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This study aimed to evaluate the efficacy of pharmacotherapy for smoking cessation among adolescent smokers by using a meta-analysis of randomized controlled trials (RCTs). PubMed, EMBASE, and Cochrane Library were searched from the inception to January 20, 2018. We included RCTs of pharmacotherapy for smoking cessation among adolescent smokers aged less than 20 years. Data were pooled using a random-effects meta-analysis. The primary outcome measures were a smoking abstinence rate and its relative risk (RR) at the longest follow-up period in each study validated by biochemical markers. Among a total of 1035 articles searched, nine RCTs, which involved 1188 adolescent smokers aged 12-20 years with 627 in the intervention group and 561 in the control group, were included in the final analysis. In the random-effects meta-analysis of all the nine trials, pharmacotherapy showed a increased abstinence rate (RR = 1.62; 95% confidence interval [CI] = 1.08 to 2.44, I2 = 0.0%), compared with the control group. Subgroup meta-analyses by follow-up period showed an increased abstinence rate at 4 weeks (RR = 1.87; 95% CI = 1.22 to 2.87; n = 4) and a nonsignificantly increased abstinence rate during the longer term follow-up periods at 8, 12, 24, and 52 weeks. The current meta-analysis suggests that pharmacotherapy can be considered as an aid for smoking cessation in the short-term period among adolescent smokers. However, further large RCTs are warranted to determine its long-term efficacy and safety. In this meta-analysis of nine RCTs with 1188 adolescent smokers aged 12-20 years, pharmacotherapy showed an increased abstinence rate, compared with the control group. In the subgroup meta-analyses by follow-up period, it showed the increased abstinence rate at 4 weeks and no efficacy on abstinence during the longer term follow-up periods up to 52 weeks. Further large RCTs are warranted to determine the long-term efficacy and safety of pharmacotherapy in adolescent smokers.

Aim The study aimed to evaluate a tailored reproductive health promotion programme based on the Precaution Adoption Process Model (PAPM) for young adults. Design This was a two‐group, non‐blinded randomized controlled trial. Methods This study was performed with women aged 18–25 who were not performing reproductive health‐related behaviour from September 2018 to November 2018 in Seoul, South Korea. The participants were stratified by stage of PAPM (1, 2 or 3) and were randomly allocated to the intervention group (n = 30) and the control group (n = 30). Women in the intervention group were given the programme, which was customized according to the stage of PAPM over 8 weeks, such as lectures, giving information, discussions, practical training, Q&A, case experience and counselling. The control group received educational material. The primary outcomes were reproductive‐health‐promoting behaviour and rate of contraception use. Results Reproductive‐health‐promoting behaviour was significantly higher in the intervention group than the control group post‐intervention, as were reproductive health beliefs, motivation and self‐efficacy.

The periodontal complex consisting of alveolar bone, cementum, and periodontal ligaments (PDL) supports human teeth through the systematic orchestration of mineralized tissues and fibrous tissues. Importantly, cementum, the outermost mineralized layer of dental roots, plays an essential role by bridging the inner ligaments from the dental root to the alveolar bone. When the periodontal complex is damaged, the regeneration of each component of the periodontal complex is necessary; however, it is still challenging to achieve complete functional regeneration. In this study, we tried to control the regeneration of cementum and PDL by using a human PDL stem cell (hPDLSC) sheet engineering technology with the pretreatment of recombinant human BMP-2 (rhBMP-2). Isolated hPDLSCs obtained from extracted human teeth were pretreated with rhBMP-2 for in vitro osteogenic differentiation and grafted on the micro/macro-porous biphasic calcium phosphate (MBCP) blocks, which represent dental roots. The MBCPs with hPDLSC sheets were implanted in the subcutaneous layer of immune-compromised mice, and rhBMP-2 pretreated hPDLSC sheets showed higher mineralization and collagen ligament deposition than the no-pretreatment group. Therefore, the rhBMP-2-hPDLSC sheet technique could be an effective strategy for the synchronized regeneration of two different tissues: mineralized tissue and fibrous tissues in periodontal complexes.

Brown adipose tissue (BAT) is responsible for energy homeostasis and adaptive thermogenesis. SUMO-specific protease 2 (SENP2) plays an essential role in adipogenesis; however, the role of SENP2 in BAT metabolism has not been explored. Here we investigated the role of SENP2 in mature brown adipocytes with a brown adipocyte-specific SENP2 knockout ( Senp2 -BKO) mouse model generated using the uncoupling protein 1 ( Ucp1 )-Cre. High-fat diet-induced insulin resistance was aggravated in Senp2 -BKO mice compared with control mice. In Senp2 -BKO mice, adaptive thermogenesis upon acute cold exposure was impaired and UCP1 expression was barely induced upon cold or β-adrenergic stimulation. SENP2-mediated deSUMOylation of estrogen-related receptor alpha (ERRα) significantly enhanced Ucp1 promoter activity through activation of the ERRα/PGC1α complex. The absence of SENP2 inhibited formation of ERRα, cAMP-response element-binding protein (CREB) and RNA Polymerase II transcriptional complex at the Ucp1 promoter following β3-adrenergic stimulation. In addition, SUMOylation of ERRα severely interfered with binding of ERRα to its DNA-binding site (ERRE) in the promoter of Ucp1 . Our findings revealed that SENP2 plays a role in the metabolic flexibility and thermogenic efficiency of BAT, particularly in response to β3-adrenergic activation. SENP2 regulates brown fat thermogenesis and metabolic flexibility Brown adipose tissue helps burn energy and generate heat, unlike white fat, which stores energy. This study explores how the SENP2 protein affects the ability of brown adipose tissue to generate heat and manage energy. The researchers used mice genetically modified to lack SENP2 specifically in their brown fat cells. They found that these mice had trouble maintaining body temperature in the cold and showed signs of insulin resistance when fed a high-fat diet. The study involved exposing these mice to cold temperatures and analyzing their brown fat tissue. The researchers discovered that SENP2, an enzyme regulating a process called deSUMOylation, influences the activity of ERRα, a protein crucial for activating genes involved in heat production. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Arginine methylation is a post-translational modification that controls the abundance of γc cytokine receptor on mature T cells by a post-transcriptional mechanism.

Trichostatin A (TSA) is a potent histone deacetylase (HDAC) inhibitor with a broad spectrum of epigenetic activities known to regulate diverse cellular mechanisms, including differentiation of mesenchymal stem cells. In this study, we demonstrate that TSA promotes proliferation and odontoblast differentiation of human dental pulp stem cells (hDPSCs) in vitro and has the ability to enhance dentin formation and odontoblast differentiation in vivo during tooth development. We observed that TSA increased the expression of proliferating cell nuclear antigen and cyclin D1 in hDPSCs at a certain concentration and the activation of JNK/c-Jun pathway was essential for TSA-dependent hDPSC proliferation. Further, TSA accelerated mineral nodule formation in vitro and increased gene expression of dentin sialophosphoprotein, dentin matrix protein 1, bone sialoprotein, and osteocalcin. In addition, TSA significantly upregulated the levels of phospho-Smad2/3, Smad4, and nuclear factor I-C, while the specific inhibitor of Smad3 inhibits TSA enhancing mineralization differentiation of hDPSCs. HDAC3 is downregulated by TSA treatment, suggesting a possible mediator of TSA-dependent pathways among the members of HDAC family. Moreover, TSA-injected embryos exhibited increased dentin thickness, larger dentin areas, and higher odontoblast numbers in their postnatal molars with stronger dentin sialoprotein expression in immunohistochemical staining. These findings indicate that TSA may serve a key role in proliferation and odontoblast differentiation of hDPSCs in dental developmental stages and can be used as an accelerator in dental hard tissue engineering.

We examined the effectiveness of using different calcium salts for bioconsolidation. Four calcium salts were chosen based on their applicability and solubility. Initial experiments demonstrated that the addition of any calcium salt had a negative effect on the urease activity of S. pasteurii. Microscopic examinations elucidated the morphological and structural differences of the calcium carbonate (CaCO₃) crystals induced. Calcite and vaterite are the prominent forms of CaCO₃ detected according to X-ray diffraction (XRD) analysis. Bioconsolidated sand samples were able to significantly resist water flow through a column compared to the non-treated samples. Also, in a tightness test, the differences in the ability to retain water within columns were observed among the samples tested. Moreover, despite the differences, the calcium salts tested still bound the sand together to form blocks. Our results further explain the influence of multiple factors in crystal formation and sand bioconsolidation effectiveness.

Staphylococcus aureus biofilms complicate the treatment of device-related infections. We hypothesized that combining rifampin with fluoroquinolones could eradicate biofilms even in antimicrobial-resistant S. aureus strains. We determined the synergistic interactions of these combinations in a biofilm model. Thirty methicillin-resistant S. aureus (MRSA) isolates with varying susceptibility profiles were evaluated. Minimum biofilm eradication concentrations (MBECs) were determined using the Calgary Biofilm Device, and the synergy was assessed using the fractional biofilm eradication concentration (FBEC) index. Scanning electron microscopy (SEM) was performed on one strain, and confocal laser scanning microscopy (CLSM) was conducted on four strains for visualizing and evaluating the biofilm viability. The MBEC90 for rifampin and levofloxacin were 512 mg/L and 256 mg/L, respectively, and exceeded 1024 mg/L for ciprofloxacin. Synergy was observed in 56.7% of strains for both the rifampin + ciprofloxacin and rifampin + levofloxacin combinations, with no difference between the combinations. A higher ciprofloxacin MBEC (≥16 mg/L) increased the likelihood of synergy with rifampin by 18-fold. SEM and CLSM analyses in a subset of strains confirmed the enhanced biofilm disruption with rifampin + ciprofloxacin compared to ciprofloxacin alone. Our findings suggest that rifampin combined with ciprofloxacin or levofloxacin may synergistically eradicate MRSA biofilms, offering a potential treatment option for device-related infections when alternatives are limited.

The platelet-rich fibrin (PRF) is known as a rich source of autologous cytokines and growth factors and universally used for tissue regeneration in current clinical medicine. However, the microstructure of PRF has not been fully investigated nor have been studied the key molecules that differ PRF from platelet-rich plasma. We fabricated PRF under Choukroun's protocol and produced its extract (PRFe) by freezing at −80°C. The conventional histological, immunohistological staining, and scanning electron microscopy images showed the microstructure of PRF, appearing as two zones, the zone of platelets and the zone of fibrin, which resembled a mesh containing blood cells. The PRFe increased proliferation, migration, and promoted differentiation of the human alveolar bone marrow stem cells (hABMSCs) at 0.5% concentration in vitro . From the results of proteome array, matrix metalloproteinase 9 (MMP9) and Serpin E1 were detected especially in PRFe but not in concentrated platelet-rich plasma. Simultaneous elevation of MMP9, CD44, and transforming growth factor β-1 receptor was shown at 0.5% PRFe treatment to the hABMSC in immunoblot. Mineralization assay showed that MMP9 directly regulated mineralization differentiation of hABMSC. Transplantation of the fresh PRF into the mouse calvarias enhanced regeneration of the critical-sized defect. Our results strongly support the new characteristics of PRF as a bioscaffold and reservoir of growth factors for tissue regeneration.

The oral mucosa is a critical barrier tissue that harbors a series of distinct immune cell subsets. Immune surveillance in the oral mucosa is important for both local and systemic immunity because the oral cavity is a heavily utilized route of pathogen entry and also serves as site of pathogen propagation. Nonetheless, composition and phenotype of the lymphocyte pool in the oral mucosa have remained poorly characterized. Utilizing a newly established protocol for mucosal immune cell isolation, here, we report that the oral mucosa features a unique cellular composition of immune cells, which differed not only from secondary lymphoid organs but also from mucosal tissues in the gut and lung. We observed profound accumulation of CD11b Ly6C monocytes in the oral mucosa that were maintained independently of T- and B-lymphocytes. Unlike the gut mucosa, the oral mucosa neither contained CD8αα T cells nor was it enriched for CD103 CD69 tissue-resident memory CD8 T cells. In fact, a major fraction of T cells circulated and trafficked through the mucosa as revealed by treatment with the S1P1 receptor antagonist, FTY720, a potent inhibitor of lymphocyte migration. Collectively, these results provide a comprehensive picture of immune cells in the oral mucosa as an active site of lymphocyte recruitment and surveillance.