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Background: Cerebral arteriovenous malformations (AVMs) have historically been considered congenital lesions with treatment options including surgery, radiation therapy, and observation. Spontaneous resolution of cerebral AVMs remains an exceedingly rare event with poorly understood pathophysiology. Materials and methods: Herein we report a retrospective case review of a 28-year-old man with alcoholic cirrhosis who presented with a seizure 3 weeks after liver transplantation. Neuroimaging confirmed the presence of a Spetzler–Martin grade 2 AVM in the right frontal lobe. Due to the recent liver transplantation, treatment was deferred at the time of initial diagnosis and the patient was observed for a course of 1 year. Follow-up imaging 1 year later showed resolution of the AVM, confirmed by a catheter angiogram. Conclusion: Spontaneous resolution of cerebral AVMs is a rare event. Treatment of chronic liver disease resulted in the normalization of angiogenic factors that likely led to AVM resolution. This case provides valuable insight into the vital role of angiogenesis in the natural history of AVMs. [ABSTRACT FROM AUTHOR]

Progression of diabetic retinopathy resists arrest even after institution of intensive glycemic control, suggesting a "metabolic memory" phenomenon, but the mechanism responsible for this phenomenon is still elusive. Gene expression and biological processes can also be regulated by long noncoding RNAs (LncRNAs), the RNAs with >200 nucleotides and no open reading frame for translation, and several LncRNAs are aberrantly expressed in diabetes. Our aim was to identify retinal LncRNAs that fail to reverse after termination of hyperglycemia. Microarray analysis was performed on retinal RNA from streptozotocin‐induced diabetic rats in poor glycemic control for 8 months, followed by in good glycemic control (blood glucose >400 mg/dL), or for 4 months, with four additional months of good glycemic control (blood glucose <150 mg/dL). Differentially expressed LncRNAs and mRNAs were identified through Volcano filtering, and their functions were predicted using gene ontology and pathway enrichment analyses. Compared with age‐matched normal rats, rats in continuous poor glycemic control had >1479 differentially expressed LncRNAs (710 downregulated, 769 upregulated), and among those, 511 common LncRNAs had similar expression in Diab and Rev groups (139 downregulated, 372 upregulated). Gene Ontology/pathway analysis identified limited LncRNAs in biological processes, but analysis based on biological processes/molecular function revealed >350 genes with similar expression in Diab and Rev groups; these genes were mainly associated with stress response, cell death, mitochondrial damage and cytokine production. Thus, identifying retinal LncRNAs and their gene targets that do not benefit from termination of hyperglycemia have potential to serve as therapeutic targets to slow down the progression of diabetic retinopathy. [ABSTRACT FROM AUTHOR]

Phlogacanthus thyrsiflorus Nees (Acanthaceae) is traditionally used in the North East Himalayan region to treat stomach issues, including gastritis. This study aimed to investigate the gastroprotective effect of 70% aqueous ethanol extract of Phlogacanthus thyrsiflorus flowers (PTE), standardized by HPTLC and LC-MS/MS, and to establish its possible mechanisms. The gastroprotective effect of PTE, at doses of 200 and 400 mg/kg body weight, was evaluated using both physical (pylorus ligation, PL; cold restraint stress, CRS) and chemical (ethanol, EtOH) ulcerogens-induced gastric ulcers in Wistar rats. Animals were randomly divided into control, ulcer control, positive control and PTE-treated groups, with PTE administered orally twice daily for 5 days. The protective effect of PTE was assessed through various gastric ulcer parameters, including gastric pH, gastric wall mucus, non-protein sulfhydryls (NP-SH) content, microvascular permeability, endogenous antioxidant markers, and gastric histopathology. HPTLC and LC-MS/MS confirmed the presence of gallic acid, naringenin, β-sitosterol and ascorbic acid in PTE. The active components of PTE showed significant dose-dependent inhibition of ulcer index, with reductions of 28.59-50.03% in PL, 27.69-53.23% in EtOH and 31.14-57.53% in CRS models (P< 0.01). Additionally, PTE at 400 mg/kg significantly increased gastric pH by 23.41%, mucus content by 33.69%, and NP-SH levels by 37.24%. PTE also demonstrated significant antioxidant potential and histopathological studies confirmed its protective effect. The study suggests that the anti-ulcer effect of PTE may be attributed to its ability to preserve adhered gastric mucus, exhibit antisecretory effects, and scavenge free radicals. [ABSTRACT FROM AUTHOR]

Aim: Hyperglycemia damages mitochondria and downregulates transcription of mtDNA-encoded genes and the long noncoding RNA LncCytB, causing mitochondrial genomic instability. The genes encoded by mtDNA are transcribed as large polycistronic transcripts, and the 5′ ends of precursor tRNAs are processed by mitochondrial-targeted ribonuclease P (MRPPs). Our aim was to investigate the role of MRPP1 in the downregulation of LncCytB in diabetic retinopathy. Methods: Using human retinal endothelial cells incubated in 20 mM D-glucose for 96 h, the gene expression and mitochondrial localization (immunofluorescence) of MRPP1 and the interaction between MRPP1 and LncCytB (determined by RNA-FISH and RNA immunoprecipitation) were quantified. The results were confirmed in retinal microvessels from streptozotocin-induced diabetic mice and from human donors with documented diabetic retinopathy. Results: Compared to normal glucose, high glucose decreased mRNA and mitochondrial localization of MRPP1 and its interaction with LncCytB. While MRPP1 overexpression prevented glucose-induced decrease in MRPP1–LncCytB interaction, LncCytB expression and mitochondrial damage (reduction in protective nucleoids in mtDNA), MRPP1-siRNA further worsened them. Similar results were obtained from retinal microvessels from diabetic mice and from human donors with diabetic retinopathy. Conclusions: Downregulation of MRPP1 in diabetes suppresses LncCytB transcription, resulting in mitochondrial functional and genomic instability, ultimately leading to the development of diabetic retinopathy. Thus, preventing MRPP1 downregulation has the potential to inhibit retinopathy and prevent the fear of vision loss in diabetic patients. [ABSTRACT FROM AUTHOR]

Objective We aim to describe a novel positioning technique using a specific surgical table to achieve the optimal angle during percutaneous glycerol rhizotomy (PGR) for trigeminal neuralgia (TN). Design This is a descriptive and photographic analysis of successful cases for future implementation. Setting This study was conducted at a single-institution, academic center. Participants The participants were adult patients with TN who underwent PGR and provided consent for publication. Main Outcome Measures Primary outcomes of this study were TN symptomatic relief and surgical complications. Results The use of a beach chair sliding headboard surgical table for PGR is plausible and ensures precise and immobile head flexion for 1 hour postglycerol injection. There were no intraoperative or postoperative complications. All patients achieved successful reduction of TN symptoms. Conclusions Utilizing this new method of intraoperative navigation with a unique surgical table in the upright position, surgeons may achieve precise head adjustments post-PGR. Head flexion has been postulated as a means of ensuring glycerol containment in Meckel's cave. This method can help standardize this procedure for future systematic studies on the importance of head positioning post-PGR. [ABSTRACT FROM AUTHOR]

Aims: Mitochondrial dysfunction is closely associated with the development of diabetic complications. In diabetic retinopathy, electron transport chain is compromised and mitochondrial DNA (mtDNA) is damaged, downregulating transcription of mtDNA-encoded cytochrome B (CYTB) and its antisense long noncoding RNA, long noncoding RNA cytochrome B (LncCytB). Our goal was to investigate the role of LncCytB in the regulation of CYTB and mitochondrial function in diabetic retinopathy. Methods: Using human retinal endothelial cells, genetically manipulated for LncCytB (overexpression or silencing), the effect of high glucose (20 mMd-glucose) on LncCytB-CYTB interactions (by chromatin isolation by RNA purification), CYTB gene expression (by real-time quantitative polymerase chain reaction), complex III activity, mitochondrial free radicals, and oxygen consumption rate (OCR, by Seahorse XF analyzer) was investigated. Key results were confirmed in the retinal microvessels from streptozotocin-induced diabetic mice. Results: High glucose decreased LncCytB-CYTB interactions, and while LncCytB overexpression ameliorated glucose-induced decrease in CYTB gene transcripts, complex III activity and OCR and increase in mitochondrial reactive oxygen species, LncCytB-siRNA further attenuated CYTB gene transcription, complex III activity, and OCR. Similar decrease in LncCytB-CYTB interactions and CYTB transcription was observed in diabetic mice. Furthermore, maintenance of mitochondrial homeostasis by overexpressing superoxide dismutase or sirtuin 1 in mice ameliorated diabetes-induced decrease in LncCytB-CYTB interactions and CYTB gene transcripts, and also improved complex III activity and mitochondrial respiration. Innovation and Conclusion: LncCytB downregulation in hyperglycemic milieu downregulates CYTB transcription, which inhibits complex III activity and compromises mitochondrial stability and OCR. Thus, preventing LncCytB downregulation in diabetes has potential of inhibiting the development of diabetic retinopathy, possibly via maintaining mitochondrial respiration. Antioxid. Redox Signal. 39, 817–828. [ABSTRACT FROM AUTHOR]

Background: Spinal tumors are rare pathology in the pediatric population. The tumors can be classified as extradural, intradural extramedullary, or intramedullary. Any of the spinal tumors can eventually lead to spinal deformity. The progressive spinal deformity can be part of the initial presentation or evolve on long follow-up, even years after the initial intervention and treatment. Summary: Management of spinal deformity associated with spinal tumors in children is not well defined. Patients with progressive symptoms and even neurological deficits need correction for their deformity when diagnosed. Patients that do not have pain or related neurological deficits should be evaluated for the severity of their deformity and followed long-term. Special consideration is needed for young patients who need multilevel surgery or have deformity at presentation. Key Messages: When considering the need for instrumentation and fusion, the surgeon should consider the age of the patient, expected future growth of the spine, neurologic status, extent of initial deformity, and the number of vertebral levels involved by tumor. Providers should also consider how surgery may fix or prevent deformity, especially when instrumentation can affect imaging at follow-up. [ABSTRACT FROM AUTHOR]

Study Design: Retrospective Cohort Study Objective: Spinal fusion, specifically constructs connected to pelvic bones, has been consistently reported as a predisposing factor to sacroiliac joint (SIJ) pain. The aim of this study is to compare SIJ outcomes in patients with constructs to the pelvis following instrumentation vs instrumentation plus fusion of the SIJ. Methods: Data of study subjects was extracted from a prospectively maintained database as well as retrospectively collected from records at a tertiary academic medical center in the United States between 2018 and 2020. Results: A cohort of 103 patients was divided into 2 groups: 65 in Group 1 [S2AI screw without fusion device] and 38 in Group 2 [S2AI screw with fusion device]. None of the patients in Group 2 developed postoperative SIJ pain compared to 44.6% in Group 1. Sacroiliac joint fusion occurred in all Group 2 but none of Group 1 patients. The postoperative Visual Analogue Scale (VAS) for lower extremity (LE) pain (.8 vs.5; P =.03) and postoperative Oswestry Disability Index (ODI) (18.7 vs 14.2; P <.01) were significantly higher in Group 1. The rate of distal junctional break, failure, and/or kyphosis (DJBFK) and time to DJBFK were not significantly different between the two groups, and the rate of DJBFK did not change in the presence of multiple covariates. Conclusion: The SIJs carry the heavy load of long lumbosacral fusion constructs extending to the pelvis. Simultaneous SIJ instrumentation and fusion decreases the risk of disability, prevents the development of postoperative SIJ pain, and may also protect the S2AI screw from loosening and failure. [ABSTRACT FROM AUTHOR]

Introduction: Mitochondrial dynamic plays a major role in their quality control, and the damaged mitochondrial components are removed by autophagy. In diabetic retinopathy, mitochondrial fusion enzyme, mitofusin 2 (Mfn2), is downregulated and mitochondrial dynamic is disturbed resulting in depolarized and dysfunctional mitochondria. Our aim was to investigate the mechanism of inhibition of Mfn2, and its role in the removal of the damaged mitochondria, in diabetic retinopathy. Methods: Using human retinal endothelial cells, effect of high glucose (20mM) on the GTPase activity of Mfn2 and its acetylation were determined. Role of Mfn2 in the removal of the damaged mitochondria was confirmed by regulating its acetylation, or by Mfn2 overexpression, on autophagosomes-autolysosomes formation and the mitophagy flux. Results: High glucose inhibited GTPase activity and increased acetylation of Mfn2. Inhibition of acetylation, or Mfn2 overexpression, attenuated decrease in GTPase activity and mitochondrial fragmentation, and increased the removal of the damaged mitochondria. Similar phenomenon was observed in diabetic mice; overexpression of sirtuin 1 (a deacetylase) ameliorated diabetes-induced inhibition of retinal Mfn2 and facilitated the removal of the damaged mitochondria. Conclusions: Acetylation of Mfn2 has dual roles in mitochondrial homeostasis in diabetic retinopathy, it inhibits GTPase activity of Mfn2 and increases mitochondrial fragmentation, and also impairs removal of the damaged mitochondria. Thus, protecting Mfn2 activity should maintain mitochondrial homeostasis and inhibit the development/progression of diabetic retinopathy. [ABSTRACT FROM AUTHOR]