Objective To study the clinical effect of total parathyroidectomy with subcutaneous autotransplantation (TPTX + AT) in the treatment of secondary hyperparathyroidism(SHPT) in patients with chronic renal failure.Methods One hundred and thirty-four patients undergoing TPTX + AT in our hospital from January 2013 to October 2014 were includud in this study.The preoperative,postoperative and follow-up intact parathyroid hormone (iPTH),serum calcium,serum phosphorus and calcium-phosphorus product were statistically analyzed.The Kidney Disease Quality of Life Short Form (KDQOL-SFTM) scale was used to evaluate quality of life before and one year after parathyroidectomy.Postoperative complications and recurrence were observed.Results Postoperative iPTH,serum calcium,serum phosphorus and calciumphosphorus product decreased significantly compared with that before surgery.The difference had statistical significance (all P ＜ 0.05).One patient died in perioperative period.Temporary injury of recurrent laryngeal nerve was found in eight patients.Early postoperative hypocalcemia was frequently seen in 124 patients (92.5％) and in 7 cases (5.2％) occured intractable hypocalcemia.The quality of life was significantly improved one year after parathyroidectomy.Recurrence developed in 5 patients after operation.Conclusions TPTX + AT is safe and effective in the treatment of SHPT in patients with chronic renal failure and can significantly improve the patient's quality of life.

Objective To detect CYP2J3 gene expression and contents of 11,12-EET in heart,liver,lung,kidney and aorta thoracalis after CYP2J3 gene transfection.Methods The rat transgenic model was developed by injecting plasmid through vena dorsalis penis.The animals were divided into control group、 pcDNA3.1 transgenic group and pcDNA3.1-CYP2J3 transgenic group.The expression of CYP2J3 mRNA was detected by RT-PCR and content of 11,12-EET was examined by the HPLC at 14 days and 28 days after injection.Results Twenty eight days after injection,both expression of CYP2J3 mRNA and the content of 11,12-EET were significantly increased as compared with that of control and pcDNA3.1 transgenic group(P

Objective To investigate the correlation between microembolic signal (MES) and immune inflammation in patients with acute ischemic stroke. Methods The consecutive patients with acute ischemic stroke were enroled. According to the results of MES, they were divided into either a positive group or a negative group. The Immune inflammatory indexes, demographics, and baseline clinical data in both groups were compared. Multivariate logistic regression analysis was used to analyze the independent influencing factors of MES in acute ischemic stroke. Results A total of 237 patients were enroled, including 52 in the MES positive group and 185 in the MES negative group. There were significant differences in the levels of triglyceride (2. 130 ± 0. 933 mmol/L vs. 1. 811 ± 0. 962 mmol/L; t = 2. 126, P = 0. 035), plasma fibrinogen (2. 946 ± 0. 255 g/L vs. 2. 833 ± 0. 322 g/L; t = 2. 332, P = 0. 021 ), Lp-PLA2 level ( 288. 265 ± 27. 855 μg/L vs. 261. 652 ± 29. 961 μg/L; t = 2. 897, P = 0. 004 ), as wel as the proportions of CD4 + CD25high Treg (8. 695% ± 1. 461% vs. 9. 445% ± 1. 397% ; t = 3. 386, P = 0. 001), artery stenosis ≥70% (21. 15% vs. 5. 41% ; χ2 = 10. 592, P = 0. 001 ) and smal arterial occlusive stroke (9. 62% vs. 23. 24% ; χ2 = 4.667, P = 0. 031) between the MES positive group and the MES negative group. Multivariate logistic regression analysis showed that the increased plasma fibrinogen level (odds ratio [OR] 3. 257, 95%confidence interval [CI] 1. 124 - 9. 438; P = 0. 030), artery stenosis ≥ 70% (OR 3. 585, 95% CI 1. 394 -9. 219; P = 0. 008), and the decreased ratio of Treg (OR 3. 801, 95% CI 1. 190 - 12. 148; P = 0. 024) were the independent risk factors for positive MES, and smal arterial occlusive stroke was its independent protective factor (OR 0. 244, 95% CI 0. 072 - 0. 829; P = 0. 024). Conclusions MES may be associated with immune inflammation. The relationship between stroke and immune inflammation should be taken seriously.

Objective:To explore the regulatory effect of exosomes derived from healthy human adipose stem cells (ADSC) on the fibrosis of localized scleroderma fibroblasts (LSFs) in vitro. Methods:From January 2021 to January 2022, fat from 10 healthy donors in Department of Plastic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences was collected by liposuction. Adipose stem cells were isolated and cultured in vitro, and exosomes (ADSC-Exo) were collected. Fibroblasts were isolated from skin tissue of 15 patients with localized scleroderma during the same period and cultured in vitro. Induced differentiation and staining, nanoparticle tracking analysis, transmission electron microscopy, PKH26 staining and Western blotting were used to identify ADSC and their exosomes. The effect of ADSC on the expression of fibrosis markers [collagen Ⅰ, collagen Ⅲ, α-smooth muscle actin (α-SMA)] in LSFs through its exosomes was examined by extracellular vesicle secretion inhibition assay. The proliferation and migration abilities of LSFs treated with ADSC-Exo were tested by CCK-8 method and scratch test. Real-time quantitative PCR, immunofluorescence staining and Western blotting were used to detect the expression levels of collagen Ⅰ, collagen Ⅲ, α-SMA, transforming growth factor β (TGF-β) and p-Smad2/3 in LSFs. Independent sample t-test was used to compare between the two groups. One-way ANOVA was used for multi-group comparison, and SNK- q test was used for pairwise comparison. Results:ADSC and LSFs were successfully isolated and cultured in vitro, and ADSC-Exo was extracted. Extracellular vesicle secretion inhibition assay demonstrated that ADSC decreased fibrotic markers of LSFs by secreting extracellular vesicles. Results of CCK-8 and scratch test showed that the proliferation and migration ability of LSFs was decreased by ADSC-Exo treatment. The results of real-time quantitative PCR, immunofluorescence staining and Western blotting showed that compared with the control group, the expressions of collagen Ⅰ, α-SMA, TGF-β and p-Smad 2/3 in the ADSC-Exo treatment group were significantly decreased. Conclusion:In vitro, ADSC-Exo can affect the biological behavior and reduce the expression of fibrosis markers in LSFs by inhibiting the TGF-β/Smad pathway.

Objective:To explore the regulatory effect of exosomes derived from healthy human adipose stem cells (ADSC) on the fibrosis of localized scleroderma fibroblasts (LSFs) in vitro. Methods:From January 2021 to January 2022, fat from 10 healthy donors in Department of Plastic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences was collected by liposuction. Adipose stem cells were isolated and cultured in vitro, and exosomes (ADSC-Exo) were collected. Fibroblasts were isolated from skin tissue of 15 patients with localized scleroderma during the same period and cultured in vitro. Induced differentiation and staining, nanoparticle tracking analysis, transmission electron microscopy, PKH26 staining and Western blotting were used to identify ADSC and their exosomes. The effect of ADSC on the expression of fibrosis markers [collagen Ⅰ, collagen Ⅲ, α-smooth muscle actin (α-SMA)] in LSFs through its exosomes was examined by extracellular vesicle secretion inhibition assay. The proliferation and migration abilities of LSFs treated with ADSC-Exo were tested by CCK-8 method and scratch test. Real-time quantitative PCR, immunofluorescence staining and Western blotting were used to detect the expression levels of collagen Ⅰ, collagen Ⅲ, α-SMA, transforming growth factor β (TGF-β) and p-Smad2/3 in LSFs. Independent sample t-test was used to compare between the two groups. One-way ANOVA was used for multi-group comparison, and SNK- q test was used for pairwise comparison. Results:ADSC and LSFs were successfully isolated and cultured in vitro, and ADSC-Exo was extracted. Extracellular vesicle secretion inhibition assay demonstrated that ADSC decreased fibrotic markers of LSFs by secreting extracellular vesicles. Results of CCK-8 and scratch test showed that the proliferation and migration ability of LSFs was decreased by ADSC-Exo treatment. The results of real-time quantitative PCR, immunofluorescence staining and Western blotting showed that compared with the control group, the expressions of collagen Ⅰ, α-SMA, TGF-β and p-Smad 2/3 in the ADSC-Exo treatment group were significantly decreased. Conclusion:In vitro, ADSC-Exo can affect the biological behavior and reduce the expression of fibrosis markers in LSFs by inhibiting the TGF-β/Smad pathway.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.