Biomedical subjects

Jie Zhao

Publications and source records attributed to Jie Zhao.

At least 19 recordsLinked to original sources

PubMed2026

Identifying potential drug targets for physical and cognitive frailty: an integrative analysis of CHARLS cohort, mendelian randomization, and gene colocalization.

With the aging of the population, frailty has become a common syndrome that severely affects the quality of life of older adults. This study aims to analyze the correlation between cognition and frailty, physical activity and frailty, and elucidate the potential pharmacological targets of cognitive frailty and physical frailty.We conducted logistic regression analyses using data from the China Health and Retirement Longitudinal Study (CHARLS) to examine the associations between total cognition and frailty, physical activity and frailty. Furthermore, summary-data-based Mendelian randomization (SMR) and two-sample Mendelian randomization (TSMR) were employed to explore potential pharmacological targets for frailty. Genes associated with physical frailty and cognitive frailty were identified, followed by analysis via colocalization analysis, phenome-wide association studies (PheWAS), and DsigDB drug prediction. Cross-sectional analysis of CHARLs revealed that total cognition(OR 0.93, 95% CI 0.92-0.95) and middle physical activity(OR 0.95, 95% CI 0.92-0.97) were negatively correlated with frailty. SMR identified 41 drug genes associated with frailty, and subsequent TSMR validation and co-localization analysis showed that 11 candidate genes exhibited strong colocalization (PP.H4 > 0.8). GRPEL 1, PABPC 4, and WBP 2NL were ultimately identified as potential drug targets associated with physical frailty, while LANCL1, LRPPRC, FADS1, and WBP2NL were identified as potential drug targets associated with cognitive frailty. Phenome-wide association analysis(PheWAS) did not reveal any significant associations between these genes and other phenotypes at the genome-wide significance threshold. Laudanosine, 25-hydroxycholesterol, and hexadecanal emerged as the top three candidate compounds for therapeutic intervention. We identified potential drug targets for physical frailty and cognitive frailty through comprehensive analysis and elucidated drugs associated with potentially relevant genetic markers, thereby laying the foundation for a deeper understanding of the mechanisms of frailty.

Humans↗

PubMed2025

A novel second-generation HIV-1 circulating recombinant form (CRF183_0107) identified among men who have sex with men in China.

OBJECTIVE: This study aimed to report a novel HIV-1 circulating recombinant form (CRF) identified among men who have sex with men (MSM) in China. DESIGN: Viral sequences were isolated from MSM patients, and the recombination and evolutionary histories of this CRF were elucidated through phylogenetic and Bayesian analyses. METHODS: Near full-length genomes (NFLGs) and partial genome sequences were amplified from RNA extracted from plasma samples of three HIV-1 seropositive MSM in Heilongjiang Province, China. Phylogenetic analysis was conducted using FastTree v2.1.9, and recombination analysis was performed using Simplot v3.5.1. The emergence time of the novel CRF was estimated by Bayesian evolutionary analysis using BEAST v1.10.4. RESULTS: Two NFLGs and two partial genome segments were successfully obtained from three MSM participants. This novel CRF was characterized by 12 mosaic gene segments, comprising 6 segments from the CRF01_AE cluster 4 and 6 segments from the CRF07_BC cluster N, and thus was designated as CRF183_0107. The estimated time of origin for the CRF01_AE and CRF07_BC components within CRF183_0107 were approximately 2009.2 and 2012.5, respectively. CONCLUSION: A novel second-generation HIV-1 recombinant, named CRF183_0107, was identified within the MSM population in China. This CRF exemplified the recombination events occurring between the CRF01_AE cluster 4 and the CRF07_BC cluster N during 2009-2012.

Humans↗

PubMed2025

Association of AGER genetic variants with chronic obstructive pulmonary disease susceptibility in Southern Chinese Han populations.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) remains a leading cause of disability and mortality among elderly populations. Studies indicate that AGER plays a critical regulatory role in the pathogenesis of respiratory disorders. However, the genetic variations in AGER to COPD susceptibility remain incompletely understood. This study employs a case-control design to investigate associations between AGER genetic variants and COPD risk in the Southern Chinese Han population. METHODS: This study enrolled 270 COPD patients and 271 healthy controls. AGER single-nucleotide polymorphisms (SNPs) were analysed using the MassARRAY iPLEX platform. Logistic regression models evaluated associations between AGER polymorphisms and COPD susceptibility, with false discovery rate (FDR) correction applied to mitigate multiple testing errors. SNP-SNP interactions were investigated through multifactor dimensionality reduction (MDR) analysis. Expression quantitative trait locus (eQTL) data from the GTEx database were further analysed to assess regulatory relationships between SNPs and AGER gene expression levels. RESULTS: This study showed that rs3134941 (G allele, OR = 0.21, 95% CI = 0.10-0.41, p (FDR) = 0.001) and rs3131300 (G allele, OR = 0.32, 95% CI = 0.20-0.49, p (FDR) = 0.0001) were significantly associated with a reduced susceptibility to COPD. MDR indicated that rs3131300 was the optimal predictive model for COPD risk. Additionally, initial mechanistic investigations utilizing the GTEx database identify rs3134941 (C > G) and rs3131300 (A > G) as significant expression quantitative trait loci for AGER mRNA in cell-cultured fibroblasts and whole blood. CONCLUSION: Our study demonstrated that AGER genetic variants might play a protective role in the progression of COPD.

Aged↗

PubMed2007

The sequence determinant causing different folding behaviors of insulin and insulin-like growth factor-1.

Although insulin and insulin-like growth factor-1 (IGF-1) belong to the insulin superfamily and share highly homologous sequences, similar tertiary structure, and a common ancestor molecule, amphioxus insulin-like peptide, they have different folding behaviors: IGF-1 folds into two thermodynamically stable tertiary structures (native and swap forms), while insulin folds into one unique stable structure. To further understand which part of the sequence determines their different folding behavior, based on previous reports from the laboratory, two peptide models, [B9A][1-4]porcine insulin precursor (PIP) and [B10E][1-4]PIP, were constructed. The plasmids encoding the peptides were transformed into yeast cells for expression of the peptides; the results showed that the former peptide was expressed as single component, while the latter was expressed as a mixture of two components (isomer 1 and isomer 2). The expression results together with studies of circular dichoism, disulfide rearrangement, and refolding lead us to deduce that isomer 1 corresponds to the swap form and the isomer 2 corresponds to the native form. We further demonstrate that the sequence 1-4 plus B9 of IGF-1 B-domain can make PIP fold into two structures, while sequence 1-5 of insulin B-chain can make IGF-1 fold into one unique structure. In other words, it is the IGF-1 B-domain sequence that 1-4 allows IGF-1 folding into two thermodynamically stable tertiary structures; this sequence plus its residue B9E can change PIP folding behavior from folding into one unique structure to two thermodynamically stable structures, like that of IGF-1.

Amino Acid Sequence↗

PubMed2006

Down-regulation Cdc42 attenuates neuronal apoptosis through inhibiting MLK3/JNK3 cascade during ischemic reperfusion in rat hippocampus.

JNK signaling pathway is activated and involved in the selective neuronal death in the hippocampal CA1 subfield following cerebral ischemia. However, little is known about upstream partner controlling the pathway. Here we reported that ischemia/reperfusion significantly elevated Cdc42 activity, enhanced assembly of the Cdc42-MLK3 complex and activation of JNK pathway. Most importantly, knock-down endogenous Cdc42 selectively suppressed the MLK3/MKK7/JNK3 cascade, and subsequently blocked the phosphorylation of c-Jun and FasL expression. Meanwhile, Bcl-2 was inactivated and the release of cytochrome c was diminished. These alterations eventually perturbed the caspase-3 activation as well as post-ischemic neuronal cell death. Taken together, our findings strongly suggest that Cdc42 serves as an upstream activator and modulates JNK-mediated apoptosis machinery in vivo, which ultimately results in neuronal apoptosis via nuclear and non-nuclear pathways. Thus, Cdc42 may be a potential therapeutic target in ischemic brain injury.

Animals↗

PubMed2006

Benign intraspinal osteoblastoma stemming from C7 lamina in cervicothoracic junction: a case report.

STUDY DESIGN: A case report of a rare benign osteoblastoma successfully treated with total en bloc excision. OBJECTIVES: To describe the clinical and radiographic features of an adolescent female patient with intraspinal osteoblastoma in cervicothoracic junction and the effect of surgical treatment. SUMMARY OF BACKGROUND DATA: A rare case of massive benign osteoblastoma stemming from left side lamina of C7 and extension to spinal canal from C6 to T1 resulting in spinal cord compressed severely is reported. And the excellent results achieved from surgical intervention are presented. METHODS: A 13-year-old girl complained of gradually increasing pain of her lower part of the neck and left shoulder radiating to the left upper extremity, and the neurologic deficits were found in physical examination. A massive neoplasm located in intraspinal cervicothoracic junction and the spinal cord compressed severely was shown in radiographs, MRI, and CT. The neoplasm was removed totally with instrumentation performed in surgical intervention. She was followed up for 2.5 years; clinical symptoms and plain radiograph and CT films were investigated. RESULTS: The specimen of the removed mass was proven osteoblastoma pathologically. Her symptoms were relieved and the neurologic deficits recovered completely. Recurrence of the tumor was not seen at the final follow-up. CONCLUSIONS: A case of massive intraspinal osteoblastoma stemming from C7 lamina was successfully treated by excised grossly with instrumentation for reconstruction of stability.

Adolescent↗

PubMed2006

Anterior debridement and bone grafting of spinal tuberculosis with one-stage instrumentation anteriorly or posteriorly.

Between 2000 and 2004, 40 cases (average age 38, range 16-65 years) of spinal tuberculosis were treated with anterior debridement and iliac bone graft with one-stage anterior or posterior instrumentation in our unit. All patients received at least 2 weeks of regular antituberculous chemotherapy before surgery. We followed up all patients for 12-48 months (mean 22 months). Local symptoms of all patients were relieved significantly 1-3 weeks postoperatively; 23 of 25 cases (92%) with neurogical deficit had excellent or good clinical results. Erythrocyte sedimentation rates (ESR) returned from 51 mm/h to 32 mm/h (average) two weeks postoperatively. Kyphosis degrees were corrected by a mean of 16 degrees . Fusion rate of the grafting bone was 72.5% one year postoperatively and 90% two years postoperatively. Severe complications did not occur. We therefore believe that patients undergoing anterior debridement and iliac bone grafting with one-stage anterior or posterior instrumentation achieve satisfactory clinical and radiographic outcomes.

Adolescent↗

PubMed2006

The treatment for multilevel noncontiguous spinal fractures.

We report the outcome of 30 patients with multilevel noncontiguous spinal fractures treated between 2000 and 2005. Ten cases were treated conservatively (group A), eight cases were operated on at only one level (group B), and 12 cases were treated surgically at both levels (group C). All cases were followed up for 14-60 months (mean 32 months). Initial mobilisation with a wheelchair or crutches in group A was 9.2 +/- 1.1 weeks, which was significantly longer than groups B and C with 6.8+/-0.7 weeks and 3.1 +/- 0.4 weeks, respectively. Operative time and blood loss in group C were significantly more than group B. The neurological deficit improved in six cases in group A (60%), six in group B (75%) and eight in group C (80%). Correction of kyphotic deformity was significantly superior in groups C and B at the operated level, and increasing deformity occurred in groups A and B at the non-operated level. From the results we believe that three treatment strategies were suitable for multilevel noncontiguous spinal fractures, and individualised treatment should be used in these patients. In the patients treated surgically, the clinical and radiographic outcomes are much better.

Adult↗

PubMed2006

Localization of an arabinogalactan protein epitope and the effects of Yariv phenylglycoside during zygotic embryo development of Arabidopsis thaliana.

Arabinogalactan proteins (AGPs) are a class of highly glycosylated proteins widely distributed in higher plants and thought to be involved in plant growth and development. In the present paper, Western blotting with the monoclonal antibodies JIM4, JIM13, and LM2 showed that JIM13 reacted best with total protein extracts from flowers and siliques of Arabidopsis thaliana. This monoclonal antibody was therefore used as a probe to localize the AGP epitope in zygotic embryos at different developmental stages. Immunofluorescent labeling with JIM13 showed that AGPs were mainly distributed in the embryo proper and the top 1 to 2 cells and basal part of suspensors. The results of immunogold labeling confirmed the JIM13 epitope distribution in the different cells of the suspensor. AGP immunofluorescence was also observed at the shoot apex meristem during transition from the globular to the heart embryo stage, but this gradually disappeared after the torpedo stage. After (beta-D-Glc)(3) Yariv phenylglycoside (betaGlcY), a synthetic reagent that specifically binds to AGPs, was added to A. thaliana ovule culture medium, the survival rate and frequency of development of ovules at the zygote stage decreased in a concentration-dependent manner, with complete inhibition at 100 microM. The frequency of embryo differentiation from the globular stage to heart or later stages also decreased sharply. When betaGlcY was removed 24 h after inoculation, the inhibitory effects were reversible in a concentration-dependent and time-dependent manner. The results show that betaGlcY can inhibit embryo development and differentiation in A. thaliana, and the inhibitory effects are concentration dependent and reversible, indicating that AGPs are involved in embryo differentiation and shoot meristem formation. The possible roles of AGPs in A. thaliana zygotic embryo development are also discussed.

Arabidopsis↗

PubMed2006

PIAS3 induction of PRB sumoylation represses PRB transactivation by destabilizing its retention in the nucleus.

Progesterone receptor (PR) plays a critical role in cell proliferation and differentiation, and its transcriptional activity is known to be modulated by cofactor proteins. In the present study, we demonstrated that in the presence of progesterone, protein inhibitor of activated STAT-3 (PIAS3) significantly inhibited the PR transcriptional activity and the expression of progesterone-responsive genes. Reduction of endogenous PIAS3 by PIAS3 small-interfering RNA enhanced PR transactivation in a ligand-dependent manner. PIAS3 interacted with PR both in vitro and in vivo and the interaction was enhanced by progesterone. Furthermore, our findings suggested that PIAS3 strongly induced PRB sumoylation at three sites, Lys-7, Lys-388 and Lys-531. In addition, novel roles in PRB nuclear retention and transactivation were identified for these sites. Our data also suggested that PIAS3 was recruited in a largely hormone-dependent manner in response to a progesterone-responsive promoter. Finally, we demonstrated that PIAS3 inhibited the DNA-binding activity of PR and influenced its nuclear export as well as PR transactivation. Taken together, these data strongly suggested that PIAS3 played an important physiological role in PR function.

Animals↗

PubMed2006

Noradrenaline deficiency in brain increases beta-amyloid plaque burden in an animal model of Alzheimer's disease.

Loss of Locus coeruleus (LC) noradrenergic (NA) neurons occurs in several neurodegenerative conditions including Alzheimer's disease (AD). In vitro and in vivo studies have shown that NA influences several features of AD disease including inflammation, neurodegeneration, and cognitive function. In the current study we tested if LC loss influenced beta amyloid (Abeta) plaque deposition. LC neuronal degeneration was induced in transgenic mice expressing mutant V717F human amyloid precursor protein (APP) by treatment with the selective neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine DSP4 (5mg/kg every 2 weeks beginning at age 3 months). At 9 months of age, when control mice show low amyloid load, DSP4-treated mice showed an approximately 5-fold increase in the average number of Abeta plaques. This was accompanied by an increase in the levels of APP C-terminal cleavage fragments. DSP4-treatment increased both microglial and astroglial activation. In vivo, DSP4-treatment decreased expression and activity of the Abeta degrading enzyme neprilysin, while in vitro NA increased phagocytosis of Abeta1-42 by microglia. These findings suggest that noradrenergic innervation from LC are needed to maintain adequate Abeta clearance, and therefore that LC degeneration could contribute to AD pathogenesis.

Alzheimer Disease↗

PubMed2006

Localization of arabinogalactan proteins in egg cells, zygotes, and two-celled proembryos and effects of beta-D-glucosyl Yariv reagent on egg cell fertilization and zygote division in Nicotiana tabacum L.

Arabinogalactan proteins (AGPs) have been implicated in a variety of plant development processes including sexual plant reproduction. As a crucial developmental event, plant sexual reproduction generally occurs inside an ovule embedded in an ovary. The inaccessibility of the egg cells, zygotes, and embryos has hindered our understanding of the importance of AGPs in the early events involving fertilization, zygotic division, and early embryogenesis. In this study, the well-established in vitro zygote and ovary culture systems, together with immunofluorescence and immunogold labelling techniques, were employed to investigate the role of AGPs in the early events of sexual reproduction in Nicotiana tabacum. Dramatic changes in AGP content during ovule development were evidenced by western blotting. Subcellular localization revealed that AGPs are localized in the plasma membrane, cell wall, and cytoplasm of pre- and post-fertilized egg cells, and cytoplasm and vacuoles of two-celled proembryos. Abundant AGPs were detected in unfertilized egg cells; however, the level of AGPs substantially decreased in fertilized egg cells. Polar distribution of AGPs in elongated zygotes was observed. The early two-celled proembryos just from zygote division displayed accumulation of AGPs at a low level, while in the elongated two-celled proembryos at the late stage, the AGP content clearly increased. Provision of betaGlcY, a synthetic phenylglycoside that specifically binds AGPs, to the in vitro cultures of isolated zygote and fertilized ovaries increased abnormal symmetrical division of zygotes. In the culture of pollinated but unfertilized ovaries, addition of betaGlcY resulted in arrest of fertilization of the egg cells, but had no effect on fertilization of the central cells. The possible roles of AGPs in fertilization, zygotic division, and proembryo development are discussed.

Cell Division↗

PubMed2006

MDM2 interacts with and downregulates a sarcomeric protein, TCAP.

Recent reports have shown that MDM2 may attenuate hypertrophy of cardiac myocytes. However, mechanism of MDM2 involving in this process is unclear. In this study, we identified a novel specific MDM2-binding protein TCAP by the yeast two-hybrid screen. It was validated by GST pull-down and co-immunoprecipitation assays. Confocal analysis showed that MDM2 and TCAP co-localized in the nucleus, and elevated MDM2 expression could alter the subcellular localization of TCAP. Notably, MDM2 downregulated the protein level of TCAP through the proteasomal pathway, and this downregulation was inhibited by p14(ARF). In addition, our results suggested that the degradation of TCAP by MDM2 was through the ubiquitin-independent pathway. Given that TCAP is a key component involving in the cardiac hypertrophy, the degradation of TCAP by MDM2 might be connected with the roles of MDM2 in cardiac hypertrophy. Further investigation will focus on the biological significance of MDM2-TCAP interaction in cardiac hypertrophy.

Connectin↗

PubMed2006

Ubc9 interacts with SOX4 and represses its transcriptional activity.

SOX4 is a member of SOX transcriptional factor family that is crucial for many cellular processes. In this study, a yeast two-hybrid screening of human mammary cDNA library identified human ubiquitin-conjugating enzyme 9 (hUbc9) that interacted with SOX4. This interaction was confirmed by GST pull-down in vitro and co-immunoprecipitation assays in vivo. Deletion mapping demonstrated that HMG-box domain of SOX4 is required to mediate the interaction with Ubc9 in yeast. Furthermore, confocal microscopy showed that Ubc9 co-localized with SOX4 in the nucleus. Luciferase assays found that Ubc9 specifically repressed SOX4 transcriptional activity in 293T cells. We further demonstrated that Ubc9 could functionally repress the transcriptional activity of endogenous SOX4 induced by progesterone in T47D cells. The C93S mutant of Ubc9, which abrogates SUMO-1 conjugation activity, did not abolish the ability to repress SOX4 activity. It shows that Ubc9 interacts with SOX4 and represses its transcriptional activity independent of its SUMO-1-conjugating activity.

High Mobility Group Proteins↗

PubMed2006

IRF-8/interferon (IFN) consensus sequence-binding protein is involved in Toll-like receptor (TLR) signaling and contributes to the cross-talk between TLR and IFN-gamma signaling pathways.

Toll-like receptor (TLR) and interferon-gamma (IFN-gamma) signaling pathways are important for both innate and adaptive immune responses. However, the cross-talk between these two signaling pathways is incompletely understood. Here we show that IFN-gamma and LPS synergistically induce the expression of proinflammatory factors, including interleukin-1 (IL-1), IL-6, IL-12, NO, and tumor necrosis factor-alpha (TNF-alpha). Comparable synergism was observed between IFN-gamma and peptidoglycan (PGN; a TLR2 ligand) and poly(I:C) (a TLR3 ligand) in the induction of IL-12 promoter activity. IFN-gamma enhanced lipopolysaccharide (LPS)-induced ERK and JNK phosphorylation but had no effect on LPS-induced NF-kappaB activation. Interestingly, we found that IRF-8-/- macrophages were impaired in the activation of LPS-induced ERK and JNK and the production of proinflammatory cytokines induced by LPS or IFN-gamma plus LPS. Retroviral transduction of IRF-8 into IRF-8-/- macrophages rescued ERK and JNK activation. Furthermore, co-immunoprecipitation experiments show that IRF-8 physically interacts with TRAF6 at a binding site between amino acid residues 356 and 305 of IRF-8. Transfection of IRF-8 enhanced TRAF6 ubiquitination, which is consistent with a physical interaction of IRF-8 with TRAF6. Taken together, the results suggest that the interaction of IRF-8 with TRAF6 modulates TLR signaling and may contribute to the cross-talk between IFN-gamma and TLR signal pathways.

Cell Line↗

PubMed2006

Identification of novel target genes of CeTwist and CeE/DA.

Twist, a basic helix-loop-helix (bHLH) transcription factor, plays an important role in mesoderm development in many organisms, including C. elegans where CeTwist is required to direct cell fate specifications of a subset of mesodermal cells. Although several target genes of CeTwist have been identified, how this protein accomplishes its function is unclear. In addition, several human genes whose mutations cause different syndromes of craniosynostosis (premature fusion of cranial sutures) have homologues in the CeTwist pathway. Identification of novel target genes of CeTwist will shed more light on the functions of CeTwist in mesoderm development, and the corresponding human homologues will be good candidates for related syndromes with unidentified mutated genes. In our study, both CeTwist and its heterodimeric partner, CeE/DA, were overexpressed from the inducible heat-shock promoter, and potential target genes were detected with Affymetrix oligonucleotide microarrays. Using transcriptional GFP reporters, we found 11 genes were expressed in cells coincident with known CeTwist target gene products. Based on subsequent validation experiments, 9 genes were defined as novel CeTwist and CeE/DA targets. Human homologues of two of these genes might be involved in craniofacial diseases, which further validates C. elegans as a good model organism for providing insights into these disorders.

Animals↗

PubMed2006

Evaluation of fusion between liposomes and erythrocytes for intracellular derivatization of amino acids in cells.

Erythrocytes were fused with liposome for intracellular derivatization of amino acids in cells. The fusion efficiency was evaluated with capillary electrophoresis (CE) and laser-induced fluorescence (LIF) detection. Reagent fluorescein isothiocyanate (FITC) was enveloped in liposomes and introduced into erythrocytes by fusion between liposomes and erythrocytes. The amino acids in the fused cells were derivated by the introduced FITC and the derivated amino acids were extracted for detection by capillary electrophoresis equipped with laser-induced fluorescence detector. The fusion conditions were investigated. It was found that incubation of liposome and erythrocytes in the presence of 13% polyethylene glycol 6000 (PEG 6000) for 15min produced the highest fusion efficiency and kept the erythrocytes stability.

Amino Acids↗

PubMed2006

Improvement of sexual function in male patients treated surgically for cervical spondylotic myelopathy.

STUDY DESIGN: A prospective follow-up study. OBJECTIVE: To analyze the recovery of sexual function loss in surgically treated male patients with cervical spondylotic myelopathy. SUMMARY OF BACKGROUND DATA: Cervical spondylotic myelopathy is common in the elder population and can lead to sexual dysfunction. Although numerous studies have shown that surgical treatment of cervical spondylotic myelopathy achieved satisfactory neurologic and functional improvement, only few researchers mentioned sexual dysfunction. METHODS: A total of 22 patients with combined cervical spondylotic myelopathy and sexual dysfunction on admission were treated with surgery. The patients' preoperative and postoperative neurologic status was recorded according to the Japanese Orthopedic Association (JOA) Scoring System. The sexual function was assessed using the International Index of Erectile Function (IIEF). Special attention was also given to the preoperative and postoperative presence or absence of a reflexogenic and psychogenic erection. RESULTS: In most cases, there was significant improvement in neurologic status after surgery, with a mean improvement of JOA score of 3.6. The difference between the preoperative and postoperative JOA score was significant (P < 0.05). Most of these patients had an abnormal psychogenic erection (18/22, 82%) before surgery, but only few had an abnormal reflexogenic erection (4/22, 18%). After surgery, most patients had improvement in sexual function, and the average IIEF score was 28.5 before and 60.2 after surgery. The difference between preoperative and postoperative IIEF scores was statistically significant (P < 0.05). CONCLUSIONS: In addition to neurologic deficits, cervical spondylotic myelopathy also causes sexual dysfunction. Most of these patients had an abnormal psychogenic erection and normal reflexogenic erection. Along with neurologic recovery, most patients had improvement in sexual function after surgery.

Adult↗