Pyogenic granuloma of the hard palate leading to alveolar cleft: a case report.

This case report describes a rare occurrence of pyogenic granuloma (PG) in the hard palate deviating from its typical gingival location that led to the formation of an alveolar cleft. The aggressive growth pattern of the lesion, with atypical progression from a pedunculated nodule to an alveolar cleft, raised concern. The diagnosis was based on magnetic resonance imaging and computed tomography findings, which revealed a tadpole-shaped lesion originating from the midline hard palate. The differential diagnosis included a minor salivary gland tumor. Surgical excision was performed under general anesthesia and resulted in a mucosal defect without nasolabial fistula formation or bone exposure. The palatal defect was packed with oxidized regenerated cellulose and closed with Vicryl Rapide sutures, both of which contributed to the patient's successful outcomes. Our comprehensive approach, extending across the stages of surgical planning, execution, and postoperative care, demonstrated the advantages of a multidisciplinary strategy for the accurate diagnosis and effective treatment of palatal PGs. This report makes a meaningful contribution to the existing literature on common oral lesions by emphasizing the importance of a broad differential diagnosis and a systematic approach to oral pathologies. It also raises clinical awareness of PGs with atypical presentations and the diagnostic challenge that they pose.

CaV 3.2 drives sustained burst-firing, which is critical for absence seizure propagation in reticular thalamic neurons.

OBJECTIVE: Genetic alterations have been identified in the CACNA1H gene, encoding the CaV 3.2 T-type calcium channel in patients with absence epilepsy, yet the precise mechanisms relating to seizure propagation and spike-wave-discharge (SWD) pacemaking remain unknown. Neurons of the thalamic reticular nucleus (TRN) express high levels of CaV 3.2 calcium channels, and we investigated whether a gain-of-function mutation in the Cacna1h gene in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) contributes to seizure propagation and pacemaking in the TRN. METHODS: Pathophysiological contributions of CaV 3.2 calcium channels to burst firing and absence seizures were assessed in vitro using acute brain slice electrophysiology and quantitative real-time polymerase chain reaction (PCR) and in vivo using free-moving electrocorticography recordings. RESULTS: TRN neurons from GAERS display sustained oscillatory burst-firing that is both age- and frequency-dependent, occurring only in the frequencies overlapping with GAERS SWDs and correlating with the expression of a CaV 3.2 mutation-sensitive splice variant. In vivo knock-down of CaV 3.2 using direct thalamic injection of lipid nanoparticles containing CaV 3.2 dicer small interfering (Dsi) RNA normalized TRN burst-firing, and in free-moving GAERS significantly shortened seizures. SIGNIFICANCE: This supports a role for TRN CaV 3.2 T-type channels in propagating thalamocortical network seizures and setting the pacemaking frequency of SWDs.

Astrocytes Provide Metabolic Support for Neuronal Synaptic Function in Response to Extracellular K.

It is an honour to have this opportunity write an article in recognition of the immense contributions of Bruce Ransom to the field of glial research. For me (BAM) personally there are many highlights both as a colleague and a friend that come to mind when I reflect on the many years that I have known Bruce. My own entry into the glial field was inspired by the early work by Ransom and his lab showing the sensitivity of astrocytes to neuronal activity. During my PhD and postdoctoral research I read these early papers and was inspired to ask the question when I first set up my independent lab in 1983: what if astrocytes also express some of the multitude of ion channels or transmitter receptors that were beginning to be described in neurons? Could they modify neuronal excitability during seizures or behaviour? As it turned out this was not only true but glial-neuronal interactions continues to be a growing and exciting field that I am still working in. I first met Bruce at the 1984 Society for Neuroscience meeting in Anaheim at my poster describing voltage gated calcium channels in astrocytes in cell culture. That was the start of a great friendship and years of discussions and collaborations. This review describes recent work from my lab led by Hyun Beom Choi that followed and was inspired by the groundbreaking studies by Bruce on electrophysiological and pH recordings from astrocytes and on glycogen mobilization in astrocytes to protect white matter axons.

Neurotoxicity screening in a multipotent neural stem cell line established from the mouse brain.

Neural stem cells (NSCs) have mainly been applied to neurodegeneration in some medically intractable neurologic diseases. In this study, we established a novel NSC line and investigated the cytotoxic responses of NSCs to exogenous neurotoxicants, glutamates and reactive oxygen species (ROS). A multipotent NSC line, B2A1 cells, was established from long-term primary cultures of oligodendrocyte-enriched cells from an adult BALB/c mouse brain. B2A1 cells could be differentiated into neuronal, astrocytic and oligodendroglial lineages. The cells also expressed genotypic mRNA messages for both neural progenitor cells and differentiated neuronoglial cells. B2A1 cells treated with hydrogen peroxide and L-buthionine-(S,R)-sulfoximine underwent 30-40% cell death, while B2A1 cells treated with glutamate and kainate showed 25-35% cell death. Cytopathologic changes consisting of swollen cell bodies, loss of cytoplasmic processes, and nuclear chromatin disintegration, developed after exposure to both ROS and excitotoxic chemicals. These results suggest that B2A1 cells may be useful in the study of NSC biology and may constitute an effective neurotoxicity screening system for ROS and excitotoxic chemicals.