Odontogenic myxoma of the jaws is a rare benign odontogenic tumor. In this case, a 61-year-old male patient had a chief complaint about maxillary anterior gingival mass and excisional biopsy result confirmed odontogenic myxoma. The clear acrylic resin custom tray was designed to minimize displacement of flabby tissue which remained after the surgery. Neutral zone and external impression technique could provide satisfactory result in terms of denture stability and retention during jaw relation record and wax denture try-in procedure. This clinical report describes fabrication of complete dentures for a patient with odontogenic myxoma in regard to flabby tissue and neutral zone.
Biopsy ; Denture Retention ; Denture, Complete ; Dentures ; Humans ; Jaw ; Jaw Relation Record ; Male ; Middle Aged ; Myxoma ; Odontogenic Tumors

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Ischemic monomelic neuropathy (IMN) is an uncommon complication of arteriovenous fistula (AVF) surgery that presents with pain, motor weakness, and sensory changes without critical ischemia. This report describes a rare case of successful IMN treatment after AVF surgery. A 61-year-old man with diabetic end-stage kidney disease was admitted for left brachiocephalic AVF surgery. Postoperatively, the patient complained of pain, motor weakness, and numbness in the left hand. However, the radial pulse remained palpable, and the overlying skin remained intact. A nerve conduction study above the wrist revealed reduced compound muscle action potential (CMAP) of the left ulnar nerve and no CMAP of the left median nerve. This study also showed the absence of sensory amplitude in both the left median and left ulnar nerves. Therefore, the patient was diagnosed with IMN. Proximalization of the arterial inflow surgery was performed to redistribute blood flow while maintaining the AVF. The patient’s neurological symptoms resolved postoperatively. Various conditions can cause hand pain after AVF surgery; however, IMN has rarely been reported. A multidisciplinary approach is needed to avoid this rare complication in patients presenting with hand pain after AVF surgery.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix. The IC50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H2O2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

Immunoglobulin A nephropathy (IgAN) is the most prevalent form of glomerulonephritis worldwide. Prediction of disease progression in IgAN can help to provide individualized treatment based on accurate risk stratification. Methods: We performed proton nuclear magnetic resonance-based metabolomics analyses of serum and urine samples from healthy controls, non-progressor (NP), and progressor (P) groups to identify metabolic profiles of IgAN disease progression. Metabolites that were significantly different between the NP and P groups were selected for pathway analysis. Subsequently, we analyzed multivariate area under the receiver operating characteristic (ROC) curves to evaluate the predictive power of metabolites associated with IgAN progression. Results: We observed several distinct metabolic fingerprints of the P group involving the following metabolic pathways: glycolipid metabolism; valine, leucine, and isoleucine biosynthesis; aminoacyl-transfer RNA biosynthesis; glycine, serine, and threonine metabolism; and glyoxylate and dicarboxylate metabolism. In multivariate ROC analyses, the combinations of serum glycerol, threonine, and proteinuria (area under the curve [AUC], 0.923; 95% confidence interval [CI], 0.667–1.000) and of urinary leucine, valine, and proteinuria (AUC, 0.912; 95% CI, 0.667–1.000) showed the highest discriminatory ability to predict IgAN disease progression. Conclusion: This study identified serum and urine metabolites profiles that can aid in the identification of progressive IgAN and proposed perturbed metabolic pathways associated with the identified metabolites.