Paranasal sinus angiosarcoma with facial paralysis as a novel manifestation: a case report and literature review.

BACKGROUND: Paranasal sinus angiosarcoma is an uncommon malignancy, with only a few reported cases worldwide. Although it exhibits multiple symptoms, facial paralysis has not been previously documented as a noticeable presentation. CASE PRESENTATION: In this case, we report a 40-year-old male who presented with facial numbness and pain for one month, weakness of his facial muscles for 15 days, and recurrent right epistaxis for 1 year. He had a history of nasal inflammatory polyps with chronic sinusitis. Computed tomography and magnetic resonance imaging showed space-occupying lesions in the right nasal cavity and maxillary sinus, with bone destruction occurring in the sinus wall and turbinate. This patient then underwent endoscopic surgery. According to the histopathological and immunohistochemical results, he was eventually diagnosed with paranasal sinus angiosarcoma in April 2021. To date, this patient has not initiated any radiotherapy or chemotherapy and has survived with lymphatic metastasis for at least 3 years. CONCLUSIONS: This manuscript suggests that paranasal sinus angiosarcoma can present with facial paralysis. Moreover, pathological and immunohistochemical tests are still vital for diagnosing paranasal sinus angiosarcoma and differential diagnosis. Additionally, regular follow-up is crucial for patients with paranasal sinus angiosarcoma, enabling monitoring of recurrence, metastasis, and recovery while contributing valuable clinical data to understanding this rare disease and associated research endeavours.

UHPLC-MS/MS-based method for quantification of verinurad in rat plasma and its application in a bioavailability study.

A rapid and sensitive UHPLC-MS/MS method was developed and fully validated for the quantification of verinurad in rat plasma. Lesinurad was used as an internal standard (IS), and simple protein precipitation was utilized to prepare the analytes from the matrix. Chromatographic separation was carried out on a Zorbax SB C18 column. The mobile phase consisted of water with 0.1% formic acid (A) and acetonitrile with 0.1% formic acid (B) at a flow rate of 0.3 mL/min. The short run time of 4 min made it possible to analyze more than 300 samples per day. The ion transitions were quantified in negative mode with multiple reaction monitoring (MRM) transitions of 347.1 â†’ 261.1 for verinurad and 404.2 â†’ 178.9 for the IS. The validated linear ranges of verinurad were 10-5000 ng/mL in rat plasma. The validated UHPLC-MS/MS method was further applied to the pharmacokinetic study of verinurad in rat plasma after intragastric (2 mg/kg) and intravenous (1 mg/kg) administrations. The pharmacokinetic study revealed that verinurad showed high clearance and high bioavailability (78.1%). To the best of our knowledge, this is the first report of the bioavailability study of verinurad.

Myo9b and RICS modulate dendritic morphology of cortical neurons.

Regulated growth and branching of dendritic processes is critical for the establishment of neuronal circuitry and normal brain functions. Rho family GTPases, including RhoA, Rac1, and Cdc42, play a prominent role in dendritic development. RhoA inhibits dendritic branching and growth, whereas Rac1/Cdc42 does the opposite. It has been suggested that the activity of RhoA must be kept low to allow dendritic growth. However, how neurons restrict the activation of RhoA for proper dendritic development is not clear. In the present study, we undertook a comprehensive loss-of-function analysis of putative RhoA GTPase-activating proteins (RhoA GAPs) in the cortical neurons. The expression of 16 RhoA GAPs was detected in the developing rat brain, and RNA interference experiments suggest that 2 of them, Myo9b and RICS, are critical regulators of dendritic morphogenesis. Knockdown of either Myo9b or RICS in cultured cortical neurons or developing cortex resulted in decreased dendrite length and number. Inhibition of RhoA/ROCK signaling restores the defects of dendritic morphology induced by knockdown of Myo9b or RICS. These data demonstrate that Myo9b and RICS repress RhoA/Rock signaling and modulate dendritic morphogenesis in cortical neurons, providing evidence for critical physiological function of RhoA GAPs in regulation of dendritic development.