Development of a social cognitive career theory scale for measuring the intention to select surgery as a career.

Background: Surgeon shortages have emerged as a prominent global issue. Although various studies have explored the factors that influence medical students in choosing surgery as a career, addressing the need for surgeons requires a multifaceted approach. However, there is currently a lack of a theoretically grounded scale to evaluate the effectiveness of surgical career development or policy promotion. Thus, this study aimed to develop a questionnaire for assessing the preference for a surgical career by adopting the Social Cognitive Career Theory (SCCT). Materials and methods: The study aimed to develop the Social Cognitive Career Theory Scale toward Surgery (SCCTSS) by adopting the framework of SCCT. The questionnaire was created through expert consensus and the content validity index (CVI) calculation. Subsequently, a pilot version of the SCCTSS was administered to 222 medical students in their clinical clerkships, and the collected data underwent item analysis. Additionally, the validation of the SCCTSS by gender was performed. Results: The SCCTSS comprised 16 items that passed expert panel evaluation, with a CVI >0.8, mean ≥ 3.00, and an interquartile range ≤1. Item analysis demonstrated that the quality of the SCCTSS met the qualifying threshold. Furthermore, the SCCTSS questionnaire effectively validated gender differences in surgical career preference. Conclusions: We developed an internally consistent and reliable scale and validated it through an expert panel method and feedback from medical students. Further research is required to evaluate the targeted interventions that may assist in recruiting medical students into the field of surgery through the application of the SCCTSS.

Trend of female first authorship in Journal of Orthopaedic Science, the official journal of the Japanese orthopaedic association from 2001 to 2021: An observational study.

BACKGROUND: Women are underrepresented in orthopaedic surgery, especially in Japan. Authorship is associated with representation and career advancement, but the academic representation of women in Japanese orthopaedic surgery has not been elucidated. This study aimed to elucidate the proportion of female first authorship and its associating factors, as well as trends in the Journal of Orthopaedic Science (JOS), the official journal of the Japanese Orthopaedic Association. METHODS: The study reviewed original articles published in JOS from 2002 to 2021 using data from PubMed on March 16, 2022. The gender of the first and last authors was determined using genderize. io, an online gender detection tool and manual search. The study used multivariable logistic regression to identify the factors associated with female first authorship and visualized the trend of predicted probability using restricted cubic spline curve. RESULTS: Among 2272 original articles, 148 (6.5%) and 79 (3.5%) had female first and last authors, respectively. Compared with 2002-2006, female first authorship significantly increased in 2012-2016 (adjusted odds ratio [aOR], 2.04; 95% confidence interval [CI], 1.09-4.05; p = 0.03) and 2017-2021 (aOR, 2.72; 95% CI, 1.46-5.276; p = 0.002). Affiliation with an institution in Japan (aOR, 0.51; 95% CI, 0.35-0.74; p < 0.001) and affiliation in orthopaedics (aOR, 0.16; 95% CI, 0.11-0.23; p < 0.001) were negatively associated with female first authorship. Around 2020, the trend showed a gradual then rapid increase in women with non-orthopaedic affiliations. Only a very small increase was observed in women with an orthopaedic affiliation. CONCLUSIONS: Female first authorship in JOS has been increasing. However, the proportion of female authors remains low. Authors outside of Japan and not affiliated with orthopaedics largely affect female authorship statistics. The results indicate the persistent gender gap in the academic representation of women in Japanese orthopaedic publications.

Recommendation for management of patients with their first episode of primary spontaneous pneumothorax, using video-assisted thoracoscopic surgery or conservative treatment.

International guidelines do not recommend surgery for the first episode of primary spontaneous pneumothorax (PSP), except in cases of persistent air leak, hemopneumothorax, bilateral pneumothorax, or occupations at risk. However, these recommendations have been challenged because of a significant reduction in the recurrence rate in emerging studies. We evaluated the rationale of recommendations by systematically reviewing RCTs and observational studies by using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) system. We searched articles in PubMed, EMBASE, and Cochrane databases up to August 15, 2020. The primary outcomes were the recurrence rate and complication rate. The secondary outcomes were hospital stay and drainage duration. Nine eligible studies with 1121 patients were retrieved and analyzed. The recurrence rate was lower in the VATS than in conservative treatment with moderate evidence (OR 0.13, 95% CI 0.09 to 0.19, P < 0.001, I2 = 0%). We did not find significant differences in complication rate (Peto OR 1.17, 95% CI 0.33 to 4.12, P = 0.80), hospital stay duration (MD - 0.48 days, 95% CI - 2.84 to 1.87, P = 0.69, very low evidence), and in drainage duration (MD - 3.99 days, 95% CI - 9.06 to 1.08, P = 0.12, very low evidence) between the two groups. Our results would suggest VATS treatment as a weak recommendation for patients with the first episode of PSP, based on our systematic review of the current evidence by using the GRADE system, indicating that different treatments will be appropriate for different patients and that patients' values and preferences should be incorporated through shared decision making.Trial REGISTRY: PROSPERO; No.: CRD42020162267.

Role of kisspeptin on cell proliferation and steroidogenesis in luteal cells in vitro and in vivo.

BACKGROUND: Kisspeptin (KISS1) and kisspeptin receptor (KISS1R) are essential gatekeepers of the reproductive system. The functions of KISS1 and KISS1R in corpus luteal cells remain ambiguous. The objective was to observe normal physiologic functions of corpus luteal cells in vivo and clarify the functions of KISS1 in vitro. METHODS: We conducted an in vivo observation of cellular patterns as well as the levels of steroidogenic enzymes and KISS1/KISS1R in corpus luteal cells obtained from female crossbred Taiwan native goats in the estrous cycle; the observation was performed using hematoxylin and eosin and immunohistochemistry staining. Subsequently, we used kisspeptin-10 (Kp-10) to stimulate temperature sensitive-caprine luteal cell line (ts-CLC-D) cells to investigate the progesterone (P4) levels, steroidogenic messenger RNA (mRNA)/protein levels, cell survival rate, intracellular Ca2+ concentration, and cell proliferation-related mRNA/protein levels in the mitogen-activated protein kinase pathway in vitro by applying immunofluorescence staining, Western blotting, 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide assay, and real-time polymerase chain reaction. RESULTS: We observed the presence of proteins and mRNAs for STAR, CYP11A1, HSD3B, KISS1, and KISS1R in the corpus luteal cells from goats in vivo. In vitro, the addition of Kp-10 reduced the P4 levels (p < 0.01) and increased cell proliferation (p < 0.05) of the ts-CLC-D cells. Furthermore, we found that the levels of proteins and mRNA for STAR, CYP11A1, and HSD3B decreased significantly when Kp-10 was added (p < 0.05). However, adding Kp-10 did not affect the mRNA levels for PLCG2, DAG1, PRKCA, KRAS, RAF1, MAP2K1, MAP2K2, MAPK3, MAPK1, and MAPK14. CONCLUSION: We determined that KISS1 could affect the P4 levels, steroidogenesis, and cell proliferation in luteal cells. However, further research is required to clarify how KISS1 regulates proliferation and steroid production in luteal cells.

Role of the kisspeptin/KISS1 receptor system in the testicular development of mice.

BACKGROUND: Kisspeptin and its receptor KISS1R have been found to be essential regulators of reproductive function. Previous data have revealed the presence of Kiss1 and Kiss1r mRNAs in the hypothalamus and the testis of humans and rodents. However, the precise location and possible physiological role of the kisspeptin/KISS1R system in the testis remain ambiguous. METHODS: We first produced an anti-KISS1R immunoglobulin Y antibody for KISS1R identification. To detect the exact sites of KISS1R and kisspeptin expression in the testis, we conducted immunohistochemistry assays on sections of testes. We used real-time polymerase chain reactions to identify Kiss1r in mice and to determine the expression levels of testicular genes. Finally, to verify the upstream regulation on the Kisspeptin/KISS1 receptor system, we treated primary mouse Leydig cells and MA-10 cells with luteinizing hormone (LH) and Br-cAMP, respectively, and examined Kiss1 and Kiss1r mRNA expression. RESULTS: Immunohistochemistry assays revealed that kisspeptin was expressed in Leydig cells and KISS1R was localized in the seminiferous tubules. With real-time polymerase chain reactions, we found Kiss1r mRNA was constitutively expressed in the mouse testis from birth until the postnatal fourth week. Furthermore, mRNA expression of Kiss1 was synchronized with that of Insl3 and Cyp19a. However, the expression of the LH receptor-encoding gene increased 1 week earlier than did Kiss1 expression. This indicated that the kisspeptin/KISS1R system in the testis may be controlled by LH and cAMP signaling pathways. Finally, we confirmed that Kiss1 mRNA expression was increased in both LH-treated primary Leydig cells and Br-cAMP-treated MA-10 cells (p < 0.05). On the other hand, cotreatment of both cell lines with Br-cAMP and a protein kinase A inhibitor RP-cAMP significantly suppressed 50% of Br-cAMP-induced Kiss1 expression (p < 0.05). CONCLUSION: We discovered that Kiss1 expression in mouse Leydig cells was induced by LH through the cAMP/PKA pathway. Based on the presence of kisspeptin receptors on spermatids, we inferred that kisspeptin- and development-related factors have synergistic effects on spermatogenesis. Nevertheless, more studies are required to elaborate the role of the kisspeptin/KISS1R system in testicular development.

Role of the Kisspeptin/KISS1 Receptor System in the Testicular Development of Mice.

BACKGROUND: Kisspeptin and its receptor KISS1R have been found to be essential regulators of reproductive function. Previous data have revealed the presence of Kiss1 and Kiss1r mRNAs in the hypothalamus and the testis of humans and rodents. However, the precise location and possible physiological role of the kisspeptin/KISS1R system in the testis remain ambiguous. METHODS: We first produced an anti-KISS1R immunoglobulin Y antibody for KISS1R identification. To detect the exact sites of KISS1R and kisspeptin expression in the testis, we conducted immunohistochemistry assays on sections of testes. We used real-time polymerase chain reactions (PCR) to identify Kiss1r in mice and to determine the expression levels of testicular genes. Finally, to verify the upstream regulation on the Kisspeptin/KISS1 receptor system, we treated primary mouse Leydig cells and MA-10 cells with luteinizing hormone (LH) and Br-cAMP, respectively and examined Kiss1 and Kiss1r mRNA expression. RESULTS: Immunohistochemistry assays revealed that kisspeptin was expressed in Leydig cells and KISS1R was localized in the seminiferous tubules. With real-time PCR, we found Kiss1r mRNA was constitutively expressed in the mouse testis from birth until the postnatal fourth week. Furthermore, mRNA expression of Kiss1 was synchronized with that of Insl3 and Cyp19a. However, the expression of the LH receptor-encoding gene increased 1 week earlier than did Kiss1 expression. This indicated that the kisspeptin/KISS1R system in the testis may be controlled by LH and cAMP signaling pathways. Finally, we confirmed that Kiss1 mRNA expression was increased in both LH-treated primary Leydig cells and Br-cAMP-treated MA-10 cells (p < 0.05). On the other hand, cotreatment of both cell lines with Br-cAMP and a protein kinase A inhibitor RP-cAMP significantly suppressed 50% of Br-cAMP-induced Kiss1 expression (p < 0.05). CONCLUSION: We discovered that Kiss1 expression in mouse Leydig cells was induced by LH through the cAMP/PKA pathway. Based on the presence of kisspeptin receptors on spermatids, we inferred that kisspeptin and development-related factors have synergistic effects on spermatogenesis. Nevertheless, more studies are required to elaborate the role of the kisspeptin/KISS1R system in testicular development.

Effects of hyperinsulinemia on acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitor via the PI3K/AKT pathway in non-small cell lung cancer cells in vitro.

Patients with lung cancer harboring activating epidermal growth factor (EGFR) mutations and pre-existing diabetes have been demonstrated to exhibit poor responses to first-line EGFR-tyrosine kinase inhibitor (TKI) therapy. Strategies for the management of acquired resistance to EGFR-TKIs in patients with advanced non-small cell lung cancer (NSCLC) are urgently required. Only a limited number of studies have been published to date on the effects of insulin on EGFR-TKI resistance in NSCLC. Hence, the aim of the present study was to investigate the roles of hyperinsulinemia and hyperglycemia in mediating gefitinib resistance in NSCLC cells with activating EGFR mutations. In the present study, the HCC4006 cell line, which harbors EGFR mutations, was co-treated with gefitinib and long-acting insulin glargine. Whether hyperinsulinemia is able to mediate EGFR-TKI resistance in the NSCLC cell line harboring activating EGFR mutations was also investigated, and the possible underlying mechanisms responsible for these actions were explored. The inhibition of cell proliferation, and the potential mechanism of gefitinib resistance, were examined using an MTS proliferation assay and western blot analysis, and through the transfection of siRNAs. Whether the inhibition of AKT is able to overcome EGFR-TKI resistance induced by long-acting insulin was also investigated. The results obtained suggested that hyperinsulinemia induced by glargine upregulated NSCLC cell proliferation and survival, and induced gefitinib resistance. By contrast, the morphology and proliferation of the cells in a medium containing a 2-fold concentration of glucose were not significantly affected. Gefitinib resistance induced by hyperinsulinemia may have been mediated via the phosphoinositide 3-kinase (PI3K)/AKT pathway rather than the mitogen-activated protein kinase extracellular signal regulated kinase (MAPK/ERK) pathway. AKT serine/threonine kinase 1 knockdown by siRNA rescued the gefitinib resistance that was induced by hyperinsulinemia. In conclusion, hyperinsulinemia, but not hyperglycemia, was identified to cause the development of gefitinib resistance in NSCLC cells with activating EGFR mutations. However, additional studies are required to investigate strategies, such as co targeting hyperinsulinemia and the PI3K/AKT pathway, for overcoming EGFR-TKI resistance in patients with NSCLC.

Dietary administration of zingerone to enhance growth, non-specific immune response, and resistance to Vibrio alginolyticus in Pacific white shrimp (Litopenaeus vannamei) juveniles.

Zingerone, one of the active components of ginger, is a phenolic alkanone with antioxidant and anti-inflammatory properties. The effects of zingerone supplementation on the growth, immunity, and disease resistance of Pacific white shrimp (Litopenaeus vannamei) juveniles were studied. Four experimental diets, including a control diet (without zingerone enrichment) and 1, 2.5, and 5 mg zingerone (kg diet)(-1) were used. After 56 days of culture, shrimp fed diets supplemented with 1, 2.5, and 5 mg zingerone (kg diet)(-1) had significantly greater weight gain and feed efficiency than the controls. Furthermore, after 56 days of culture, shrimp fed all doses of the zingerone diet had higher survival rates compared to the controls after 24-72 h of challenge by the pathogen, Vibrio alginolyticus. Significantly increased phenoloxidase levels were found in shrimp fed the zingerone diets at all doses, and respiratory bursts, lysozyme and phagocytic activities of shrimp fed 2.5 and 5 mg zingerone (kg diet)(-1) also significantly increased. Neither the total hemocyte count nor superoxide dismutase activity of the experimental and control groups revealed significant differences at any dose. The results indicate that zingerone can be recommended as a supplement to shrimp feed to increase growth, immunity, and disease resistance against the pathogen, V. alginolyticus. Use of zingerone as appetizer and immunostimulant in shrimp is promising.