Three-dimensional structure and cytokine distribution of platelet-rich fibrin

OBJECTIVES: Previous reports have revealed that several cytokines (including platelet-derived growth factor-BB, transforming growth factors-β1 and insulin-like growth factor-1) can enhance the rate of bone formation and synthesis of extracellular matrix in orthopaedics or periodontology. This study aimed to determine the concentration of cytokines within platelet-rich fibrin microstructures and investigate whether there are differences in the different portions of platelet-rich fibrin, which has implications for proper clinical use of platelet-rich fibrin gel. METHODS: Whole blood was obtained from six New Zealand rabbits (male, 7 to 39 weeks old, weight 2.7-4 kg); it was then centrifuged for preparation of platelet-rich fibrin gels and harvest of plasma. The resultant platelet-rich fibrin gels were used for cytokine determination, histological analyses and scanning electron microscopy. All plasmas obtained were subject to the same cytokine determination assays for the purpose of comparison. RESULTS: Cytokines platelet-derived growth factor-BB and transforming growth factor-β1 formed concentration gradients from high at the red blood cell end of the platelet-rich fibrin gel (p=1.88×10-5) to low at the plasma end (p=0.19). Insulin-like growth factor-1 concentrations were similar at the red blood cell and plasma ends. The porosities of the platelet-rich fibrin samples taken in sequence from the red blood cell end to the plasma end were 6.5% ± 4.9%, 24.8% ± 7.5%, 30.3% ± 8.5%, 41.4% ± 12.3%, and 40.3% ± 11.7%, respectively, showing a gradual decrease in the compactness of the platelet-rich fibrin network. CONCLUSION: Cytokine concentrations are positively associated with platelet-rich fibrin microstructure and portion in a rabbit model. As platelet-rich fibrin is the main entity currently used in regenerative medicine, assessing cytokine concentration and the most valuable portion of PRF gels is essential and recommended to all physicians

Gender-Differential Associations between Attention Deficit and Hyperactivity Symptoms and Youth Health Risk Behaviors

Attention deficit and hyperactivity disorder (ADHD) is one of the common developmental disorders that generally receives clinical attention at learning ages, and some symptoms may persist in young adulthood.1 Past research has demonstrated a consistent association between ADHD and youth health risk behaviors (e.g., cigarette smoking), which often develop during adolescence and contribute to early morbidity and mortality among young adults.2 However, ADHD symptoms are not routinely screened in adolescents and emerging adults during their visits to healthcare providers.3 The six-item Adult Self-Report Scale (ASRS-6) for ADHD has been validated in the young population for screening purposes.4 This short form is time-saving and also provides a comparable predictivity of ADHD diagnosis as that of the original long version.5 Although accumulating evidence has demonstrated the association between ADHD symptoms and youth health risk behaviors, this issue has scarcely been explored in the Taiwanese youth population.6 Therefore, this study was conducted to validate the psychometric property of the Chinese version of ASRS-6 and examine the gender-stratified association between ADHD symptoms and youth health risk behaviors

Dementia Assessment Using Mandarin Speech with an Attention-based Speech Recognition Encoder

Dementia diagnosis requires a series of different testing methods, which is complex and time-consuming. Early detection of dementia is crucial as it can prevent further deterioration of the condition. This paper utilizes a speech recognition model to construct a dementia assessment system tailored for Mandarin speakers during the picture description task. By training an attention-based speech recognition model on voice data closely resembling real-world scenarios, we have significantly enhanced the model's recognition capabilities. Subsequently, we extracted the encoder from the speech recognition model and added a linear layer for dementia assessment. We collected Mandarin speech data from 99 subjects and acquired their clinical assessments from a local hospital. We achieved an accuracy of 92.04% in Alzheimer's disease detection and a mean absolute error of 9% in clinical dementia rating score prediction.Comment: submitted to IEEE ICASSP 202

Estrogen Modulates the Sensitivity of Lung Vagal C Fibers in Female Rats Exposed to Intermittent Hypoxia

Obstructive sleep apnea is mainly characterized by intermittent hypoxia (IH), which is associated with hyperreactive airway diseases and lung inflammation. Sensitization of lung vagal C fibers (LVCFs) induced by inflammatory mediators may play a central role in the pathogenesis of airway hypersensitivity. In females, estrogen interferes with inflammatory signaling pathways that may modulate airway hyperreactivity. In this study, we investigated the effects of IH on the reflex and afferent responses of LVCFs to chemical stimulants and lung inflammation in adult female rats, as well as the role of estrogen in these responses. Intact and ovariectomized (OVX) female rats were exposed to room air (RA) or IH for 14 consecutive days. On day 15, IH enhanced apneic responses to right atrial injection of chemical stimulants of LVCFs (e.g., capsaicin, phenylbiguanide, and α,β-methylene-ATP) in intact anesthetized females. Rats subjected to OVX prior to IH exposure exhibited an augmented apneic response to the same dose of stimulants compared with rats subjected to other treatments. Apneic responses to the stimulants were completely abrogated by bilateral vagotomy or perivagal capsaicin treatment, which blocked the neural conduction of LVCFs. Electrophysiological experiments revealed that in IH-exposed rats, OVX potentiated the excitability of LVCFs to stimulants. Moreover, LVCF hypersensitivity in rats subjected to OVX prior to IH exposure was accompanied by enhanced lung inflammation, which was reflected by elevated inflammatory cell infiltration in bronchoalveolar lavage fluid, lung lipid peroxidation, and protein expression of inflammatory cytokines. Supplementation with 17β-estradiol (E2) at a low concentration (30 μg/ml) but not at high concentrations (50 and 150 μg/ml) prevented the augmenting effects of OVX on LVCF sensitivity and lung inflammation caused by IH. These results suggest that ovarian hormones prevent the enhancement of LVCF sensitivity and lung inflammation by IH in female rats, which are related to the effect of low-dose estrogen

Topical application of marine briarane-type diterpenes effectively inhibits 12-O-tetradecanoylphorbol-13-acetate-induced inflammation and dermatitis in murine skin

<p>Abstract</p> <p>Background</p> <p>Skin is the largest organ in the body, and is directly exposed to extrinsic assaults. As such, the skin plays a central role in host defense and the cutaneous immune system is able to elicit specific local inflammatory and systemic immune responses against harmful stimuli. 12-O-tetradecanoylphorbol-13-acetate (TPA) can stimulate acute and chronic inflammation and tumor promotion in skin. TPA-induced dermatitis is thus a useful <it>in vivo </it>pharmacological platform for drug discovery. In this study, the inhibitory effect of briarane-type diterpenes (BrDs) from marine coral <it>Briareum excavatum </it>on TPA-induced dermatitis and dendritic cell (DC) function was explored.</p> <p>Methods</p> <p>Evans blue dye exudation was used to determine vascular permeability. H&E-stained skin section was used to determine the formation of edema in mouse abdominal skin. We also used immunohistochemistry staining and western blot assays to evaluate the activation of specific inflammation makers and key mediators of signaling pathway in the mouse skin. Furthermore, mouse bone marrow DCs were used to determine the relationship between the chemical structure of BrDs and their regulation of DC function.</p> <p>Results</p> <p>BrD1 remarkably suppressed TPA-induced vascular permeability and edema in skin. At the biochemical level, BrD1 inhibited TPA-induced expression of cyclooxygenase-2, inducible nitric oxide synthase and matrix metalloproteinase-9, the key indicators of cutaneous inflammation. This inhibition was apparently mediated by interference with the Akt/NF-κB-mediated signaling network. BrD1 also inhibited TNF-α and IL-6 expression in LPS-stimulated BMDCs. The 8, 17-epoxide of BrDs played a crucial role in the inhibition of IL-6 expression, and replacement of the C-12 hydroxyl group with longer esters in BrDs gradually decreased this inhibitory activity.</p> <p>Conclusions</p> <p>Our results suggest that BrDs warrant further investigation as natural immunomodulatory agents for control of inflammatory skin diseases.</p

Sedimentological characteristics and seafloor failure offshore SW Taiwan

In this study, analysis results reveal two main deposition zones are located at the flank of upper Gaoping Submarine Canyon and Lower Fangliao Basin offshore SW Taiwan. The non-event related sediments deposited in past 150 years (i.e., 632 Mt km-2) was delivered and transported from Gaoping River by suspension process with tides and coastal currents and gradually spread out offshore. Meanwhile, the total mass of accumulation sediments is 1922 Mt km-2, accounting for 40% Gaoping Riverâs sediment load and suggesting that the deposition process is mainly controlled by natural hazards. Sedimentation rates in much of the study area, except in the main deposition zones, are less than 0.5 cm yr-1 (5 m kyr-1). Compared with the studies at the instability seafloor caused by high sedimentation rates (~30 m kyr-1), the offshore southwestern Taiwan is relatively stable. In this study, we also discovered a series of sediment waves located on the upper continental slope between Gaoping and Fangliao Submarine Canyons, which is related to the creeping process on seafloor. In summary, our results reveal the fluid activities, existence of weak layers and earthquake triggering are potential factors which might induced seafloor failures offshore southwestern Taiwan

A novel sol-gel Bi2-xHfxO3+x/2 radiopacifier for mineral trioxide aggregates (MTA) as dental filling materials

Funding Information: The authors would like to thank Taipei Medical University Hospital for financially sup-porting this work under grant no. 110TMU-TMUH-16 and partially supported by MOST 109-2221-E-038-014. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.Mineral trioxide aggregate (MTA) is well known as an effective root canal filling material for endodontics therapy. Within MTA, bismuth oxide (Bi2O3) serving as the radiopacifier still has biocompatibility concerns due to its mild cytotoxicity. In the present study, we tried to modify the Bi2O3 radiopacifier by doping hafnium ions via the sol-gel process and investigated the effects of different doping ratios (Bi2-xHfxO3+x/2, x = 0–0.3) and calcination temperatures (400–800 °C). We mixed various precursor mixtures of bismuth nitrate (Bi(NO3)3·5H2O) and hafnium sulfate (Hf(SO4)2) and controlled the calcination temperatures. The as-prepared Hf-doped Bi2O3 radiopaci-fier powders were investigated by thermogravimetric analysis (TGA), X-ray diffraction (XRD), field-emission scanning electron microscopy (FESEM), and transmission electron microscopy (TEM). Portland cement/radiopacifier/calcium sulfate (75/20/5) were mixed and set by deionized water (powder to water ratio = 3:1). Changes in radiopacity, diametral tensile strength (DTS), and in vitro cell viability of the hydrated MTA-like cement were carried out. The experimental results showed that the group containing radiopacifier from sol-gelled Bi/Hf (90/10) exhibited significantly higher radiopacity (6.36 ± 0.34 mmAl), DTS (2.54 ± 0.29 MPa), and cell viability (84.0±8.1%) (p < 0.05) when compared to that of Bi/Hf (100/0) powders. It is suggested that the formation of β-Bi7.78Hf0.22O12.11 phase with hafnium addition and calcining at 700 °C can prepare novel bismuth/haf-nium composite powder that can be used as an alternative radiopacifier for root canal filling mate-rials.publishersversionPeer reviewe

AMG 837: A Novel GPR40/FFA1 Agonist that Enhances Insulin Secretion and Lowers Glucose Levels in Rodents

Agonists of GPR40 (FFA1) have been proposed as a means to treat type 2 diabetes. Through lead optimization of a high throughput screening hit, we have identified a novel GPR40 agonist called AMG 837. The objective of these studies was to understand the preclinical pharmacological properties of AMG 837. The activity of AMG 837 on GPR40 was characterized through GTPγS binding, inositol phosphate accumulation and Ca2+ flux assays. Activity of AMG 837 on insulin release was assessed on isolated primary mouse islets. To determine the anti-diabetic activity of AMG 837 in vivo, we tested AMG 837 using a glucose tolerance test in normal Sprague-Dawley rats and obese Zucker fatty rats. AMG 837 was a potent partial agonist in the calcium flux assay on the GPR40 receptor and potentiated glucose stimulated insulin secretion in vitro and in vivo. Acute administration of AMG 837 lowered glucose excursions and increased glucose stimulated insulin secretion during glucose tolerance tests in both normal and Zucker fatty rats. The improvement in glucose excursions persisted following daily dosing of AMG 837 for 21-days in Zucker fatty rats. Preclinical studies demonstrated that AMG 837 was a potent GPR40 partial agonist which lowered post-prandial glucose levels. These studies support the potential utility of AMG 837 for the treatment of type 2 diabetes

SLC2A10 genetic polymorphism predicts development of peripheral arterial disease in patients with type 2 diabetes. SLC2A10 and PAD in type 2 diabetes

<p>Abstract</p> <p>Background</p> <p>Recent data indicate that loss-of-function mutation in the gene encoding the facilitative glucose transporter GLUT10 (<it>SLC2A10</it>) causes arterial tortuosity syndrome via upregulation of the TGF-β pathway in the arterial wall, a mechanism possibly causing vascular changes in diabetes.</p> <p>Methods</p> <p>We genotyped 10 single nucleotide polymorphisms and one microsatellite spanning 34 kb across the <it>SLC2A10 </it>gene in a prospective cohort of 372 diabetic patients. Their association with the development of peripheral arterial disease (PAD) in type 2 diabetic patients was analyzed.</p> <p>Results</p> <p>At baseline, several common SNPs of <it>SLC2A10 </it>gene were associated with PAD in type 2 diabetic patients. A common haplotype was associated with higher risk of PAD in type 2 diabetic patients (haplotype frequency: 6.3%, <it>P </it>= 0.03; odds ratio [OR]: 14.5; 95% confidence interval [CI]: 1.3- 160.7) at baseline. Over an average follow-up period of 5.7 years, carriers with the risk-conferring haplotype were more likely to develop PAD (<it>P </it>= 0.007; hazard ratio: 6.78; 95% CI: 1.66- 27.6) than were non-carriers. These associations remained significant after adjustment for other risk factors of PAD.</p> <p>Conclusion</p> <p>Our data demonstrate that genetic polymorphism of the <it>SLC2A10 </it>gene is an independent risk factor for PAD in type 2 diabetes.</p