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      • KCI등재

        Prevalence of dental anxiety in 10-14 years old children and its implications

        Kakkar, Mayank,Wahi, Astha,Thakkar, Radhika,Vohra, Iqra,Shukla, Arvind Kumar The Korean Dental Society of Anesthsiology 2016 Journal of Dental Anesthesia and Pain Medicine Vol.16 No.3

        Background: The aim of this study was to provide insight on dental fear amongst schoolchildren and evaluate the association between caries experience and fear of dental procedures. Methods: A sample size of 250 students (both sexes) of ages 10-14 years were enrolled in the study. Before dental examination, each participant was informed about the study and given the Children's Fear Survey Schedule - Dental Subscale (CFSS-DS) questionnaire. Children who scored greater than 38 were included in the 'with dental fear' group and those who scored less than 38 were assigned to the 'without dental fear' group. All oral check-ups were carried out on the school premises according to WHO criteria. Results: There were 105 children (42%) who experienced dental fear. As CFSS-DS scores increased, scores on the Decayed, Missing and Filled Surfaces Index (DMFS) also increased. Scores were highest on "injections" followed by "dentist drill" and "feeling of choking". Children were significantly less anxious about items of dental treatment if they had experienced that particular form of treatment. Female participants were found to be more dentally anxious than the male participants. Conclusions: The data revealed dental fear in 10-14 years old children and showed that dental fear scores decreased with increase in age and experience.

      • Folic acid inhibits necrosis and apoptosis in ischemic and reperfusion induced injury in rat liver

        Chattopadhyay, Pronobesh,Shukla, Gunjan,Wahi, Arun Kumar Kyung Hee Oriental Medicine Research Center 2009 Oriental pharmacy and experimental medicine Vol.9 No.1

        Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. On the basis of our findings it may be concluded that folic acid afforded significant protection from necrosis and apoptosis in I/R injury.

      • KCI등재

        Folic acid inhibits necrosis and apoptosis in ischemic and reperfusion induced injury in rat liver

        Pronobesh Chattopadhyay,Gunjan Shukla,Arun Kumar Wahi 경희대학교 융합한의과학연구소 2009 Oriental Pharmacy and Experimental Medicine Vol.9 No.1

        Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. On the basis of our findings it may be concluded that folic acid afforded significant protection from necrosis and apoptosis in I/R injury. Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. On the basis of our findings it may be concluded that folic acid afforded significant protection from necrosis and apoptosis in I/R injury.

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