported. The early clinical manifestations of this case were intermittent epistaxis and subsequent massive epistaxis. Imaging examination revealed that there were masses in the nasal cavity and paranasal sinus, accompanied by bleeding and destruction of the skull base. Renal CT examination showed a tumor in the right kidney, and considered the patient suffering from renal cell carcinoma. The patient underwent a nasal side incision to remove the tumor, the patient's pathological return; nasal nephrogenic clear-cell carcinoma.

AADS: Augmented autonomous driving simulation using data-driven algorithms.

Simulation systems have become essential to the development and validation of autonomous driving (AD) technologies. The prevailing state-of-the-art approach for simulation uses game engines or high-fidelity computer graphics (CG) models to create driving scenarios. However, creating CG models and vehicle movements (the assets for simulation) remain manual tasks that can be costly and time consuming. In addition, CG images still lack the richness and authenticity of real-world images, and using CG images for training leads to degraded performance. Here, we present our augmented autonomous driving simulation (AADS). Our formulation augmented real-world pictures with a simulated traffic flow to create photorealistic simulation images and renderings. More specifically, we used LiDAR and cameras to scan street scenes. From the acquired trajectory data, we generated plausible traffic flows for cars and pedestrians and composed them into the background. The composite images could be resynthesized with different viewpoints and sensor models (camera or LiDAR). The resulting images are photorealistic, fully annotated, and ready for training and testing of AD systems from perception to planning. We explain our system design and validate our algorithms with a number of AD tasks from detection to segmentation and predictions. Compared with traditional approaches, our method offers scalability and realism. Scalability is particularly important for AD simulations, and we believe that real-world complexity and diversity cannot be realistically captured in a virtual environment. Our augmented approach combines the flexibility of a virtual environment (e.g., vehicle movements) with the richness of the real world to allow effective simulation.

Increasing miR-150 and lowering HMGA2 inhibit proliferation and cycle progression of colon cancer in SW480 cells.

OBJECTIVE: High mobility group protein A2 (HMGA2) is a kind of oncogene that regulates cell proliferation and cycle. HMGA2 up-regulation is related to the occurrence of multiple tumors including colorectal cancer. MiR-150 is found down-regulated in colorectal cancer tissue. Bioinformatics analysis shows the complementary targeted relationship between miR-150 and the 3'-UTR of HMGA2. This study explores the role of microRNA-150 (miR-150) in regulating HMGA2 expression, colorectal cancer cell proliferation, and cycle. PATIENTS AND METHODS: Colorectal cancer patients were enrolled to collect cancer and para-carcinoma tissues. MiR-150 and HMGA2 expressions were tested in tissue. MiR-150, HMGA2, and Cyclin A levels in colorectal cancer cell line SW480, and normal colorectal epithelial cell line FHC were compared. The targeted relationship between miR-150 and the 3'-UTR of HMGA2 was evaluated by dual luciferase reporter gene assay. SW480 cells were divided into five groups, including miR-control, miR-150 mimic, small interfere normal control (si-NC), si-HMGA2, and miR-150 mimic + si-HMGA2. Cell cycle was determined by using flow cytometry. The cell proliferation was detected by using the cell counting kit 8 (CCK-8) test. RESULTS: HMGA2 expression was significantly increased, while miR-150 levels were significantly declined in colorectal cancer tissue compared with that in para-carcinoma tissue (p<0.05). HMGA2 and Cyclin A levels were higher significantly, whereas miR-150 expression was lower significantly in SW480 cells compared to that in FHC cells (p<0.05). MiR-150 targeted band to the 3'-UTR of HMGA. MiR-150 mimic and/or si-HMGA2 significantly reduced HMGA2 and Cyclin A expressions, blocked cell cycle in the G0/G1 phase, and attenuated cell proliferation. CONCLUSIONS: We observed that miR-150 down-regulated Cyclin A expression to block colorectal cancer cell cycle and inhibit proliferation through targeted inhibiting HMGA2.

[Clinicopatholigic features of renal cell carcinoma associated with chromosome X inversion harboring gene fusions involving TFE3].

Objective: To study the clinicopathologic features, immunophenotype, characteristic FISH pattern and prognosis of renal cell carcinoma (RCC) associated with chromosome X inversion harboring gene fusions involving TFE3. Methods: Ten cases of NONO-TFE3 RCC and four cases of RBM10-TFE3 RCC were investigated at Nanjing Jinling Hospital from 2009 to 2016 by clinicopathological findings, immunohistochemistry, and genetic analysis. Results: Morphologically, the distinct pattern of secretory endometrioid subnuclear vacuolization was overlapped with clear cell papillary RCC, and often accompanied by sheets of epithelial cells in NONO-TFE3 RCC. Most cases of RBM10-TFE3 RCC presented with the biphasic feature that acinar, tubular and papillary patterns of epithelioid cells combined with sheets of small cells with "pseudorosette-like" architectures. In addition, cytoplasmic vacuolization, nuclear groove, and psammoma bodies were also observed. Immunohistochemically, all NONO-TFE3 RCC cases were immunoreactive for TFE3, CD10, RCC markers, and PAX8, and negative for CK7, Cathepsin K, Melan A, HMB45, Ksp-cadherin, vimentin, and CD117. All 4 cases of RBM10-TFE3 RCC showed moderate to strong immunoreactivity for TFE3, Cathepsin K, CD10, Ksp-cadherin, E-cadherin, P504s, RCC marker, PAX8, and vimentin but negative for TFEB, HMB45 and CK7. CKpan and Melan A were at least focally expressed. The antibody to Ki-67 showed labeling of 3%-8% (mean 5%). There were some expression discrepancies of immunochemistry between different histological patterns. PAX8, CKpan, P504s, and Ksp-cadherin were expressed in epithelioid areas but not in small-cell areas. Ki-67 labeling index of epithelioid areas was higher than that in small-cell areas. In molecular analysis, NONO-TFE3 fusion transcripts were identified in 6 patients. The fusion points were between exon 7 of NONO and exon 6 of TFE3 in 5 patients and between exon 9 of NONO and exon 5 of TFE3 in one patient. All 4 cases of RBM10-TFE3 RCC demonstrated to have RBM10-TFE3 fusion transcripts and the fusion points were between exon 5 of TFE3 and exon 17 of RBM10. Using TFE3 break-apart FISH assay, all 10 cases of NONO-TFE3 RCC showed characteristic patterns of equivocal split signals with a distance of nearly 2 signal diameters. All 4 cases of RBM10-TFE3 RCC showed colocalized or subtle split signals with a distance of <1 signal diameter, which was considered as negative results. Long-term follow-up was available for 7 patients of NONO-TFE3 RCC and 4 patients of RBM10-TFE3 RCC. All patients were alive with no evidence of disease. Conclusions: Two rare genotypes, NONO-TFE3 RCC and RBM10-TFE3 RCC, are reported in this study. Both of these two tumors show specific morphology and good prognosis, along with the positive TFE3 staining and the equivocal or false-negative TFE3 FISH results, which could be missed. PCR detection or next-generation sequencing can determine the genotype.