UC San Diego

Encephaloceles are considered rare with an approximate incidence of 1 in 35,000, and sphenoid encephaloceles are even more uncommon.2 Two types of sphenoid encephaloceles exist: medial perisellar encephaloceles, and lateral sphenoidal encephaloceles. Surgical correction of the lateral sphenoid recess encephalocele is achieved via one of two endoscopic approaches: extended sphenoidotomy or transpterygopalatine. Extended sphenoidotomy is preferred if the angle between the access door and lateral extension of bone defect is greater than 35°1. Otherwise, the transpterygopalatine approach is used. Intraoperative video demonstrating an extended sphenoidotomy approach to correcting a lateral recess sphenoidal encephalocele has not previously been published. Here we present a case of a 41-year-old female who presented with meningitis, a cerebrospinal fluid leak, and an incidental sphenoid mass. Brain MRI redemonstrated the mass in the sphenoid sinus consistent with an encephalocele occupying Sternbergs Canal. The patient consented to the procedure. The video demonstrates the skull base approach, encephalocele extraction, collagen inlay, and nasal septal bone and vascularized pedicled nasoseptal flap placement. Postoperative imaging confirmed the placement of the collagen inlay and nasal septal bone autograft. The patient recovered from surgery and was discharged on post-operative day 3 with no cerebrospinal fluid (CSF) leak recurrence. Postoperative follow up demonstrated viable nasoseptal graft without evidence of CSF leak. For patients with favorable anatomy, an extended sphenoidotomy approach to lateral sphenoid sinus encephalocele resection is a preferred alternative to the transpterygoid approach. This surgical video demonstrates the technique for managing lateral sphenoid sinus encephaloceles occupying Sternbergs canal, including endonasal approach, encephalocele resection and posterior sphenoid wall repair.

Despite ART, we detected occasional microglia containing cell-associated HIV RNA and HIV DNA integrated into open regions of the hosts genome (∼0.005%) should be corrected to: Despite ART, we detected occasional microglia containing cell-associated HIV RNA and HIV DNA integrated into open regions of the hosts genome (∼0.5%).

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Aberration of the "gut-liver axis" contributes to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Here, we use multi-omics to analyze the gut microbiota composition and metabolic profile of patients with type-2 diabetes mellitus (T2DM). T2DM patients were screened for liver disease by blood tests, ultrasound, and liver stiffness measurements. Stool microbiota was analyzed by 16S rRNA gene sequencing; metabolomic profiling by Nuclear Magnetic Resonance spectroscopy and Ultra-High Performance-Mass Spectrometry. Microbiome and metabolic signatures were analyzed in the whole cohort and in matched subsets to identify signatures specific for steatosis (MASLD±) or fibrosis (Fibrosis±). Gut permeability was assessed in-vitro using monolayers of MDCK cells and trans-epithelial electric resistance (TEER). Cytokine profile was assessed in serum and stools.Overall, 285 patients were enrolled: 255 serum, 252 urine and 97 stool samples were analyzed. Anaeroplasma and Escherichia/Shigella ASVs were higher, while Butyricicoccus ASVs were lower in those with normal liver. In MASLD±, Butyricicoccus ASV was significantly higher in those with steatosis. In the Fibrosis±, Butyricicoccus ASV was significantly lower in those with fibrosis. Glycochenodeoxycholic acid-3-sulfate (G-UDCA-3S) appeared to be higher in MASLD with fibrosis. Fecal water from patients with MASLD and fibrosis caused the greatest drop in the TEER vs those with normal liver; this was reversed with protease inhibitors. Finally, fecal IL-13 was lower in MASLD with fibrosis. We identified microbiome signatures which were specific for steatosis and fibrosis and independent of other metabolic risk factors. Moreover, we conclude that protease-related gut permeability plays a role in those MASLD patients with fibrosis, and that disease progression is linked to a gut-liver axis which is at least partially independent of T2DM.