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Background:Parkinson's disease (PD) is one of the most common neurodegenerative movement disorders and its incidence is increasing worldwide along with population aging. Previous clinical and histologic studies suggest that the neurodegenerative process, which affects the brain, may also affect the retina of PD patients.Objective:The objective of this study was to determine the thickness changes of retina nerve fibers and macular volume with optical coherence tomography (OCT) in PD patients.Materials and Methods:The spectral domain OCT was used to assess the thickness of retinal nerve fiber layer (RNFL) and macular volume from 34 PD patients and 50 healthy age-matched controls.Results:Compared with healthy age-matched controls, the RNFL thickness of PD patients was much thinner (P < 0.05) in all retinal quadrants, with temporal thinning being more than nasal thinning. Macular volumes were diminished in both perifoveal and outer macular regions in all sectors (P < 0.05) with preserved foveal volume. The degree of tissue loss corroborated with the severity of disease as objectively assessed by standardized rating scales (UPDRS).Conclusion:There is generalized retinal nerve degeneration in patients of PD and the degree of loss correlated with the severity and duration of disease.

Hepatocellular carcinoma (HCC) is one of the most lethal and prevalent cancers in many developing countries including India. Among the various etiological factors being implicated in the cause of HCC, the most important cause, however, is hepatitis B virus (HBV) infection. Among all HBV genes, HBx is the most critical carcinogenic component, the molecular mechanisms of which have not been completely elucidated. Despite its clinical significance, there exists a very elemental understanding of the molecular, cellular, and environmental mechanisms that drive disease pathogenesis in HCC infected with HBV. Furthermore, there are only limited therapeutic options, the clinical benefits of which are insignificant. Therefore, the quest for novel and effective therapeutic regimen against HBV-related HCC is of paramount importance. This review attempts to epitomize the current state of knowledge of this most common and dreaded liver neoplasm, highlighting the putative treatment avenues and therapeutic research strategies that need to be implemented with immediate effect for tackling HBV-related HCC that has plagued the medical and scientific fraternity for decades. Additionally, this review proposes a novel "five-point" management algorithm for HBV-related HCC apart from portraying the unmet needs, principal challenges, and scientific perspectives that are relevant to controlling this accelerating global health crisis.

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Asthma has been an inflammatory disorder accompanied by tissue remodeling and protease-antiprotease imbalance in lungs. The SNPs of alpha-1 antitrypsin (α 1 AT) and tissue inhibitor of metalloproteinase-1 (TIMP-1) genes were studied for their association with asthma. Genotyping of α 1 AT and TIMP-1 genes was performed in 202 asthmatics and 204 controls. Serum levels of α 1AT, TIMP-1 and cytokines were estimated to find if the interplay between genotypes and cellular biomarkers determines the pathogenesis of asthma. The analysis of results showed significantly low level of α 1AT in the serum of asthmatics as compared to controls (P = 0.001), whereas cytokines were elevated in patients. No significant difference was observed in the concentration of TIMP-1 in patients and controls. Genotyping led to the identification of 3 SNPs (Val213Ala, Glu363Lys, and Glu376Asp) in α 1 AT gene. The novel SNP Glu363Lys of α 1 AT was found to be associated with asthma (P = 0.001). The analysis of TIMP-1 gene showed the occurrence of seven SNPs, including a novel intronic SNP at base G3774A. The allele frequency of G3774A and Phe124Phe was significantly higher in asthmatics as compared to controls. Thus, the SNP Glu363Lys of α 1 AT and G3774A and Phe124Phe of TIMP-1 could be important genetic markers for use in better management of the disease.