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Background: It is important to ensure that both the qualitative and quantitative aspects of clinical education are maintained during the pandemic. Understanding students' views on clinical rotations and the extent of their perceived pandemic-related stress would thus be useful for designing and implementing effective clerkship programs. Therefore, this study aimed to investigate perceived stress and perceptions regarding clinical clerkship among incoming clinical students (third year) and senior clinical students (fourth year) during the COVID-19 pandemic. Methods: After completing orientation programs at the beginning of the academic year, we surveyed students on their perceived stress, their general perspectives regarding the appropriate scope of clinical clerkship, and their preferences regarding level of participation in clerkship. We examined the differences in stress and clerkship-related perceptions based on the students' study year and sex using independent t-test, chi-squared test, and Fisher's exact test. In addition, the influences of stress, sex, and study year on clerkship-related perceptions were examined using multinomial logistic regression. Results: The independent t-test indicated that third-year students experienced lower stress than did fourth-year students. Clerkship-related perceptions also differed significantly between third- and fourth-year students. Multinomial logistic regression analyses on the scope of and participation levels in clinical clerkship revealed that third-year students had significantly lower odds of preferring a limited range of clinical rotations and lower engagement in clerkships compared to fourth-year students. Conclusion: The COVID-19 pandemic has affected clinical education and, consequently, medical students' inclination toward active participation in clinical rotations. It is thus essential to understand students' views and provide them with relevant intra-pandemic educational supports. [ABSTRACT FROM AUTHOR]

Background: Chronic cerebral hypoperfusion (CCH) is known to induce Alzheimer's disease (AD) pathology, but its mechanism remains unclear. The purpose of this study was to identify the cerebral regions that are affected by CCH, and to evaluate the development of AD pathology in a rat model of CCH. Methods: A rat model of CCH was established by bilaterally ligating the common carotid arteries in adult male rats (CCH group). The identical operations were performed on sham rats without arteries ligation (control group). Regional cerebral glucose metabolism was evaluated at 1 and 3 months after bilateral CCA ligation using positron emission tomography with F-18 fluorodeoxyglucose. The expression levels of amyloid β40 (Aβ40), amyloid β42 (Aβ42), and hyperphosphorylated tau were evaluated using western blots at 3 months after the ligation. Cognitive function was evaluated using the Y-maze test at 3 months after the ligation. Results: At 1 month after the ligation, cerebral glucose metabolism in the entorhinal, frontal association, motor, and somatosensory cortices were significantly decreased in the CCH group compared with those in the control group. At 3 months after the ligation, cerebral glucose metabolism was normalized in all regions except for the anterodorsal hippocampus, which was significantly decreased compared with that of the control group. The expression of Aβ42 and the Aβ42/40 ratio were significantly higher in the CCH group than those in the control group. The phosphorylated-tau levels of the hippocampus in the CCH group were significantly lower than those in the control group. Cognitive function was more impaired in the CCH group than that in the control group. Conclusion: Our findings suggest that CCH causes selective neurodegeneration of the anterodorsal hippocampus, which may be a trigger point for the development of AD pathology. [ABSTRACT FROM AUTHOR]

To determine the degree to which nurses are aware of cervical cancer and to describe nurses' experiences of caring for patients with cervical cancer. To promote quality of nursing care of cervical cancer, we need to explore their perceptions and nursing experience in doing cervical-cancer care. This study was a qualitative descriptive design. Interviews were conducted with 14 registered nurses. The interviews were audiotaped, transcribed and analyzed. Content analysis was performed. Fourteen nurses who had been working at wards and cancer education centers were recruited in this study. Nine key themes emerged from three categories such as nurses’ awareness of cervical cancer, awareness of cervical cancer patient and caring experience. Nurses expressed fear of cervical cancer and helplessness in the face of a life-threatening prognosis. Nurses stated that they might have prejudice about cervical cancer, since it is caused by a sexually transmitted disease. They also recalled that patients with cervical cancer were more sensitive and demanding. Our findings provide a comprehensive and in-depth perspective in understanding the experience of caring for cervical cancer patients. Clinical nurses showed complex emotional reactions to cervical cancer, and expressed prejudice against the sex life of cervical-cancer patients. More education is required to ensure that clinical nurses can provide a nurse-led intervention with patients by managing nurses’ fear, prejudice, and the care burden. [ABSTRACT FROM AUTHOR]

Background: In June 2016, the Republic of Korea included free human papillomavirus (HPV) vaccinations for all 12-year-old girls in its national immunization program. Purpose: This study investigated perceptions of nurses on HPV vaccination and their intent to vaccinate preteens at the best ages. Methods: Recruited for the survey were 514 health teachers (181, 35.2%), public health nurses (168, 32.7%), and clinical nurses (165, 32.1%). Factor-analysis was conducted to validate the Vaccine-Hesitancy Scale for Korean nurses. Related variables associated with vaccine-acceptance were examined using the Kruskal–Wallis test and Spearman’s rho coefficients, due to lack of normalization. Results: Factor-analysis results showed that two factors of positive acceptance (7 items) and negative acceptance (3 items) accounted for 67.46% of the total variance, and explained 47.4% and 20.1%, respectively. Nurses who positively accepted HPV vaccine differed significantly in agreement to vaccinate girls or boys. For the proper vaccination age, a significant difference emerged between answers for girls and vaccine-acceptance scores, whereas no difference emerged between answers for boys and the scores. The vaccinated status of respondents significantly related to higher HPV vaccine acceptance, although age, religion, marital status, education, and working duration did not. Conclusions: This study showed that vaccine-acceptance levels reflect nurses’ attitudes and opinions about HPV vaccination for girls and boys. [ABSTRACT FROM AUTHOR]

Introduction: White matter lesions (WMLs), detected as hyperintensities on T2-weighted MRI, represent small vessel disease in the brain and are considered a potential risk factor for memory and cognitive impairment in older adults. The purpose of this study was to evaluate the association between WMLs and cerebral amyloid-β (Aβ) burden in patients with cognitive impairment. Methods: A total of 83 patients with cognitive impairment, who underwent brain MRI and F-18 florbetaben PET, were included prospectively: 19 patients were cognitively unimpaired, 30 exhibited mild cognitive impairment (MCI), and 34 exhibited dementia. The Fazekas scale was used to quantify WMLs on T2-weighted brain MR images. Cerebral Aβ burden was quantitatively estimated using volume-of-interest analysis. Differences in cerebral Aβ burden were evaluated between low-WML (Fazekas scale ≤1) and high-WML (Fazekas scale ≥2) groups. The relationship between the Fazekas rating and cerebral Aβ burden was evaluated using linear regression analysis after adjusting for age and sex. Results: In the overall cohort, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.011) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.299, P = 0.006). In patients with MCI, the high-WML group exhibited significantly higher Aβ burden compared with the low-WML group (P = 0.019) and cerebral Aβ burden was positively correlated with Fazekas rating (β = 0.517, P = 0.003). Conclusion: The presence of WMLs was associated with cerebral Aβ burden in patients with MCI. Our findings suggest that small vessel disease in the brain is related to Alzheimer’s disease pathology. [ABSTRACT FROM AUTHOR]

Accumulating evidence suggests that the glutamatergic system plays a major role in the pathophysiology of obsessive compulsive disorder (OCD) and empathic processing. Particularly, genetic influence of glutamate transporter gene (SLC1A1) on OCD has been frequently replicated in previous studies, but several studies did not replicate the result. Therefore, we aimed to replicate the associations between the SLC1A1 and OCD in a Korean population. In addition, we investigated the influence of SLC1A1 on trait empathy, impairments in which are characteristic of OCD. Six single-nucleotide polymorphisms (SNP) of SLC1A1 were genotyped in 615 patients with OCD and 508 healthy controls. The interpersonal reactivity index (IRI)—which consists of four subscales (perspective taking, PT; fantasy seeking, FS; empathic concern, EC; personal distress, PD)—was assessed from 277 patients with OCD and 395 controls. There were no significant associations between OCD and SNPs or haplotypes of SLC1A1. Patients with OCD exhibited significantly lower PT and higher PD scores than controls. The C-T-G haplotype at rs301430-rs301434-rs3087879 of SLC1A1 was significantly associated with higher PD scores after adjusted for age, sex, and OCD status. Our results suggest that six common SNPs of SLC1A1 may not contribute to the development of OCD, but may contribute to certain aspect of trait empathy such as personal distress. However, insufficient sample size and limited number of SLC1A1 SNPs may have reduced the likelihood of detecting significant associations. Therefore, further studies with larger sample size and more tag SNPs of the SLC1A1 gene were warranted. [ABSTRACT FROM AUTHOR]

Background and aim: Tumor burden is important to predict clinical behaviors of cancer such as lymph node metastasis (LNM). Tumor size has been used as a parameter of tumor burden such as indication of endoscopic resection in early gastric cancer (EGC) to predict LNM. Thus, we aimed to investigate whether tumor area can be more helpful to predict clinical behaviors than longest diameter of tumor in EGC. Patients and methods: 3,059 patients who underwent gastrectomy for EGC were reviewed retrospectively. Tumor area was calculated by multiplying long and short diameter of the tumor in surgical specimen. Longest diameter means maximal longitudinal diameter of tumor in specimen. Clinicopathologic features were compared between longest diameter and area using area under receiver operating characteristic (AUROC) curves. Results: Longest diameter and area of tumor showed a strong correlation (correlation coefficient 0.859, p<0.01). The cutoff value for prediction of LNM was 20 mm of longest diameter of tumor and 270 mm2 of tumor area. There was no significant difference between longest diameter and area for prediction of LNM (AUC 0.850 vs. 0.848, respectively). In differentiated-type EGC and undifferentiated-type EGC, there was no significant difference between longest diameter and area for prediction of LNM. Among mucosal or submucosal cancer prediction value of LNM between longest diameter and area was not significantly different. Conclusion: Tumor area may not be more helpful to predict LNM than longest diameter in EGC. Therefore, the longest diameter of tumor may be sufficient as an indicator of tumor burden in EGC. [ABSTRACT FROM AUTHOR]

Even when structural abnormalities are not observed on the brain magnetic resonance images (MRI) of very low-birth-weight (VLBW) infants, such infants are at increased risk for poor neurodevelopment. The aim of the present study was to evaluate cerebral glucose metabolism in VLBW infants without apparent structural abnormalities on MRI. Methods: Thirty-six VLBW infants who underwent F-18 fluorodeoxyglucose (F-18 FDG) brain PET and MRI were prospectively enrolled, while infants with evidence of parenchymal brain injury on MRI were excluded. The regional glucose metabolic ratio and asymmetry index were calculated. The asymmetry index more than 10% (right > left asymmetry) or less than -10% (left > right asymmetry) were defined as abnormal. Regional cerebral glucose metabolism were compared between right and left cerebral hemispheres, and between the following subgroups: multiple gestations, premature rupture of membrane, bronchopulmonary dysplasia, and low-grade intraventricular hemorrhage. Results: In the individual analysis, 21 (58.3%) of 36 VLBW infants exhibited asymmetric cerebral glucose metabolism. Fifteen infants (41.7%) exhibited right > left asymmetry, while six (16.7%) exhibited left > right asymmetry. In the regional analysis, right > left asymmetry was more extensive than left > right asymmetry. The metabolic ratio in the right frontal, temporal, and occipital cortices and right thalamus were significantly higher than those in the corresponding left regions. In the subgroup analyses, the cerebral glucose metabolism in infants with multiple gestations, premature rupture of membrane, bronchopulmonary dysplasia, or low-grade intraventricular hemorrhage were significantly lower than those in infants without these. Conclusion: VLBW infants without structural abnormalities have asymmetry of cerebral glucose metabolism. Decreased cerebral glucose metabolism are noted in infants with neurodevelopmental risk factors. F-18 FDG PET could show microstructural abnormalities not detected by MRI in VLBW infants. [ABSTRACT FROM AUTHOR]

Background: Although cognitive impairment is not a consistent feature of multiple system atrophy (MSA), increasing evidence suggests that cognitive impairment is common in MSA with predominant parkinsonism (MSA-P). It is assumed that the cognitive impairment in MSA-P is caused by the striatal dysfunction and disruption of striatofrontal connections. The aim of this study was to evaluate the relationship between regional glucose metabolism in the frontal cortex and striatum in patients with MSA-P using [18F]FDG brain PET. Methods: Twenty-nine patients with MSA-P and 28 healthy controls underwent [18F]FDG brain PET scan. The [18F]FDG brain PET images were semiquantitatively analyzed on the basis of a template in standard space. The regional glucose metabolism of the cerebral cortex and striatum were compared between MSA-P and healthy control groups. The correlations between age, symptom duration, H&Y stage, UPDRS III score, MMSE score, and glucose metabolism in the cerebellum and striatum to glucose metabolism in the frontal cortex were evaluated by multivariate analysis. Results: The glucose metabolism in the frontal cortex and striatum in MSA-P patients were significantly lower than those in healthy controls. Glucose metabolism in the striatum was the most powerful determinant of glucose metabolism in the frontal cortex in MSA-P. Only age and glucose metabolism in the cerebellum were independent variables affecting the glucose metabolism in the frontal cortex in healthy controls. Conclusion: The decrease in frontal glucose metabolism in MSA-P is related to the decrease in striatal glucose metabolism. This result provided evidence of striatofrontal deafferentiation in patients with MSA-P. [ABSTRACT FROM AUTHOR]

Complete reconstruction of damaged periodontal pockets, particularly regeneration of periodontal ligament (PDL) has been a significant challenge in dentistry. Tissue engineering approach utilizing PDL stem cells and scaffolding matrices offers great opportunity to this, and applying physical and mechanical cues mimicking native tissue conditions are of special importance. Here we approach to regenerate periodontal tissues by engineering PDL cells supported on a nanofibrous scaffold under a mechanical-stressed condition. PDL stem cells isolated from rats were seeded on an electrospun polycaprolactone/gelatin directionally-oriented nanofiber membrane and dynamic mechanical stress was applied to the cell/nanofiber construct, providing nanotopological and mechanical combined cues. Cells recognized the nanofiber orientation, aligning in parallel, and the mechanical stress increased the cell alignment. Importantly, the cells cultured on the oriented nanofiber combined with the mechanical stress produced significantly stimulated PDL specific markers, including periostin and tenascin with simultaneous down-regulation of osteogenesis, demonstrating the roles of topological and mechanical cues in altering phenotypic change in PDL cells. Tissue compatibility of the tissue-engineered constructs was confirmed in rat subcutaneous sites. Furthermore, in vivo regeneration of PDL and alveolar bone tissues was examined under the rat premaxillary periodontal defect models. The cell/nanofiber constructs engineered under mechanical stress showed sound integration into tissue defects and the regenerated bone volume and area were significantly improved. This study provides an effective tissue engineering approach for periodontal regeneration—culturing PDL stem cells with combinatory cues of oriented nanotopology and dynamic mechanical stretch. [ABSTRACT FROM AUTHOR]

Mesoporous bioactive nanoparticles (MBNs) have been developed as promising additives to various types of bone or dentin regenerative material. However, biofunctionality of MBNs as dentin regenerative additive to dental materials have rarely been studied. We investigated the uptake efficiency of MBNs-NH2 with their endocytosis pathway and the role of MBNs-NH2 in odontogenic differentiation to clarify inherent biofunctionality. MBNs were fabricated by sol-gel synthesis, and 3% APTES was used to aminate these nanoparticles (MBNs-NH2) to reverse their charge from negative to positive. To characterize the MBNs-NH2, TEM, XRD, FTIR, zeta(ξ)-potential measurements, and Brunauer–Emmett–Teller analysis were performed. After primary cultured rat dental pulp stem cells (rDPSCs) were incubated with various concentrations of MBNs-NH2, stem cell viability (24 hours) with or without differentiated media, internalization of MBNs-NH2 in rDPSCs (~4 hours) via specific endocytosis pathway, intra or extracellular ion concentration and odontoblastic differentiation (~28 days) were investigated. Incubation with up to 50 μg/mL of MBNs-NH2 had no effect on rDPSCs viability with differentiated media (p>0.05). The internalization of MBNs-NH2 in rDPSCs was determined about 92% after 4 hours of incubation. Uptake was significantly decreased with ATP depletion and after 1 hour of pre-treatment with the inhibitor of macropinocytosis (p<0.05). There was significant increase of intracellular Ca and Si ion concentration in MBNs-NH2 treated cells compared to no-treated counterpart (p<0.05). The expression of odontogenic-related genes (BSP, COL1A, DMP-1, DSPP, and OCN) and the capacity for biomineralization (based on alkaline phosphatase activity and alizarin red staining) were significantly upregulated with MBNs-NH2. These results indicate that MBNs-NH2 induce odontogenic differentiation of rDPSCs and may serve as a potential dentin regenerative additive to dental material for promoting odontoblast differentiation. [ABSTRACT FROM AUTHOR]

Magnetism is an intriguing physical cue that can alter the behaviors of a broad range of cells. Nanocomposite scaffolds that exhibit magnetic properties are thus considered useful 3D matrix for culture of cells and their fate control in repair and regeneration processes. Here we produced magnetic nanocomposite scaffolds made of magnetite nanoparticles (MNPs) and polycaprolactone (PCL), and the effects of the scaffolds on the adhesion, growth, migration and odontogenic differentiation of human dental pulp cells (HDPCs) were investigated. Furthermore, the associated signaling pathways were examined in order to elucidate the molecular mechanisms in the cellular events. The magnetic scaffolds incorporated with MNPs at varying concentrations (up to 10%wt) supported cellular adhesion and multiplication over 2 weeks, showing good viability. The cellular constructs in the nanocomposite scaffolds played significant roles in the stimulation of adhesion, migration and odontogenesis of HDPCs. Cells were shown to adhere to substantially higher number when affected by the magnetic scaffolds. Cell migration tested by in vitro wound closure model was significantly enhanced by the magnetic scaffolds. Furthermore, odontogenic differentiation of HDPCs, as assessed by the alkaline phosphatase activity, mRNA expressions of odontogenic markers (DMP-1, DSPP,osteocalcin, and ostepontin), and alizarin red staining, was significantly stimulated by the magnetic scaffolds. Signal transduction was analyzed by RT-PCR, Western blotting, and confocal microscopy. The magnetic scaffolds upregulated the integrin subunits (α1, α2, β1 and β3) and activated downstream pathways, such as FAK, paxillin, p38, ERK MAPK, and NF-κB. The current study reports for the first time the significant impact of magnetic scaffolds in stimulating HDPC behaviors, including cell migration and odontogenesis, implying the potential usefulness of the magnetic scaffolds for dentin-pulp tissue engineering. [ABSTRACT FROM AUTHOR]

The first cell lineage determination in embryos takes place when two cell populations are set apart, each differentiating into the trophectoderm (TE) and inner cell mass (ICM), respectively. It is widely believed that position/polarity cues play a key role in triggering this differentiation, but it remains unclear how extracellular cues are transduced into cell fate determination. Here, we provide evidence that supports that neogenin is implicated in relaying extracellular cues into the first cell fate determination in preimplantation mouse embryos. A polarized and transient distribution of neogenin was manifested in early blastomeres. Neogenin up-regulation by its overexpression accelerated ICM development in the blastocyst concomitant with the activation of the ICM-specific transcription factors Oct3/4, Sox2, and Nanog while its depletion by small hairpin RNAs (shRNAs) caused a developmental abnormality of poorly endowed ICM accompanied by the deactivation of Oct3/4, Sox2, and Nanog. Treatment with netrin-1 among neogenin ligands further impaired both embryonic development and ICM formation while repulsive guidance molecule c (RGMc) led to opposite consequences, enhancing ICM formation. From this study, we propose a model whereby neogenin interprets its own expression level to control the first cell fate determination in response to extracellular cues. [ABSTRACT FROM AUTHOR]

Magnetic nanofibrous scaffolds of poly(caprolactone) (PCL) incorporating magnetic nanoparticles (MNP) were produced, and their effects on physico-chemical, mechanical and biological properties were extensively addressed to find efficacy for bone regeneration purpose. MNPs 12 nm in diameter were citrated and evenly distributed in PCL solutions up to 20% and then were electrospun into nonwoven nanofibrous webs. Incorporation of MNPs greatly improved the hydrophilicity of the nanofibers. Tensile mechanical properties of the nanofibers (tensile strength, yield strength, elastic modulus and elongation) were significantly enhanced with the addition of MNPs up to 15%. In particular, the tensile strength increase was as high as ∼25 MPa at 15% MNPs vs. ∼10 MPa in pure PCL. PCL-MNP nanofibers exhibited magnetic behaviors, with a high saturation point and hysteresis loop area, which increased gradually with MNP content. The incorporation of MNPs substantially increased the degradation of the nanofibers, with a weight loss of ∼20% in pure PCL, ∼45% in 10% MNPs and ∼60% in 20% MNPs. Apatite forming ability of the nanofibers tested in vitro in simulated body fluid confirmed the substantial improvement gained by the addition of MNPs. Osteoblastic cells favored the MNPs-incorporated nanofibers with significantly improved initial cell adhesion and subsequent penetration through the nanofibers, compared to pure PCL. Alkaline phosphatase activity and expression of genes associated with bone (collagen I, osteopontin and bone sialoprotein) were significantly up-regulated in cells cultured on PCL-MNP nanofibers than those on pure PCL. PCL-MNP nanofibers subcutaneously implanted in rats exhibited minimal adverse tissue reactions, while inducing substantial neoblood vessel formation, which however, greatly limited in pure PCL. In vivo study in radial segmental defects also signified the bone regeneration ability of the PCL-MNP nanofibrous scaffolds. The magnetic, bone-bioactive, mechanical, cellular and tissue attributes of MNP-incorporated PCL nanofibers make them promising candidate scaffolds for bone regeneration. [ABSTRACT FROM AUTHOR]

A phase II study of NK cell therapy in treatment of patients with recurrent breast cancer has recently been reported. However, because of the complexities of tumor microenvironments, effective therapeutic effects have not been achieved in NK cell therapy. Radioiodine (I-131) therapy inhibits cancer growth by inducing the apoptosis and necrosis of cancer cells. Furthermore, it can modify cancer cell phenotypes and enhance the effect of immunotherapy against cancer cells. The present study showed that I-131 therapy can modulate microenvironment of breast cancer and improve the therapeutic effect by enhancing NK cell cytotoxicity to the tumor cells. The susceptibility of breast cancer cells to NK cell was increased by precedent I-131 treatment in vitro. Tumor burden in mice treated with I-131 plus NK cell was significantly lower than that in mice treated with NK cell or I-131 alone. The up-regulation of Fas, DR5 and MIC A/B on irradiated tumor cells could be the explanation for the enhancement of NK cell cytotoxicity to tumor cells. It can be applied to breast cancer patients with iodine avid metastatic lesions that are non-responsive to conventional treatments. [ABSTRACT FROM AUTHOR]

Background: Although cognitive impairment is not a consistent feature of multiple system atrophy (MSA), increasing evidence suggests that cognitive impairment is common in MSA with predominant parkinsonism (MSA-P). It is assumed that the cognitive impairment in MSA-P is caused by the striatal dysfunction and disruption of striatofrontal connections. The aim of this study was to evaluate the relationship between regional glucose metabolism in the frontal cortex and striatum in patients with MSA-P using [18F]FDG brain PET., Methods: Twenty-nine patients with MSA-P and 28 healthy controls underwent [18F]FDG brain PET scan. The [18F]FDG brain PET images were semiquantitatively analyzed on the basis of a template in standard space. The regional glucose metabolism of the cerebral cortex and striatum were compared between MSA-P and healthy control groups. The correlations between age, symptom duration, H&Y stage, UPDRS III score, MMSE score, and glucose metabolism in the cerebellum and striatum to glucose metabolism in the frontal cortex were evaluated by multivariate analysis., Results: The glucose metabolism in the frontal cortex and striatum in MSA-P patients were significantly lower than those in healthy controls. Glucose metabolism in the striatum was the most powerful determinant of glucose metabolism in the frontal cortex in MSA-P. Only age and glucose metabolism in the cerebellum were independent variables affecting the glucose metabolism in the frontal cortex in healthy controls., Conclusion: The decrease in frontal glucose metabolism in MSA-P is related to the decrease in striatal glucose metabolism. This result provided evidence of striatofrontal deafferentiation in patients with MSA-P., Competing Interests: The authors declare that they have no conflict of interest.

Fibroblast growth factor18 (FGF18) belongs to the FGF family and is a pleiotropic protein that stimulates proliferation in several tissues. Bone marrow mesenchymal stem cells (BMSCs) participate in the normal replacement of damaged cells and in disease healing processes within bone and the haematopoietic system. In this study, we constructed FGF18 and investigated its effects on rat BMSCs (rBMSCs). The proliferative effects of FGF18 on rBMSCs were examined using an MTS assay. To validate the osteogenic differentiation effects of FGF18, ALP and mineralization activity were examined as well as osteogenic differentiation-related gene levels. FGF18 significantly enhanced rBMSCs proliferation (p<0.001) and induced the osteogenic differentiation by elevating ALP and mineralization activity of rBMSCs (p<0.001). Furthermore, these osteogenic differentiation effects of FGF18 were confirmed via increasing the mRNA levels of collagen type I (Col I), bone morphogenetic protein 4 (BMP4), and Runt-related transcription factor 2 (Runx2) at 3 and 7 days. These results suggest that FGF18 could be used to improve bone repair and regeneration.