Periodontal bone defects, primarily caused by periodontitis, are highly prevalent in clinical settings and manifest as bone fenestration, dehiscence, or attachment loss, presenting a significant challenge to oral health. In regenerative medicine, harnessing developmental principles for tissue repair offers promising therapeutic potential. Of particular interest is the condensation of progenitor cells, an essential event in organogenesis that has inspired clinically effective cell aggregation approaches in dental regeneration. However, the precise cellular coordination mechanisms during condensation and regeneration remain elusive. Here, taking the tooth as a model organ, we employed single-cell RNA sequencing to dissect the cellular composition and heterogeneity of human dental follicle and dental papilla, revealing a distinct Platelet-derived growth factor receptor alpha (PDGFRA) mesenchymal stem/stromal cell (MSC) population with remarkable odontogenic potential. Interestingly, a reciprocal paracrine interaction between PDGFRA⁺ dental follicle stem cells (DFSCs) and CD31⁺ Endomucin⁺ endothelial cells (ECs) was mediated by Vascular endothelial growth factor A (VEGFA) and Platelet-derived growth factor subunit BB (PDGFBB). This crosstalk not only maintains the functionality of PDGFRA⁺ DFSCs but also drives specialized angiogenesis. In vivo periodontal bone regeneration experiments further reveal that communication between PDGFRA⁺ DFSC aggregates and recipient ECs is essential for effective angiogenic-osteogenic coupling and rapid tissue repair. Collectively, our results unravel the importance of MSC-EC crosstalk mediated by the VEGFA and PDGFBB-PDGFRA reciprocal signaling in orchestrating angiogenesis and osteogenesis. These findings not only establish a framework for deciphering and promoting periodontal bone regeneration in potential clinical applications but also offer insights for future therapeutic strategies in dental or broader regenerative medicine.
Receptor, Platelet-Derived Growth Factor alpha/metabolism* ; Humans ; Neovascularization, Physiologic/physiology* ; Dental Sac/cytology* ; Single-Cell Analysis ; Transcriptome ; Mesenchymal Stem Cells/metabolism* ; Bone Regeneration ; Animals ; Dental Papilla/cytology* ; Periodontium/physiology* ; Stem Cells/metabolism* ; Regeneration ; Angiogenesis

Objective: To explore the effects of microRNA-34a on regulating silent information regulator 1 (SIRT1) and influence of SIRT1 on myocardial damage of rats with severe burns at early stage. Methods: (1) Twenty-four Sprague-Dawley (SD) rats were divided into sham injury (SI) group, simple burns (SB) group and SIRT1 agonist (SA) group according to the random number table (the same grouping method below), with 8 rats in each group. Rats in groups SB and SA were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burns) on the back, and rats in group SI were sham injuried on the back. Immediately after injury, rats in groups SI and SB were intraperitoneally injected with normal saline of 50 mL/kg, and rats in group SA were intraperitoneally injected with normal saline of 50 mL/kg and 1 mg/mL resveratrol of 50 mg/kg. At 6 h post injury, abdominal aortic blood was collected to make serum and myocardial tissue of rats was collected. (2) Myocardial cells of twelve neonatal SD rats were collected and divided into microRNA-34a mimic control (MMC) group, microRNA-34a mimic (MM) group, microRNA-34a inhibitor control (MIC) group, and microRNA-34a inhibitor (MI) group, which were respectively transfected with gene sequences of mimic control, mimic, inhibitor control, and inhibitor of microRNA-34a. The microRNA-34a expression level and protein expression level of SIRT1 in myocardial cells were respectively detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Another batch of myocardial cells were divided into microRNA-34a inhibitor control+ burn serum (MCB) group, microRNA-34a inhibitor+ burn serum (MB) group, and microRNA-34a inhibitor+ burn serum + EX527 (MBE) group. Myocardial cells in group MCB were transfected with gene sequence of inhibitor control, and myocardial cells in the later groups were transfected with gene sequence of inhibitor of microRNA-34a. After transfection of 48 h, myocardial cells in group MBE were cultured in Dulbecco′s modified Eagle′s medium (DMEM) solution for 6 hours, with serum in group SB of volume fraction of 10% and final amount-of-substance concentration of 1 mol/L, and myocardial cells in the other 2 groups were cultured in DMEM solution with serum from rats of group SB of volume fraction of 10%. The protein expression levels of myocardial cells of SIRT1, cleaved-caspase-3, and Bax were detected by Western blotting. (3) Myocardial tissue from (1) was collected to detect expression levels of microRNA-34a and mRNA of SIRT1 in groups SI and SB by real-time fluorescence quantitative RT-PCR. Morphology of myocardial tissue of rats in groups SI, SB, and SA was observed with biological image navigator. The mRNA expression levels of interleukin 1β (IL-1β) and tumor necrosis factor (TNF-α) of rats in groups SI, SB, and SA were detected by real-time fluorescence quantitative RT-PCR. The expression levels of cleaved-caspase-3, and Bax of myocardial tissue of rats in groups SI, SB, and SA were detected by Western blotting. Data were processed with one-way analysis of variance and least-significant difference test. Results: (1) After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MM was 4.67±0.92, significantly higher than 1.03±0.04 in group MMC (P<0.01); the protein expression level of SIRT1 of myocardial cells in group MM was 0.35±0.06, significantly lower than 1.12±0.11 in group MMC (P<0.01). After transfection of 48 h, the expression level of microRNA-34a of myocardial cells in group MI was 0.26±0.07, significantly lower than 1.33±0.07 in group MIC (P<0.01); the protein expression level of SIRT1 of myocardial cells in group MIC was 1.12±0.16, significantly lower than 1.74±0.34 in group MI (P<0.01). At 6 h after culture, compared with those in group MCB, the SIRT1 protein expression level of myocardial cells in group MB was significantly increased (P<0.05), while cleaved-caspase-3 and Bax protein expression levels of myocardial cells in group MB were significantly decreased (P<0.05). Compared with those in group MB, the SIRT1 protein expression level of myocardial cells in group MBE was with no significantly statistical difference (P>0.05), and cleaved-caspase-3 and Bax protein expression levels were significantly increased (P<0.05). (2) At 6 h post injury, compared with that in group SI, the microRNA-34a expression level of myocardial tissue in group SB was significantly increased (P<0.01), and the mRNA expression level of SIRT1 of myocardial tissue in group SB was significantly decreased (P<0.01). At 6 h post injury, myocardial cells in group SI arranged neatly with normal nucleus and no inflammatory cells infiltration; myocardial cells in group SB arranged disorderly, with no abnormal nucleus, and obvious inflammatory cells infiltration; myocardial cells in group SA arranged neatly, with normal nucleus and little inflammatory cells infiltration. At 6 h post injury, compared with those in group SB, the mRNA expression levels of IL-1β and TNF-α, and the protein expression levels of cleaved-caspase-3 and Bax of myocardial tissue in groups SI and SA were significantly decreased (P<0.01). Conclusions The microRNA-34a expression level of myocardial tissue of rats with severe burns at early stage increases, which decreases the expression level of SIRT1, and increases the expression levels of IL-1β, TNF-α, cleaved-caspase-3 and Bax, leading to obvious myocardial damage. Activation of SIRT1 can alleviate myocardial damage of rats with severe burns at early stage through decreasing expression levels of IL-1β, TNF-α, cleaved-caspase-3, and Bax.

Objective To probe the correlation between preoperative pulmonary dysfunction and postoperative pulmonary complications in patients of orthotopic liver transplantation. Methods From August 2008 to June 2009, 71 orthotopic liver transplantation patients were studied. Preoperative pulmonary function and its relationship with postoperative pulmonary complications were analyzed.Results Preoperatively 65 out of 71 patients had abnormal lung functions, suffering from pulmonary diffusing capacity reduction (65 cases, 91.5% ), followed by reduction of restrictive ventilation function (30 cases, 42. 2% ), small airway function reduction ( 28 cases, 39.4% ), and obstructive ventilatory function reduction (21 cases, 29. 6% ). The incidence of postoperative pulmonary complications was 56. 3% including: pulmonary atelectasis, pneumonia, acute respiratory failure. The incidence of posttransplantation pulmonary complications in patients with pulmonary restrictive or obstructive ventilation function reduction was higher than in normal group (x2 = 6.703, P= 0.010; x2 = 4.768, P = 0.029), and there was significant difference in pulmonary complication rate between groups of moderate and severe diffusing capacity reduction and mild reduction and normal range (x2 = 8.478, P = 0.004 ).Conclusions Preoperative pulmonary function abnormality in patients before liver transplantation such as pulmonary ventilatory function reduction (VCmax ＜ 80% or FEV1.0 ＜ 80% ) and moderate to severe pulmonary diffusing capacity reduction (TLCOSB ＜ 60% ) predicts higher incidence of postoperative pulmonary complications.

Objective To develop an embedded system by using time-triggered system and ATmega128.Methods Making use of the minimum system structure of ATmega128,a multitask system,which could be implanted into AVR CPU,was designed based on the singlechip with 8 bits and 51series.Results Time-Triggered Embedded System kept the controlling precision on ms degree and ensured a sensitive and rapid response to keyboard input.Conclusion Software designed by Time-Triggered Embedded System has advantage in real time,so it is applicable to minitype real time control system.

Objective To study the diagnosis and treatment for the syndrome of inappropriate antidiuretic hormone secretion in neurosurgery.Methods Retrospective analyze clinical situation, treatment, and process of final diagnosis in 6 SIADH cases.Result Diagnosis of SIADH and differential diagnosis with CSWS is very difficult.In clinic the experimental therapy of restricting water and natrium is a important method of differential diagnosis,but also a effective therapy.Conclusion Speciality of SIADH is (1)hyponatremia(Na +≤128 mmol/L),natriuresis(Na +≥80 mmol/24h),(2)ADH assay is no significant for SIADH and CSWS,(3)no hypervolemia and edema exhibition,(4)restrict water is effective in treatment.

Objective To study the diagnosis and treatment of the inappropriate antidiuretic hormone secretion(SIADH) syndrome after cerebral injury. Methods A retrospective analysis was conducted on 12 patients suffered from SIADH after cerebral injury. The clinical features were similar to common hyponatremia, no specific manifestation. Most of the hyponatremia were detected by routine examination. The first of all,sodium losing in these patients with hyponatremia was routine supplied according the amont of true salt losing.If natremia was not raised or still more descended 2～3 days after treatment, and amount of supplying salt was correspond to that of natriuresis, SIADH should be considered,using restricting water therapy,substituted for salt supplement.furosemide plus albumin were the first choice for dehydration therapy. Results 24～48h after restricting water and natrium, 12 patient's natremia level was back up in different degree. Except for 2 death whose natremia was not corrected completely, 8 patient's natremia was corrected completely in 1 week, 1 patient's in 14 days, and 1 in 3 months after injury. Conclusions Diagnosis of SIADH is very difficult before treatment, but effective treatment can be obtained if we adopt correcting strategy. In these patients, the diagnosis of SIADH was confirmed with the course of treatment,we call it as therapeutic diagnosis.