Roles of human periodontal ligament stem cells in osteogenesis and inflammation in periodontitis models: Effect of 1α,25-dihydroxyvitamin D3.

Periodontitis is a chronic inflammatory disease caused by Porphyromonas gingivalis and other bacteria, and human periodontal ligament stem cells (hPDLSCs) are a promising candidate for the treatment of periodontal supporting tissue defects. This study aimed to investigate the effect of 1α,25-dihydroxyvitamin D3 [1,25(OH)2VitD3] on osteogenic differentiation of hPDLSCs in an in vitro periodontitis model and whether it can improve inflammatory status. hPDLSCs were in vitro isolated and identified. After treatment with 1,25(OH)2VitD3 and ultrapure pure Porphyromonas gingivalis lipopolysaccharide (LPS-G), the viability of hPDLSCs was detected using Cell Counting Kit-8, the expressions of osteogenic markers and inflammatory genes using Western blotting and quantitative reverse transcription PCR (qRT-PCR), the levels of inflammatory factors in cells using enzyme linked immunosorbent assay (ELISA), and the fluorescence signal intensity of osteoblastic markers and inflammatory genes in cells using immunofluorescence assay. It was found that 1,25(OH)2VitD3 reversed the inhibition of hPDLSCs proliferation by LPS-G; LPS-G exhibited inhibitory effect on ALP, Runx2, and OPN expressions, and such inhibitory effect was significantly weakened when co-acting with 1,25(OH)2VitD3. Meanwhile, LPS-G upregulated the expressions of inflammatory genes IL-1ß and Casp1, whereas 1,25(OH)2VitD3 antagonized such an effect and improved the inflammatory status. In conclusion, 1,25(OH)2VitD3 can reverse the inhibitory effect of LPS-G on hPDLSCs proliferation and osteogenic differentiation and suppress LPS-G-induced upregulation of inflammatory gene expressions.

p38 mitogen-activated protein kinase gene silencing rescues rat hippocampal neurons from ketamine-induced apoptosis: An in vitro study.

Ketamine (KTM) is an anesthetic drug with several advantages, including the elevation of cardiac output and blood pressure. However, KTM may also induce the apoptosis of hippocampal neurons. Notably, p38 mitogen­activated protein kinase (p38MAPK) has previously been studied for its role in neuronal injury. Therefore, the present study evaluated the effect of lentivirus­mediated p38MAPK gene silencing on KTM­induced apoptosis of rat hippocampal neurons. Hippocampal neurons were extracted from neonatal Sprague­Dawley rats, and then treated with KTM, p38MAPK­short hairpin RNA or SB203580 (an inhibitor of p38MAPK). Next, the expression levels of p38MAPK and apoptosis­associated genes, including caspase­3, B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein (Bax), were detected. In addition, cell viability and apoptosis were determined using an MTT assay and flow cytometry, respectively. Finally, telomerase activity of hippocampal neurons was detected by ELISA. The results revealed that silencing of p38MAPK in KTM­treated cells decreased the expression levels of p38MAPK, caspase­3 and Bax, and the extent of p38MAPK phosphorylation, while it increased the expression of Bcl­2. Furthermore, silencing p38MAPK promoted cell viability, cell cycle progression and the telomerase activity of hippocampal neurons, and inhibited the apoptosis of hippocampal neurons. Taken together, the results suggested an inhibitory role of lentivirus­mediated p38MAPK gene silencing on KTM­induced apoptosis of rat hippocampal neurons. Thus, p38MAPK gene silencing may serve as a potential target for preventing the KTM­induced apoptosis of hippocampal neurons.

Clinical application of endothelial injury marker in hypertensive patients.

PURPOSE: Endothelial damages are one of the most important causes of persistent hypertensive complications. The aim of our study was to discuss the relationship between the molecular markers of endothelial damage, thrombomodulin, and complications in hypertension. METHODS: A total 132 cases of hypertensive patients, including 13 patients with damage of target organs, were selected as research subjects. And grouping was based on different levels of blood pressure. The blood pressure and thrombomodulin levels were detected among all cases, and their drinking, smoking, and other medical records were tracked. RESULTS: Higher plasma concentration of thrombomodulin was demonstrated in subjects with hypertensive complications compared with without complications [24.5 (18.1,37.55) vs 12.1 (9.1,22.3) TU/mL, P = .001, respectively]. The optimum thrombomodulin cutoff value was determined to be more than 15.5 TU/mL, with a sensitivity of 92.3% and a specificity of 63%. With the increase in blood pressure level, thrombomodulin levels in three groups gradually raised [6.15(5.475,12.75) vs 9.75(7.725,13.35) vs 16.45 (10.125,23.725) TU/mL, P = .007, respectively]. CONCLUSION: With the increase in blood pressure and the occurrence of complications, thrombomodulin showed an increasing trend, which was caused by an increase in the degree of endothelial injury. So, thrombomodulin may serve as a clinically meaningful marker of the progression of hypertension.

Tangeretin alters neuronal apoptosis and ameliorates the severity of seizures in experimental epilepsy-induced rats by modulating apoptotic protein expressions, regulating matrix metalloproteinases, and activating the PI3K/Akt cell survival pathway.

PURPOSE: Epilepsy is complex neural disarray categorized by recurring seizures. Despite recent advances in pharmacotherapies for epilepsy, its treatment remains a challenge due to the contrary effects of the drugs. As a result, the identification of novel anti-epileptic drugs (AEDs) with neuroprotective properties and few side effects is of great value. Thus, the present study assessed the treatment effects of tangeretin using a rat model of pilocarpine-induced epilepsy. MATERIALS AND METHODS: Separate groups of male Wistar rats received oral administrations of tangeretin at 50, 100, or 200mg/kg for 10 days and then, on the 10th day, they received an intraperitoneal injection of pilocarpine (30mg/kg). Subsequently, neuronal degeneration and apoptosis were assessed using Nissl staining and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay procedures. Additionally, the expressions of phosphatidylinositol-3-kinase (PI3K/Akt) pathway proteins, cleaved caspase-3, Bad, Bcl-2, Bcl-xL, and Bax were determined using Western blot analyses. RESULTS: Tangeretin reduced the seizure scores and latency to first seizure of the rats and effectively activated the pilocarpine-induced suppression of PI3K/Akt signaling. Additionally, tangeretin effectively regulated the levels of apoptosis-inducing factor (AIF) in mitochondria as well as the expressions of apoptotic pathway proteins. Seizure-induced elevations in the activities and expressions of matrix metalloproteinases (MMPs)-2 and -9 were also modulated. CONCLUSION: The present results indicate that tangeretin exerted potent neuroprotective effects against pilocarpine-induced seizures via the activation of PI3K/Akt signaling and the regulation of MMPs.

[Comparative study on bilateral temporomandibular joint of patients with unilateral multiple symptoms in cone-beam computed tomography].

PURPOSE: To investigate bilateral temporomandibular joint of patients with unilateral multiple symptoms in cone-beam computed tomography (CBCT) and explore the reference planes that may be different,providing reference for the diagnosis of temporomandibular disorders and comparative study. METHODS: 50 cases with unilateral multiple symptoms（except for cases with unilateral single symptom）were examined by CBCT and the following indexes were observed and analyzed,including horizontal angles of the cross-sectional condyle after the reconstruction in the same patient, joint space, macroaxis diameter of condyle and vertical angles of condyle, which were commonly used at oblique position parallelled to the long axis of condyle, the gradient of articular tubercle and the joint space,which could be obtained at sagittal and oblique position vertical to the long axis of condyle.The data obtained was analyzed by paired t test with SPSS13.0 software package. RESULTS: There was significant difference between the bilateral measured value of joint space when the angle was 60° in sagittal plane (P<0.05).The difference was more significant when the angle was 120° in parallel plane and 90° in sagittal plane (P<0.01). The other measured parameters were not significant different. CONCLUSIONS: For patients with TMD, it is more easily to observe differences between the bilateral measured value of joint space in the sagittal or vertical plane,where the increase of the front joint space can be seen and construction was more significant.

[Mastoid surgery for secretory otitis media with mixed hearing loss].

OBJECTIVE: To analyze the therapeutic effect of mastoid surgery for secretory otitis media with mixed hearing loss. METHODS: A retrospective analysis was conducted of the data from 26 cases (43 ears) of secretory otitis media with bone conduction hearing loss collected from 2001 to 2008. Thirty-two ears were treated with mastoid surgery and myringotomy with insertion of ventilation tubes. All the patients received medications after the operation. RESULTS: All the patients showed obvious improvement after mastoid surgery. The average pure tone of air conduction hearing threshold was about 25 dB after the surgery, with the average pure tone of bone conduction hearing threshold of about 15 dB. The patients were followed up for 1-2 years during which no significant change in hearing was recorded, and no middle ear effusion in the tympanic cavity was found after removal of the ventilation tubes. CONCLUSION: Persistent secretory otitis media can be associated with mixed hearing loss, and mastoid surgery can significantly enhance the hearing level to produce positive therapeutic effects.