Enoki, Yuki

写真a

Affiliation

Faculty of Pharmacy, Department of Pharmacy 薬効解析学講座 ( Shiba-Kyoritsu )

Position

Assistant Professor/Senior Assistant Professor
 

Research Areas 【 Display / hide 】

  • Life Science / Clinical pharmacy

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Books 【 Display / hide 】

  • 「ニガテさん」のための薬物動態

    榎木裕紀, 松元一明, じほう, 2021.07,  Page： 230

    Scope: 第4章 患者背景によるADMEの変化に注目できる！ー高齢者の薬物動態ー,  Contact page： 154-161

  • スペシャル・ポピュレーションの抗菌薬投与設計

    榎木裕紀, 松元一明, じほう, 2020.07,  Page： 226

    Scope: 8.四肢切断患者,  Contact page： 212-219

  • Molecular mechanism of muscle wasting in CKD

    Watanabe H, Enoki Y, Maruyama T, Recent Advances of Sarcopenia and Frailty in CKD, 2020.01

    　View Summary

    © Springer Nature Singapore Pte Ltd. 2020. Chronic kidney disease (CKD), a chronic catabolic condition, is characterized by muscle wasting and a decreased muscle endurance. Many insights have made into the molecular mechanisms of muscle atrophy in CKD. A persistent imbalance between protein synthesis and degradation causes a loss of muscle mass. A decrease in insulin/IGF-1-Akt-mTOR signaling and an increased ubiquitin-proteasome system (UPS) have emerged as inducers of muscle loss. During muscle wasting, abnormal levels of reactive oxygen species (ROS) and inflammatory cytokines are detected in skeletal muscle. These increased ROS and inflammatory cytokine levels induce the expression of myostatin. The binding of myostatin to its receptor ActRIIB stimulates the expression of Foxo-dependent atrogenes. An impaired mitochondrial function also contributes to reduced muscle endurance. Increased glucocorticoid, angiotensin II, parathyroid hormone, and protein-bound uremic toxin levels that are observed in CKD all have a negative effect on muscle mass and endurance. The loss of skeletal muscle mass during the progression of CKD further contributes to the development of renal failure. Some potential therapeutic approaches based on the molecular mechanisms of muscle wasting in CKD are currently in the testing stages using animal models and clinical settings.

  • Uremic Solutes and Sarcopenia

    Watanabe H., Kato H., Enoki Y., Maeda H., Maruyama T., Uremic Toxins and Organ Failure, 2020.01

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    Sarcopenia in chronic kidney disease (CKD) is characterized by muscle wasting and decreased muscle endurance. Many insights have been made into the molecular mechanisms of muscle atrophy in CKD. A persistent imbalance between protein synthesis and degradation causes a loss of muscle mass. A decrease in insulin/IGF-1-Akt-mTOR signaling and an increased ubiquitin–proteasome system have emerged as inducers of muscle loss. During muscle wasting, abnormal levels of reactive oxygen species (ROS) and inflammatory cytokines are detected in skeletal muscle. The increased ROS and inflammatory cytokine induce the expression of myostatin, a negative regulator of muscle growth. An impaired mitochondrial function also contributes to reduced muscle endurance. Uremic toxins such as indoxyl sulfate, p-cresyl sulfate, and parathyroid hormone have a negative effect on muscle mass and endurance by affecting protein synthesis and degradation in addition to mitochondrial function in skeletal muscle. Some potential therapeutic approaches based on the molecular mechanisms of muscle wasting in CKD are currently in the testing stages.

  • 調剤と情報-高齢者の低栄養と薬-

    ENOKI YukiMATSUMOTO Kazuaki, JIHO, 2018.10

    Scope: 高齢者が低栄養になるとどうなる？-体内動態の変化と服薬上のリスク-

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Papers 【 Display / hide 】

  • Application of epithelial lining fluid drug concentrations to MIC(i)-Based PK/PD modeling of cefepime/nacubactam in a murine model of CPE pneumonia.

    Mizukami Y, Takahashi M, Suzuki K, Duan S, Ikegami S, Muraishi T, Satake N, Okamoto Y, Igarashi Y, Enoki Y, Taguchi K, Matsumoto K

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 32 ( 1 ) 102889 2026.01

    ISSN  1341-321X

  • Impact of Chronic Kidney Disease on the Onset of Sepsis: A Systematic Review

    Osa Sumika, Enoki Yuki, Endo Ayuka, Kumamoto Kanako, Kobayashi Keita, Komiya Chihiro, Satake Natsuki, Kawakami Junichi, Yagi Tatsuya, Taguchi Kazuaki, Matsumoto Kazuaki

    Biological and Pharmaceutical Bulletin (The Pharmaceutical Society of Japan)  49 ( 1 ) 99 - 107 2026

    ISSN  0918-6158

    　View Summary

    <p>Patients with chronic kidney disease (CKD) who develop sepsis experience worse prognoses; however, the impact of CKD on the incidence of sepsis has not been systematically investigated. A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A comprehensive search of Medical Literature Analysis and Retrieval System Online, Web of Science, the Cochrane Register of Controlled Trials, and ClinicalTrials.gov was performed for literature published prior to May 22, 2025, comparing the onset of sepsis in patients with or without CKD. The risk of bias was determined using the Risk of Bias in Nonrandomized Studies of Interventions tool. This study was registered with the International Prospective Register of Systematic Reviews (CRD42023465075). A total of 14 studies met the inclusion criteria for the systematic review. Of these, 5 examined community-acquired sepsis, 2 focused on intensive care unit-acquired sepsis, and the rest investigated surgery-acquired sepsis. Most studies enrolled populations aged over 65 years; 2 assessed age-related sepsis risk. One study evaluated sepsis occurrence in patients with end-stage CKD, while 3 studies stratified this association by estimated glomerular filtration rate (eGFR). Nearly all studies demonstrated an increased risk of sepsis among patients with CKD, with the risk progressively increasing as eGFR declined. Additionally, 2 studies reported that CKD elevated the risk of sepsis regardless of age, and all included studies indicated a low risk of bias. We indicate that patients with CKD may have a higher risk of developing sepsis than individuals without CKD.</p>

  • Development and external validation of a population pharmacokinetic model and optimal Vancomycin dosing regimen for overweight and obese patients.

    Komatsu T, Tomizawa A, Samura M, Suzuki A, Ishigo T, Fujii S, Ibe Y, Yoshida H, Tanaka H, Fujihara H, Yamaguchi F, Ebihara F, Maruyama T, Yagi Y, Hamada Y, Nagumo F, Takuma A, Chiba H, Nishi Y, Igarashi Y, Enoki Y, Otori K, Matsumoto K

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 31 ( 12 ) 102838 2025.12

    ISSN  1341-321X

  • Oral β-lactam combinations are effective in vitro against Mycobacterium avium, regardless of clarithromycin susceptibility.

    Yoshikawa M, Nishimura T, Misawa K, Shimamura R, Suzuki K, Kashimura S, Igarashi Y, Enoki Y, Taguchi K, Hasegawa N, Namkoong H, Matsumoto K

    Microbiology spectrum 13 ( 11 ) e0201225 2025.11

  • Evaluating the necessity of two-point sampling for vancomycin area under the curve in follow-up therapeutic drug monitoring.

    Suzuki A, Fujihara H, Yamaguchi F, Yoshida H, Tanaka H, Yagi Y, Maruyama T, Hamada Y, Ishigo T, Fujii S, Nagumo F, Samura M, Chiba H, Ebihara F, Takuma A, Komatsu T, Tomizawa A, Nishi Y, Igarashi Y, Enoki Y, Matsumoto K

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 31 ( 11 ) 102821 2025.11

    ISSN  1341-321X

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Papers, etc., Registered in KOARA 【 Display / hide 】

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Reviews, Commentaries, etc. 【 Display / hide 】

  • Betulinic acid ameliorates cast‐immobilized skeletal muscle atrophy but not denervation‐induced skeletal muscle atrophy

    Yuki Enoki, Yuki Kanezaki, Isamu Takahata, Kazuaki Taguchi, Kazuaki Matsumoto

    JCSM Communications (Wiley)  7 ( 1 ) 30 - 39 2024.01

    ISSN  29961394

    　View Summary

    <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Terpenoids have gained attention as therapeutic agents for skeletal muscle atrophy owing to their various physiological activities. In this study, we screened four terpenoids for their therapeutic potential against muscle atrophy in cultured cells and evaluated the effectiveness of betulinic acid in two disuse muscle atrophy models.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>C2C12 cells were used as the skeletal muscle model in cell culture experiments. Betulinic acid (100 mg/kg, twice daily) was administered to two different mouse models of muscle atrophy (established using the sciatic denervation and casting methods) for 7 days.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>In myotube experiments, the mRNA expression of atrogin‐1 and myostatin was significantly suppressed by betulinic and ursolic acids (<jats:italic>P</jats:italic> < 0.05). In the differentiation phase of C2C12 myotubes, the mRNA expression levels of myoD and myogenin were significantly increased by betulinic acid (<jats:italic>P</jats:italic> < 0.05). In addition, apelin and irisin were also significantly increased by betulinic acid (<jats:italic>P</jats:italic> < 0.05 and 0.01, respectively). Consequently, betulinic acid was administered to the aforementioned muscle atrophy models. Betulinic acid did not inhibit the decrease in skeletal muscle weight observed in the denervation model. However, it significantly inhibited the decrease in tibialis anterior (TA) and extensor digitorum longus (EDL) weights and grip strength observed in the cast‐immobilized skeletal muscle atrophy model (TA: Cast + Veh vs. Cast + Bet = 42.6 ± 1.0 vs. 46.0 ± 0.8 mg, <jats:italic>P</jats:italic> < 0.01; EDL: Cast + Veh vs. Cast + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg, <jats:italic>P</jats:italic> < 0.01; grip strength: Cast + Veh vs. Cast + Bet = 222 ± 4.8 vs. 245 ± 3.6 g, <jats:italic>P</jats:italic> < 0.05). In addition, betulinic acid administration partially inhibited the decrease in skeletal muscle cross‐sectional area.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Betulinic acid alleviated muscle atrophy in the cast model of muscle atrophy and has therapeutic potential for the treatment of immobilized disuse skeletal muscle atrophy.</jats:p></jats:sec>

  • Evaluation of <i>in vitro</i> antibacterial activities of therapeutic drugs against <i>Clostridioides difficile</i>, and measurement of fecal concentrations in <i>Clostridioides difficile</i> infection mouse models.

    Tashiro Sho, Mizukami Yuki, Enoki Yuki, Taguchi Kazuaki, Matsumoto Kazuaki

    Proceedings for Annual Meeting of The Japanese Pharmacological Society (Japanese Pharmacological Society)  95 ( 0 ) 1-YIA-30 2022

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    <p><b>[Background, Purpose]</b> Metronidazole (MNZ), vancomycin (VCM), and fidaxomicin (FDX) are standard therapeutic drugs against <i>Clostridioides difficile</i> infection (CDI). MNZ resulted in lower clinical cure rate compared with VCM. Detail information about antibacterial activities of the drugs and reasons for MNZ inferiority are not clear. Therefore, we evaluated the <i>in vitro</i> antibacterial activities, and measured fecal concentrations in CDI mouse models. </p><p><b>[Method] </b>Minimum inhibitory concentration (MIC) against seven strains of <i>C. difficile</i> were determined. Time-kill curves and post-antibiotic effect (PAE) were determined against <i>C. difficile</i> ATCC<sup>®</sup>43255. In addition, fecal concentrations in CDI mouse models were measured. </p><p><b>[Results] </b>MNZ, VCM, and FDX geometric mean MIC were 0.91, 1.81, and 0.34 µg/mL, respectively. MNZ exhibited concentration-dependent and rapid antibacterial activities at low concentrations ranged from 0.5 to 2.0 µg/mL. On the other hands, VCM and FDX exhibited time-dependent and slow antibacterial activities at high concentrations ranged from 0.5 to 32 µg/mL.<b> </b>MNZ showed the shortest PAE (1.9 h).<b> </b>In addition, maximal fecal concentration of MNZ (21.7 µg/g) was significantly lower than that of VCM (222.7 µg/g) at the dose of 40 mg/kg. </p><p><b>[Conclusion] </b>MNZ exhibited noteworthy antibacterial activities against <i>C. difficile</i>. However, MNZ PAE was short, and the fecal exposure was significantly small. We think the two characteristics are responsibility for the MNZ inferiority in clinical cure rate.</p>

  • Clostridioides difficile感染症に対するメトロニダゾールとバンコマイシンの有効性及び安全性評価

    三澤 可奈, 池谷 修, 榎木 裕紀, 田口 和明, 松元 一明, 宇野 俊介, 上蓑 義典, 長谷川 直樹

    日本化学療法学会雑誌 ((公社)日本化学療法学会)  68 ( Suppl.A ) 339 - 339 2020.09

    ISSN  1340-7007

  • A post-transplantation patient in whom a specific interval was required until the blood concentration of fluconazole reached a steady state

    Sakamoto Yasutaka, Matsumoto Kazuaki, Isono Hikaru, Koike Hirofumi, Enoki Yuki, Taguchi Kazuaki, Hagihara Maki, Matsumoto Kenji, Nakajima Hideaki, Sahashi Yukiko

    Proceedings for Annual Meeting of The Japanese Pharmacological Society (Japanese Pharmacological Society)  93 ( 0 ) 2 - O-036 2020

    Other, Joint Work

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    <p>[Introduction]</p><p>Fluconazole is anti-fungal agent widely used to prophylaxis and treatment. In the ECIL6 Guidelines, it is recommended that the dose of FLCZ for treatment should be established as ≥10 to 15 mg/mL, which is a trough level. We report a patient in whom a specific interval was required until the blood concentration of FLCZ reached a steady state.</p><p>[Case]</p><p>The patient was a 50-year-old male. To treat acute lymphocytic leukemia, remission induction and consolidation therapies were performed. After remission was achieved, umbilical cord blood transplantation was conducted. On Day 18, graft survival was confirmed. A blood culture test on Day 27 detected yeast-like fungus. Micafungin (MCFG) at 150 mg, used for empiric therapy, was switched to liposomal amphotericin B (L-AMB) at 3 mg/kg. On Day 36, renal hypofunction was noted, and L-AMB was switched to MCFG at 150 mg. On Day 65, there was a decrease in the β-D-glucan level from ≥600 to 375.2 pg/mL, and MCFG at 150 mg was switched to FLCZ at 200 mg. On Day 71, the trough level of FLCZ was 21.0 mg/mL, and its concentration 2 hours after administration was 24.4 mg/mL. The β-D-glucan level was 232.1 pg/mL. On Day 79, the trough and 2-hour levels of FLCZ were 30.6 and 32.1 mg/mL, respectively, and the β-D-glucan level was 167.6 pg/mL. On Day 85, the trough level of FLCZ was 38.4 mg/mL, and the β-D-glucan level was 161.4 pg/mL. Subsequently, blood culture was negative, and FLCZ administration was continued until Day 229. During the administration period, the creatinine clearance ranged from 33.0 to 45.9 mL/min.</p><p>[Discussion]</p><p>The half-life of FLCZ is approximately 30 hours. Its clearance depends on the renal function. In the present case, a target trough level was achieved in the early phase, but the blood concentration of FLCZ increased with the prolongation of the administration period. Therefore, the appearance of central nervous toxicity must be considered. In the future, it may be necessary to establish individualized, optimized FLCZ dosimetry in accordance with the renal function for the optimal use of FLCZ.</p>

  • Factorial Analysis of Clostridioides Difficile Colitis and Pseudomembranous Colitis Using JADER

    Takaya Risako, Misawa Kana, Tashiro Sho, Enoki Yuki, Taguchi Kazuaki, Matsumoto Kazuaki

    BPB Reports (公益社団法人 日本薬学会)  3 ( 1 ) 1 - 6 2020

    Other, Joint Work

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    <p>Clostridioides difficile (C. difficile) colitis and pseudomembranous colitis are known as healthcare-associated intestinal infections. In this study, the incidence of C. difficile colitis and pseudomembranous colitis was investigated using the Japanese Adverse Drug Event Report (JADER). Using JADER data between April 2004 and September 2017, the patient who developed C. difficile colitis and pseudomembranous colitis were investigated. During the study period, 375 cases of C. difficile colitis and 903 cases of pseudomembranous colitis were reported. The numbers of reported cases of both C. difficile colitis and pseudomembranous colitis were largest in those in their 70s, accounting for 24.7% and 25.6%, respectively. Patients in their 60s-90s comprised the majority of all patients with both C. difficile colitis and pseudomembranous colitis. Both C. difficile colitis and pseudomembranous colitis were caused by antibiotics in many patients, and signals of all antibiotics were detected. In C. difficile colitis, signals of immunosuppressants, corticosteroids, and alkylating drugs were also detected among drugs other than antibiotics. For pseudomembranous colitis, the use of molecularly targeted drugs, antimetabolic drugs, and corticosteroids was reported other than antibiotics. Using JADER, we revealed risk factors for the development of C. difficile colitis and pseudomembranous colitis, and firstly revealed that molecularly targeted drugs other than antibiotics could also be potential risk factors. Our findings may be useful for the early detection of drug-induced C. difficile colitis and pseudomembranous colitis.</p>

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Presentations 【 Display / hide 】

  • 多剤耐性菌・真菌・抗酸菌を含む病原性細菌に対するMA-T水溶液の殺菌・消毒効果の評価

    島田 そら, 水上 雄貴, 榎木 裕紀, 田口 和明, 松元 一明

    日本集中治療医学会雑誌, 

    2025.09
    , 

    (一社)日本集中治療医学会

  • 慢性腎臓病による病態関連因子がもたらす骨格筋萎縮

    榎木 裕紀, 本間 杏花, 五十嵐 裕貴, 松元 一明

    日本筋学会学術集会プログラム・抄録集, 

    2025.08
    , 

    (一社)日本筋学会

  • 抗菌薬投与によるMycobacterium abscessusの細胞壁脂質とコロニー形態の変化

    島村 莉奈, 西村 知泰, 吉川 万衣子, 三澤 可奈, 榎木 裕紀, 田口 和明, 松元 一明, 長谷川 直樹

    日本感染症学会総会・学術講演会・日本化学療法学会学術集会合同学会プログラム・抄録集, 

    2025.04
    , 

    日本感染症学会・日本化学療法学会

  • 模擬微小重力による筋芽細胞増殖抑制はメカノセンシティブチャネルを介した細胞外からのCa2+取り込み能低下に起因する

    市原 彩夏, 榎木 裕紀, 松元 一明, 南沢 享, 谷端 淳

    宇宙航空環境医学, 

    2025.03
    , 

    日本宇宙航空環境医学会

  • 腸球菌感染症に対するバンコマイシンの目標PK/PDパラメータ値に関する基礎研究

    林 侑孝, 高橋 実秀, 榎木 裕紀, 田口 和明, 山口 哲央, 舘田 一博, 松元 一明

    日本化学療法学会雑誌, 

    2025.01
    , 

    (公社)日本化学療法学会

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

  • 肺および肝線維化に対する骨格筋由来細胞外小胞による新規治療法の開発

    2025.06
    -
    2028.03

    Grants-in-Aid for Scientific Research, Grant-in-Aid for Challenging Research (Exploratory), Principal investigator

    　View Summary

    申請者は萎縮した骨格筋が腎臓の線維化を抑制するという興味深い現象を確認した。この機序の全貌は全く未解明であるが、申請者は骨格筋萎縮下で産出されたマウス血清中の脂質二重膜構造を有する細胞外小胞が強力な抗線維化作用を有している可能性を見出し、その細胞外小胞が新規抗線維化治療薬としてのモダリティとして優れているのではないかと考えた。そこで坐骨神経切断による廃用性筋萎縮モデルマウス血清由来細胞外小胞のブレオマイシン誘発肺線維症モデルおよび四塩化炭素誘発肝線維化モデルに対しする抗線維化効果について検討する。

  • Elucidation of the Exacerbation Mechanism Mediated by Skeletal Muscle-Derived Exosomes in Sepsis with Sarcopenia

    2022.04
    -
    2025.03

    日本学術振興会, Grants-in-Aid for Scientific Research, Enoki Yuki, Grant-in-Aid for Early-Career Scientists, No Setting

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    Although patients with skeletal muscle atrophy exhibit a poorer prognosis in sepsis, the underlying mechanisms remain largely undefined. To investigate this relationship, the applicant established a murine model of skeletal muscle atrophy induced by sciatic nerve transection (DN) and examined its impact on sepsis progression. The results demonstrated that DN mice exhibited aggravated sepsis, accompanied by an increased proportion of splenic T cells expressing the immune checkpoint molecule cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Furthermore, when exosomes isolated from the atrophied skeletal muscle of septic DN mice were applied to splenocytes from healthy mice, there was a notable increase in CTLA-4+CD4+ T cells. These findings suggest that exacerbation of sepsis in the context of skeletal muscle atrophy may be mediated by excessive activation of immunosuppressive pathways driven by exosomes derived from atrophied skeletal muscle.

  • Strategy for the treatment of CKD-induced sarcopenia based on the crosstalk between myokine and uremic toxins

    2018.04
    -
    2021.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, ENOKI YUKI, Grant-in-Aid for Early-Career Scientists , Principal investigator

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    In a mouse model of chronic kidney disease (CKD), the skeletal muscle weight and the cross-sectional area of the muscle fiber appeared to gradually decrease after the CKD surgery; expression of apelin-a skeletal muscle-derived secretory factor also decreased in the skeletal muscles. The administration of charcoal, a uremic toxin adsorbent, suppressed the decrease in apelin and skeletal muscle mass. Furthermore, apelin suppressed the decrease in skeletal muscle mass in CKD mice. The findings suggest that uremic toxin-mediated downregulation of apelin may play an important role in the pathophysiology of CKD-induced sarcopenia. Apelin, therefore could be a promising therapeutic target for CKD-induced sarcopenia.

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Awards 【 Display / hide 】

  • 第13回日本化学療法学会東日本支部 支部長賞（臨床）

    劉小茜、長邑花、榎木裕紀、田口和明、松元一明, 2022.01, 日本化学療法学会東日本支部, リネゾリドによる血液毒性に与える腎障害またはトラフ値の影響

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • 第13回日本化学療法学会東日本支部 支部奨励賞（基礎）

    三澤可奈、西村知泰、榎木裕紀、田口和明、宇野俊介、上蓑義典、松元一明、長谷川直樹, 2022.01, 日本化学療法学会東日本支部, Mycobacterium abscessus complexに対するNacubactamとβラクタム薬の併用効果

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • 第31回日本医療薬学会年会 Young Investigator’s Award

    長邑花、榎木裕紀、田口和明、松元一明, 2021.10, 日本医療薬学会, 廃用性筋萎縮による敗血症病態増悪における骨格筋由来エクソソームの関与

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • 第28回日本血液代替物学会年次大会優秀発表賞

    渡部佑樹、田口和明、榎木裕紀、酒井宏水、小田切優樹、松元一明, 2021.10, 日本血液代替物学会, 一酸化炭素結合型ヘモグロビン小胞体の急性呼吸窮迫症候群に対する有用性評価

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • MRSAフォーラム2020 一般演題優秀賞

    田代渉、北廣夕貴、森山大夢、濱村有那、高畑勇、川邊理奈、榎木裕紀、田口和明、松元一明, 2021.07, MRSAフォーラム, MRSA菌血症に対するダプトマイシンとバンコマイシンの有効性及び安全性の評価：システマティックレビュー＆メタ解析

    Type of Award： Award from Japanese society, conference, symposium, etc.

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Courses Taught 【 Display / hide 】

  • STUDY OF MAJOR FIELD (PHARMACODYNAMICS)

    2025

  • SEMINAR (PHARMACODYNAMICS)

    2025

  • RESEARCH FOR BACHELOR'S THESIS 1

    2025

  • PRIOR LEARNING FOR CLINICAL PRACTICE 4

    2025

  • PRIOR LEARNING FOR CLINICAL PRACTICE 1

    2025

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