Objective:To establish an animal model of trans-sutural distraction osteogenesis in SD rats.Methods:A self-designed V-shaped distraction device(distractor)was fabricated with the traction force(N)of 0,1.3,2.2,3.0,4.3 and 5.0 corresponding to the distraction length(mm)of 5,4,3,2,1 and 0 respectively,meeting the trans-sutural distraction osteogenesis requirements in skull of 5-week-old SD rats.The distractor was plased into the sagittal suture of 12 SD rats.Continuous sampling was conducted 1,3,5 and 7 days respectively(n=3)after operation.The tissue changes in the trans-sutural distraction area were observed by HE and Masson's trichrome staining.Inflammation levels were determined using Arg-1 immunofluorescence staining.The early angiogenesis was clarified through co-staining with CD31 and EMCN.Results:A stable trans-sutural distraction osteogenesis model was estab-lished,5 mm distraction osteogenesis width was observed completely within 7 days of distraction.Significant new bone formation was observed at 7 days after operation.Arg-1 expression increased and was concentrated at the bone margins,overlapping with the areas of new bone formation.EMCN expression gradually decreased,and by day 7 CD31 was predominant,indicating the basic maturation of blood vessels.Conclusion:This study successfully constructed a stable and effective trans-sutural distraction osteogenesis animal model,and provides an experimental basis for the investigation of its early continuous histological changes.

This study investigated the association between serum 25(OH)D 3 levels and cardiovascular risk-related indicators. 4 727 participants aged 20 and above from the National Health and Nutrition Examination Survey 2015-2018 database were enrolled. Body mass index, hypersensitive C-reactive protein, high density lipoprotein cholesterol, systolic blood pressure, waist-height ratio, and total cholesterol were selected as the research indicators. Weighted multiple linear regression models, subgroup analyses, smooth curve fitting, and saturation threshold effect analyses were employed to explore the relationship between serum 25(OH)D 3 and these indicators. The results showed that after full adjustment for covariates, every 1 nmol/L increase in serum 25(OH)D 3, the changes in β (95% CI) values for body mass index(BMI), hypersensitive C-reactive protein(hs-CRP), systolic blood pressure(SBP), waist-height ratio(WHtR), high density lipoprotein cholesterol(HDL-C), and total cholesterol(TC) were -0.05 (-0.06, -0.04) kg/m 2, -0.01 (-0.02, -0.01) mg/L, -0.02 (-0.04, -0.01) mmHg, -0.000 7 (-0.000 8, -0.000 6), 0.10 (0.08, 0.11) mg/dl, and 0.08 (0.04, 0.12) mg/dl, respectively. Female participants were more sensitive to changes in serum 25(OH)D 3, while participants aged 60 and above were relatively less sensitive. The relationship between serum 25(OH)D 3 and these indicators partially exhibited nonlinear patterns across different gender and age subgroups. The saturation threshold effect analysis revealed 8 meaningful inflection points. In summary, vitamin D has a close association with cardiovascular risk-related indicators.

This study investigated the association between serum 25(OH)D 3 levels and cardiovascular risk-related indicators. 4 727 participants aged 20 and above from the National Health and Nutrition Examination Survey 2015-2018 database were enrolled. Body mass index, hypersensitive C-reactive protein, high density lipoprotein cholesterol, systolic blood pressure, waist-height ratio, and total cholesterol were selected as the research indicators. Weighted multiple linear regression models, subgroup analyses, smooth curve fitting, and saturation threshold effect analyses were employed to explore the relationship between serum 25(OH)D 3 and these indicators. The results showed that after full adjustment for covariates, every 1 nmol/L increase in serum 25(OH)D 3, the changes in β (95% CI) values for body mass index(BMI), hypersensitive C-reactive protein(hs-CRP), systolic blood pressure(SBP), waist-height ratio(WHtR), high density lipoprotein cholesterol(HDL-C), and total cholesterol(TC) were -0.05 (-0.06, -0.04) kg/m 2, -0.01 (-0.02, -0.01) mg/L, -0.02 (-0.04, -0.01) mmHg, -0.000 7 (-0.000 8, -0.000 6), 0.10 (0.08, 0.11) mg/dl, and 0.08 (0.04, 0.12) mg/dl, respectively. Female participants were more sensitive to changes in serum 25(OH)D 3, while participants aged 60 and above were relatively less sensitive. The relationship between serum 25(OH)D 3 and these indicators partially exhibited nonlinear patterns across different gender and age subgroups. The saturation threshold effect analysis revealed 8 meaningful inflection points. In summary, vitamin D has a close association with cardiovascular risk-related indicators.

Objective:To investigate the effect of the transcriptional coactivator Mediator 1 (Med1) on mouse hair regeneration, and to explore potential mechanisms.Methods:Med1 flox/flox C57BL/6J mice were mated with K14-Cre mice, and the mice with epidermis-specific knockout of Med1 gene, namely K14-Cre-expressing Med1 flox/flox mice (knockout group) , were obtained by using the Cre-Loxp system, while Med1 flox/flox mice without K14-Cre expression served as control group. Mice in the two groups (3 mice in each group) were raised together for 8 weeks followed by dorsal hair removal. Hair regeneration was observed for 12 consecutive days after hair removal. After 12 days, all mice in the two groups were sacrificed, their depilated and non-depilated dorsal skin tissues were resected, and total RNA was extracted from the tissues. Real-time quantitative PCR was performed to determine the mRNA expression of hair keratin genes, vitamin D receptor/β-catenin pathway-related genes, and genes associated with maintenance of hair follicle stem cell proliferation and quiescence. Paraffin-embedded sections of depilated and non-depilated mouse skin tissues were prepared, and immunofluorescence staining was conducted to determine the number of stem cells in the hair follicle bulge. Two-independent-sample t test was used for comparisons between two groups. Results:From days 0 to 12 after depilation, hair regeneration was delayed in the depilated skin area in the knockout group compared with the control group. Real-time quantitative PCR showed significantly decreased mRNA relative expression levels of hair keratin genes Ha1 and Krt2-16, vitamin D receptor/β-catenin pathway-related genes S100a3, Dlx3 and Tubb3, and genes associated with maintenance of hair follicle stem cell proliferation and quiescence including Lhx2, Sox9 and Nfatc1 in the depilated skin tissues in the knockout group (22.09 ± 12.32, 2.07 ± 0.20, 0.02 ± 0.01, 12.36 ± 2.12, 1.75 ± 0.46, 0.39 ± 0.02, 4.42 ± 0.76, 0.44 ± 0.07, respectively) compared with the control group (70.53 ± 9.46, 7.76 ± 0.49, 0.05 ± 0.01, 26.16 ± 2.96, 2.60 ± 0.14, 0.71 ± 0.09, 11.93 ± 0.42, 0.75 ± 0.04, respectively; t = 5.40, 18.64, 3.89, 6.57, 3.04, 6.10, 15.03, 6.18, respectively, all P < 0.05) . Immunofluorescence staining showed that the number of CD34 +K15 + hair follicle stem cells in the hair follicle bulge in both depilated and non-depilated skin tissues was significantly lower in the knockout group than in the control group. Conclusion:Med1 gene knockout may down-regulate the expression of downstream genes of the vitamin D receptor/β-catenin pathway and genes associated with maintenance of hair follicle stem cell proliferation and quiescence (Sox9, Nfatc1 and Lhx2) , and reduce the number of hair follicle stem cells, leading to hair follicle differentiation disorder and hair regeneration delay.

We presented an adolescent with recurrent intracranial hemorrhage and skin lesion. The diagnosis was unclear and the treatment was difficult. Through a multidisciplinary effort type Ⅰ interferon disease was suspected and later, an interferon-stimulated gene was further detected. Considering the high morbidity and fatality rate of recurrent intracranial hemorrhage, tofacitinib and hydroxychloroquine were administered. After treatment, the livedo reticularis was significantly regressed. Unfortunately, the intracranial hemorrhage recurred due to a pre-existing cerebral aneurysm, leading to death of the patient. The diagnosis and treatment of this case highlight the importance of multidisciplinary collaboration in the diagnosis and treatment of difficult and rare diseases.

To strengthen the Party′s overall leadership over public hospitals is the cornerstone to ensure nonprofit and sustainable development of public hospitals.It is a vital guarantee to promote the Party construction work at public hospitals by establishing and improving the hospital′s internal management organization, management system, rules of procedure and handling system. This study aimed to establish the operation system of the rules of procedure of the Party committee meeting of public hospitals by building an office automation platform. This system could connect functions covering topics determination, meeting convening, resolution implementation, and supervision in an effort to achieve a closed-loop management and to realize the controllability, feedback and traceability of the decision-making process. The closed-loop management could not only ensures that the decision-making process be scientific and standardized, but also the decision-making efficiency, for reference in the Party committees of other public hospitals in improving their efficiency and quality of debate and decision making.

Objective    To investigate the safety and effectiveness of the multi-artery graf tstrategy for coronary bypass (MICS-CABG) with small incision in the left chest, and to provide experience for the promotion of this technique. Methods    The clinical data of 64 patients with MICS-CABG in Department of Cardiac Surgery of Peking University Third Hospital from December 2015 to November 2019 were retrospectively analyzed. There were 54 males and 10 females, aged 36-77 (61.1±8.7) years. The left lateral thoracic incision (5-8 cm) was made through the 5th intercostal incision, and the operation was performed under off-pump CABG. With the help of the chest wall suspension device and the heart fixator, the proximal anastomosis of the ascending aorta, anastomosis of the target vessels of the left anterior descending (LAD), left circumflex (LCX) and right coronary artery (RCA) systems were completed. The number of grafts was 2-4 (2.3±0.5) including 2 grafts in 45 patients, 3 grafts in 17 patients and 4 grafts in 2 patients. Three patients were treated with percutaneous intervention (PCI) hybridization and 62 patients were treated with total artery bypass graft. Coronary angiography was performed within 7 days after the operation to evaluate the graft patency rate. The incidence of major adverse cardiac and cerebrovascular events (MACCE) was recorded in the follow-up. The MACCE rate was calculated by Kaplan-Meier method. Results    None of the patients was transferred to thoracotomy and no intra-aortic balloon counterpulsation (IABP) or extracorporeal membrane oxygenation (ECMO) was used during the operation.  Incision infection was in 1 patient and reoperation in 2 patients (all were postoperative hemorrhage). Within 30 days after surgery, MACCE occurred in 1 patient, including 1 patient of non-fatal myocardial infarction. The overall patency rate of angiography bypass was 96.2%, and the patency rate of anterior descending branch bypass was 98.2%. Follow-up was performed from 12 to 60 months (median follow-up time was 28 months). The loss rate was 7.8% (5/64). The incidence of MACCE was 84.9% (95%CI 79.5%-90.3%). Conclusion    The MICS-CABG can achieve completed re-vascularization and totally artery-CABG and the short-term and medium-term clinical results of the operation are good.

Prostate cancer is a complex, heterogeneous disease that mainly affects the older male population with a high-mortality rate. The mechanisms underlying prostate cancer progression are still incompletely understood. Beta-adrenergic signaling has been shown to regulate multiple cellular processes as a mediator of chronic stress. Recently, beta-adrenergic signaling has been reported to affect the development of aggressive prostate cancer by regulating neuroendocrine differentiation, angiogenesis, and metastasis. Here, we briefly summarize and discuss recent advances in these areas and their implications in prostate cancer therapeutics. We aim to provide a better understanding of the contribution of beta-adrenergic signaling to the progression of aggressive prostate cancer.

Prostate cancer is a complex, heterogeneous disease that mainly affects the older male population with a high-mortality rate. The mechanisms underlying prostate cancer progression are still incompletely understood. Beta-adrenergic signaling has been shown to regulate multiple cellular processes as a mediator of chronic stress. Recently, beta-adrenergic signaling has been reported to affect the development of aggressive prostate cancer by regulating neuroendocrine differentiation, angiogenesis, and metastasis. Here, we briefly summarize and discuss recent advances in these areas and their implications in prostate cancer therapeutics. We aim to provide a better understanding of the contribution of beta-adrenergic signaling to the progression of aggressive prostate cancer.
Cell Differentiation/genetics* ; Disease Progression ; Humans ; Male ; Neoplasm Metastasis ; Neovascularization, Pathologic/pathology* ; Neuroendocrine Cells/pathology* ; Prostatic Neoplasms/pathology* ; Receptors, Adrenergic, beta ; Signal Transduction

OBJECTIVETo screen for KIT gene mutations in two Han Chinese pedigrees affected with Piebaldism.

METHODSClinical data of the pedigrees was collected. Genomic DNA was extracted from blood samples collected from the pedigrees and 120 unrelated healthy controls. All coding exons of the KIT gene were subjected to PCR amplification and direct sequencing.

RESULTSTwo missense mutations, c.1861G>A(p.Ala621Thr) and c.1872G>A(p.Met624Ile), were identified respectively in the two pedigrees. Neither mutation was found among healthy members from the respective pedigree and the 120 unrelated healthy controls. c.1872G>A is a novel mutation.

CONCLUSIONMutations of the KIT gene may affect the structure and function of the transmembrane receptor KIT, which lead to the disease.