Objective To investigate the effects of lncRNA/Hedgehog signaling pathway-mediated autophagy on chondrocyte function in osteoarthritis(OA).Methods Established an LPS-induced inflammatory chondrocyte model in OA chondrocytes(SW1353),and identified it through collagen Ⅱ immunofluorescence staining and toluidine blue staining,dividing the groups into Normal,LPS,LPS/lncRNA HHIP-AS1 inhibitor,and LPS/Scr groups.RT-qPCR was used to detect lncRNA HHIP-AS1 and HHIP expression in chondrocytes,Western blot was used to assess HHIP,Gli1,Gli2,LC3B-Ⅰ/Ⅱ,and p62 protein expression,TUNEL staining and flow cytometry(FC)were used to detect cell apoptosis,and immunofluorescence assay(IFA)was used to detect autophagy LC3B expression.Results When SW1 cells were treated with LPS,compared with normal chondrocytes,after LPS induction,the volume of chondrocytes increased,the number of vacuoli in the cytoplasm increased,the volume of the nucleus increased,the morphology of some cells was irregular,and the number relatively decreased.Toluidine blue staining and type Ⅱ collagen immunohistochemical staining decreased.LPS stimulation would induce cell death and autophagy.lncRNA HIP-AS1 and HHIP were upregulated(P<0.05),the key molecules of the Hedgehog signaling pathway HHIP,Gli1 and Gli2 were continuously upregulated(P<0.05),chondrocytes treated with LPS showed obvious apoptosis(P<0.05),and LC3B(green)accumulated.The biosynthesis and processing of LC3B increased(the levels of LC3B Ⅰ and Ⅱ increased),the degradation of p62 increased(P<0.05),and the lncRNA HIP-AS1 inhibitor reduced LPS-induced apoptosis of OA chondrocytes(decreased apoptosis rate)and autophagy(decreased autophagy rate of chondrocytes treated with LPS).The biosynthesis and processing of LC3B decreased(the levels of LC3B Ⅰ and Ⅱ decreased),and the degradation of p62 weakened),and the difference was statistically significant(P<0.05).Conclusion The lncRNA HHIP-AS1 may inhibit LPS-induced OA chondrocyte apoptosis and autophagy by regulating the Hedgehog signaling pathway.

Purpose To evaluate the predictive performance of mean apparent propagator-magnetic resonance imaging(MAP-MRI)combined with habitat analysis for determining O6-methylguanine-DNA methyltransferase(MGMT)promoter methylation status in glioma.Materials and Methods This retrospective study analyzed MRI and clinical data from 55 patients with surgically confirmed glioma at Fujian Medical University Union Hospital from January 2019 to December 2023.All patients underwent structural and diffusion-weighted imaging.Three-dimensional volumes of interest were delineated in the tumor solid region using ImageJ software.The nn-FAE tool was used to segment the tumor solid region into two habitat subregions based on mean diffusivity(MD)maps:high-MD and low-MD habitats.Average diffusion parameter values were extracted from the entire tumor solid region and each habitat subregion.Differences in parameters between methylated and unmethylated groups were compared,and the area under the curve was calculated.Results Among 55 patients,significant differences were observed in all MAP-MRI parameters and MD in the tumor solid region and low-MD habitat,as well as all parameters in the high-MD habitat between methylated and unmethylated groups(t/Z=-3.780-3.153,all P<0.05).The return-to-origin probability(RTOP)in the low-MD habitat demonstrated the highest diagnostic performance,with the area under the curve improving from 0.771 before habitat analysis to 0.827 after habitat analysis.In the high-grade subgroup,significant differences were observed in return-to-axis probability(RTAP)and RTOP in the tumor solid region;RTOP,non-Gaussianity,non-Gaussianity axial,and RTAP in the low-MD habitat;and non-Gaussianity in the high-MD habitat(t/Z=-2.820--1.976,all P<0.05).RTOP in the low-MD habitat again showed optimal diagnostic efficacy(the area under the curve 0.725 before habitat analysis,0.798 after).Multivariate analysis identified RTAP and RTOP in the tumor solid region and low-MD habitat as independent predictors of MGMT methylation.Conclusion MAP-MRI diffusion parameters demonstrate the ability to predict MGMT promoter methylation status in glioma,with superior performance compared with diffusion tensor imaging.Habitat imaging further enhances the predictive efficacy of MAP-MRI parameters for MGMT promoter methylation.

Purpose To evaluate the predictive performance of mean apparent propagator-magnetic resonance imaging(MAP-MRI)combined with habitat analysis for determining O6-methylguanine-DNA methyltransferase(MGMT)promoter methylation status in glioma.Materials and Methods This retrospective study analyzed MRI and clinical data from 55 patients with surgically confirmed glioma at Fujian Medical University Union Hospital from January 2019 to December 2023.All patients underwent structural and diffusion-weighted imaging.Three-dimensional volumes of interest were delineated in the tumor solid region using ImageJ software.The nn-FAE tool was used to segment the tumor solid region into two habitat subregions based on mean diffusivity(MD)maps:high-MD and low-MD habitats.Average diffusion parameter values were extracted from the entire tumor solid region and each habitat subregion.Differences in parameters between methylated and unmethylated groups were compared,and the area under the curve was calculated.Results Among 55 patients,significant differences were observed in all MAP-MRI parameters and MD in the tumor solid region and low-MD habitat,as well as all parameters in the high-MD habitat between methylated and unmethylated groups(t/Z=-3.780-3.153,all P<0.05).The return-to-origin probability(RTOP)in the low-MD habitat demonstrated the highest diagnostic performance,with the area under the curve improving from 0.771 before habitat analysis to 0.827 after habitat analysis.In the high-grade subgroup,significant differences were observed in return-to-axis probability(RTAP)and RTOP in the tumor solid region;RTOP,non-Gaussianity,non-Gaussianity axial,and RTAP in the low-MD habitat;and non-Gaussianity in the high-MD habitat(t/Z=-2.820--1.976,all P<0.05).RTOP in the low-MD habitat again showed optimal diagnostic efficacy(the area under the curve 0.725 before habitat analysis,0.798 after).Multivariate analysis identified RTAP and RTOP in the tumor solid region and low-MD habitat as independent predictors of MGMT methylation.Conclusion MAP-MRI diffusion parameters demonstrate the ability to predict MGMT promoter methylation status in glioma,with superior performance compared with diffusion tensor imaging.Habitat imaging further enhances the predictive efficacy of MAP-MRI parameters for MGMT promoter methylation.

OBJECTIVETo investigate the origin of a rare supernumerary chromosome in a patient with premature ovarian failure (POF), and to explore the relationship between this abnormal karyotype and pathogenesis of POF.

METHODSGTG banding karyotyping, Q-banding and fluorescence in situ hybridization (FISH) were employed for the investigation.

RESULTSThe extra chromosome was identified as i(Y)(q10) by FISH with a panel of sex chromosome probes. The patient's karyotype was described as: 47,XX,+ ish mar i(Y)(q10) (DXZ1-, SRY-, DYZ3+, DYZ1++, wcpY+).

CONCLUSIONCo-occurrence of the supernumerary i(Y)(q10) with a female kryotype is extremely rare. This supernumerary chromosome may cause failure of X chromosomes synapsis during pachytene of meiosis I, which may trigger apoptosis of many oocytes and result in POF of the patient. Q-banding, FISH and multiple probes have been critical for accurate diagnosis of the unknown chromosome.

Chromosome Aberrations ; Chromosomes, Human, Pair 10 ; Chromosomes, Human, Y ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotype ; Primary Ovarian Insufficiency ; genetics