Alzheimer's disease (AD) has been proposed as type III diabetes mellitus (DM). Prognosis and early stage diagnosis of AD is essentially required in diabetic patients to avoid extensive irreversible neuronal damage. Also, simple medication regimes including therapeutics for maintaining glucose levels and simultaneous resistance to neuronal damage are quintessential. In the present study, secretome and hippocampus proteome modulations were investigated for serum-based markers that have correlations with DM-mediated neurological alterations which extend to AD. Concurrently, the therapeutic effect of hesperidin on DM and DM-mediated neurodegeneration was investigated. Twenty one male Wistar rats were separated into three groups, namely, healthy control, diabetic (65 mg kg À1 STZ i.p., single) and diabetic administered with hesperidin (STZ i.p. + 50 mg kg À1 hesperidin orally, for four weeks).Secretome and hippocampus proteome profiling was accomplished by two dimensional electrophoresis, and proteins showing differential expression were characterized by MALDI-TOF MS PMF and validated by relative expression analysis. APO A-IV and secretory AGK were found to have prognostic and/or diagnostic potential in detecting the early stage of DM-associated AD. A novel protein, 'WajidSaima_Diabetes protein' (WSDP), was found to have a probable role in neural homeostasis. The therapeutic potential of hesperidin in DM and DM-mediated neuronal fluctuations has successfully been determined through proteomic resolution. Our study emphasizes the DM-mediated neuronal fluctuations that expedite AD.

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The intriguing molecular pathways involved in oral carcinogenesis are still ambiguous. The oral squamous cell carcinoma (OSCC) ranks as the most common type constituting more than 90% of the globally diagnosed oral cancers cases. The elevation in the OSCC incidence rate during past 10 years has an alarming impression on human healthcare. The major challenges associated with OSCC include delayed diagnosis, high metastatic rates, and low 5-year survival rates. The present work foundations on reverse genetic strategy and involves the identification of genes showing expressional variability in an OSCC case lacking addictive proclivities for tobacco, betel nut, and/or alcohol, major etiologies. The expression modulations in the identified genes were analyzed in 16 patients comprising oral pre-cancer and cancer histo-pathologies. The genes SCCA1 and KRT1 were found to down regulate while DNAJC13, GIPC2, MRPL17, IG-Vreg, SSFA2, and UPF0415 upregulated in the oral pre-cancer and cancer pathologies, implicating the genes as crucial players in oral carcinogenesis.

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Background and purpose Human papillomavirus (HPV) has been shown to be associated with oral malignancies. The purpose of this study was to detect HPV and a high‐risk type HPV16 viral DNA in 24 cases with oral squamous cell carcinoma (OSCC) and 15 cases with non‐OSCC persistent oral lesions (POL) residing in North India. The diagnosis was determined by the histopathological characteristics of the oral biopsy. Results All oral lesions were HPV‐DNA positive, and the HPV16‐positive ratios of OSCC and non‐OSCC POLs were 50% and 53%, respectively. Approximately 62% of moderately differentiated OSCC and 36% of well‐differentiated OSCC were HPV16 positive. Evaluated odds and prevalence ratios >1 indicated a higher prevalence of HPV16 infection in patients with tobacco, areca nut, and/or alcohol habits, compared with nonaddicts. The obtained P‐values were higher than 0.05, indicating that the relationship is statistically insignificant, which may be due to lower number of POL cases. This study could not conclude that HPV16 infection plays an essential role in malignant transformation of the oral mucosa, raising a need for further experimental endeavors. Conclusions This study indicates that HPV16 infection in OSCC and non‐OSCC POLs frequently occurred in people with tobacco smoking, tobacco‐areca nut chewing, and alcohol intake. These fallacious habits may increase HPV16 infection in the oral cavity.