Morphometric evaluation of alveolar bone after orthodontic treatment of multiple impacted teeth in the unilateral maxillary anterior region.

INTRODUCTION: This study aimed to investigate the height and thickness of alveolar bone by cone-beam computed tomography imaging after orthodontic treatment in the unilateral maxillary anterior region and speculate on reasons for the difference in alveolar bone morphology. METHODS: This study selected 11 patients (3 males and 8 females; mean age, 9.42 ± 1.45 years). Cone-beam computed tomography was performed for these 11 patients before and after treatment using Dolphin Imaging software (Dolphin Imaging and Management Solutions, Chatsworth, Calif). Labial and palatal alveolar bone thickness (BT) at root apices and different levels along the roots and loss of alveolar bone height was measured for each impacted tooth and its contralateral homonymous tooth. RESULTS: After orthodontic therapy, all 3 impacted anterior teeth had different degrees of loss of labial alveolar bone height compared with the normal side (central incisor: -1.5 mm, P <0.005; lateral incisor: -1.06 mm, P <0.01; canine: -0.59 mm, P < 0.01). The lateral incisors also showed palatal alveolar bone height loss compared with the unaffected side (-0.8 mm, P <0.005). Alveolar BT at root apices of impacted canines was 1.14 mm thicker than the normal side (P <0.005). Central and lateral incisors were similar to the normal side. The thickness of the alveolar bone at 8, 10, and 12 mm of the impacted canine position was still larger than that on the healthy side, whereas the difference in average thickness between the healthy and affected side had been significantly reduced compared with pretreatment measurements. CONCLUSIONS: There is satisfactory retention of alveolar bone height in canines after orthodontic treatment; however, alveolar bone loss is slightly worse at central and lateral incisors. Retention of alveolar BT was normal for impacted anterior teeth, whereas excess apical alveolar BT at the canines, although still present, was substantially less significant than had been observed before treatment.

Quantitative proteomic analysis shows involvement of the p38 MAPK pathway in bovine parainfluenza virus type 3 replication.

BACKGROUND: Bovine parainfluenza virus type 3 (BPIV3) infection often causes respiratory tissue damage and immunosuppression and further results in bovine respiratory disease complex (BRDC), one of the major diseases in dairy cattle, caused huge economical losses every year. However, the pathogenetic and immunoregulatory mechanisms involved in the process of BPIV3 infection remain unknown. However, the pathogenetic and immunoregulatory mechanisms involved in the process of BPIV3 infection remain unknown. Proteomics is a powerful tool for high-throughput identification of proteins, which has been widely used to understand how viruses interact with host cells. METHODS: In the present study, we report a proteomic analysis to investigate the whole cellular protein alterations of MDBK cells infected with BPIV3. To investigate the infection process of BPIV3 and the immune response mechanism of MDBK cells, isobaric tags for relative and absolute quantitation analysis (iTRAQ) and Q-Exactive mass spectrometry-based proteomics were performed. The differentially expressed proteins (DEPs) involved in the BPIV3 invasion process in MDBK cells were identified, annotated, and quantitated. RESULTS: A total of 116 proteins, which included 74 upregulated proteins and 42 downregulated proteins, were identified as DEPs between the BPIV3-infected and the mock-infected groups. These DEPs included corresponding proteins related to inflammatory response, immune response, and lipid metabolism. These results might provide some insights for understanding the pathogenesis of BPIV3. Fluorescent quantitative PCR and western blotting analysis showed results consistent with those of iTRAQ identification. Interestingly, the upregulated protein MKK3 was associated with the p38 MAPK signaling pathway. CONCLUSIONS: The results of proteomics analysis indicated BPIV3 infection could activate the p38 MAPK pathway to promote virus replication.

A reliable quantitative method for determining CBD content and release from transdermal patches in Franz cells.

INTRODUCTION: There are several cannabidiol (CBD) transdermal patches available on the market. However, none are FDA-approved. Furthermore, not much evidence has been published about CBD release and skin permeation from such patches, so the effectiveness and reliability remain unclear. OBJECTIVES: We aimed to develop a method to determine the in vitro release and skin permeation of CBD from transdermal patches using Franz cell diffusion in combination with quantitative 1 H-NMR (qNMR). MATERIALS AND METHODS: The study was conducted on CBD patches with known CBD content and six different commercially available or market-ready CBD patches using a Franz cell with a Strat-M™ membrane and with samples taken directly from the transdermal patch for qNMR analysis. RESULTS: The use of qNMR yielded an average recovery of 100% ± 7% when samples with known CBD content were tested. Results from the testing of six commercially available patches indicated that five out of six patches did not contain the CBD amount stated by the manufacturer according to a ± 10% variance margin, of which four patches were under-labeled and one was over-labeled. The release rate of patches was determined, and significant differences between the patches were shown. Maximum release of CBD was calculated to occur after 39 to 70 h. CONCLUSION: The established method was proven to be a reliable means of determining the quantity and release of CBD from transdermal patches and can be used to verify CBD content and release rate in transdermal patches.

Silicone-Ionic Liquid Elastomer Composite with Keratin as Reinforcing Agent Utilized as Pressure Sensor.

Development of a flexible pressure sensor is crucial for the future improvement of the wearable electronic devices designed to detect dynamic human motion. In this study, a novel pressure sensor with remarkably improved force sensing characteristics is obtained through combined usage of polydimethylsiloxane (PDMS) and ionic liquid (IL). Keratin is dispersed homogeneously in the PDMS matrix to serve as a reinforcing filler. High conductivity IL is employed as sensitivity-enhancing constituent in the elastomer, and the effect of the amount of IL on elastomers' pressure-sensing performance is investigated. The elastomer with 70 parts per hundred rubber (phr) IL shows excellent pressure-sensing performance. This novel pressure sensor demonstrates high linear sensitivity (0.037 kPa-1 ) in the large pressure region of 0-10 kPa. Response and recovery times are 8 and 11 ms, respectively, which are much shorter than previously reported. Moreover, the pressure sensor could distinguish different pressures via stable sensing signals in the pressure range of 0 to 50 kPa. The excellent performance of the novel pressure sensor has application potential in various fields, such as health monitoring and soft robotics.

Peroxiredoxin I deficiency increases keratinocyte apoptosis in a skin tumor model via the ROS-p38 MAPK pathway.

Keratinocyte hyperproliferation is an essential link in skin cancer pathogenesis. Peroxiredoxin I (Prx I) is known to regulate cancer cell proliferation, differentiation, and apoptosis, but its role in skin cancer remains unclear. This study aimed to elucidate the role and mechanism of Prx I in skin cancer pathogenesis. Dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) were used to create a skin tumor model of the initiation/promotion stage of cancer. The role of Prx I in H2O2-induced keratinocyte apoptosis was also investigated. After DMBA/TPA treatment, Prx I deficiency was significantly associated with less skin tumors, lower Bcl-2 expression, and higher p-p38 and cleaved caspase-3 expressions in Prx I knockout tumors than in wild-type controls. H2O2 stimulation caused more cellular apoptosis in Prx I knockdown HaCaT cells than in normal HaCaT cells. The signaling study revealed that Bcl-2, p-p38, and cleaved caspase-3 expressions were consistent with the results in the tumors. In conclusion, the deletion of Prx I triggered the DMBA/TPA-induced skin tumor formation in vivo and in vitro by regulating the reactive oxygen species (ROS)-p38 mitogen-activated protein kinase (MAPK) pathway. These findings provide a theoretical basis for treating skin cancer.

Mitochondrial dysfunction and endoplasmic reticulum stress in calf hepatocytes are associated with fatty acid-induced ORAI calcium release-activated calcium modulator 1 signaling.

The store-operated Ca2+ entry (SOCE) moiety ORAI calcium release-activated calcium modulator 1 (ORAI1) located in the endoplasmic reticulum (ER) participates in key cellular functions such as protein folding, transport, and secretion, and lipid metabolism. We used an in vitro approach to test whether exogenous fatty acids alter ORAI1 signaling and to explore potential consequences on mitochondrial dysfunction and ER stress. First, hepatocytes isolated from 4 healthy female calves (1 d old, 40-50 kg) were challenged with a 1.2 mM mixture of oleic, linoleic, palmitic, stearic, and palmitoleic acids for 0.5, 1, 3, 6, 9, and 12 h to measure oxidative stress [intracellular reduced glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and hydrogen peroxide] and ER stress (protein abundance of PERK, IRE, ATF6, and GRP78). Concentrations of GSH and SOD decreased at 0.5 h, and MDA and hydrogen peroxide increased at 1 h; ER stress proteins increased at 6 h. To determine whether ER stress was caused by oxidative stress, primary calf hepatocytes were treated with the same 1.2 mM fatty acid mix or the reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC) for 6 h. We found that NAC prevented an increase in ER stress protein abundance. Next, the role of ORAI1 on ER stress was measured by transfecting hepatocytes with small interfering (si)ORAI1 or the ORAI1 inhibitor BTP2, followed by a challenge with 1.2 mM fatty acids for 3 h. Without inhibiting ORAI1, exogenous fatty acids upregulated ORAI1 mRNA and protein abundance, oxidative stress, ER stress proteins, and protein abundance of marker indicators of an opened mitochondrial permeability transition pore (mPTP). Inhibition with BPT2 or silencing via siORAI1 abrogated oxidative stress, including increased GSH concentration and SOD activity, decreased MDA, hydrogen peroxide, and ROS concentration; ER stress protein abundance was downregulated, and mitochondrial function was restored. Last, changes in markers of mPTP opening were evaluated by culturing hepatocytes for 6 h with the sarcoendoplasmic Ca2+ ATPase inhibitor thapsigargin or the calcium ionophore ionomycin. We detected an increase in VDAC1, CLPP, and CypD protein abundance, all of which indicated opening of the mPTP. Overall, data from these in vitro studies suggest that ORAI1 mediates ER stress induced by high concentrations of fatty acids, in part through alleviating mitochondrial dysfunction caused by oxidative stress.

[Cerebral Autoregulation in Patients with Unilateral Carotid Artery Stenosis].

Objective To investigate cerebral autoregulation(CA)in patients with severe unilateral carotid artery stenosis by near infrared spectroscopy. Methods Thirty patients who underwent general anesthesia in our hospital from January 2015 to February 2017 were enrolled in this study.The stenosis group included 15 patients with severe unilateral internal carotid artery stenosis,and the control group included 15 patients without carotid artery stenosis.Both groups were matched in sex and age.Cerebral tissue oxygenation index(TOI)and mean arterial pressure were recorded continuously under stable general anesthesia.The Pearson correlation coefficient(r)was calculated to judge the CA status. Results TOI was not significantly different between the stenosis side and the non-stenosis side in the stenosis group(66.52±6.50 vs. 65.23±4.50;t=0.93, P=0.368)or between the stenosis side in the stenosis group and the stenosis side in the control group(66.52±6.50 vs. 64.22±3.87;t=1.18, P=0.248).The r values of stenosis side and non-stenosis side in the stenosis group were 0.36±0.12 and 0.17±0.11,respectively,and the r values of the stenosis side in the stenosis group and the stenosis side of the control group were 0.36±0.12 and 0.13±0.08,respectively.In the stenosis group,5 patients had transient ischemic attack and 2 patients had a history of stroke within 3 months before operation.When an r value of 0.342 was used as the judgment point of CA abnormality,the sensitivity and specificity were 0.625 and 0.909,respectively. Conclusion Within the range of normal blood pressure fluctuation,cerebral blood flow is linked to blood pressure at the stenosis side in patients with severe unilateral carotid artery stenosis.

Molecular Strategies for Improved Dielectric Elastomer Electrical Breakdown Strengths.

Dielectric elastomer transducers (actuators and generators) possess great commercial potential because they allow for novel transducer designs and applications due to-amongst others-their flexibility and low weight. On the other hand, the flexibility and inherent softness of dielectric elastomers also pose restrictions on their use, since the thin elastomers may undergo destructive deformations under large loads or in large electrical fields. In order to design better dielectric elastomers, it is crucial to understand the underlying phenomena of how thin and elastic dielectric elastomer films undergo electrical breakdown. This understanding will allow for the design of dielectric elastomers with high electrical breakdown strength and thus open up the use of films in transducers at higher electrical fields and forces. Here, the study couples intrinsic electrical breakdown strengths with well-described polymer and network characteristics, namely Kuhn parameters and cross-linking density. The universality of the developed model is illustrated by comparison over a wide range of silicone-based elastomers, such as prestretched elastomers and synthesized cross-linked bottlebrush polymers, representing both filled and unfilled elastomers. This study paves a robust way for the molecular design of elastomers into high-intrinsic electrical breakdown strength dielectric elastomers.

Simple Preparation of Thiol-Ene Particles in Glycerol and Surface Functionalization by Thiol-Ene Chemistry (TEC) and Surface Chain Transfer Free Radical Polymerization (SCT-FRP).

Thiol-ene (TE)-based polymer particles are traditionally prepared via emulsion polymerization in water (using surfactants, stabilizers, and cosolvents). Here, a green and simple alternative is presented with excellent control over particle size, while avoiding the addition of stabilizers. Glycerol is applied as a dispersing medium for the preparation of off-stoichiometric TE microparticles, where sizes in the range of 40-400 µm are obtained solely by changing the mixing speed of the emulsions prior to crosslinking. Control over surface chemistry is achieved by surface functionalization of excess thiol groups via photochemical thiol-ene chemistry resulting in a functional monolayer. In addition, surface chain transfer free radical polymerization is used for the first time to introduce a thicker polymer layer on the particle surface. The application potential of the system is demonstrated by using functional particles as adsorbent for metal ions and as a support for immobilized enzymes.

EFFICACY OF INTRAVITREAL INJECTION OF CONBERCEPT IN POLYPOIDAL CHOROIDAL VASCULOPATHY: Subgroup Analysis of the Aurora Study.

PURPOSE: To evaluate the efficacy of different doses of conbercept in patients with polypoidal choroidal vasculopathy in the AURORA study. METHODS: Retrospective subgroup analyses of 12-month data from the AURORA study. Fifty-three patients (32 in 0.5-mg group and 21 in 2.0-mg group) diagnosed with polypoidal choroidal vasculopathy in AURORA study were retrospectively evaluated. Efficacy outcomes were compared between the two dosage groups. RESULTS: At Month 12, mean changes in best-corrected visual acuity from baseline were 14.4 ± 14.1 letter scores for the 0.5-mg group and 14.2 ± 21.0 letter scores for the 2.0-mg group; mean central retinal thickness decreased by 104.5 ± 127.3 µm in the 0.5-mg group and 140.7 ± 127.9 µm in the 2.0-mg group; mean total macular volume decreased by 0.9 ± 2.3 mm and 1.0 ± 1.2 mm in the 0.5-mg and 2.0-mg groups, respectively. The mean subretinal fluid thickness decreased by 111.9 ± 122.5 µm and 76.3 ± 112.6 µm in the 0.5-mg and 2.0-mg groups, respectively. The mean pigment epithelial detachment height decreased by 79.3 ± 217.8 µm and 61.3 ± 161.5 µm in the 0.5-mg and 2.0-mg groups, respectively. The mean area of polyps decreased by 0.46 ± 0.76 mm and 0.55 ± 1.34 mm in the 0.5-mg and 2.0-mg groups, respectively. The mean total lesion area decreased by 2.51 ± 5.94 mm (P = 0.088) and 4.62 ± 5.51 mm in the 0.5-mg group and 2.0-mg groups, respectively. Complete regression of polyps was observed in 56.5% of patients in the 0.5-mg group and 52.9% of those in the 2.0-mg group, whereas partial regression was observed in 26.1% and 35.3% of patients in the 0.5-mg and 2.0-mg groups, respectively. CONCLUSION: Intravitreal injection of conbercept appears to significantly improve visual acuity and anatomical outcomes in patients with polypoidal choroidal vasculopathy.