Treatment of Unilateral TMJ Ankylosis in a Pediatric Patient with Temporalis Fascia Flap A Case Report.

The definite cause of temporomandibular joint (TMJ) ankylosis is still an unknown fact. TMJ ankylosis may result from, infection, trauma or insufficient surgical treatment of the mandibular condyle region. Different techniques have been described so far for the treatment of TMJ ankylosis, but no technique has successfully given uniform results. Relapse causing limited mouth opening, infection, open bite, reankylosis are the complications. Many authors agree that aggressive physiotherapy immediately after the surgical procedure, interpositional graft as spacer and wide bone resection are the basic principles in treating TMJ ankylosis. In this article, we discussed a case of unilateral TMJ ankylosis, in a 9-year-old boy, treated with the intre-positional gap arthroplasty with superficial temporalis fascia flap.

Single Family Members with Multiple Impacted teeth: A Rare Case Report.

Multiple impacted teeth of idiopathic origin are a rare dental anomaly. Various local and systemic causative factors have been implicated in the literature; however, it is unknown at present about the localization of the genetic defect in the phenotype of failure of eruption. Retained primary teeth is a well-known process, but multiple permanent and supernumerary teeth that too asymptomatic is surely a rare possibility. This article aims in to consolidate and organize the available information regarding the tooth eruption failure and to collaborate the current evidence with the report of three adult sibling’s cases of failure of eruption of multiple permanent teeth in a family without a known cause.

Development of melanocye-keratinocyte co-culture model for controls and vitiligo to assess regulators of pigmentation and melanocytes.

Background: There is a need to develop an in vitro skin models which can be used as alternative system for research and testing pharmacological products in place of laboratory animals. Therefore to study the biology and pathophysiology of pigmentation and vitiligo, reliable in vitro skin pigmentation models are required. Aim: In this study, we used primary cultured melanocytes and keratinocytes to prepare the skin co-culture model in control and vitiligo patients. Methods: The skin grafts were taken from control and patients of vitiligo. In vitro co-culture was prepared after culturing primary melanocytes and keratinocytes. Co- cultures were treated with melanogenic stimulators and inhibitors and after that tyrosinase assay, MTT assay and melanin content assay were performed. Results: Melanocytes and keratinocytes were successfully cultured from control and vitiligo patients and after that co-culture models were prepared. After treatment of co-culture model with melanogenic stimulator we found that tyrosinase activity, cell proliferation and melanin content increased whereas after treatment with melanogenic inhibitor, tyrosinase activity, cell proliferation and melanin content decreased. We also found some differences in the control co-culture model and vitiligo co-culture model. Conclusion: We successfully constructed in vitro co-culture pigmentation model for control and vitiligo patients using primary cultured melanocytes and keratinocytes. The use of primary melanocytes and keratinocytes is more appropriate over the use of transformed cells. The only limitation of these models is that these can be used for screening small numbers of compounds.

Crosstalk between RXR, LXR and VDR within blood mononuclear cellular model.

An accumulation of data from in vitro to in vivo model system has established a pivotal role of three crucial ligand activated nuclear receptors RXR, LXR-α and VDR for their ability to regulate an array of genes involved in regulation of fundamental cellular processes to patho-physiological situations. Keeping in view RXR as a common heterodimeric partner for LXR-α and VDR, the present study was designed to dissect the interrelationship between these three nuclear receptors in peripheral blood mononuclear cellular model. The present study revealed that all the three nuclear receptors displayed auto regulation in response to their specific ligands; Both LXR-α and VDR regulated the expression of their heterodimeric partner RXR; and VDR was regulated by LXR-α through its ability to modulate SREBP response element present in the promoter region of VDR gene. Based on these findings, the role of these nuclear receptors could be better understood in various nuclear receptor mediated pathological processes.

Cellular AATF gene encodes a novel miRNA that can contribute to HIV-1 latency.

HIV-1 encoded microRNA hiv1-miR-H1 is known to induce CD4+ lymphopenia through its ability to downregulate cellular AATF gene. The present study directed to examine the target sites of this miRNA on AATF gene revealed the existence of a novel miRNA designated as hmiR-che-1 which had the inherent capacity to target HIV-1 genome especially regions coding for hiv1-miR-H1 as well as Vpr gene. Further, the expression of AATF gene coupled with its encoded microRNA hmiR-che-1 exhibited characteristic antagonism with the expression of hiv1-miR-H1 within the lymphocytes, derived from asymptomatic as well as symptomatic AIDS subjects. Based upon these observations, we propose that the widely recognised HIV-1 latency in CD4+ T-lymphocytes may arise, because of the orchestrated balance that may exist between the expression levels of hiv1-miR-H1 and hmiR-che-1 within lymphocytes infected with HIV-1.

Cellular AATF gene: armour against HIV-1.

Outcome of HIV-1 infection at the cellular level is decided by the orchestrated balance that exists between cellular nucleic acid-based adaptive immune mechanism involving non-coding micro RNAs (miRNAs) and offensive tactics of HIV-1 to suppress this host cellular immunity. In this context, the review explains the importance of a novel miRNA encoded exclusively and conspicuously by HIV-1 genome that has the ability to specifically target cellular AATF gene recognized to play a crucial role in the maintenance of adaptive immunity at nucleic acid level against HIV-1 invasion.