Objective To analyze the changes in the protein expression profile of peripheral blood mononuclear cells in systemic lupus erythematosus patients. Methods Peripheral blood was obtained from SLE patients and healthy controls, then mononuclear cells were isolated and the total protein was extracted by one-step method. Two-dimensional gel electrophoresis was performed and then stained with silver. Protein maps were analyzed and differentially expressed protein spots were detected using ImageMaster 2D Platinum 5.0 software. Results Match rates of (71±4)% and (72±4)% was obtained from gels from controls and pati-ents respectively. 791±17 spots were detected from control gels and 781±17 from patient gels. Eleven protein spots were up-regulated and 9 were down-regulated in SLE patients. Five proteins were identified by MS analysis, some of which had previously been shown to play a potential role in the pathogenesis of SLE. Conclusion There are significant changes in the protein expression of peripheral blood mononuclear cells in systemic lupus erythematosus patients. This study could be used as a preliminary work for better understanding of the pathogenesis and immune regulation pathways of SLE from an integrated lymphocyte protein profile perspective.

OBJECTIVE: To explore the molecular basis for an individual with Ax28 phenotype of the ABO subtype. METHODS: The ABO group antigens on red blood cells of the proband were identified by monoclonal antibodies. The ABO antibody in serum was detected by standard A, B, O cells. Exons 1 to 7 of the ABO gene were respectively amplified by PCR and directly sequenced. Amplicons for exons 5 to 7 were also sequenced after cloning. RESULTS: Weakened A antigen was detected on red blood cells from the proband. Both anti-A and anti-B antibodies were detected in the serum. Heterozygous 261G/del was detected in exon 6, while heterozygous 467C/T and 830T/C were detected in exon 7 by direct DNA sequencing. After cloning and sequencing, two alleles (O01 and Ax28) were obtained. Compared with A102, the sequence of Ax28 contained one nucleotide changes (T to C) at position 830, which resulted in amino acid change (Val to Ala) at position 277. CONCLUSION The novel mutation c.830T>C of the galactosaminyltransferase gene may give rise to the Ax28 phenotype.
ABO Blood-Group System ; genetics ; Alleles ; Amino Acid Substitution ; Exons ; Galactosyltransferases ; genetics ; Genotype ; Humans ; Phenotype ; Polymorphism, Single Nucleotide ; Sequence Deletion

Objective:To explore the feasibility and advantages of different MRI sequences in delineating target volumes in lung cancer with obstructive pneumonia or atelectasis (OC).Methods:Fourteen patients with OC underwent CT localization and MRI scan. CT, T 1WI, fat suppression T 2WI, LAVA, LAVA+ C images were collected respectively. CT and MRI images were fused in the treatment planning system, and GTV-p was target delineated on CT and MRI respectively. Results:CT showed tumor and OC boundaries in 2 patients, fat suppression T 2WI showed tumor and OC boundaries in 10 patients, LAVA showed tumor and OC boundaries in 12 patients, and LAVA+ C showed tumor and OC boundaries in 10 patients. Fat suppression T 2WI, LAVA, and LAVA+ C sequences showed similar resolving ability ( P>0.05). The GTV of T 2WI, LAVA, and LAVA+ C sequences decreased significantly compared with ST-GTV ( P<0.05), and T 2WI_GTV and LAVA_GTV were similar ( P>0.05). The GTV value of LAVA+ C was the smallest among all sequences. Conclusions:The application of MRI fat compression T 2WI, LAVA, and LAVA+ C sequences to the radiotherapy target volume delineation in lung cancer patients with OC improved the accuracy, among which the boundary resolution of LAVA was better than that of fat compression T 2WI, and LAVA+ C showed the best effect on tiny blood vessels.

Lung cancer is the malignant tumor with the highest morbidity and mortality worldwide, most lung cancer patients were diagnosed at an advanced stage. Using low-dose computed tomography(CT) for lung cancer screening in high-risk patients were proved to decrease lung cancer mortality and find out more early-stage patients. However, CT is of high false-positive rate which requires long-term follow-up or invasive examination to confirm the diagnosis. Serum tumor markers have become the focus of early diagnosis of lung cancer due to their characteristics of minimally invasive and good stability. Lung cancer-related antigens can be captured by the immune system to produce autoantibodies. These autoantibodies can appear in the early stage of lung cancer development with high concentration and stably exist. Therefore, the detection of serum autoantibodies can be effective in the early screening and early diagnosis of lung cancer. Here, we provide a systematic review of the production and detection methods of tumor autoantibodies and their application in the diagnosis and screening of malignant tumors, especially lung cancer.

Objective To assess the effects of repeated mild traumatic brain injury(rmTBI)in the parietal cortex on neuronal morphology and synaptic plasticity in the medulla oblongata of mice.Methods Thirty-two male ICR mice were randomly divided into sham operation group(n=8)and rmTBI group(n=24).The mice in the latter group were subjected to repeated mild impact injury of the parietal cortex by a free-falling object.The mice surviving the injuries were evaluated for neurological deficits using neurological severity scores(NSS),righting reflex test and forced swimming test,and pathological changes of the neuronal cells in the medulla oblongata were observed with HE and Nissl staining.Western blotting and immunofluorescence staining were used to detect the expressions of neuroligin 1(NLG-1)and postsynaptic density protein 95(PSD-95)in the medulla oblongata of the mice that either survived rmTBI or not.Results None of the mice in the sham-operated group died,while the mortality rate was 41.67%in rmTBI group.The mice surviving rmTBI showed significantly reduced NSS,delayed recovery of righting reflex,increased immobility time in forced swimming test(P<0.05),and loss of Nissl bodies;swelling and necrosis were observed in a large number of neurons in the medulla oblongata,where the expression levels of NLG-1 and PSD-95 were significantly downregulated(P<0.05).The mice that did not survive rmTBI showed distorted and swelling nerve fibers and decreased density of neurons in the medulla oblongina with lowered expression levels of NLG-1 and PSD-95 compared with the mice surviving the injuries(P<0.01).Conclusion The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.

Objective To assess the effects of repeated mild traumatic brain injury(rmTBI)in the parietal cortex on neuronal morphology and synaptic plasticity in the medulla oblongata of mice.Methods Thirty-two male ICR mice were randomly divided into sham operation group(n=8)and rmTBI group(n=24).The mice in the latter group were subjected to repeated mild impact injury of the parietal cortex by a free-falling object.The mice surviving the injuries were evaluated for neurological deficits using neurological severity scores(NSS),righting reflex test and forced swimming test,and pathological changes of the neuronal cells in the medulla oblongata were observed with HE and Nissl staining.Western blotting and immunofluorescence staining were used to detect the expressions of neuroligin 1(NLG-1)and postsynaptic density protein 95(PSD-95)in the medulla oblongata of the mice that either survived rmTBI or not.Results None of the mice in the sham-operated group died,while the mortality rate was 41.67%in rmTBI group.The mice surviving rmTBI showed significantly reduced NSS,delayed recovery of righting reflex,increased immobility time in forced swimming test(P<0.05),and loss of Nissl bodies;swelling and necrosis were observed in a large number of neurons in the medulla oblongata,where the expression levels of NLG-1 and PSD-95 were significantly downregulated(P<0.05).The mice that did not survive rmTBI showed distorted and swelling nerve fibers and decreased density of neurons in the medulla oblongina with lowered expression levels of NLG-1 and PSD-95 compared with the mice surviving the injuries(P<0.01).Conclusion The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.

BACKGROUND: Tissue engineering is increasingly viewed as a promising avenue for functional cartilage reconstruction.However, chondrocyte dedifferentiation during in vitro culture remains an obstacle for clinical translation of tissue engineered cartilage. Re-differentiated induction have been employed to induce dedifferentiated chondrocytes back to their original phenotype. Regrettably, these strategies have been proven to be only moderately effective. METHODS: To explore underlying mechanism, RNA transcriptome sequencing was conducted on primary chondrocytes (P0), dedifferentiated chondrocytes (P5), and redifferentiated chondrocytes (redifferentiation-induction of P5, P5.R). Based on multiple bioinformatics analysis, LGR5 was identified as a target gene. Subsequently, stable cell lines with LGR5 knocking-down and overexpression were established using P0 chondrocytes. The phenotypic changes in P1 and P5 chondrocytes with either LGR5 knockdown or overexpression were assessed to ascertain the potential influence of LGR5 dysregulation on chondrocyte phenotypes. Regulatory mechanism was then investigated using bioinformatic analysis, protein–protein docking, immunofluorescence co-localization and immunoprecipitation. RESULTS: The current study found that dysregulation of LGR5 can significantly impact the dedifferentiated phenotypes of chondrocytes (P5). Upregulation of LGR5 appears to activate the PI3K/AKT signal via increasing the phosphorylation levels of AKT (p-AKT1). Moreover, the increase of p-AKT1 may stabilize b-catenin and enhance the intensity of Wnt/b-catenin signal, and help to restore the dedifferentated phenotype of chondrocytes. CONCLUSION LGR5 can modulate the phenotypes of chondrocytes in P5 passage through PI3K/AKT signaling pathway.

Objective:To evaluate the nutritional status of patients with decompensated liver cirrhosis and explore the correlation with malnutrition and the risk factors of depressed mood.Methods:190 cirrhotic patients admitted to the Department of Gastroenterology of the First Hospital of Shanxi Medical University from June to September 2023 were selected according to the inclusion and exclusion criteria. Eligible patients were divided into subgroups based on the presence or absence of malnutrition as determined by subjective global assessment (SGA). The Center for Epidemiological Studies Depression (CES-D) scale was used to assess patients' propensity for depressed mood. Relevant clinical data were also collected and analyzed.Results:A total of 185 patients were included, of which 126 were in the non-malnutrition group and 59 malnutrition group. There were significant between-group differences in terms of CES-D results, age, body mass index, platelets, D-dimer, serum sodium, third lumbar skeletal muscle index, grip strength, triceps skinfold thickness, and upper arm muscle circumference (all P<0.05). Correlation analysis showed that grip strength, triceps skinfold thickness, upper arm muscle circumference, serum sodium, and depressed mood tendency status were correlated with the development of cirrhotic malnutrition ( P<0.05). The diagnostic model for malnutrition in cirrhosis using these five indicators showed the area under the curve of 81.9%. Conclusions:Depression is closely related to the development of malnutrition in patients with liver cirrhosis. Independent risk factors for malnutrition in cirrhosis include serum sodium≤135 mmol/L, grip strength, triceps skinfold thickness, lower-than-normal upper arm circumference , and the tendency of depression , which demonstrate the combined contribution to the diagnosis of malnutrition in cirrhosis.

Objective To explore the characteristics of trunk muscle activity in persons with Parkinson's disease (PD) in search of better treatments for abnormal posture.Methods Ninety persons with PD of different severity and 8 normal controls were studied using surface electromyography (sEMG).A sixteen-lead sEMG instrument was used to collect sEMG amplitudes from the bilateral thoracic erector spinae,lumbar erector spinae,external oblique and rectus abdominis muscles when the subjects were lying,standing and walking.Results Compared with the control group,a significant increase was observed in the sEMG amplitude of the lumbar erector spinal muscle [(18.56±14.57) μV] and rectus abdominis muscles [(24.00±18.80)μV] of the PD group when lying.Significant relative increases in (P＜0.05),of the external oblique muscles were observed [(27.87± 11.49)μV] when standing (P＜0.05),and in the thoracic erector spinae muscle [(58.74±29.69)μV] and external oblique muscles [(59.01± 25.20) μV] increased when walking (P＜0.05).Compared with the control group,the sEMG activity of the external oblique muscles was significantly elevated in PD patients at Hoehn and Yahr stage 1 to 1.5 when walking.One or more of the trunk muscle groups showed significantly greater activity in the PD patients in Hoehn and Yahr stage 2 or 3 in all three positions.Conclusions The sEMG activities of the extensor and flexor muscles increase simultaneously in PD patients.More trunk muscles are involved in PD patients with higher H-Y grades.These findings provide a neurophysiological basis for the customizaton of rehabilitation therapy for patients with Parkinson's disease and for the precise selection of muscles for botulinum toxin injection.

Some primary bone tumors are prone to hematogenous metastasis and after that, the therapeutic effect is not that good and prognosis is poor. Circulating tumor cells (CTC) shed from the tumor cells of primary or metastatic focus and then enter into blood circulation. CTC may appear in the early stage of the tumor, which can implant in distant organs to form metastatic sites and self-implant in the primary sites leading to the tumor recurrence; CTC are closely related with the prognosis of patients with tumors. In most primary bone tumors, CTC are heterogeneous compared with primary tumor cells. Studying CTC from various aspects can provide a basis for the early diagnosis and treatment of primary bone tumors. This review summarizes the current researches of CTC in common primary bone tumors, and expects the future of research direction and application practice in clinic.