Background:

The details about the research productivity in the neurology specialty from India is lacking. We analyzed the publishing trends and the research productivity of neurology-related articles in the Journal of the Association of Physicians of India (JAPI).

Materials and Methods:

We carried the bibliometric analysis of articles related to neurology specialty from JAPI published between 2000 and 2011. Data were derived from the journal's website and the articles were analyzed for type (original article, case reports, etc.), disease (infection, vascular, etc.), place, and timelines for publication.

Results:

Out of total 2977 articles published, 256 articles belong to neurology. Neurology contributed to 7--20% of the published articles per year in JAPI. Case reports (52%) constitute the majority type of articles followed by Original Articles (20%), Correspondence and Images (15% each). Infections (27%), structural disorders (19%), cerebrovascular and peripheral nervous system disorders (16% each) contribute the majority of research articles in Neurology. Mumbai (15%), Delhi (13%), and Chennai (9%) are the top three contributors followed by Lucknow and Varanasi. All types of articles took about 9--10 months for acceptance and another 4--5 months for publication. Letters to the Editor were published faster when compared to other articles (P=0.0035).

Conclusion:

Neurology specialty contributes an average 14% of articles per annum in JAPI. Infections, vascular, structural, and peripheral nervous system disorders together account for 80% of published literature with a small representation from other diseases. Mumbai and Delhi are the leading contributors toward research productivity in neurology.

Oral lichen planus (OLP) is a chronic mucocutaneous disease of uncertain etiopathogenesis. Several factors including stress, genetics, systemic diseases, viruses, dental restorative materials and drugs have been implicated as causative agents. The disease seems to be mediated by an antigen specific mechanism, activating cytotoxic T cells, and non specific mechanisms like mast cell degranulation and matrix metalloproteinase activation. Further clarity on the pathogenesis will aid in modifying therapeutic interventions, thus significantly reducing the morbidity of OLP patients.

Background

TGF-beta is one of the key cytokines implicated in various disease processes including cancer. TGF-beta inhibits growth and promotes apoptosis in normal epithelial cells and in contrast, acts as a pro-tumour cytokine by promoting tumour angiogenesis, immune-escape and metastasis. It is not clear if various actions of TGF-beta on normal and tumour cells are due to differential gene regulations. Hence we studied the regulation of gene expression by TGF-beta in normal and cancer cells.

Results

Using human 19 K cDNA microarrays, we show that 1757 genes are exclusively regulated by TGF-beta in A549 cells in contrast to 733 genes exclusively regulated in HPL1D cells. In addition, 267 genes are commonly regulated in both the cell-lines. Semi-quantitative and real-time qRT-PCR analysis of some genes agrees with the microarray data. In order to identify the signalling pathways that influence TGF-beta mediated gene regulation, we used specific inhibitors of p38 MAP kinase, ERK kinase, JNK kinase and integrin signalling pathways. The data suggest that regulation of majority of the selected genes is dependent on at least one of these pathways and this dependence is cell-type specific. Interestingly, an integrin pathway inhibitor, RGD peptide, significantly affected TGF-beta regulation of Thrombospondin 1 in A549 cells.

Conclusion

These data suggest major differences with respect to TGF-beta mediated gene regulation in normal and transformed cells and significant role of non-canonical TGF-beta pathways in the regulation of many genes by TGF-beta.