Mitochondrial DNA transcription and mitochondrial genome-encoded long noncoding RNA in diabetic retinopathy.

In diabetic retinopathy, mitochondrial DNA (mtDNA) is damaged and mtDNA-encoded genes and long noncoding RNA cytochrome B (LncCytB) are downregulated. LncRNAs lack an open reading frame, but they can regulate gene expression by associating with DNA/RNA/protein. Double stranded mtDNA has promoters on both heavy (HSP) and light (LSP) strands with binding sites for mitochondrial transcription factor A (TFAM) between them. The aim was to investigate the role of LncCytB in mtDNA transcription in diabetic retinopathy. Using human retinal endothelial cells incubated in high glucose, the effect of regulation of LncCytB on TFAM binding at mtDNA promoters was investigated by Chromatin immunoprecipitation, and binding of LncCytB at TFAM by RNA immunoprecipitation and RNA fluorescence in situ hybridization. High glucose decreased TFAM binding at both HSP and LSP, and binding of LncCytB at TFAM. While LncCytB overexpression ameliorated decrease in TFAM binding and transcription of genes encoded by both H- and L- strands, LncCytB-siRNA further downregulated them. Maintenance of mitochondrial homeostasis by overexpressing mitochondrial superoxide dismutase or Sirtuin-1 protected diabetes-induced decrease in TFAM binding at mtDNA and LncCytB binding at TFAM, and mtDNA transcription. Similar results were obtained from mouse retinal microvessels from streptozotocin-induced diabetic mice. Thus, LncCytB facilitates recruitment of TFAM at HSP and LSP, and its downregulation in diabetes compromises the binding, resulting in the downregulation of polypeptides encoded by mtDNA. Regulation of LncCytB, in addition to protecting mitochondrial genomic stability, should also help in maintaining the transcription of mtDNA encoded genes and electron transport chain integrity in diabetic retinopathy.

Privacy-preserving blockchain-based federated learning for brain tumor segmentation.

Improved data sharing between healthcare providers can lead to a higher probability of accurate diagnosis, more effective treatments, and enhanced capabilities of healthcare organizations. One critical area of focus is brain tumor segmentation, a complex task due to the heterogeneous appearance, irregular shape, and variable location of tumors. Accurate segmentation is essential for proper diagnosis and effective treatment planning, yet current techniques often fall short due to these complexities. However, the sensitive nature of health data often prohibits its sharing. Moreover, the healthcare industry faces significant issues, including preserving the privacy of the model and instilling trust in the model. This paper proposes a framework to address these privacy and trust issues by introducing a mechanism for training the global model using federated learning and sharing the encrypted learned parameters via a permissioned blockchain. The blockchain-federated learning algorithm we designed aggregates gradients in the permissioned blockchain to decentralize the global model, while the introduced masking approach retains the privacy of the model parameters. Unlike traditional raw data sharing, this approach enables hospitals or medical research centers to contribute to a globally learned model, thereby enhancing the performance of the central model for all participating medical entities. As a result, the global model can learn about several specific diseases and benefit each contributor with new disease diagnosis tasks, leading to improved treatment options. The proposed algorithm ensures the quality of model data when aggregating the local model, using an asynchronous federated learning procedure to evaluate the shared model's quality. The experimental results demonstrate the efficacy of the proposed scheme for the critical and challenging task of brain tumor segmentation. Specifically, our method achieved a 1.99% improvement in Dice similarity coefficient for enhancing tumors and a 19.08% reduction in Hausdorff distance for whole tumors compared to the baseline methods, highlighting the significant advancement in segmentation performance and reliability.

Consensus Review on Strategies to Improve Delivery Across the BBB Including Focused Ultrasound.

Drug delivery to the central nervous system (CNS) has been a major challenge for CNS tumors due to the impermeability of the blood brain barrier (BBB). There have been a multitude of techniques aimed at overcoming the BBB obstacle aimed at utilizing natural transport mechanisms or bypassing the BBB which we review here. Another approach that has generated recent interest in the recently published literature is to use new technologies (Laser Interstitial Thermal Therapy, LITT; or Low Intensity Focused Ultrasound, LIFU) to temporarily increase BBB permeability. This review overviews the advantages, disadvantages, and major advances of each method. LIFU has been a major area of research to allow for chemotherapeutics to cross the BBB which has a particular emphasis in this review. While most of the advances remain in animal studies, there are an increasing number of translational clinical trials which will have results in the next few years.

A Nod for Meckel: A Novel Surgical Position Utilizing Meckel's Cave Anatomy for Percutaneous Glycerol Rhizotomy in Trigeminal Neuralgia.

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.

Improvement in Hearing Loss Following Posterior Fossa Arachnoid Cyst Fenestration: A Case Study.

Arachnoid cysts are abnormal intradural collections of cerebrospinal fluid. For posterior fossa arachnoid cysts (PFACs), symptoms vary greatly, often relating to cranial nerve impingement and/or hydrocephalus. Literature on long-term symptomatic and radiographic follow-up of PFACs is lacking. This case study describes a 32-year-old man who presented with headaches and left-sided hearing loss and was found to have a large left-sided cerebellopontine angle arachnoid cyst with syrinx and ventriculomegaly. After PFAC fenestration and excision, his headaches resolved and his hearing markedly improved. At the one-year postoperative evaluation, symptom improvement persisted, and MRI demonstrated a stable decreased cyst and near-complete resolution of his syrinx.

Three-column osteotomy in long constructs has lower rates of proximal junctional kyphosis and better restoration of lumbar lordosis than anterior column realignment.

PURPOSE: Three-column osteotomies (TCOs) and minimally invasive techniques such as anterior column realignment (ACR) are powerful tools used to restore lumbar lordosis and sagittal alignment. We aimed to appraise the differences in construct and global spinal stability between TCOs and ACRs in long constructs. METHODS: We identified consecutive patients who underwent a long construct lumbar or thoracolumbar fusion between January 2016 and November 2021. "Long construct" was any construct where the uppermost instrumented vertebra (UIV) was L2 or higher and the lowermost instrumented vertebra (LIV) was in the sacrum or ileum. RESULTS: We identified 69 patients; 14 (20.3%) developed PJK throughout follow-up (mean 838 days). Female patients were less likely to suffer PJK (p = 0.009). TCO was more associated with open (versus minimally invasive) screw/rod placement, greater number of levels, higher UIV, greater rate of instrumentation to the ilium, and posterior (versus anterior) L5-S1 interbody placement versus the ACR cohort (p < 0.001, p < 0.001, p < 0.001, p < 0.001, p = 0.005, respectively). Patients who developed PJK were more likely to have undergone ACR (12 (32.4%) versus 2 (6.3%, p = 0.007)). The TCO cohort had better improvement of lumbar lordosis despite similar preoperative measurements (ACR: 16.8 ± 3.78°, TCO: 23.0 ± 5.02°, p = 0.046). Pelvic incidence-lumbar lordosis mismatch had greater improvement after TCO (ACR: 14.8 ± 4.02°, TCO: 21.5 ± 5.10°, p = 0.042). By multivariate analysis, ACR increased odds of PJK by 6.1-times (95% confidence interval: 1.20-31.2, p = 0.29). CONCLUSION: In patients with long constructs who undergo ACR or TCO, we experienced a 20% rate of PJK. TCO decreased PJK 6.1-times compared to ACR. TCO demonstrated greater improvement of some spinopelvic parameters.

Impaired Removal of the Damaged Mitochondria in the Metabolic Memory Phenomenon Associated with Continued Progression of Diabetic Retinopathy.

Retinopathy fails to halt even after diabetic patients in poor glycemic control try to institute tight glycemic control, suggesting a "metabolic memory" phenomenon, and the experimental models have demonstrated that mitochondria continue to be damaged/dysfunctional, fueling into the vicious cycle of free radicals. Our aim was to investigate the role of removal of the damaged mitochondria in the metabolic memory. Using human retinal endothelial cells (HRECs), incubated in 20 mM D-glucose for 4 days, followed by 5 mM D-glucose for 4 additional days, mitochondrial turnover, formation of mitophagosome, and mitophagy flux were evaluated. Mitophagy was confirmed in a rat model of metabolic memory where the rats were kept in poor glycemic control (blood glucose ~ 400 mg/dl) for 3 months soon after induction of streptozotocin-induced diabetes, followed by 3 additional months of good control (BG < 150 mg/dl). Reversal of high glucose by normal glucose had no effect on mitochondrial turnover and mitophagosome formation, and mitophagy flux remained compromised. Similarly, 3 months of good glycemic control in rats, which had followed 3 months of poor glycemic control, had no effect on mitophagy flux. Thus, poor turnover/removal of the damaged mitochondria, initiated during poor glycemic control, does not benefit from the termination of hyperglycemic insult, and the damaged mitochondria continue to produce free radicals, suggesting the importance of mitophagy in the metabolic memory phenomenon associated with the continued progression of diabetic retinopathy.

Knowledge Review of Spinal Deformity and the Need for Fusion and Fixation following Treatment for Spinal Tumors among the Pediatric Age Group.

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.

Mitochondrial Genome-Encoded Long Noncoding RNA Cytochrome B and Mitochondrial Dysfunction in Diabetic Retinopathy.

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 mM d-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.

Impaired mitochondrial dynamics and removal of the damaged mitochondria in diabetic retinopathy.

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.

Improved Outcomes with Concurrent Instrumentation and Fusion of the Sacroiliac Joint in Patients with Long Lumbosacral Constructs.

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.

Mitochondrial Genome-Encoded Long Noncoding RNA and Mitochondrial Stability in Diabetic Retinopathy.

Mitochondria experience genomic and functional instability in diabetes, and mitochondrial dysfunction has a critical role in the development of diabetic retinopathy. Diabetes also alters expressions of many long noncoding RNAs (LncRNAs), the RNAs with >200 nucleotides and no open reading frame. LncRNAs are mainly encoded by the nuclear genome, but mtDNA also encodes three LncRNAs. Our goal was to investigate the effect of hyperglycemia on mtDNA-encoded LncRNA cytochrome B (LncCytB) in mtDNA stability in diabetic retinopathy. Retinal endothelial cells, transfected with LncCytB-overexpressing plasmids or siRNA, incubated in 5 mmol/L d-glucose (normal glucose [NG]) or 20 mmol/L d-glucose (high glucose [HG]) for 4 days, were analyzed for LncCytB expression by strand-specific PCR and its mitochondrial localization by RNA fluorescence in situ hybridization. Damage-sensitive mtDNA regions were examined by micrococcal nuclease (MNase) digestion sequencing and LncCytB occupancy at mtDNA by chromatin isolation by RNA purification. Protective nucleoids in mtDNA were analyzed by SYBR Green-MitoTracker Red staining and confirmed in isolated mitochondria by flow cytometry. Compared with NG, HG downregulated LncCytB by >50% but had no significant effect on the other mtDNA-encoded LncRNAs. mtDNA packaging was impaired, MNase sensitivity was increased, and LncCytB occupancy at mtDNA was decreased. While LncCytB overexpression ameliorated mtDNA damage and decrease in nucleoids and copy numbers, LncCytB-siRNA exacerbated damage and further reduced nucleoids. Retinal microvessels from streptozotocin-induced diabetic mice and human donors with diabetic retinopathy presented a similar decrease in LncCytB and mtDNA nucleoids. Thus, LncCytB has a major role in maintaining mitochondrial genomic stability, and its downregulation in the hyperglycemic milieu contributes to increased vulnerability of mtDNA to damage.

Blockchain and homomorphic encryption based privacy-preserving model aggregation for medical images.

Medical healthcare centers are envisioned as a promising paradigm to handle the massive volume of data for COVID-19 patients using artificial intelligence (AI). Traditionally, AI techniques require centralized data collection and training models within a single organization. This practice can be considered a weakness as it leads to several privacy and security concerns related to raw data communication. To overcome this weakness and secure raw data communication, we propose a blockchain-based federated learning framework that provides a solution for collaborative data training. The proposed framework enables the coordination of multiple hospitals to train and share encrypted federated models while preserving data privacy. Blockchain ledger technology provides decentralization of federated learning models without relying on a central server. Moreover, the proposed homomorphic encryption scheme encrypts and decrypts the gradients of the model to preserve privacy. More precisely, the proposed framework: (i) train the local model by a novel capsule network for segmentation and classification of COVID-19 images, (ii) furthermore, we use the homomorphic encryption scheme to secure the local model that encrypts and decrypts the gradients, (iii) finally, the model is shared over a decentralized platform through the proposed blockchain-based federated learning algorithm. The integration of blockchain and federated learning leads to a new paradigm for medical image data sharing over the decentralized network. To validate our proposed model, we conducted comprehensive experiments and the results demonstrate the superior performance of the proposed scheme.

Alkyl-substituted N-methylaryl-N'-aryl-4-aminobenzamides: A new series of small molecule inhibitors for Wip1 phosphatase.

The wild-type p53 induced phosphatase 1 (Wip1), a member of the serine/threonine-specific PP2C family, is overexpressed in numerous human cancers. Wip1 dephosphorylates p53 as well as several kinases (such as p38 MAPK, ATM, Chk1, and Chk2) in the DNA damage response pathway that are responsible for maintaining genomic stability and preventing oncogenic transformation. As a result, Wip1 is an attractive target for synthetic inhibitors that could be further developed into therapeutics to treat some cancers. In this study, we report a series of alkyl-substituted N-methylaryl-N'-aryl-4-aminobenzamides and their inhibitory activity of the Wip1 phosphatase. A straightforward synthetic route was developed to synthesize the target compounds from commercially available starting materials. Three different portions (R1, R2, R3) of the core scaffold were extensively modified to examine structure-activity relationships. This study revealed interesting trends about a new molecular scaffold to inhibit Wip1.

Partial replacement of cement with induction furnace dust for enhancing concrete properties with and without Aspergillus niger fungus: a green building approach.

Induction furnace dust (IFD) is a waste product of the alloy-making process whose disposal by landfill process becomes unsafe due to the presence of heavy metals in high concentrations. It further reduces the fertility of soil and pollutes the air making it harmful for human health. However, efforts can be made to utilize this dust in construction material as it has the same oxides (silica, aluminium oxide, and magnesium oxide) as found in cement, bricks, fine aggregates, coarse aggregates, etc. This study is aimed at the utilization of pre-treated induction furnace dust with Aspergillus niger fungus to replace cement for the construction of concrete structures through Taguchi design of experiments (DOE). The purpose of Aspergillus niger fungus is to reduce the heavy metal concentration from IFD to prevent the surroundings from getting toxic. The optimization of operating parameters such as dust replacement (5%, 10%, and 15%), curing days (7, 14, and 28 days), and cell count of fungus (104, 106, and 108 CFU/ml of distilled water) is done using Multi-objective Genetic Algorithm (G.A.) for effective compressive strength and water absorption capacity of cubes. The best results have been found in the case of IFD treated with Aspergillus niger fungus having dust replacement, curing time, and cell count of 14.96%, 28 days, and 9.22 × 107 CFU/ml of distilled water respectively for concrete production.

Both cis and trans-acting genetic factors drive somatic instability in female carriers of the FMR1 premutation.

The fragile X mental retardation (FMR1) gene contains an expansion-prone CGG repeat within its 5' UTR. Alleles with 55-200 repeats are known as premutation (PM) alleles and confer risk for one or more of the FMR1 premutation (PM) disorders that include Fragile X-associated Tremor/Ataxia Syndrome (FXTAS), Fragile X-associated Primary Ovarian Insufficiency (FXPOI), and Fragile X-Associated Neuropsychiatric Disorders (FXAND). PM alleles expand on intergenerational transmission, with the children of PM mothers being at risk of inheriting alleles with > 200 CGG repeats (full mutation FM) alleles) and thus developing Fragile X Syndrome (FXS). PM alleles can be somatically unstable. This can lead to individuals being mosaic for multiple size alleles. Here, we describe a detailed evaluation of somatic mosaicism in a large cohort of female PM carriers and show that 94% display some evidence of somatic instability with the presence of a series of expanded alleles that differ from the next allele by a single repeat unit. Using two different metrics for instability that we have developed, we show that, as with intergenerational instability, there is a direct relationship between the extent of somatic expansion and the number of CGG repeats in the originally inherited allele and an inverse relationship with the number of AGG interruptions. Expansions are progressive as evidenced by a positive correlation with age and by examination of blood samples from the same individual taken at different time points. Our data also suggests the existence of other genetic or environmental factors that affect the extent of somatic expansion. Importantly, the analysis of candidate single nucleotide polymorphisms (SNPs) suggests that two DNA repair factors, FAN1 and MSH3, may be modifiers of somatic expansion risk in the PM population as observed in other repeat expansion disorders.

Learning High-Dimensional Evolving Data Streams With Limited Labels.

In the context of streaming data, learning algorithms often need to confront several unique challenges, such as concept drift, label scarcity, and high dimensionality. Several concept drift-aware data stream learning algorithms have been proposed to tackle these issues over the past decades. However, most existing algorithms utilize a supervised learning framework and require all true class labels to update their models. Unfortunately, in the streaming environment, requiring all labels is unfeasible and not realistic in many real-world applications. Therefore, learning data streams with minimal labels is a more practical scenario. Considering the problem of the curse of dimensionality and label scarcity, in this article, we present a new semisupervised learning technique for streaming data. To cure the curse of dimensionality, we employ a denoising autoencoder to transform the high-dimensional feature space into a reduced, compact, and more informative feature representation. Furthermore, we use a cluster-and-label technique to reduce the dependency on true class labels. We employ a synchronization-based dynamic clustering technique to summarize the streaming data into a set of dynamic microclusters that are further used for classification. In addition, we employ a disagreement-based learning method to cope with concept drift. Extensive experiments performed on many real-world datasets demonstrate the superior performance of the proposed method compared to several state-of-the-art methods.

An Online Semantic-Enhanced Graphical Model for Evolving Short Text Stream Clustering.

Due to the popularity of social media and online fora, such as Twitter, Reddit, Facebook, and Wechat, short text stream clustering has gained significant attention in recent years. However, most existing short text stream clustering approaches usually work on static data and tend to cause a "term ambiguity" problem due to the sparse word representation. Beyond, they often exploit short text streams in a batch way and are difficult to find evolving topics in term-changing subspaces. In this article, we propose an online semantic-enhanced graphical model for evolving short text stream clustering (OSGM), by exploiting the word-occurrence semantic information and dynamically maintaining evolving active topics in term-changing subspaces in an online way. Compared to the existing approaches, our online model is not only free of determining the optimal batch size but also lends itself to handling large-scale data streams efficiently. It is also able to handle the "term ambiguity" problem without incorporating features from external resources. More importantly, to the best of our knowledge, it is the first work to extract evolving topics in term-changing subspaces automatically in an online way. Extensive experiments demonstrate that the proposed model yields better performance compared to many state-of-the-art algorithms on both synthetic and real-world datasets.

Spontaneous resolution of cerebral arteriovenous malformation after liver transplant: illustrative case.

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.