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Background and Objective: Gentamicin can cause cell destruction by generating active oxygen species leading to hepatotoxicity. This study was done to determine the effect of Dianthus carryophyllu extract on the Gentamicin induced hepatotoxicity in Wistar rats.

Methods: In this experimental study, 49 mature wistar rats, were randomly allocated into 7 groups including, control; Sham (saline interaperitonely); experimental group 1 was treated with 100 mg/kg/bw clove essence; experimental group 2 were received 100 mg/kg/bw of Gentamicin; and experimental groups 3, 4 and 5 were received 100 mg/kg/bw of Gentamicin along with 25, 50 and 100 mg/kg/bw of hydro alcoholic extract of Dianthus carryophyllu (clove), respectively for 28 days. Blood samples were taken and serum activities of Alanine Aminotransferase (ALT), Aspartate aminotransferase (AST), alkaline phosphatase (ALP) and serum concentration of total protein and albumin were measured.

Results: The serum level of aspartate transaminase and Alanine transaminase significantly increased in experimental group 2 in compared to the sham and control groups (P<0.05). Alkaline Phosphatase concentration significantly reduced in experimental groups 2 and 3 in comparision with sham and control groups (P<0.05). Albumin and total protein concentration significantly reduced in experimental groups 2 and 3 in compare to the sham and control groups (P<0.05). In histological examination, cell necrosis, fat accumdation and mononocular cell accumulation reduced in experimental groups 5 in compare to Gentamicin treated group.

Conclusion: Dianthus carryophyllu hydro alcoholic extract is able to protect against enzyme alterations and hepatotoxicity induced by Gentamicin.

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Background and Objective: Permanent first molars are susceptible to caries due to their particular anatomical form, early development and lack of knowledge of parents about their permanence. This study was conducted to determine the index of first permanent dental careis (DMF6) and some of its related factors in 12 year-old students.
Methods: This descriptive-analytical study was carried out on 400 students (200 females and 200 males) using combined method (stratified and cluster sampling) from public and non-governmental schools in Gorgan, northern Iran during 2015-16. First permanent molar examination was carried out. The parents' education level, frequency of toothbrushing and daily consumption of sugar-containing snack foods was recorded in a questionnaire. Each decayed, missing and filled first permanent molar tooth was given number one. These numbers were combined to compute the DMF6 index for each individual.
Results: The DMF6 index was zero in 19.5% and the DMF6 index was determined to be between
1 and 4 in 80.5% of the children. The mean DMF6 index was 2.23±0.07 and significantly higher in girls (2.39±0.10) than in boys (2.07±0.11) (P<0.05). The DMF6 index decreased with increasing parental education and the frequency of brushing and reducing consumption of sugary meals.
Conclusion: Dental caries prevalence among 12-years-old students in north of Iran is higher (2.23) than global standard until 2020 (lower than 1). Gender of child, parent’s education, frequency of toothbrushing and consumption of sugar-containing snack foods plays an important role in the rate of dental caries.

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Background and Objective: Familial hypercholesterolemia (FH) is one of the most common inherited familial diseases that cause lipid accumulation in tendons and arteries by increasing the level of low density plasma lipoprotein (LDL). The main cause of FH is a mutation in the low-density lipoprotein receptor (LDLR) gene. This study was performed to evaluate common mutations in LDLR gene in FH patients.
Methods: This descriptive study was performed on 100 patients with suspected familial hypercholesterolemia referred to Sepehr laboratory according to the Simon Broom international standard in Karaj city, Iran during 2015. After complate the questionnaire form and drawing the family tree, it was found that 17 of them had a history of disease in at least one of the first degree relatives. The presence of changes was investigated using PCR-SSCP method, and after identifying the suspected cases direct DNA sequencing was performed.
Results: Among of 17 patients with a history of FH disease, 13 patients had a heterozygote mutation in the LDLR gene. Mutations included: c.97C>T, c.445G>T, c.651-653 (DEL3), c.652-654 (DEL3), c.682G>T, c.925-931 (DEL7), c.936-940 (DEL5), c.986G>T, c.2054C>T, c.2177C>T and c.313+1G>A. Four patients did not have mutations in their LDLR gene. In two patients the common polymorphism c.1959T>C was identified.
Conclusion: The LDLR gene was involved in the development of FH in the study population. However, another gene or locus may be involved in the outbreak of this disease in the studied population.