To address the challenges faced by current brain midline segmentation techniques, such as insufficient accuracy and poor segmentation continuity, this paper proposes a deep learning network model based on a two-stage framework. On the first stage of the model, prior knowledge of the feature consistency of adjacent brain midline slices under normal and pathological conditions is utilized. Associated midline slices are selected through slice similarity analysis, and a novel feature weighting strategy is adopted to collaboratively fuse the overall change characteristics and spatial information of these associated slices, thereby enhancing the feature representation of the brain midline in the intracranial region. On the second stage, the optimal path search strategy for the brain midline is employed based on the network output probability map, which effectively addresses the problem of discontinuous midline segmentation. The method proposed in this paper achieved satisfactory results on the CQ500 dataset provided by the Center for Advanced Research in Imaging, Neurosciences and Genomics, New Delhi, India. The Dice similarity coefficient (DSC), Hausdorff distance (HD), average symmetric surface distance (ASSD), and normalized surface Dice (NSD) were 67.38 ± 10.49, 24.22 ± 24.84, 1.33 ± 1.83, and 0.82 ± 0.09, respectively. The experimental results demonstrate that the proposed method can fully utilize the prior knowledge of medical images to effectively achieve accurate segmentation of the brain midline, providing valuable assistance for subsequent identification of the brain midline by clinicians.
Humans ; Brain/diagnostic imaging* ; Deep Learning ; Image Processing, Computer-Assisted/methods* ; Algorithms ; Magnetic Resonance Imaging/methods* ; Neural Networks, Computer

OBJECTIVE: To analyze the serological and molecular biological characteristics of 5 patients with cis AB blood group, and to explore the safe transfusion strategy. METHODS: Serological identification of the samples' blood group was performed using anti-A, anti-B, anti-D, anti-A1, anti-H typing reagents and ABO reagent erythrocytes. Molecular biological identification of the samples' blood group was performed using PCR-SSP or gene sequencing. RESULTS: The serological identification results of blood group in 5 patients all showed inconsistent forward and reverse typing, presenting as A₂B₃ or A₂B_w. ABO gene sequencing of samples 1, 2 and 3 showed 261delG in exon 6 and 467C>T, 803G>C in exon 7. The genotypes of samples 1, 2 and 3 were determined to be cisAB/O . PCR-SSP genotyping was performed on sample 4 and 5，and the results were both cisAB/O . CONCLUSION Patients with cisAB alleles have inconsistent serological manifestations, and genetic testing is necessary to ensure the safety and effectiveness of blood transfusion.
Humans ; ABO Blood-Group System/genetics* ; Blood Transfusion ; Blood Grouping and Crossmatching ; Genotype ; Blood Group Antigens/genetics* ; Alleles ; Male ; Female

Recent studies have indicated that the expression of ubiquitin-specific protease 51 (USP51), a novel deubiquitinating enzyme (DUB) that mediates protein degradation as part of the ubiquitin‒proteasome system (UPS), is associated with tumor progression and therapeutic resistance in multiple malignancies. However, the underlying mechanisms and signaling networks involved in USP51-mediated regulation of malignant phenotypes remain largely unknown. The present study provides evidence of USP51's functions as the prominent DUB in chemoresistant triple-negative breast cancer (TNBC) cells. At the molecular level, ectopic expression of USP51 stabilized the 78 kDa Glucose-Regulated Protein (GRP78) protein through deubiquitination, thereby increasing its expression and localization on the cell surface. Furthermore, the upregulation of cell surface GRP78 increased the activity of ATP binding cassette subfamily B member 1 (ABCB1), the main efflux pump of doxorubicin (DOX), ultimately decreasing its accumulation in TNBC cells and promoting the development of drug resistance both in vitro and in vivo. Clinically, we found significant correlations among USP51, GRP78, and ABCB1 expression in TNBC patients with chemoresistance. Elevated USP51, GRP78, and ABCB1 levels were also strongly associated with a poor patient prognosis. Importantly, we revealed an alternative intervention for specific pharmacological targeting of USP51 for TNBC cell chemosensitization. In conclusion, these findings collectively indicate that the USP51/GRP78/ABCB1 network is a key contributor to the malignant progression and chemotherapeutic resistance of TNBC cells, underscoring the pivotal role of USP51 as a novel therapeutic target for cancer management.

Patients suffering from nerve injury often experience exacerbated pain responses and complain of memory deficits. The dorsal hippocampus (dHPC), a well-defined region responsible for learning and memory, displays maladaptive plasticity upon injury, which is assumed to underlie pain hypersensitivity and cognitive deficits. However, much attention has thus far been paid to intracellular mechanisms of plasticity rather than extracellular alterations that might trigger and facilitate intracellular changes. Emerging evidence has shown that nerve injury alters the microarchitecture of the extracellular matrix (ECM) and decreases ECM rigidity in the dHPC. Despite this, it remains elusive which element of the ECM in the dHPC is affected and how it contributes to neuropathic pain and comorbid cognitive deficits. Laminin, a key element of the ECM, consists of α-, β-, and γ-chains and has been implicated in several pathophysiological processes. Here, we showed that peripheral nerve injury downregulates laminin β1 (LAMB1) in the dHPC. Silencing of hippocampal LAMB1 exacerbates pain sensitivity and induces cognitive dysfunction. Further mechanistic analysis revealed that loss of hippocampal LAMB1 causes dysregulated Src/NR2A signaling cascades via interaction with integrin β1, leading to decreased Ca²⁺ levels in pyramidal neurons, which in turn orchestrates structural and functional plasticity and eventually results in exaggerated pain responses and cognitive deficits. In this study, we shed new light on the functional capability of hippocampal ECM LAMB1 in the modulation of neuropathic pain and comorbid cognitive deficits, and reveal a mechanism that conveys extracellular alterations to intracellular plasticity. Moreover, we identified hippocampal LAMB1/integrin β1 signaling as a potential therapeutic target for the treatment of neuropathic pain and related memory loss.
Animals ; Laminin/genetics* ; Hippocampus/metabolism* ; Neuralgia/metabolism* ; Cognitive Dysfunction/etiology* ; Male ; Peripheral Nerve Injuries/metabolism* ; Extracellular Matrix/metabolism* ; Integrin beta1/metabolism* ; Pyramidal Cells/metabolism* ; Signal Transduction

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OBJECTIVE: To explore the relationship between the geriatric nutritional risk index (GNRI) and cognitive function. METHODS: A cross-sectional study method was conducted. People aged ≥ 60 years from the National Health and Nutrition Examination Survey (NHANES) databases from 1999 to 2002 and 2011 to 2014 were included as study subjects. The participants were divided into three groups based on their GNRI scores: a medium-high risk group (82 ≤ GNRI < 92), a low risk group (92 ≤ GNRI < 98), and a no-risk group (GNRI ≥ 98). Demographic characteristics (gender, age, race, education), chronic diseases [chronic bronchitis, emphysema, thyroid problems, coronary heart disease, angina pectoris, stroke, hypertension, diabetes mellitus, and depression score on the patient health questionnaire (PHQ-9)], lifestyle habits (history of smoking, hours of sleep), etc., were collected. Cognitive function was assessed using the consortium to establish a registry for Alzheimer's disease word learning subtest (CERAD-WL), animal fluency test (AFT), and digit symbol substitution test (DSST) for the 2011-2014 data, while only the DSST was used for the 1999-2002 data. Differences in the above information among the GNRI cohorts were compared. Factors affecting cognitive function in the population were analyzed using multifactorial Logistic regression. RESULTS: 2 653 participants from 2011 to 2014 and 2 380 participants from 1999 to 2002 were enrolled, with a total of 5 033 participants in the study. There were statistically significant differences in age, stroke, diabetes mellitus, DSST score, AFT score, CERAD score test 1 recall (Cst1), and CERAD score test 2 recall (Cst2) among the GNRI groups. Multifactorial Logistic regression analysis of data from 2011 to 2014 showed that in model 3 (DSST score, age, gender, race, marriage, education, hours of sleep, history of smoking, emphysema, thyroid problems, chronic bronchitis, coronary heart disease, angina pectoris, hypertension, diabetes mellitus, depression score on the PHQ-9, and stroke) adjusted for all covariates, GNRI was a protective factor for DSST [odds ratio (OR) = 1.03, 95% confidence interval (95%CI) was 1.00 to 1.05, P = 0.03]; Logistic regression analyse for 1999 to 2002 and 2011 to 2014 showed a significant association even after adjustment for covariates (OR = 1.02, 95%CI was 1.00 to 1.03, P = 0.02). Subgroup Logistic regression analyses of the total population from 2011 to 2014 showed a significant association between GNRI and DSST scores (OR = 1.02, 95%CI was 1.01 to 1.03, P < 0.001), with significant associations in the age subgroups of 60 to 64 years old, across gender, non-Hispanic Whites and Blacks, by education, and by marital status associations were significant (all P < 0.05). Subgroup Logistic regression analyse of the total populations from 1999 to 2002 and 2011 to 2014 showed a significant association between the GNRI and DSST score (OR = 1.01, 95%CI was 1.01 to 1.02, P < 0.001), but did not show a significant year difference (interaction P = 0.503), and the newly found in the smoking population the association was also more significant (P < 0.01). CONCLUSION The GNRI correlates with the presence of cognitive functions related to processing speed, sustained attention, and executive function, and may be able to serve as an indicator for the assessment or prediction of related cognitive functions.
Humans ; Cross-Sectional Studies ; Aged ; Middle Aged ; Nutrition Surveys ; Cognition ; Female ; Male ; Nutritional Status ; Risk Factors ; Geriatric Assessment

Objective To study the effect of reactive oxygen species(ROS)/p38 MAPK cascade reaction on the formation of kidney stones(KS)in rats and explore the mechanism.Methods Fifty SD rats were randomly divided into control group(normal feeding),N-acetylcysteine(NAC)group(intraperitoneally injected 200 mg/kg NAC),KS group(constructed calcium oxalate KS model),KS+NAC group(constructed calcium oxalate KS model,intraperitoneally injected 200 mg/kg NAC),KS+NAC+tunicamycin(TM)group(constructed calcium oxalate KS model,intraperitoneally injected 200 mg/kg NAC and 1 mg/kg TM),with 10 rats in each group.After 4 weeks of administration,24 hours urine volume and oxalic acid(Ox)of each group were measured,serum creatinine(Cr),urea nitrogen(BUN)and uric acid(UA)levels were detected by automatic biochemical analyzer.HE staining and Von Kossa staining were used to observe the histopathological changes and crystal deposition of the kidney.TUN EL staining was used to detect apoptosis of renal tissue cells.The activity of superoxide dismutase(SOD)and the content of malondialdehyde(MDA)in renal tissue were measured by the kit.DHE fluorescent probes detected the levels of reactive oxygen species(ROS)in kidney tissue.Immunohistochemical staining was used to detect the expressions of microtubule-associated protein 1 light chain 3 B(LC3B)and glucose regulatory protein 78(GRP78)in renal tissue,and the protein expression of LC3 Ⅱ/LC3 Ⅰ,Beclin1,GRP78,CCAAT/enhancer binding protein homologous protein(CHOP)in renal tissue was determined by Western blotting.Results Compared with the KS group,Ox in KS+NAC group decreased(P＜0.05),BUN,Cr and UA levels decreased(P＜0.05),renal tubule dilatation and calcium oxalate crystallization decreased,TUNEL positive cell rate decreased(P＜0.05),SOD activity increased and MDA content decreased(P＜0.05),ROS levels decreased(P＜0.05),LC3B and GRP78 positive staining levels decreased(P＜0.05),the relative protein expressions of p-p38 MAPK/p38 MAPK,LC3 Ⅱ/LC3 Ⅰ,Beclin1,GRP78 and CHOP were down-regulated(P＜0.05).Compared with the KS+NAC group,Ox in KS+NAC+TM group increased(P＜0.05),BUN,Cr and UA levels also increased(P＜0.05),renal tubule dilated significantly,calcium oxalate crystals increased,TUNEL positive cell rate increased(P＜0.05),SOD activity decreased and MDA content increased(P＜0.05),ROS levels increased(P＜0.05),LC3B and GRP78 positive staining levels increased(P＜0.05),the relative protein expressions of p-p38 MAPK/p38 MAPK,LC3 Ⅱ/LC3 Ⅰ,Beclin1,GRP78 and CHOP were also up-regulated(P＜0.05).Conclusion ROS/p38 MAPK cascade is involved in promoting KS formation in rats,which is related to the activation of endoplasmic reticulum stress-mediated autophagy pathway.

Objective To explore the efficacy of microvascular technology combined with perforator flap repair in the treatment of soft tissue defects in hand injuries.Method 98 patients with hand injury soft tissue defects admitted to our hospital from August 2018 to February 2023 were selected as the study subjects.The patients were randomly divided into a control group and an observation group using a random number table method,with 49 cases in each group.The control group was treated with thoracoabdominal pedicle flap repair,while the observation group was treated with microvascular technology combined with perforator flap repair.Compare the efficacy,visual analogue scale(VAS)score,histopathological score,total finger mobility(TAM)score,sensory function grading,and comprehensive quality of life assessment questionnaire 74(GQOLI-74)score between two groups before and after treatment.Result After 6 months of surgery,the therapeutic effect of the observation group was significantly higher than that of the control group(95.92％vs 79.59％)(P＜0.05).On postoperative days 3 and 7,the VAS score of the observation group was significantly lower than that of the control group,while the histopathological score was significantly higher than that of the control group(P＜0.05).After 6 months of surgery,the TAM score and sensory function grading in the observation group were(3.37±0.43)and(4.17±0.12)levels,respectively,higher than those in the control group(2.27±0.26)and(3.32±0.12)levels(P＜0.05).After 6 months of surgery,the psychological,physical,social,and material function scores of the observation group were significantly higher than those of the control group(P＜0.05).Conclusion The combination of microvascular technology and perforator flap repair has a significant therapeutic effect on patients with hand injury tissue injury,which can improve their hand sensation and motor function,alleviate pain,and improve tissue healing and quality of life.

Objective To evaluate the predictors of biochemical recurrence after laparoscopic radical prostatectomy.Methods The study cohort consisted of 416 consecutive prostatecancer patients who underwent radical prostatectomy in Zhongshan Hospital,Fudan University between Jan 2016 and Jun 2018.No patient received adjuvant therapy until documented biochemical recurrence.Biochemical recurrence-free survival(BCRFS)was estimated using the Kaplan-Meier method.Univariable and multivariable Cox proportional hazards regression models were utilized to determine variables predictive of biochemical recurrence.Results The median follow-up period was 174 weeks(inter quartile range 133-209 weeks).The overall biochemical recurrence rate was 21.39%(88/416).The time to biochemical recurrence was(51.11±47.71)weeks.Until the end of follow-up,the biochemical recurrence rates were 10%(1/10),6.12%(3/49),16.41%(43/262)and 43.16%(41/95)for low-risk,medium-risk,high-risk and locally advanced prostate cancer,respectively.On multivariable analysis,tumor invasion of the seminal vesicles(HR:2.119,95%CI:1.154-3.891,P=0.016);Seminal vesicle invasion(HR:1.824,95%CI:1.034-3.220,P=0.038),Gleason score≥8(HR:2.746,95%CI:1.268-5.943,P=0.010),prostate-specific antigen(PSA)=10-20 ng/mL(HR:4.240,95%CI:2.550-7.050,P<0.001);PSA>20 ng/mL(HR:6.341,95%CI:3.296-12.202,P<0.001)were the main predictors of biochemical recurrence.Conclusion Laparoscopic radical prostatectomy provides effective control of biochemical recurrence during the mid-term follow-up period.Tumor invasion of the seminal vesicles,seminal vesicle invasion,GS≥8,PSA=10-20 ng/mL,PSA>20 ng/mL were important predictors of biochemical recurrence after radical prostatectomy.