125I Radioactive Particles Drive Protective Autophagy in Hepatocellular Carcinoma by Upregulating ATG9B.

Background and Aims: 125I radioactive particles implantation have demonstrated efficacy in eradicating hepatocellular carcinoma (HCC). However, progressive resistance of HCC to 125I radioactive particles has limited its wide clinical application. Methods: We investigated the cellular responses to 125I radioactive particles treatment and autophagy-related 9B (ATG9B) silencing in HCC cell lines and Hep3B xenografted tumor model using Cell Counting Kit-8 reagent, western blotting, immunofluorescence, flow cytometry, transmission electron microscopy and immunohistochemistry. Results: In this study, we demonstrated that 125I radioactive particles induced cell apoptosis and protective autophagy of HCC in vitro and in vivo. Inhibition of autophagy enhanced the radiosensitivity of HCC to 125I radioactive particles. Moreover, 125I radioactive particles induced autophagy by upregulating ATG9B, with increased expression level of LC3B and decreased expression level of p62. Furthermore, ATG9B silencing downregulated LC3B expression and upregulated p62 expression and enhanced radiosensitivity of HCC to 125I radioactive particles in vitro and in vivo. Conclusions: Inhibition of ATG9B enhanced the antitumor effects of 125I particle radiation against HCC in vitro and in vivo. Our findings suggest that 125I particle radiation plus chloroquine or/and the ATG9B inhibitor may be a novel therapeutic strategy for HCC.

Mutation screening of eight genes and comparison of the clinical data in a Chinese cohort with congenital hypothyroidism.

BACKGROUND: Congenital hypothyroidism (CH) is a common neonatal endocrine disorder, characterized by irreversible intellectual disability and short stature if left untreated. It can be divided into thyroid dysgenesis (TD), including athyreosis, ectopy and hypoplasia, and dyshormonogenesis (DH), also referring to gland in situ (GIS), in which patients have eutopic thyroids with normal size or goiter. This study aims to analyze the clinical and genetic data of 375 Chinese CH patients without DUOX2 and thyroid transcription factor (TTF) variants, and to explore the mutation frequencies of the eight genes and the inheritance pattern of CH. METHODS: Targeted next generation sequencing (NGS) and statistical analysis were performed for mutation screening on eight CH-related genes and the comparison of clinical data in a cohort of 606 Chinese CH patients from Henan Province. RESULTS: A total of 104 variants were detected in genes required for thyroid formation (TSHR, GLIS3, BOREALIN, NTN1, JAG1 and TUBB1) and thyroid hormone synthesis (TG and TPO) in 83 subjects. Monogenic variants were the most prevalent with a percentage of 75.00% (78/104) followed by oligogenic variants (25.00%, 26/104). No differences were found in various clinical data between patients with and without variants. However, it should be noted that only initial L-T4 dose was statistically different between patients with monogenic variants and oligogenic variants. CONCLUSIONS: Our results suggested that apart from Mendelian monogenic inheritance, oligogenic inheritance of CH could not be excluded and also involves other factors, such as penetrance, epigenetic mechanisms and environmental factors.

Two Chinese siblings of combined oxidative phosphorylation deficiency 14 caused by compound heterozygous variants in FARS2.

BACKGROUND: As a rare mitochondrial disease, combined oxidative phosphorylation deficiency 14 (COXPD14) is caused by biallelic variants in the phenylalanyl-tRNA synthetase 2, mitochondrial gene (FARS2) with clinical features of developmental delay, an elevated lactate level, early-onset encephalopathy, liver failure, and hypotonia. The objectives of this study were to analyze the clinical and molecular features of two Chinese siblings affected with COXPD14, and to review relevant literature. METHODS: Mutation screening was performed by whole exome sequencing (WES) in combination with Sanger sequencing validation to identify the disease-causing variants of the two patients. RESULTS: The two siblings presented with severe clinical features and both progressed aggressively and failed to survive after treatment abandonment. We identified two compound heterozygous FARS2 variants c.925G>A p.Gly309Ser and c.943G>C p.Gly315Arg in this proband, which were inherited from the unaffected father and mother, respectively. In addition, Sanger sequencing confirmed that the elder affected sister carried the same compound heterozygous variants. The c.925G>A p.Gly309Ser variant is known and commonly reported in COXPD14 patients, while c.943G>C p.Gly315Arg is a novel one. Neither of the variants was found in 100 Chinese healthy controls. Both variants were classified as "deleterious" and were located in the highly conserved regions of the protein. The above results suggested that the two variants were likely causative in this COXPD14-affected pedigree. CONCLUSIONS: Our study expands the mutation spectrum of FARS2 and highlights the importance of genetic testing in the diagnosis of diseases with a wide variety of phenotypes, especially in the differential diagnosis of diseases.

Measurement of the Correlation Degree between Rural Family Fertility Willingness and the Development of China's Labor Original Equipment Manufacturing Industry.

At present, China is facing problems such as the decline of fertility rate, gender imbalance, serious aging, and the reduction of youth and working population, which will have an adverse impact on the long-term development of social economy. Based on the literature review, combined with China's financial family data, combined with the innovative calculation model of the correlation between rural family fertility willingness and labor original equipment manufacturing (OEM) industrial development, through the empirical analysis of rural families, this paper investigates the relationship between fertility willingness and the development and endogeneity of labor OEM industry and finds that female labor participation has a significant negative impact on the number of children in rural families. Spouse labor participation has a negative effect on the number of children in rural families. The regression coefficient of women's willingness to have two children for career development is significant and negative (c 1=-0.181, P=-0.003 < 0.01), and that of women's family status is significant and negative (c 1=-0.998, P=0.031 < 0.01). The relative opportunity cost of birth of individual operators is more concentrated in the range of 50%-80%. The results show that the development of labor OEM industry is significantly influenced by the fertility willingness of rural families. This paper concludes that differentiated policies and measures should be taken according to the type of industrial promotion.

The first Chinese case of Vici syndrome with novel compound heterozygous sequence variants in EPG5.

BACKGROUND: Vici syndrome (VICIS) refers to a clinical spectrum of multiple organ systems characterized by corpus callosum agenesis, hypopigmentation, cataracts, cardiomyopathy and immunodeficiency. The aims of this study were to describe detailed clinical and molecular features of two Chinese female siblings and to review several previous findings. METHODS: Targeted sequencing panel involving all known disease-causing genes of monogenic disorders combined with Sanger sequencing validation were performed to identify the likely pathogenic sequence variants of the proband with VICIS. RESULTS: The proband diagnosed as VICIS presented with neonatal pneumonia, myocardial damage, hypotonia, maxillofacial malformations, hearing impairment, failure to thrive and died 40 days after birth. Two novel missense variants in ectopic P-granules autophagy protein 5 homologue (EPG5, NM_020964.3) were identified in this proband. The two likely pathogenic variants c.1609G > A (p.(E537K)) and c.5764C>G (p.(P1922A)) were assessed as damaging by bioinformatic analysis. As these variants were absent in 150 unrelated Chinese normal controls and inherited from asymptomatic parents in the co-segregation analysis, the compound heterozygous EPG5 variants were responsible for the clinical features of this patient. Finally, she was genetically diagnosed with VICIS. CONCLUSIONS: To our knowledge, this is the first Chinese case of VICIS. Our report identified novel compound heterozygous EPG5 sequence variants in the proband with VICIS, highlighting the rarity and high mortality rate of VICIS and emphasizing on the importance of high-throughput sequencing in confirmed diagnosis of monogenic diseases, which could further facilitate the development of genetic counselling and prenatal diagnosis.

A Novel Homozygous VPS13B Splice-Site Mutation Causing the Skipping of Exon 38 in a Chinese Family With Cohen Syndrome.

Background: Cohen syndrome (CS) is a clinically heterogeneous disorder characterized by extensive phenotypic variation with autosomal recessive inheritance. VPS13B was identified to be the disease-causing gene for CS. The objectives of the present study were to screen likely pathogenic mutations of the patient with developmental delay and mental retardation, and to determinate the effect of this splice-site mutation by reverse transcription analysis. Methods: Whole exome sequencing (WES) in combination with Sanger sequencing were performed to identify the causative mutations of this CS family. Subsequently, the impact of the intronic variant on splicing was analyzed by reverse transcription and the construction of expression vector. Results: A novel homozygous splice-site mutation (c.6940+1G>T) in the VPS13B gene was identified in this proband. Sanger sequencing analysis of the cDNA demonstrated that the c.6940+1G>T variant could cause the skipping of entire exon 38, resulting in the loss of 208 nucleotides and further give rise to the generation of a premature in-frame stop codon at code 2,247. Conclusions: The homozygous VPS13B splicing variant c.6940+1G>T was co-segregated with the CS phenotypes in this family and was identified to be the cause of CS after comprehensive consideration of the clinical manifestations, genetic analysis and cDNA sequencing result.

Molecular and clinical characteristics of congenital hypothyroidism in a large cohort study based on comprehensive thyroid transcription factor mutation screening in Henan.

BACKGROUND: Congenital hypothyroidism (CH), the most common neonatal endocrine disorder worldwide, can be caused by variants in thyroid transcription factor (TTF) genes including NKX2-1, FOXE1, PAX8, NKX2-5 and HHEX. This study aims to perform targeted next-generation sequencing (NGS) panel for comprehensive mutation screening on these genes in a cohort of 606 CH patients with various types from Henan Province, China, to investigate the mutation rate of TTF genes, and to analyze the clinical, biochemical and molecular characteristics of our CH cohort. METHODS: High-throughput sequencing combined with statistical calculation were applied for mutation screening and analyses of the clinical data. RESULTS: Twenty-two likely disease-causing monoallelic mutations in the TTF genes were identified in our cohort (3.63%, 22/606). Mutated PAX8 was the most predominant genetic alteration among these TTF mutations. Interestingly, PAX8 defects were only found in TD cases and variants in the five TTF genes were detected in gland in situ (GIS) patients. CH patients with the same genotype may have significant phenotypic variability and permanent CH (PCH) patients in the GIS group were significantly fewer than those in the TD group. CONCLUSIONS: Our study showed the estimated TTF mutation rate among CH cases was 3.63% in Henan Province and genetic alternations in TTF genes played a role not only in TD but also in GIS, especially in goiter. Although we speculated that the five TTF genes may be involved in certain steps of thyroid hormone biosynthesis, more researches are needed to verify the conclusions of the present study.

Identification and analyzes of DUOX2 mutations in two familial congenital hypothyroidism cases.

BACKGROUND: Mutations in DUOX2 are the frequent cause of congenital hypothyroidism (CH), a common neonatal metabolic disorder characterized by great phenotypic variability. CH can be traditionally subclassified into two subtypes: thyroid dysgenesis (TD) and thyroid dyshormonogenesis. The objectives of this study were to analyze the genetic data of two familial CH cases, to elucidate the pathogenesis from the perspective of genetics and to review and summarize the previous findings. METHODS: Targeted regions sequencing (TRS) technology covering all exons and intron-exon boundaries of 35 known and potential CH-related candidate target genes in combination with Sanger sequencing were performed to identify the likely pathogenic mutations of the six patients with familial CH. RESULTS: In family 1, two DUOX2 missense mutations, namely, c.1060C>T/p.R354W in exon 10 and c.3200C>T/p.S1067L in exon 25, were found. Patient 1 (P1), P2 and P3 were transient CH (TCH) patients with eutopic thyroid glands of normal size and function. In family 2, only the mutation c.3200C>T/p.S1067L was identified. P4, P5, and P6 were diagnosed with permanent CH (PCH), which requires lifelong levothyroxine (L-T4) treatment. Furthermore, both P4 and P5 harbored properly located thyroid glands, whereas P6 had a mildly reduced gland. P1, P3, P6, and other family members carrying monoallelic or biallelic DUOX2 mutations showed no obvious abnormal clinical symptoms or signs, while P2, P4, and P5 showed umbilical hernias. CONCLUSIONS: The present study suggests that the phenotypic features resulting from DUOX2 mutations vary greatly. The p.R354W and p.S1067L alterations or the combination of the two alterations in DUOX2 are probably only predisposing to CH and DUOX2 may be involved in the morphogenesis of the human thyroid gland. Simultaneously, the compensation of DUOX1 for the loss of DUOX2, undetectable pathogenic mutations, the effects of environmental factors, epigenetic mechanisms and the involvement of multiple genes cannot be excluded in the explanation of these genetic results.

Compound heterozygous DYSF variants causing limb-girdle muscular dystrophy type 2B in a Chinese family.

BACKGROUND: The dysferlin gene or the DYSF gene encodes the Ca2+ -dependent phospholipid-binding protein dysferlin, which belongs to the ferlin family and is associated with muscle membrane regeneration and repair. Variants in the DYSF gene are responsible for limb-girdle muscular dystrophy type 2B (LGMD2B), also called limb-girdle muscular dystrophy recessive 2 (LGMDR2), a rare subtype of muscular dystrophy involving progressive muscle weakness and atrophy. The present study aimed to identify the variants responsible for the clinical symptoms of a Chinese patient with limb girdle muscular dystrophies (LGMDs) and to explore the genotype-phenotype associations of LGMD2B. METHODS: A series of clinical examinations, including blood tests, magnetic resonance imaging scans for the lower legs, electromyography and muscle biopsy, was performed on the proband diagnosed with muscular dystrophies. Whole exome sequencing was conducted to detect the causative variants, followed by Sanger sequencing to validate these variants. RESULTS: We identified two compound heterozygous variants in the DYSF gene, c.1058 T>C, p.(Leu353Pro) in exon 12 and c.1461C>A/p.Cys487* in exon 16 in this proband, which were inherited from the father and mother, respectively. In silico analysis for these variants revealed deleterious results by PolyPhen-2 (Polymorphism Phenotyping v2; http://genetics.bwh.harvard.edu/pph2), SIFT (Sorting Intolerant From Tolerant; https://sift.bii.a-star.edu.sg), PROVEAN (Protein Variation Effect Analyzer; http://provean.jcvi.org/seq_submit.php) and MutationTaster (http://www.mutationtaster.org). In addition, the two compound heterozygous variants in the proband were absent in 100 control individuals who had an identical ethnic origin and were from the same region, suggesting that these variants may be the pathogenic variants responsible for the LGMD2B phenotypes for this proband. CONCLUSIONS: The present study broadens our understanding of the mutational spectrum of the DYSF gene, which provides a deep insight into the pathogenesis of LGMDs and accelerates the development of a prenatal diagnosis.

A Novel CD40L Mutation Associated with X-Linked Hyper IgM Syndrome in a Chinese Family.

Background: Mutations in CD40 ligand gene (CD40L) affecting immunoglobulin class-switch recombination and somatic hypermutation can result in X-Linked Hyper IgM Syndrome (HIGM1, XHIGM), a kind of rare serious primary immunodeficiency disease (PID) characterized by the deficiency of IgG, IgA and IgE and normal or increased serum concentrations of IgM. The objective of this study is to explain genotype-phenotype correlation and highlight the mutation responsible for a Chinese male patient with XHIGM.Methods: Whole exome sequencing (WES) and Sanger sequencing validation were performed to identify and validate the likely pathogenic mutation in the XHIGM family.Results: The results of the sequencing revealed that a new causative mutation in CD40L (c.714delT in exon 5, p.F238Lfs*4) which leads to the change in amino acids (translation terminates at the third position after the frameshift mutation) appeared in the proband. As his mother in the family was carrier with this heterozygous mutation, the hemizygous mutation in this patient came from his mother indicating that genetic mode of XHIGM is X-linked recessive inheritance.Conclusion: This study broadens our knowledge of the mutation in CD40L and lays a solid foundation for prenatal diagnosis and genetic counseling for the XHIGM family.

Targeted regions sequencing identified four novel PNPLA1 mutations in two Chinese families with autosomal recessive congenital ichthyosis.

BACKGROUND: Autosomal recessive congenital ichthyosis (ARCI) is a rare genetically heterogeneous cutaneous disease predominantly characterized by erythroderma, generalized abnormal scaling of the whole body and a collodion membrane at birth. Numerous causative genes have been demonstrated to be responsible for ARCI including PNPLA1 which can cause ARCI type 10. The objectives of this study are to describe clinical features of three ARCI patients from two Chinese unrelated families and to identify the underlying causative mutations. METHODS: Genomic DNA was extracted from peripheral venous blood obtained from the two Chinese ARCI families in Shandong province. Subsequently, targeted regions sequencing (TRS) followed by Sanger sequencing was conducted to identify and validate the likely pathogenic mutations of the ARCI families. RESULTS: Genetic analyses revealed four novel PNPLA1 variants that are predicted to be probably to lead to ARCI in three patients of two families. Patient 1 in one family was in compound heterozygous status for c.604delC/p.Arg202Glyfs*27 and c.820dupC/p.Arg274Profs*15, whereas c.738_742delinsCCCACAGATCCTGC/ p.Gly247_Tyr248delinsProGlnIleLeuHis, and c.816dupC/p.Arg274Profs*15 were found in patient 2 and 3 of the other family. In addition, these variants cosegregate in the two pedigrees and are all within highly conserved regions of the PNPLA1 protein, which indicate that the four mutations are likely pathogenic. CONCLUSION: Our findings not only broaden the mutational spectrum of PNPLA1, but also contribute to establishing genotype-phenotype correlations for different forms of ARCI.

A novel ATRX mutation causes Smith­Fineman­Myers syndrome in a Chinese family.

Smith­Fineman­Myers syndrome (SFMS) is a rare inherited disorder characterized mainly by mental retardation and anomalies in the appearance of patients. SFMS is caused by a mutation in the α­thalassemia/mental retardation syndrome X­linked (ATRX) gene and has an X­linked recessive pattern. In the present study, a novel ATRX mutation was identified, and the association between its genotype and the phenotype was explored in a Chinese Han family with SFMS. This study aimed to lay a foundation for prenatal diagnosis for this family. Briefly, genomic DNA was extracted from peripheral blood samples obtained from the family. High­throughput genetic sequencing was employed to detect the whole exome; subsequently, Sanger sequencing was performed to verify the candidate mutations. Clinical analysis of the proband was also accomplished. Consequently, a novel missense ATRX mutation was identified comprising a single nucleotide change of C to T, which caused an amino acid substitution at codon 172 in exon 7 (c.515C>T; p.Thr172Ile) of the proband. This mutation was found to co­segregate in the present SFMS pedigree and was located in a highly conserved region of the ATRX protein, thus suggesting that it may be a pathogenic mutation. Taken together, these findings provided novel information that may lead towards an improved understanding of the genetic and clinical features of patients with SFMS, thereby facilitating a more accurate prenatal diagnosis of SFMS.

Clinical efficacy of computed tomography-guided iodine-125 seed implantation therapy for patients with metastatic epidural spinal cord compression: A retrospective study.

BACKGROUND: This study evaluated the clinical efficacy of computed tomography (CT)-guided radioactive iodine-125 (125 I) seed implantation in patients with metastatic epidural spinal cord compression (MESCC). MATERIALS AND METHODS: A cohort of 22 patients with MESCC were retrospectively enrolled. All patients underwent CT-guided 125 I seed implantation therapy via standard procedures. Clinical indexes, including the University of Texas MD Anderson Cancer Center (MDA) criteria for tumor responses, numerical rating scale (NRS) for the degree of pain, Karnofsky Performance Status (KPS) for quality of life, American Spinal Injury Association (ASIA) impairment scale, grade of ESCC, and radiation dose, were evaluated and recorded pre- and post-operation. A follow-up evaluation was performed at least 3 months after the operation. Finally, pre- and post-operative differences in these clinical indexes were compared. Overall survival was recorded. RESULTS: Operations were successfully performed on all patients. A median of 48 (range, 7-103) seeds were implanted in lesions, and the postoperative target verified dose D90 was 11,072.4 ± 1773.5 cGy. Patients were followed for a median of 6 months (range, 3-38 months). The median survival time was 10 months; the response rate was 18/22 (82%); the local control rates at 3, 6, and 12 months were 91.3%, 81.9%, and 81.9%, respectively; and the survival rates were 80%, 50.0%, and 21.9% at 6, 12, and 18 months, respectively. The ESCC grade was significantly lower (P < 0.05). Based on the ASIA impairment scale, the nerve functional reservation, recovery, and decline rates were 63.7% (14/22), 27.3% (6/22), and 9% (2/22), respectively. The NRS and KPS were both significantly improved in the 3rd month of follow-up (P < 0.05). CONCLUSION: CT-guided 125 I seed implantation represents an effective and safe palliative care for patients with MESCC, which can effectively relieve pain and spinal cord compression and improve nerve function and quality of life.

Whole exome sequencing reveals two novel compound heterozygous mutations in TWNK as a cause of the hepatocerebral form of mitochondrial DNA depletion syndrome: a case report.

BACKGROUND: Although Mitochondrial DNA depletion syndrome (MDS) can be classified into three forms: myopathic, encephalomyopathic and hepatocerebral form, it is difficult to identify its form due to its clinical heterogeneity. Therefore, it is very important to conduct molecular genetic analysis on suspected patients. This study presented a male 38 weeks and 5 days infant with liver cytolysis and leukodystrophy. CASE PRESENTATION: A male infant proband was admitted to the department of NICU for feeding intolerance, irregular rhythm of respiration, hypoglycemia, lactic acidosis, liver cytolysis and neurological abnormalities. He was onset of mild jaundice with leukodystrophy and high lactate and phenylderivatives for urine organic acids on the 7th day. Whole exome sequencing (WES) and Sanger sequencing were performed to screen and confirm the suspicious pathogenic mutations. The results revealed this proband carried two compound heterozygous mutations in TWNK: c.1186 C > T / p.Pro396Ser and c.1844 G > C / p.Gly615Ala inherited by an autosomal recessive form from his parents, of which protein conservative analysis and structural modeling supported the pathogenicity of the two mutations. Unfortunately, the conditions described above were not improved until he was discharged from the hospital on the 23rd day and died at 4 months of age. CONCLUSIONS: In this study, we investigated a Chinese family with the hepatocerebral form of MDS and conducted WES and Sanger sequencing to explore the causative mutations for this proband born from non-consanguineous and healthy parents. We identified two novel TWNK c.1186 C > T/ c.1844 G > C compound heterozygous mutations which were probably the disease-causing mutations of hepatocerebral form of MDS and described the clinical manifestations of the proband, which expanded the phenotypic spectrum of MDS caused by variants in TWNK. This study also emphasized WES technology can provide the genetic diagnosis of Mendelian genetic disease.

Photocatalytic Activation of Saturated C-H Bond Over the CdS Mixed-Phase Under Visible Light Irradiation.

Selective activation of saturated C-H bond in hydrocarbons to produce high-value-added chemicals is of great significance for chemical synthesis and transformation. Herein, we present a facile procedure to achieve Ni-doped CdS nanoparticles with mixed (cubic and hexagonal) phases, as well as its application to the photocatalytic activation of saturated primary C-H bond of toluene and its derivatives. The photocatalytic oxidation rate of toluene into benzaldehyde of formation reached up to 216.7 µmolh-1g-1 under visible light irradiation. The excellent photocatalytic performance of Ni(II)-doped CdS [Ni(II)/CdS] can be attributed to its unique structural assembly with cubic and hexagonal phases and also the addition of Ni ions, together taking effect in promoting the separation of photogenerated charge carriers. The possible reaction mechanism for the photocatalytic selective oxidation is illustrated in this work. The band width of the as-prepared mixed phase CdS is reduced, which can effectively expand the response range and improve photocatalytic performance.

[Is 18F-PET-CT the First Choice for Preoperative Screening 
for Ia Non-small Cell Lung Cancer?]

BACKGROUND: The preferred therapy for patients with pulmonary nodules which highly suspected as lung cancer by low-dose spiral computed tomography (CT) is surgery, but the best screening method of whole body is not clear yet. The aim of this study is to investigate the differences in the progression-free survival (PFS) of patients with Ia stage non-small cell lung cancer after screening of positron emission computed tomography (PET)-CT and conventional imaging (B-ultrasound/CT/MRI/ECT, BCME). METHODS: A total of 300 cases of Ia stage non-small cell lung cancer were collected, of which 170 cases were performed PET-CT and 130 cases were performed BCME before operation. The basic characteristics of the two groups were analyzed by propensity score matching (PSM), and 114 cases of each group were included in the study. The survival analysis was carried out by the Kaplan-Meier survival curve and the Cox regression analysis. RESULTS: There was no significant difference between each group analyzed by PSM. The PFS of PET-CT and BCME were (44.9±27.2) months and (44.1±33.1) months (χ2=1.284, P=0.257). Both of the method ssucceed in screening. It is not the PFS influence factors. The false positive of PET-CT and BCME were 10 cases and 8 cases (χ2=0.241, P=0.623). CONCLUSIONS: Both PET-CT and BCME can be used as a screening method for Ia stage non-small cell lung cancer according to individualized choice of patients.

Assessment of the cancer risk factors of solitary pulmonary nodules.

There are no large samples or exact prediction models for assessing the cancer risk factors of solitary pulmonary nodules (SPNs) in the Chinese population. We retrospectively analyzed the clinical and imaging data of patients with SPNs who underwent computer tomography guided needle biopsy in our hospital from Jan 1st of 2011 to March 30th of 2016. These patients were divided into a development data set and a validation data set. These groups included 1078 and 344 patients, respectively. A prediction model was developed from the development data set and was validated with the validation data set using logistic regression. The predictors of cancer in our model included female gender, age, pack-years of smoking, a previous history of malignancy, nodule size, lobulated and spiculated edges, lobulation alone and spiculation alone. The Area Under the Curves, sensitivity and specificity of our model in the development and validation data sets were significantly higher than those of the Mayo model and VA model (p < 0.001). We established the largest sampling risk prediction model of SPNs in a Chinese cohort. This model is particularly applicable to SPNs > 8 mm in size. SPNs in female patients, as well as SPNs featuring a combination of lobulated and spiculated edges or lobulated edges alone, should be evaluated carefully due to the probability that they are malignant.