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  1. Ghasak Ghazi Faisal, Faridah Md Khalid, Yusri Yazid
    MyJurnal
    Introduction: Smoking is a well-known cause of oral disease and oral cancer. Several dysplastic cytological changes occur before the appearance of the clinical lesion. This study aimed to investigate the cytopathological effects of smoking in clinically normal oral mucosa of cigarette smokers.
    Materials and Methods: A total of 40 cigarette smokers and 40 nonsmokers (control group) were included in this study. All participants had clinically normal oral mucosa. Oral smears were obtained from the side of the tongue and floor of the mouth using a Cytobrush. The smears were stained by Papanicolaou stain and examined under light microscope for inflammation, hyperkeratinization and dysplasia.
    Results: There was a significantly higher rate(p<0.005) of inflammation 63%, hyperkeratiniztion 62% and mild dysplasia 26% among smokers than non-smokers where the rates were 35%, 12% and 2% respectively.
    Conclusion: Smoking causes significant cytopathological changes in normal oral mucosa, the detection of which is important to prevent progression into carcinoma. The procedure is fast, painless and inexpensive.
    KEYWORDS: Papanicolaou stain, brush biopsy, cigarette smokers, dysplasia, oral mucosa
  2. Marwan Saad Azzubaidi, Al-Ani, Imad Matloub, Anil Kumar Saxena, Ghasak Ghazi Faisal
    MyJurnal
    Introduction: The oil extract of black cumin seeds Nigella sativa (NSO) demonstrated considerable
    preservation of spatial cognitive functions in rats subjected to chronic brain hypoperfusion (CBH). The hippocampal CA1 region pyramidal cells are the earliest neurons suffering neurodegeneration following CBH. Objective: The current study was devoted to assess the protective effects of Nigella sativa (NSO) treatment on CA1 hippocampal pyramidal cells of rats subjected to chronic brain hypoperfusion (CBH) that was achieved through permanent two vessel occlusion (2VO) procedure. Methods: Twenty four rats were equally divided into three groups; sham control, untreated 2VO and NSO treated group (2VO with daily oral NSO treatment. After the 10th postoperative week coronal sections of the hippocampus were collected for histopathological and electron microscopical examinations. Results: The number of viable pyramidal cells within CA1 hippocampal region in sham control and NSO treated groups was significantly higher than that of untreated 2VO group, while the difference was not significant when comparing the viable pyramidal cells number of sham control with NSO treated groups. Furthermore, 2VO group showed marked intracellular ultrastructural distortions that were less pronounced in NSO treated group. Conclusion: NSO displayed a robust potential to protect hippocampal pyramidal cells from CBH induced neurodegeneration putting forward its prospective neuroprotective activity against age related cognitive decline of Alzheimer’s disease and vascular dementia.
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