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Background: Vascular Dementia (VaD) is the second most prevalent cause of dementia, arising from the blockage of blood vessels in the brain. One event responsible for the blockage or narrowing of small blood vessels is transient ischemic attack (TIA), and these changes resolve within 24 hours in humans. The molecular mechanism underlying these changes in recovery in small vessels still needs to be investigated. To address this gap, we have developed a mouse model by administering endothelin‐1 (ET‐1) into the lateral ventricles. This disrupts small vessel integrity, which leads to learning and memory deficits after 3 days of a single ET‐1 injection. Intriguingly, there is a subsequent recovery in these deficits after 30 days, mimicking the clinical scenario of TIAs. Bulk RNA sequencing from microvessels was performed to elucidate further the factors involved in recovery mechanisms. Method: ET‐1 injection was given to 4 groups of C57BL6/J mice, and mice were sacrificed at different time points of 3, 15, and 30 days along with saline counterparts. Microvessels were extracted from the pooled cortex and hippocampus, followed by RNA isolation. RNA samples were subjected to the cDNA library preparation, and RNA sequencing was conducted using the Illumina NovaSeq 6000® instrument. Transcriptomic analysis was carried out in the Linux environment. Differential gene expression was performed using R. Result: We observed biological processes such as vasculature development, angiogenesis, and wound healing start upregulating after 3 days of a single ET‐1 injection, whereas several processes involved in ion transport chains were downregulated. Further, biological processes for muscle development, mitochondrial electron transport chain, and neuronal development were upregulated after 15 days of a single ET‐1 injection. No biological processes were affected after 30 days of a single ET‐1 injection, suggesting a possible complete recovery from ET‐1‐mediated vascular insult by the 30th day. Conclusion: Our results highlight the temporal dynamics of biological processes in response to a single ET‐1 injection. It offers valuable insight for understanding the mechanism behind the recovery and factors involved in this process after vascular insult, paving the way for therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: Vascular pathology is often seen in cases of mixed dementia affecting elderly population including Alzheimer's disease (AD). AD is generally characterized by the presence of amyloid‐β (Aβ) plaques and tau deposits. However, many factors influence the onset and progression of AD pathology. In the present study, we are looking for brain vascular pathology like blood brain barrier (BBB) breach by vascular insult and associated microglial activation in small vessels increase risk of developing pathology over age. It is often hypothesized that in presence of increased Aβ, vascular insults could synergistically trigger neuroinflammation leading to cognitive impairment accelerating neurodegeneration. Method: Learning and memory deficits were performed in slow progressing APPswe mice injected with 2µg/2μl of ET‐1(endothelin‐1) bilaterally into lateral ventricles after 30 days of ET‐1 injection. BBB structural changes were assessed by immunohistochemistry for markers of endothelial cells and pericytes. Aβ plaque load and vascular deposition of Aβ were tested to understand the effect of vascular insult on AD pathology in double transgenic J20 mice. Further, microglial activation was estimated using specific markers. Result: BBB breaching was increased after vasoconstriction following ET‐1 injection after 30 days with increasing age causing memory deficits in AD mice. The extent of structural changes in BBB increased with age indicating the susceptibility with mutation. Aβ plaque load and glial activation was increased in J20 mice after ET‐1 injection. Conclusion: APP mutation increases susceptibility to ET‐1 induced single vascular insult bringing about BBB leakage, memory deficits, increased Aβ aggregation and glial activation with increasing age given enough time of 30 days to rescue. However, there was rescue in case of wild type mice. [ABSTRACT FROM AUTHOR]

The invention and application of engine driven or rotary instruments in operative treatment of carious lesions has resulted in removal of considerable toothe structure. However, with the introduction of adhesive materials for restorations, and the advent of minimal cavity design this principle has been challenged and is now considered to be too destructive to the tooth structure during caries removal. A number of techniques are available for cutting tooth tissue. The chemo mechanical method of caries removal/treatment is considered to be less painful when compared to the traditional treatment method (use of drill). The present study was carried to study the effect of an indigenously developed caries removal agent viz. Carie Care™ & its effectiveness as a chemo mechanical caries removal agent. [ABSTRACT FROM AUTHOR]

The invention and application of engine driven or rotary instruments in operative treatment of carious lesions has resulted in removal of considerable toothe structure. However, with the introduction of adhesive materials for restorations, and the advent of minimal cavity design this principle has been challenged and is now considered to be too destructive to the tooth structure during caries removal. A number of techniques are available for cutting tooth tissue. The chemo mechanical method of caries removal/treatment is considered to be less painful when compared to the traditional treatment method (use of drill). The present study was carried to study the effect of an indigenously developed caries removal agent viz. Carie Care (TM) & its effectiveness as a chemo mechanical caries removal agent. How to cite this article: Venkataraghavan K, Kush A, Lakshminarayana CS, Diwakar L, Ravikumar P, Patil S, Karthik S. Chemomechanical Caries Removal: A Review & Study of an Indigenously Developed Agent (Carie Care (TM) Gel) In Children. J Int Oral Health 2013; 5(4):84-90.