Needs and gaps of faculty development for medical schools.

PURPOSE: Current faculty development (FD) programs are mostly limited to medical education and often lack a comprehensive and systematic structure. Therefore, the present study aimed to explore the current status and needs of FD programs in medical schools to provide a basis for establishing FD strategies. METHODS: We conducted an online survey of medical school FD staff and professors regarding FD. Frequency, regression, and qualitative content analyses were conducted. FD programs were categorized into the classification frameworks. RESULTS: A total of 17 FD staff and 256 professors at 37 medical schools participated. There are gaps between the internal and external FD programs offered by medical schools and their needs, and there are gaps between the programs the professors participated in and their needs. Recent internal and external FD programs in medical schools have focused on educational methods, student assessment, and education in general. Medical schools have a high need for leadership and self-development, and student assessment. Furthermore, professors have a high need for leadership and self-development, and research. The number of participants, topics, and needs of FD programs varied depending on the characteristics of individual professors. CONCLUSION: Medical schools should expand their FD programs to meet the needs of individuals and the changing demands of modern medical education. The focus should be on comprehensive and responsive programs that cover various topics, levels, and methods. Tailored programs that consider professors' professional roles, career stages, and personal interests are essential for effective FD.

Ginsenosides Rh1, Rg2, and Rg3 ameliorate dexamethasone-induced muscle atrophy in C2C12 myotubes.

High doses or prolonged use of the exogenous synthetic glucocorticoid dexamethasone (Dex) can lead to muscle atrophy. In this study, the anti-atrophic effects of ginsenosides Rh1, Rg2, and Rg3 on Dex-induced C2C12 myotube atrophy were assessed by XTT, myotube diameter, fusion index, and western blot analysis. The XTT assay results showed that treatment with Rh1, Rg2, and Rg3 enhanced cell viability in Dex-injured C2C12 myotubes. Compared with the control group, the myotube diameter and fusion index were both reduced in Dex-treated cells, but treatment with Rh1, Rg2, and Rg3 increased these parameters. Furthermore, Rh1, Rg2, and Rg3 significantly downregulated the protein expression of FoxO3a, MuRF1, and Fbx32, while also upregulating mitochondrial biogenesis through the SIRT1/PGC-1α pathway. It also prevents myotube atrophy by regulating the IGF-1/Akt/ mTOR signaling pathway. These findings indicate that Rh1, Rg2, and Rg3 have great potential as useful agents for the prevention and treatment of muscle atrophy.

The Mechanism of the Anti-Obesity Effects of a Standardized Brassica juncea Extract in 3T3-L1 Preadipocytes and High-Fat Diet-Induced Obese C57BL/6J Mice.

Obesity is a global health concern. Recent research has suggested that the development of anti-obesity ingredients and functional foods should focus on natural products without side effects. We examined the effectiveness and underlying mechanisms of Brassica juncea extract (BJE) in combating obesity via experiments conducted in both in vitro and in vivo obesity models. In in vitro experiments conducted in a controlled environment, the application of BJE demonstrated the ability to suppress the accumulation of lipids induced by MDI in 3T3-L1 adipocytes. Additionally, it downregulated adipogenic-related proteins peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer-binding protein-α (C/EBP-α), adipocyte protein 2 (aP2), and lipid synthesis-related protein acetyl-CoA carboxylase (ACC). It also upregulated the heat generation protein peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and fatty acid oxidation protein carnitine palmitoyltransferase-1 (CPT-1). The oral administration of BJE decreased body weight, alleviated liver damage, and inhibited the accumulation of lipids in mice with diet-induced obesity resulting from a high-fat diet. The inhibition of lipid accumulation by BJE in vivo was associated with a decreased expression of adipogenic and lipid synthesis proteins and an increased expression of heat generation and fatty acid oxidation proteins. BJE administration improved obesity by decreasing adipogenesis and activating heat generation and fatty acid oxidation in 3T3-L1 cells and in HFD-induced obese C57BL/6J mice. These results suggest that BJE shows potential as a natural method for preventing metabolic diseases associated with obesity.

Identification of marker compounds in fermented Benincasa hispida and validation of the method for its analysis.

Fermentation is a process that improves health functionality by inducing the production and increase of bioactive compounds. In this study, to standardize the fermentation process for Benincasa hispida, marker compounds that are increased or produced during fermentation were identified based on UPLC-QTOF-MS/MS. Analysis method verification and content analysis were conducted using HPLC-PDA. The marker compounds produced or increased in content were identified as 2-furoic acid, 2,3-dihydroxybenzoic acid, and rubinaphthin A by comparing their retention times, UV and MS spectra, and molecular formulas with those reported in previous studies. In addition, the increase in the content of the marker compounds by fermentation was confirmed, and the analytical method was validated by measuring its specificity, linearity, limit of detection and quantitation, precision, and accuracy. These results suggest that the developed fermentation process, marker compound identification, and verified analysis method can be applied to develop potential functional food ingredients from fermented B. hispida.

Plant sources, extraction techniques, analytical methods, bioactivity, and bioavailability of sulforaphane: a review.

Sulforaphane (SFN) is an isothiocyanate commonly found in cruciferous vegetables. It is formed via the enzymatic hydrolysis of glucoraphanin by myrosinase. SFN exerts various biological effects, including anti-cancer, anti-oxidation, anti-obesity, and anti-inflammatory effects, and is widely used in functional foods and clinical medicine. However, the structure of SFN is unstable and easily degradable, and its production is easily affected by temperature, pH, and enzyme activity, which limit its application. Hence, several studies are investigating its physicochemical properties, stability, and biological activity to identify methods to increase its content. This article provides a comprehensive review of the plant sources, extraction and analysis techniques, in vitro and in vivo biological activities, and bioavailability of SFN. This article highlights the importance and provides a reference for the research and application of SFN in the future.

Is it feasible and effective to provide faculty development programs online for clinical teachers?

PURPOSE: Seoul National University College of Medicine operates a faculty development program for clinical teachers at multiple affiliated teaching hospitals. In 2020, the program was moved online due to coronavirus disease 2019. The purpose of this study was to determine whether it is feasible and effective to provide faculty development programs online in terms of clinical teachers' participation and satisfaction in comparison with offline programs. METHODS: Clinical teachers participated in the clinical teaching methods programs offline in 2019 and online in 2020. We analyzed participation rate and satisfaction level. All surveys items were rated on a 5-point Likert scale. We also interviewed instructors about the advantages and drawbacks of the online program. RESULTS: The participation rate of the online program (89.5%) was significantly higher than that of the offline program (67.8%). The overall satisfaction level for the online program (4.37) was similar to that for the offline program (4.50). CONCLUSION: Faculty development programs online are feasible and effective in medical education. We need to design training content that fits online programs, consider various online training methods to reinforce the strengths of online programs, and support participants to make good use of these programs.

Detection of mechanical complications related to the potential risk of sudden cardiac death in patients with pulmonary arterial hypertension by computed tomography.

BACKGROUND: We explored the value of cardiac computed tomography (CT) for the detection and prediction of mechanical complications related to the risk of sudden cardiac death (SCD) in pulmonary arterial hypertension (PAH) patients. METHODS: PAH patients (n=60, mean age 47±15, 31.7% male) with pulmonary artery (PA) enlargement (≥40mm) by echocardiography were studied with cardiac CT. Complications explored were the presence of left main coronary artery (LM) compression, airway compression, PA dissection and PA thrombosis in relation to diameters of main PA (MPA) which were measured in (1) axial plane (MPAAx) and (2) LM oblique view (MPALMobq). RESULTS: Mechanical complications were found in 21 patients (35.0%): LM compression in 20 patients; airway compression in 3 patients; and PA thrombosis in 4 patients. Patients with complications had more dilated MPALMobq than patients without complication (59.4±13.0mm vs. 42.4±7.0mm, p<0.001). The area under the receiver operating characteristic curve for MPALMobq was 0.889 (95% confidence interval: 0.795 to 0.983, p<0.001) with the highest discriminating sensitivity and specificity being 90.5% and 69.2%, respectively at MPALMobq of 45mm. MPAAx failed to predict the presence of mechanical complications (p>0.05). CONCLUSION: MPALMobq≥45mm was significantly associated with the presence of mechanical complications of PAH. Evaluation with CT should be considered in PAH patients with dilated MPA.

Screening of Mechanical Complications of Dilated Pulmonary Artery Related to the Risk for Sudden Cardiac Death in Patients with Pulmonary Arterial Hypertension by Transthoracic Echocardiography.

BACKGROUND: In patients with pulmonary arterial hypertension (PAH), the mechanical complications of pulmonary artery (PA) enlargement are related to sudden cardiac death (SCD). The aim of this study was to investigate the prevalence of PA enlargement, the correlation of main PA (MPA) diameter with other echocardiographic parameters, and the role of transthoracic echocardiography in screening for such complications. METHODS: Among 298 patients who were followed for PAH, patients with PA enlargement (>40 mm) by transthoracic echocardiography were consecutively enrolled in a prospective manner. The presence of left main and airway compression, PA dissection, or PA thrombus was determined with cardiac computed tomography. RESULTS: Forty-six patients (15.4%; mean age, 49 ± 14 years; 32.6% men) with dilated MPAs were enrolled. Mechanical complications were present in 16 patients (34.8%). Those with complications had more dilated MPAs compared with patients without (mean PA diameter, 55.6 ± 12.2 vs 46.7 ± 4.3 mm; P = .012). Other echocardiographic parameters of the right heart, such as right ventricular systolic pressure, showed no differences (P > .05 for all). The area under the receiver operating characteristic curve for MPA diameter was 0.750 (95% CI, 0.577-0.923; P = .009), with the highest sensitivity and specificity values for the presence of complications being 85.7% and 58.6%, respectively, according to an MPA diameter of 46.5 mm. CONCLUSIONS: Mechanical complications related to sudden cardiac death in patients with PAH with dilated PAs are common. The overall performance of transthoracic echocardiography as a screening tool for predicting such complications appears reasonable. Given the burden of sudden cardiac death, measurement of PA diameter should be routinely included over the course of follow-up, especially in patients with PAH.

Rapid visual identification of PCR amplified nucleic acids by centrifugal gel separation: Potential use for molecular point-of-care tests.

Recently, nucleic acid amplification and detection techniques have progressed based on advances in in microfluidics, microelectronics, and optical systems. Nucleic acids amplification based point-of-care test (POCT) in resource-limited settings requires simple visual detection methods. Several biosensing methods including lateral flow immunoassays (LFIA) were previously used to visually detect nucleic acids. However, prolonged assay time, several washing steps, and a need for specific antibodies limited their use. Here we developed a novel, rapid method to visualize amplified nucleic acids with naked eyes in clinical samples. First, we optimized conditions based on separation using very low centrifugal force and a density medium to detect human papillomavirus (HPV)-16 DNA in cervical specimens. After DNA extraction, HPV16 PCR was performed with biotin-labeled forward primer and Cy3-labeled reverse primer. PCR amplicon was mixed with streptavidin-magnetic beads, introduced into the density medium. After two-minute centrifugation, the result was visually identified. This system showed identical results with commercial HPV real-time PCR for 30 clinical samples and could detect up to 10(2)copies/mL of HPV DNA without any optical instruments. This robust and sensitive visual detection system is suitable for non-specialist personnel and point-of-care diagnosis in low-resource settings.

Antiplatelet activity of beta-carboline alkaloids from Perganum harmala: a possible mechanism through inhibiting PLCgamma2 phosphorylation.

Beta-carboline alkaloids including harmalol, harmaline, norharmane, harmol, harmine and harmane are important constituents of the medicinal plant, Perganum harmala L. (Zygophylaceae), which has been used in traditional medicine. In the present study, the antiplatelet activities of six beta-carboline alkaloid compounds were investigated in vitro. At a concentration of 200 microM, these compounds have no effect on arachidonic acid (AA)-, thrombin- and U46619 (a thromboxane A2 mimic)-stimulated platelet aggregation. On the contrary, it was revealed that collagen-induced platelet aggregation could be inhibited by these compounds with different potencies (harmane and harmine were most potent, harmol had medium potency, and harmol, norharmane, harmalol and harmaline had a weak, non significant effect), indicating a selective inhibition on collagen-mediated platelet activation. Consistently, further study revealed that collagen-mediated phospholipase (PL) Cgamma2 and protein tyrosine phosphorylation, cytosolic calcium mobilization and arachidonic acid liberation were completely inhibited by harmane and harmine in a concentration-dependent manner, while the other compounds were only partially or not effective at all. Taken together, these results indicate that three of these six beta-carboline alkaloids can selectively affect collagen-induced platelet aggregation with different potencies; in particular, harmane and harmine were most potent, and their antiplatelet activities may be mediated by inhibiting PLCgamma2 and protein tyrosine phosphorylation with sequential suppression of cytosolic calcium mobilization and arachidonic acid liberation, indicating that harmane and harmine have a potential to be developed as a novel agent for atherothrombotic diseases.

Antiplatelet activity of epigallocatechin gallate is mediated by the inhibition of PLCgamma2 phosphorylation, elevation of PGD2 production, and maintaining calcium-ATPase activity.

We have previously reported that green tea catechins displayed a potent antithrombotic effect by inhibition of platelet aggregation. In the present study, the antiplatelet and antithrombotic activities of epigallocatechin gallate (EGCG), the major catechin derived from green tea, were extensively investigated. EGCG inhibited arterial thrombus formation and U46619-, collagen-, and arachidonic acid (AA)-induced washed rabbit platelet aggregation in a concentration-dependent manner, with IC50 values of 61 +/- 3, 85 +/- 4, and 99 +/- 4 microM, respectively. In line with the inhibition of collagen-induced platelet aggregation, EGCG revealed blocking of the collagen-mediated phospholipase (PL) Cgamma2 and protein tyrosine phosphorylation, and it caused concentration-dependent decreases of cytosolic calcium mobilization, AA liberation, and serotonin secretion. In addition, the platelet aggregation, intracellular Ca2+ mobilization, and protein tyrosine phosphorylation induced by thapsigargin, a Ca2(+)-ATPase pump inhibitor, were completely blocked by EGCG. Contrary to the inhibition of AA-induced platelet aggregation, EGCG failed to inhibit cyclooxygenase and thromboxane (TX) A2 synthase activities, but it concentration-dependently elevated AA-mediated PGD2 formation. In contrast, epigallocatechin (EGC), a structural analogue of EGCG lacking a galloyl group in the 3' position, slightly inhibited collagen-stimulated cytosolic calcium mobilization, but failed to affect other signal transductions as did EGCG in activated platelets and arterial thrombus formation. These results suggest that antiplatelet activity of EGCG may be attributable to its modulation of multiple cellular targets, such as inhibitions of PLCgamma2, protein tyrosine phosphorylation and AA liberation, and elevation of cellular PGD2 levels, as well as maintaining Ca2(+)-ATPase activity, which may underlie its beneficial effect on the atherothrombotic diseases.

Antithrombotic and antiplatelet activities of Korean red ginseng extract.

The antithrombotic and antiplatelet activities of Korean red ginseng extract (KRGE) were examined on rat carotid artery thrombosis in vivo and platelet aggregation in vitro and ex vivo. The KRGE significantly prevented rat carotid arterial thrombosis in vivo in a dose-dependent manner. Administration of the KRGE to rats significantly inhibited adenosine diphosphate (ADP)- and collagen-induced platelet aggregation ex vivo, although it failed to prolong coagulation times such as activated partial thromboplastin and prothrombin time indicating that the antithrombotic effect of the red ginseng may be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, the red ginseng inhibited the U46619-, arachidonic acid-, collagen- and thrombin-induced rabbit platelet aggregations in vitro in a concentration-dependent manner, with IC(50) values of 390 +/- 15, 485 +/- 19, 387 +/- 11 and 335 +/- 15 microg/ml, respectively. Consistently, serotonin secretion was also inhibited by ginseng in the same pattern. These results suggest that the red ginseng has a potent antithrombotic effect in vivo, which may be due to the antiplatelet rather than the anticoagulation activity, and the red ginseng intake may be beneficial for individuals with high risks of thrombotic and cardiovascular diseases.

Antiplatelet and antithrombotic activities of Korean Red Ginseng.

The antiplatelet and antithrombotic activities of Korean Red Ginseng (KRG) were examined on rat carotid artery thrombosis in vivo, and platelet aggregation in vitro and ex vivo. Administration of KRG to rats not only prevented carotid artery thrombosis in vivo in a dose-dependent manner, but also significantly inhibited ADP- and collagen-induced platelet aggregation ex vivo, while failed to prolong coagulation times such as activated partial thromboplastin time (APTT) and prothrombin time (PT), indicating the antithrombotic effect of KRG might be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, KRG inhibited U46619-, arachidonic acid-, collagen- and thrombin-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 620 +/- 12, 823 +/- 22, 722 + 21 and 650 +/- 14 microg/mL, respectively. Accordingly, KRG also inhibited various agonists-induced platelet serotonin secretions as it suppressed platelet aggregation. These results suggest that KRG has a potent antithrombotic effect in vivo, which may be due to antiplatelet rather than anticoagulation activity, and KRG intake may be beneficial to the individuals with high risks of thrombotic and cardiovascular diseases.