BACKGROUND:Pudendal neuralgia (PN) lacks specific treatments and severely affects patients' quality of life. Although pudendal nerve pulsed radiofrequency (PRF) can alleviate symptoms, its overall efficacy is not satisfactory. Ganglion impar neurolysis (GIN) has been widely employed for perineal pain management. We hypothesize that combining PRF with GIN may enhance therapeutic outcomes for PN compared to PRF monotherapy. To the best of our knowledge, no relevant reports have been found. OBJECTIVE:To assess whether GIN improves PRF treatment efficacy for PN. STUDY DESIGN:A retrospective cohort study. SETTING:This is a single-center retrospective study conducted at the Department of Pain Medicine, Peking University People's Hospital in Beijing, China. METHODS:We conducted a retrospective analysis of 84 women patients with PN treated from January 2020 through February 2024. The patients were divided into 2 groups: PRF Group (n = 40) received only pudendal nerve PRF; PRF + GIN Group (n = 44) received PRF combined with GIN. We recorded the posttreatment differences in Visual Analog Scale (VAS) scores, Overall Improvement in Pain (OIP) values, Hospital Anxiety and Depression Scales scores (anxiety: HADS-A; depression: HADS-D), and Pain Catastrophizing Scale scores (PCS) of the 2 groups at time points up to posttreatment month 6. RESULTS:At one, 2, 3, and 6 months posttreatment, the VAS scores in both groups were lower than pretreatment levels (P < 0.05). At 6 months posttreatment, the mean (SD) VAS score in the PRF+GIN Group (2.09 [1.38]) was lower than that in the PRF Group (3.81 [1.85]) (P < 0.05). The mean (SD) OIP value in the PRF+GIN group (73.72% [17.27%]) was higher than that in the PRF Group (56.13% [26.90%]) (P < 0.05). At 3 and 6 months posttreatment, the HAD scores and PCS scores in both groups were lower than pretreatment levels (P < 0.05). At 6 months posttreatment, the mean (SD) HADS-A and HADS-D scores in the PRF+GIN Group-3.91 (2.70) and 3.37 (2.18), respectively-were lower than those in the PRF group-6.54 (3.75) and 5.55 (3.25), respectively (P < 0.05); the mean (SD) PCS score in the PRF+GIN Group 12.16 (6.16) was lower than that in the PRF Group 19.52 (9.92) (P < 0.05). No severe complications were observed at any posttreatment time point. LIMITATIONS:This single-center study has a small sample size, a short follow-up period, and lacks patients who are men. CONCLUSIONS:GIN enhances short-term pudendal nerve PRF efficacy for PN, with no significant adverse reactions.

Contextual fear generalization is a hallmark of psychiatric disorders including post-traumatic stress disorder (PTSD), generalized anxiety disorder and panic disorder. Among these disorders, PTSD is particularly associated with contextual fear generalization. However, the mechanisms by which fear responses extend to similar contexts remain unclear. Here we tested whether corticotropin-releasing hormone (CRH) neurons in the dorsal bed nucleus of the stria terminalis (dBNST) contribute to contextual fear generalization. Using a contextual fear generalization paradigm with variable shock timing, we observed that intense foot shock conditioning enhanced freezing responses in both the training context and the generalization context in adult male mice, accompanied by elevated dBNST activity. Fiber photometry showed that dBNST CRH neurons were strongly engaged by foot shock and exhibited clear activity changes around freezing onset during both training and generalization tests. Functionally, chemogenetic inhibition of dBNST CRH neurons reduced freezing responses in the generalization test, whereas activation increased generalized freezing and promoted contextual fear generalization. Mechanistically, local pharmacological blockade of CRH receptor 1 (CRHR1) within the dBNST reduced freezing responses in the generalization test, indicating that CRHR1-dependent signaling within the dBNST contributes to fear generalization. Together, these findings identify dBNST CRH neurons and local CRHR1 signaling as key components underlying contextual fear generalization.

Background Genital inflammation is the most common gynecological issue among prepubertal girls. However, research on the vulvovaginal microecology of prepubertal girls (≤12 years old) is scarce compared to that of adult women. Notably, the vaginal microbiota of prepubertal girls differs from that of healthy adults, with fewer lactobacilli (key for microecological balance). Estrogen levels, which fluctuate with age, influence vaginal microbiota composition. This study aimed to explore the characteristics of vulvovaginal microecology in prepubertal girls across different age groups and its correlation with age, providing a theoretical basis for clinical diagnosis and treatment of genital tract infections in this population. Methods A total of 371 prepubertal girls aged≤12 years old who visited the gynecological outpatient department from January 2016 to December 2022 were selected. These girls were divided into three groups according to their ages. Then, the results of their vulvovaginal microecology were analyzed. Results A total of 84 cases (84/371, 22.6%) were clinically diagnosed with vulvovaginitis, including 43 cases (43/84, 51.2%) of bacterial vaginosis (BV), 38 cases (38/84, 45.2%) of vulvovaginal candidiasis (VVC), 2 cases (2/84, 2.4%) of Vaginal trichomoniasis (TV), and 1 case (1/84, 1.2%) of mixed vulvovaginitis (BV + VVC). In this study, it was found that VVC infection was significantly different among different age groups of prepubertal girls (P< 0.001), and the infection rate was higher in the 9 - 12 years old group. There was also a statistically significant difference in BV infection among different age groups of prepubertal girls (P< 0.001). The infection rate was the highest in the 7-9 years old group and the lowest in the 9 - 12 years old group. There were differences in the composition ratios of microbiota suppression, BV - type abnormal microbiota, non - BV - type abnormal microbiota, and total abnormal microbiota among different age groups (P< 0.001). Microecological analysis showed that the composition ratios of factors were absolutely diffrent such as dominant bacteria (eg., Gram - positive large bacilli) and pH > 4.5 among different age groups (P < 0.001). Conclusion There are differences in the composition of the vulvovaginal microecology and genital tract infections among prepubertal girls of different ages. Assisting in diagnosis through vulvovaginal microecology can better guide clinicians to carry out targeted treatment for genital tract infections in prepubertal girls, and improve the clinical cure rate.

Maternal embryonic leucine zipper kinase (MELK) is a cell cycle regulator, yet its role in embryonic cortical development remains unclear. We identified ultra-rare, predicted loss-of-function MELK variants in ASD individuals, prompting this functional investigation. Published human single-cell transcriptomics showed that MELK expression is enriched in neural progenitors and correlates with the G2/M phase. Using in utero electroporation in mouse cortex, we found that Melk knockdown reduced the proportion of progenitors in G2/M phase. Knockdown also caused impaired multipolar-to-bipolar transition and shorter leading processes. Complementing these findings, transcriptomic analysis of FACS-sorted Melk-knockdown cortical cells revealed downregulation of G2/M-related genes and cytoskeletal regulators linked to neuronal morphogenesis. Together, these findings identify MELK as a critical regulator of both G2/M phase progression and neuronal morphogenesis during cortical development, providing a mechanistic link to neurodevelopmental conditions.

Individuals with psychiatric disorders can show differences in plasma high-density lipoprotein cholesterol (HDL-C), although whether they share a common genomic basis is unclear. This study relied on publicly summarized data from genome-wide association studies for HDL-C and major psychiatric disorders to evaluate shared genetic architecture. Correlation between traits was summarized via linkage disequilibrium score regression. Using a bivariate causal mixture model, polygenicity was quantified alongside sharing versus trait-specificity. Jointly associated loci were mapped with a conjunctional false discovery rate approach. Analyses indicated polygenic overlap between HDL-C and several psychiatric disorders; the pattern differed across disorders. Mapped signals were primarily noncoding in available annotations, consistent with regulatory mechanisms. These findings did not establish causality or immediate clinical utility. They were compatible with attention to metabolic health in psychiatric care when clinically indicated and motivated prospective validation across diverse populations to support equitable applicability and clarify clinical significance.

Major depression is a prevalent and devastating psychiatric disorder. However, our understanding of the underlying molecular mechanisms is limited. Here, we found reduced expression of zinc finger protein with Krüppel-associated box and SCAN domains 4 (Zkscan4) in the hippocampi of patients with major depressive disorder and stress-susceptible mice. Zkscan4 disruption ( Zkscan4 −/− ) was sufficient to induce depression-like behaviors following subthreshold social stress. Zkscan4 regulated excitatory synaptic transmission mainly through direct interaction with the Htr2a promoter and the recruitment of glucocorticoid receptors for the transcriptional repression of 5-hydroxytryptamine receptor 2a (Htr2a). Reduced excitatory synaptic transmission in the hippocampus and stress susceptibility in Zkscan4 −/− mice were restored by pharmacological inhibition, genetic knockdown of Htr2a, or overexpression of the amino-terminal SCAN domain of Zkscan4 (Zkscan4 1–133 ) in cornus ammonis region 3. Our findings demonstrate an essential role of Zkscan4 in promoting stress resilience, suggesting a potential antidepressant effect of Zkscan4 1–133 .

Maternal Embryonic Leucine Zipper Kinase (MELK) regulates cell cycle progression, but its role in neurodevelopmental disorders is unclear. We identified loss-of-function MELK variants in autism spectrum disorder (ASD) patients, suggesting MELK haploinsufficiency contributes to ASD pathogenesis. Single-cell analysis revealed preferential MELK expression in proliferating neural progenitors during neurodevelopment, correlating with the expression of G2/M-phase regulators. In vivo MELK knockdown induced neuronal mislocalization and premature cell cycle exit without concomitant differentiation. Additionally, MELK deficiency impaired neuronal polarity transition. Our findings establish MELK as a critical regulator of G2/M progression and neuronal maturation during cortical neurogenesis, providing mechanistic insights into ASD etiology.

[This corrects the article DOI: 10.3389/fpsyt.2024.1396716.].

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by social interaction deficits, restricted interests and repetitive behaviors. The co-occurrence of motor impairments exacerbates the severity and societal impact of ASD, but the underlying mechanism remains to be elucidated. Research on the comorbidities of ASD including motor impairments could benefit in the life quality improvement in patients with ASD. Here we aimed at investigating the motor behaviors in mice with Trio deletion in Purkinje cells (PCs), and further exploring the cellular and molecular mechanisms. The protein level of Calbindin as PCs’ marker was determined. Behaviors including spontaneous locomotion activity, rotarod, beam balance and gait were tested in mice with the ages of 12-week and 20-week. Magnetic resonance imaging (MRI) scanning with T2 and DTI sequencing was performed in 12-week old mice. Although Triofl/fl; Pcp2-Cre mice showed significant impairments of spontaneous locomotion activity in both 12-week and 20-week ages, only the 20-week but not 12-week Triofl/fl; Pcp2-Cre mice showed extra mild abnormal motor, fine motor coordination, and gait. The decreased expression of Calbindin existed in both 12-week and 20-week old mice compared with control. Differentially expressed genes analysis from RNA-Seq and Gene Co-expression Network Analysis (GCNA) showed that Syne1 and its co-expressed genes were upregulated in Triofl/fl; Pcp2-Cre mice compared to controls. In addition, abnormal ADC values suggested the long-term chronic damage in the cerebellum. Together, our findings indicate that the motor dysfunction in ASD are affected by Trio deletion in PCs with delayed in onset, accompanied with alterations in MRI, histological, and epigenetic level.

Melicope pteleifolia is a plant belonging to the Melicope genus of the Rutaceae family. Known for a bitter taste and cold nature, its stems and tender branches with leaves possess properties of clearing heat, detoxifying, dispelling wind, and removing dampness and can be used to treat sore throat, malaria, jaundice hepatitis, rheumatic bone pain, eczema, dermatitis, and sores and ulcers. In this study, 19 compounds were isolated from the chloroform and n-butanol extracts of M. pteleifolia leaves by using liquid chromatography-mass spectrometry(LC-MS) and proton nuclear magnetic resonance(~1H-NMR)-guided separation techniques. The compounds were identified as isoleptonol(1), leptaones B-E(2-5), friedelin(6), evodionol(7), ethyl p-hydroxybenzoate(8), litseachromolaevane A(9), quercetin-7,3',4'-trimethyl ether(10), kokusaginin(11), 8-(1-hydroxyethyl)-5,6,7-trimethoxy-2,2-dimethyl-2H-1-benzopyran(12), ethyl p-hydroxycinnamate(13), 3-hydroxy-9-methyl-6H-benzo\[c\]chromen-6-one(14), agrimonolide(15), 7-hydroxycoumarin(16), scopoletin(17), isoscutellarein(18), and agrimonolide 6-O-glucoside(19). Among these, the new compounds included one chromene and four meroterpenoid(1-5). The anti-inflammatory activities of the newly identified compounds 1-5 were screened in vitro, showing that the five compounds(1-5) exhibited inhibitory effects on nitric oxide(NO) production in BV2 cells induced by lipopolysaccharide(LPS)/interferon(IFN)-γ, with IC_(50) values ranging from 12.25 to 36.48 μmol·L~(-1).

Autism spectrum disorders (ASDs) are a group of neurodevelopmental disorders with high heritability. Nevertheless, the involvement of genetic variants in ASDs is not fully understood. One gene of interest is TRIO, which encodes a large protein that aids in GDP-to-GTP exchange as a Ras homologous (Rho) guanine nucleotide exchange factor (GEF), facilitating cytoskeleton reorganization. Thus, it plays crucial roles in neuronal migration, neurite outgrowth, and synaptic transmission. De novo mutations in TRIO have been extensively reported in the pathogenesis of ASDs. However, no evidence currently supports the genetic association between common variants in TRIO and ASDs. To investigate the role of common genetic variations in autism risk, we analyzed 12 tagging single-nucleotide polymorphisms (SNPs) in the TRIO gene. These tagging SNPs captured an average of 75% of all common variations in TRIO with a minor allele frequency (MAF) > 5%. Using the family-based association study in 239 Chinese Han autism trios, we identified the significant association of three SNPs (rs32593, rs33005, and rs27479) with autism. To confirm the association, the sample size was expanded to 427 trios by recruiting 188 additional trios. Our findings across all 427 trios confirmed that A allele of rs32593, G allele of rs33005, and C allele of rs27479 showed a preferential transmission to the affected offspring (rs32593: A > G, Z = 2.600, p = 0.0093; rs33005: G > T, Z = 2.978, p = 0.0029; rs27479: C > A, Z = 3.214, p = 0.0013) after Bonferroni's correction (p < 0.0042). Haplotype analyses showed that one haplotype (A-G) constructed from rs32593 and rs33005 was significantly associated with autism (p = 0.0064; Global p = 0.022). These results suggested that the common variants in TRIO might be involved in the susceptibility to autism in the Chinese Han population.

Cognitive dysfunction is a core feature of schizophrenia (SCZ), yet its mechanisms remain poorly understood. We investigated the functional role of NKAPL (nuclear factor κB activating protein-like)-an SCZ risk-associated gene-and the single nucleotide polymorphism rs1635 in cognitive deficits related to SCZ. We used Nkapl transgenic mouse models to explore the impact of NKAPL on SCZ-related cognitive deficits. NKAPL acts as a transcriptional repressor of the γ-aminobutyric acid (GABA) metabolizing enzyme succinic semialdehyde dehydrogenase (SSADH). Nkapl deletion in medial prefrontal cortex (mPFC) interneurons led to increased SSADH levels, reduced GABA concentration in the synaptic cleft, impaired inhibitory synaptic transmission, and cognitive deficits. Furthermore, the rs1635 mutation (T153N) caused similar effects as the Nkapl knockout. Reexpression of wild-type NKAPL or genetic knockdown of SSADH in mPFC interneurons restored the synaptic dysfunction and cognitive deficits in Nkapl-/- mice. Our study indicates the potential role of NKAPL and SSADH in mPFC interneurons in neuronal mechanisms of learning and memory in mice.

Postherpetic neuralgia (PHN) is a common complication of herpes zoster, which seriously affects patients' quality of life. This study analysed the synergistic effect of neuromodulation and opioid dilution analgesics in the treatment of PHN. 120 patients with PHN from Affiliated Hospital of Southwest Medical University between December 2020 and December 2023 were categorized into PR and PO groups, both groups were treated with pulsed radiofrequency, PO group was added with Oxycodone hydrochloride. VAS scores, inflammatory factor indexes [tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-10 (IL-10)], immune indexes [percentage of CD4+ T cells, CD8+ T cells, CD4+ /CD8+] and clinical efficacy were mainly evaluated. Secondary indicators included sleep quality (PSQI) scores, anxiety self-assessment (SAS) scores, disease control time, adverse reactions and recurrence rates. Post-treatment, both groups' indicators were significantly improved. IL-2 and IL-10 levels, CD4+ T cells percentage, CD4+ /CD8+ and clinical efficacy were higher in PO group than PR group. VAS score, TNF-α and IL-1β levels, CD8+ T cells percentage, PSQI score, SAS score, disease control time, adverse reaction and recurrence rate were lower than PR group (P<0.05). The combination treatment efficacy of PHN is remarkable and is worth promoting its use in the clinic.

Basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), as certain forms of non-melanoma skin cancer (NMSC) or keratinocyte carcinoma, are the most common forms of malignant neoplasms worldwide (Sharp et al., 2024). BCC and cSCC have been identified as two major components of NMSC, comprising one-third of all malignancies (Burton et al., 2016). Generally speaking, patients with NMSC tend to have relatively favorable survival outcomes, while different histopathological subtypes of NMSC exhibit distinct biological behaviors (Stătescu et al., 2023). Keratinocyte carcinoma, although not considered as deadly as melanoma, tends to metastasize if left untreated (Civantos et al., 2023; Nanz et al., 2024). cSCC can evolve locally, then aggressively metastasize, invade, and even lead to fatal consequences in a subset of patients (Winge et al., 2023). A solid, pigmented, smooth plaque or a hyperkeratotic papule with or without central ulceration and hemorrhage appears to be characteristic of cSCC (Thompson et al., 2016; Zhou et al., 2023). Of note, a rare type of intraepidermal cSCC in situ often appears as a velvety, demarcated, slightly raised erythematous plaque on the genitalia of men (Yamaguchi et al., 2016). Accounting for approximately 16.0% of scalp tumors and with a rising incidence, cSCC is now the second most common NMSC in humans (Verdaguer-Faja et al., 2024). According to the latest statistics, up to 2%‒5% of cSCCs in situ may gradually progress into invasive cSCCs in the final step (Rentroia-Pacheco et al., 2023). Several risk factors for the carcinogenesis and development of cSCC have been identified, including age, accumulative exposure to ultraviolet light radiation A and B, human papillomavirus infection, arsenic ingestion, chronic scarring, xeroderma pigmentosa, a relevant history of ionizing radiation, androgenetic alopecia in males, and immunosuppression therapy (Martinez and Otley, 2001; Welsch et al., 2012; Mortaja and Demehri, 2023).

Background: Autism is a severe neurodevelopmental disorder characterized by social interaction deficits, impairments in communication, and restricted and repetitive stereotyped behavior and activities. Family and twin studies suggested an essential role of genetic factors in the etiology of autism spectrum disorder (ASD). Also, other studies found SORCS3 and GSDME (DFNA5) might be involved in brain development and susceptible to ASD. Methods: In this study, 17 genome-wide significant SNPs reported in previous ASD genome-wide association studies (GWAS) and 7 SNPs in strong linkage disequilibrium with known ASD GWAS hits were selected to investigate the association between these SNPs and autism in the Han Chinese population. Then, 10 tagSNPs in SORCS3 and 11 tagSNPs in GSDME were selected to analyze the association between these SNPs and autism. The selected 24 SNPs and tagSNPs were genotyped using the Agena MassARRAY SNP genotyping assay in 757 Han Chinese autism trios. Results: Rs1484144 in NAA11 was significantly associated with autism; significance remained after the Bonferroni correction (P < 0.0022). Also, rs79879286, rs12154597, and rs12540919 near GSDME, as well as rs9787523 and rs3750261 in SORCS3, were nominally associated with autism. Conclusion: Our study suggests that rs1484144 in NAA11 is a significant SNP for autism in the Han Chinese population, while SORCS3 and GSDME might be the susceptibility genes for autism in this population.

Schizophrenia is a severe psychiatric disorder with high heritability, characterized by positive and negative symptoms as well as cognitive abnormalities. Dysfunction in glutamate synapse is strongly implicated in the pathophysiology of schizophrenia. However, the precise role of the perturbed glutamatergic system in contributing to the cognitive abnormalities of schizophrenia at the synaptic level remains largely unknown. Although our previous work found that Opcml promotes spine maturation and Opcml-deficient mice exhibit schizophrenia-related cognitive impairments, the synaptic mechanism remains unclear. By using whole-cell patch clamp recording, we found that decreased neuronal excitability and alterations in intrinsic membrane properties of CA1 PNs in Opcml-deficient mice. Furthermore, Opcml deficiency leads to impaired glutamatergic transmission in hippocampus, which is closely related to postsynaptic AMPA/NMDA receptors dysfunction, resulting in the disturbances of E/I balance. Additionally, we found that the aripiprazole which we used to ameliorate abnormal cognitive behaviors also rescued the impaired glutamatergic transmission in Opcml-deficient mice. These findings will help to understand the synaptic mechanism in schizophrenia pathogenesis, providing insights into schizophrenia therapeutics with glutamatergic disruption.

Autism Spectrum Disorders (ASDs) are reported as a group of neurodevelopmental disorders. The structural changes of brain regions including the hippocampus were widely reported in autistic patients and mouse models with dysfunction of ASD risk genes, but the underlying mechanisms are not fully understood. Here, we report that deletion of Trio, a high-susceptibility gene of ASDs, causes a postnatal dentate gyrus (DG) hypoplasia with a zigzagged suprapyramidal blade, and the Trio-deficient mice display autism-like behaviors. The impaired morphogenesis of DG is mainly caused by disturbing the postnatal distribution of postmitotic granule cells (GCs), which further results in a migration deficit of neural progenitors. Furthermore, we reveal that Trio plays different roles in various excitatory neural cells by spatial transcriptomic sequencing, especially the role of regulating the migration of postmitotic GCs. In summary, our findings provide evidence of cellular mechanisms that Trio is involved in postnatal DG morphogenesis.

BACKGROUND Gitelman syndrome (GS) is an uncommon autosomal recessive inherited disease caused by inactivating mutations in the SLC12A3 gene located on chromosome 16q13, resulting in distal tubular dysfunction. Most cases are detected during routine examinations in adulthood, due to hypokalemia and alkalosis. GS needs to be distinguished from diseases that cause hypokalemia, such as Classic Bartter syndrome and hyperthyroidism. In individual cases, GS and hyperthyroidism occur simultaneously, which is prone to misdiagnosis. CASE REPORT A 51-year-old woman with intermittent palpitations and lower limb fatigue for 4 years received a diagnosis of hypokalemia at a local hospital. Treatment with potassium supplementation did not improve the patient's palpitations and fatigue. After coming to our hospital for examination, it was found that the patient had hyperthyroidism. After receiving treatment of hyperthyroidism remission and sufficient potassium replacement, the patient's serum potassium level remained low. Meanwhile, the patient had hypomagnesemia and metabolic alkalosis. Subsequently, according to our suggestion, the patient continued to take oral supplements of potassium and magnesium, while also started on spironolactone. We convinced the patient to undergo genetic testing and discovered compound heterozygous mutations in the SLC12A3 gene, which presented a definitive diagnosis of GS. In the following 3 months, the patient's serum potassium level was within the normal range, and the dose of methimazole was reduced. CONCLUSIONS As a rare disease, GS may have only mild or occasional manifestations, making it prone to misdiagnosis. GS remains therapeutically challenging, and future progress in treatment will depend on further research of the disease.

AbstractAlthough the association between persistent hypertension and the compromise of both micro‐ and macro‐circulatory functions is well recognized, a significant gap in quantitative investigations exploring the interplay between microvascular and macrovascular injuries still exists. In this study, the authors looked into the relationship between brachial‐ankle pulse wave velocity (baPWV) and hypertensive retinopathy in treated hypertensive adults. The authors conducted a cross‐sectional study of treated hypertensive patients with the last follow‐up data from the China Stoke Primary Prevention Trial (CSPPT) in 2013. With the use of PWV/ABI instruments, baPWV was automatically measured. The Keith‐Wagener‐Barker classification was used to determine the diagnosis of hypertensive retinopathy. The odds ratio (OR) and 95% confidence interval (CI) for the connection between baPWV and hypertensive retinopathy were determined using multivariable logistic regression models. The OR curves were created using a multivariable‐adjusted restricted cubic spline model to investigate any potential non‐linear dose‐response relationships between baPWV and hypertensive retinopathy. A total of 8514 (75.5%) of 11,279 participants were diagnosed with hypertensive retinopathy. The prevalence of hypertensive retinopathy increased from the bottom quartile of baPWV to the top quartile: quartile 1: 70.7%, quartile 2: 76.1%, quartile 3: 76.7%, quartile 4: 78.4%. After adjusting for potential confounders, baPWV was positively associated with hypertensive retinopathy (OR = 1.05, 95% CI, 1.03–1.07, p < .001). Compared to those in the lowest baPWV quartile, those in the highest baPWV quartile had an odds ratio for hypertensive retinopathy of 1.61 (OR = 1.61, 95% CI: 1.37–1.89, p < .001). Two‐piece‐wise logistic regression model demonstrated a nonlinear relationship between baPWV and hypertensive retinopathy with an inflection point of 17.1 m/s above which the effect was saturated .