Objective: This study aims to investigate the mediating role of parental non-involvement in relation to goals of progress with academic dishonesty in students. Methods: This is a correlational study in which the relationships between the variables of the proposed model were investigated using the structural equation modeling method. The statistical population included all female high school students in Semnan City, in the academic year 2020. Using the convenience sampling method, 350 people were selected as the sample. The academic dishonesty questionnaire, goals of progress questionnaire, and Family non-involvement questionnaire were used as measurement tools. Correlation coefficients (using the SPSS software) and structural equation modeling analysis (using AMOS statistical software) were employed to investigate the variables of the academic dishonesty prediction model. Results: The findings indicated that the data fit the model, and the results showed that goals of progress had a direct effect on academic dishonesty and Family non-involvement. In addition, Family non-involvement had a direct effect on academic dishonesty. Finally, goals of progress through the mediating variable had an indirect effect on academic dishonesty. Conclusion: To increase students’,academic honesty, a set of internal, external, individual, and Family factors of students should be considered.

The focus of this study is primarily on “the discrepancy in mentality as an important factor affecting Family problems and divorce”. For this purpose, some minor studies were conducted each of which experimentally examined different aspects of mental discrepancy in Iranian families. Almost all of these studies showed that permanent disputes and divorces resulted from the differences in their world-views, thinkings, and impressions in their mutual affairs. At last, the theory of Homogamy with two major revisions were used to explain the reasons and causes of Family problems and divorce which were confirmed in minor studies and cases.

Background: Lung cancer is one the leading cause of cancer-related death worldwide, with more than 1. 2 million deaths each year. In addition to genetic mutations, epigenetic modifications may contribute to the induction and progression of cancer. The term epigenetic refers to several molecular mechanisms and pathways that regulate gene expression without changing the DNA sequence. These mechanisms include alterations in the histone modification, the methylation status of DNA, chromatin remodeling, and microRNAs. Cancer cells exhibit changes in histone modification patterns at individual genes. Epigenetic deregulation can affect several aspects of tumor cell biology comprising cell growth, cell differentiation, and cell death. Histones are highly conserved alkaline proteins that can become post-translationally modified at the amino acid residues located on their N and C-terminal tails. There are four core histones include histone 2 A, histone 2 B, histone 3, and histone 4, and one linker histone, histone 1. Histone modifying enzymes, such as histone acetyltransferases (HATs), histone deacetylases (HDACs), histone methyltransferases (HMTs), histone demethylases (HDMs), is often responsible for the aberrant histone modifications. HDACs and HATs are two counteracting enzyme families whose enzymatic activity controls the acetylation state of protein lysine residues. Aberrant histone acetylation is associated with several solid cancers. In mammals, HDACs form three groups based on their sequence homology and are classified as HDACs I, II, and III. These enzymes have a critical role in modulating the balance between pro-and anti-apoptotic proteins. Dysregulation of HDACs and aberrant deacetylation have been implicated in the pathogenesis of various cancers. Overexpression of these enzymes correlates with tumorigenesis. Two known mechanisms, methylation and histone deacetylation seem to be the best candidate mechanisms for inactivation of CIP/KIP (p21CIP1/WAF1, p27KIP1, and p57KIP2) and INK4 (p15INK4b, p16INK4a, p18INK4c, and p19INKd) families. Histone deacetylation is a general mechanism for the inactivation of the CIP/KIP Family in various cancers such as gastric cancer, human colon cancer cell line HT-29, human breast cancer MDA231 cell line, human non-small cell lung cancer c ell line, A549 cells. HDAC inhibitors have been considered to be a novel class of cancer treatment agent. These compounds include trichostatin A (TSA), butyrate, trapoxin (TPX), MS-27-275 (a synthetic benzamide derivative) and apicidin. Previously, we reported the effect of trichostatin A on hepatocellular carcinoma (HCC). The present study was aimed to investigate the effect of TSA on histone deacetylase 1 (HDAC 1), CIP/KIP (p21CIP1/WAF1, p27KIP1, and p57KIP2), cell growth inhibition and apoptosis induction in lung cancer COR-L105 cell line. Methods: First, the lung cancer COR-L105 cells were cultured in DMEM supplemented with sodium butyrate, sodium bicarbonate, sodium pyruvate, 10% FBS and antibiotics (penicillin G and streptomycin) at 37° C in 5% CO2 overnight and then seeded into 96-well plates (3× 105 cells per well). After 24 h, the medium was replaced with an experimental medium containing various concentrations of TSA (0, 1, 2. 5, 5, 7. 5, 10, and 20 μ M). The control groups received DMSO only, at a concentration of 0. 05  %. After a period of 24 and 48h, the cells were investigated by MTT assay according to Standard protocols to determine cell viability. Therefore, MTT solution was added to each well for 4 h at 37℃ and then the MTT solution was changed by DMSO and shaken for 10 min to dissolve all of the crystals. Finally, the optical density was detected by a microplate reader at a wavelength of 570 nM. Each experiment was repeated three times (triplicates). To determine apoptotic cells, the COR-L105 cells were cultured at a density of 3 × 105 cells/well and incubated overnight and then treated with TSA (2. 5 μ M) for different periods (24 and 48 h). Subsequently, the treated and untreated cells were harvested by trypsinization, washed with cold PBS, and resuspended in Binding buffer (1x). Finally, Annexin-V-(FITC) and PI were used according to the protocol to determine the apoptotic cells by FACScan flow cytometry (Becton Dickinson, Heidelberg, Germany). Real-time quantitative RT-PCR amplification and analysis were achieved to quantitatively estimate the expression of histone deacetylase 1(HDAC 1) and CIP/KIP (p21CIP1/WAF1, p27KIP1, and p57KIP2) in TSA (25 µ M)-treated COR-L105 cells at different times. After treatment times, Total RNA was isolated by RNeasy mini kit (Qiagen) according to the manufacturer’ s protocol and then treated by RNase free DNase (Qiagen) to eliminate the genomic DNA. The RNA concentration was determined using a Biophotometer (Eppendorf). Total RNA (100 ng) was reverse-transcribed to cDNA by using the RevertAid™ First Strand cDNA Synthesis Kit (Fermentas) according to the manufacturer’ s instructions. Real-time RT-PCR was performed by the Maxima SYBR Green RoxqPCR master mix kit (Fermentas). The primer sequences are shown in Table1. Real-time PCR reactions were performed using the Steponeplus (Applied Biosystem). Data were analyzed using the comparative Ct (Δ Δ ct) method, the relative expression level of the genes were calculated by determining a ratio between the amount of these genes and that of endogenous control. GAPDH was used as a reference gene for internal control. Results: To test the effect of TSA (0, 1, 2. 5, 5, 7. 5, 10, and 20 μ M) on the lung cancer COR-L105 cell viability, MTT assay was utilized. Our findings showed that the rate of cell growth inhibition was significantly increased in than that of control groups after 24 and 48 h. Results showed that the number of viable cells decreased significantly, as the concentration of the compounds and duration increased; indicating a dose-and duration-dependent relationship (p<0. 001). The IC50 values were determined with approximately 2. 5 μ M for TSA. Flow cytometric analysis was achieved to determine whether TSA (2. 5 μ M) can induce apoptosis in the lung cancer COR-L105 line. The percentage of treated and un-treated COR-L105 apoptotic cells was evaluated by staining with annexin V-FITC and PI after 24 and 48 h of treatment. After treatment with TSA, the apoptosis percentage increased significantly. The effect of TSA (2. 5 μ M) on the histone deacetylase 1(HDAC 1) and CIP/KIP (p21CIP1/WAF1, p27KIP1, and p57KIP2) gene expression was investigated by quantitative real-time RT-PCR analysis. The result indicated that the treatment of lung cancer COR-L105 cells with TSA (2. 5 μ M) for 24 and 48 h reactivated the p21CIP1/WAF1, p27KIP1, and p57KIP2 gene, down-regulated HDAC 1 significantly. Conclusion: TSA can down-regulate HDAC 1 and up-regulate p21CIP1/WAF1, p27KIP1, and p57KIP2 gene expression and induce apoptosis in lung cancer COR-L105 cell line.

Along with different and deep problems that the contemporary Family has challenged in Iran, Internet penetration and use of modern communication technologies in the Family have made these problems and challenges more complex and obscure. The challenges which are to some extent rooted in the transformation of Family relations in Iran. This research was conducted to study the relationship between the use of modern communication technologies and Family relations. The study population was Shiraz high school students from all 10 city regions. Using classified random sampling method, 400 students were selected and responded to the questionnaire. The theoretical framework of this study is a combination of the "networked Family" and the "Family boundaries" theories. One of the innovations in this research is the use of two mediating variables called Family time and Family network, which has been inspired by the theoretical framework. Generally, the results of this research indicate that there is no direct relationship between the type and extent of the use of new technologies of communication with Family relations, but this relationship is realized through the path of mediating variables, namely, the time of Family and Family network. Finally, Family time and Family network variables have a positive effect on Family relationships, with a beta of 0.473 and 0.273, and in general they are able to explain 30% of the Family relationship variable.

The purpose of this research was to study the mediating role of Family communication in relation with Family spirituality and Family resilience. In order to examine the mediating role of the Family communication, 398 parents of students in Kermanshah participated in the study. They were selected through a multi cluster sampling. These parents answered Family Resilience Assessment Scale (FRAS), Family Communication Scale (FCS), Sanctification of Marriage Scale and, Sanctification of Parenting Scale. Results of pearson correlation and simultaneous regression analyses (enter method) showed that Family communication has a directly (b=0.20) and an indirectly (b=0.13) effect on Family resilience. In sum, the results of the study confirm the mediating of Family communication patterns for Family spirituality and Family resilience.

One of the achievements of sociology in the last century was resorting to the theory of social capital. Although a consensus on the meaning of social capital has not yet been achieved among sociologists and social sciences thinkers, its meaning variations have paved the way for being looked from new perspectives. This article first, with due attention to theroots of the concept of social capital, redefines it to cover Family capital.Then, it introduces three components which constitute the concept of Family capital and dicuss the threats addressed to it in the framework of challenges facing Iranian society. Finally, it presents some recommendations for enhancing Family capital. Since this article approaches Family affairs from social  capital perspective for the first time, it also emphasizes the necessity of conducting research in this field  in the future.

According to general aggression model, it is expected that antisocial and prosocial tendencies can be affected by Family-related variables. The present study sought to predict aggression and moral identity based on Family cohesion, Family communication patterns and Family social support. The research design was correlational and the population of the study was comprised of male high school students in Estahban in 2018-19 school year. The sample consisted of 253 individuals who were selected through cluster sampling method. The research instruments included Aggression Questionnaire (Buss & Perry, 1992), Self-Importance of Moral Identity Scale (Aquino & Reed, 2002), Social Support Questionnaire (Vaux et al., 1986), Revised Family Communication Patterns Scale (Koerner et al., 2002), Family Cohesion Questionnaire (Samani, 2002) and Crowne & Marlowe Social Desirability Scale (1982). Data were analyzed via Pearson correlation, partial correlation and multiple regression by SPSS22. Results revealed that conversation orientation as a communication pattern and Family cohesion correlated to aggression negatively and to moral identity positively. Furthermore, conformity orientation as another communication pattern and Family social support correlated to aggression positively and to moral identity negatively. Family social support, conformity orientation and conversation orientation could account for 71% of variance in aggression. In addition, conversation orientation and Family cohesion could account for 13% percent of variance in moral identity. The positive relationship between social support and aggression and its negative association with moral identity was contrary to expectations. Nevertheless, this study has confirmed the role of Family variables in aggression and moral identity.