The effect of the virtual social network-based psycho-education on the hope of family caregivers of clients with severe mental disorders

Psycho-education may have a positive effect on family caregivers of clients with mental disorders, and promote positive psychological states such as hope. The present study aims to investigate the effect of virtual social network-based psycho-education on the hope of family caregivers of clients with severe mental disorders.This study is a quasi-experimental research with a control and experimental groups. The participants of the study were 72 family caregivers of clients with severe mental disorders (36 in each group). Data were collected using demographic questionnaire and Adult Hope Scale before the study, immediately after the end of the training (first post-test), and 4 weeks afterwards (second post-test). The experimental group received psycho-education through Telegram App for four weeks.The results of the demographic questionnaire showed that both groups were homogeneous. The results of the Adult Hope Scale indicated that the mean score of both control and experimental groups were statistically significant and increased in the experimental group (P < 0.001). In addition, the changes of hope score in the experimental group were statistically significant in the first post-test than the pre-test, and in the second post-test than the first post-test and pre-test (P < 0.001).The findings of this study suggested that virtual social network-based psycho-education promotes the hopes of the family caregivers of clients with severe mental disorders. Due to the low cost and fast access of people to virtual networks, the content of this educational program can be widely used for family caregivers.     

Molecular analysis of human adenoviruses in hospitalized children <5 years old with acute gastroenteritis in Tehran,Iran

Human adenoviruses (HAdVs), especially AdV-40 and 41, are common causes of nonbacterial sporadic and outbreak gastroenteritis in children. The present study aimed to describe the frequency and genetic analysis of HAdVs in hospitalized children <5 years old with acute gastroenteritis. A total of 376 stool samples obtained from June 2015 to December 2017 were investigated for the presence of HAdVs by polymerase chain reaction. The HAdV DNA was detected in 16 (4.3%) out of 376 stool samples. Based on the hexon hypervariable region (HVR), B, C, and F HADV species including five types HAdV-1, 2, 3, 6, and 41 were identified, among which enteric AdV species F (EAdV-41) was the most dominant. Moreover, our findings showed the presence of genomic type cluster 1 (GTC1) pattern in Iranian type 41 strains, which was closely similar to the D1 prototype strain (Tak) and D28. In this regard, a recombination was found in AdV-41 strains presenting the hexon sequence that belonged to GTC1, while fiber sequence clustered with GTC2.     

The enhancement of vincristine cytotoxicity by combination with feselol

Urinary bladder cancer is one of the most common cancers worldwide. Human transitional cell carcinoma (TCC) cells are epithelial-like adherent cells originally established from a primary bladder carcinoma. Studies have shown that TCC cells are resistant to some chemotherapeutic agents such as vincristine (VCR). In the present study, the effect of feselol, a sesquiterpene coumarin isolated from the fruits of Ferula badrakema, was investigated on VCR effectiveness. Our results demonstrated that feselol itself did not have any cytotoxic effect on TCC cells. In order to check its combinatorial effects, TCC cells were exposed to various combined concentrations of feselol and VCR. Then, morphological changes were monitored and cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay for three consequent days. Results showed that the combination of 40 μg/ml VCR with 16 μg/ml feselol increased the cytotoxicity of VCR by 28.32% after 48 h. This effect might be due to inhibition of P-glycoprotein in TCC cells by feselol.     

Smoking status in Iranian male adolescents: A cross-sectional study and a meta-analysis

The present study aimed to estimate the prevalence of smoking status and its associated factors in Iranian adolescents and a meta-analysis of recent cross-sectional studies in order to estimate the corresponding prevalence for all Iranian adolescents.     

Marginal bone loss over 5 years in an adult Danish population

PURPOSE: To evaluate marginal bone loss on the individual and tooth level, with focus on the importance of the baseline marginal bone level. MATERIALS AND METHODS: In 1997, 616 randomly selected individuals (mean age 42 years, range 21-63 years) underwent a full-mouth radiographic survey. In 2003, the survey was repeated for 473 of the same individuals (239 females and 234 males). The marginal bone level of each tooth was measured in mm from the cemento-enamel junction to the marginal bone. These measurements were used to calculate marginal bone loss during the 5-year period, and to analyse the average marginal bone loss for the individual, and tooth group in relation to age and to baseline marginal bone level, calculated as the average between measurements in 1997 and 2003 to circumvent regression to the mean. RESULTS: Marginal bone loss rate was on average 0.1 mm per year. For the individual, marginal bone loss was associated with both baseline marginal bone level and age. A significant difference was shown (p < 0.05) in marginal bone loss between different age groups, with a stronger association between marginal bone loss and baseline marginal bone level in the youngest age group. Moreover, marginal bone loss differed between tooth groups (p < 0.001), with molars and premolars losing marginal bone more rapidly than incisors and canines and showing a stronger association with baseline marginal bone level. CONCLUSIONS: Marginal bone loss over a 5-year period is associated with age and baseline marginal bone level. Younger individuals with a reduced marginal bone level were at high risk for further bone loss. Molars and premolars exhibit more rapid marginal bone loss than incisors and canines.     

The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

The removal of apoptotic cells is an innate function of tissue macrophages; however, its role in disease progression is unclear. The present study was designed to investigate the role of macrophage CD36, a recognized receptor of apoptotic cells and oxidized lipids, in two models of kidney injury: unilateral ureteral obstruction (UUO) and ischemia reperfusion. To differentiate the macrophage CD36-specific effects in vivo, we generated CD36 chimeric mice by bone marrow transplantation and evaluated the two models. Fibrosis severity was substantially decreased after UUO with a corresponding decrease in matrix synthesis in macrophage CD36-deficient mice. Despite a reduction in fibrosis severity, a 56% increase in apoptotic cells was found without an increase in apoptotic effectors. In addition, a substantial reduction was observed in tumor necrosis factor-α and transforming growth factor-β1 mRNA levels and intracellular bioactive oxidized lipid levels in CD36-deficient macrophages. To validate the functional role of macrophage CD36, we performed unilateral ischemia reperfusion, followed by contralateral nephrectomy. Similarly, we found that the severity of fibrosis was reduced by 55% with a corresponding improvement in kidney function by 88% in macrophage CD36-deficient mice. Taken together, these data suggest that macrophage CD36 is a critical regulator of oxidative fibrogenic signaling and that CD36-mediated phagocytosis of apoptotic cells may serve as an important pathway in the progression of fibrosis.Studies in various organ systems, including the kidney, provide strong evidence that macrophages control fibrosis progression and resolution.^1–4 During both acute and chronic kidney injury, the interstitial macrophage population is heterogenous and polarized into distinct subsets. In vitro studies have dissected classically activated (M1) and alternatively activated (M2) macrophages on the basis of cytokine activation patterns as follows: M1 macrophages express proinflammatory cytokines such as IL-1β, tumor necrosis factor (TNF)α, and IL-6, whereas M2 macrophages suppress expression of the proinflammatory mediators.⁵ Studies in solid-organ injury suggest that this M2 population is further subdivided into reparative, regulatory, and profibrotic phenotypes.^6–8 However, studies suggest that complex tissue microenvironments are not adequately mirrored by the M1/M2 paradigm and that macrophage activation is more versatile and dynamic in response to the surrounding milieu.^9–12 Therefore, further delineation of tissue macrophage phenotypes should be based on functional outcome during kidney injury.Phagocytosis is an inherent function of tissue macrophages for the removal of apoptotic cells and cellular debris during acute and chronic injury; however, the implications of this event on macrophage function during tissue remodeling and fibrosis are not known.¹³ When a cell undergoes apoptosis or necrosis, several damage-associated molecular patterns are expressed for recognition by a host of pattern recognition receptors on macrophages.¹⁴ CD36 is a class B scavenger receptor expressed on the surface of several cell types, including macrophages, platelets, microvascular endothelial cells, and renal tubular cells. Although several in vitro studies have identified CD36 as an important macrophage receptor of apoptotic cell recognition and phagocytosis, few studies have examined its in vivo role during chronic injury.^15–17 Our previous work demonstrated that CD36 is important in promoting fibrosis but did not differentiate the specific roles of CD36-bearing cells.¹⁸ Here, we hypothesized that macrophage CD36 plays a critical role in promoting fibrogenesis through oxidative and inflammatory pathways after kidney injury. The results of this study provide evidence that the CD36 receptor identifies a profibrotic M2 macrophage phenotype and suggests that CD36-dependent phagocytosis of apoptotic cells is an important step in fibrogenic signaling in chronic kidney disease progression.     

Histopathological investigation of neuroprotective effects of Nigella sativa on motor neurons anterior horn spinal cord after sciatic nerve crush in rats

The aim of this study was designed to evaluate the possible protective effects of Nigella sativa (NS) on the neuronal injury in the sciatic nerve of rats. The rats were randomly allotted into one of the three experimental groups: A (control), B (only trauma) and C (trauma and treated with NS); each group contain 10 animals. Sciatic nerve injury was performed by placing an aneurysm clip on the left leg. Rats were neurologically tested over 24 h after trauma. The rats in NS-treated group was given NS (in a dose of 400 mg/kg body weight) once a day orally for 30 days starting just after trauma. Control and untreated (only trauma) rats were injected with the same volume of isotonic NaCl as the treated animals that received NS. Tissue samples were obtained for histopathological investigation. To date, no histopathological changes of neurodegeneration in the sciatic nerve after trauma in rats by NS treatment have been reported. Results showed in the group B (only trauma), the neurons of sciatic nerve tissue became extensively dark and degenerated with picnotic nuclei. Treatment of NS markedly reduced degenerating neurons after trauma and the distorted nerve cells were mainly absent in the NS-treated rats. The morphology of neurons in groups treated with NS was well protected, but not as neurons of the control group. The number of neurons in sciatic nerve tissue of group B (only trauma) was significantly less than both control and treated with NS groups. The morphology of neurons revealed that the number of neurons were significantly less in group B compared to control (P < 0.001) and group C (P < 0.01) rats’ motor neurons anterior horn spinal cord tissue. We conclude that NS therapy causes morphologic improvement on neurodegeneration in sciatic nerve after trauma in rats.     

Constraints on task-based control of behaviour following frontal lobe damage: A single-case study

What factors determine stimulus-driven responses in patients with utilization behaviour? We examined this question by assessing the influence of an irrelevant cue on visual search in a patient showing evidence of utilization behaviour (F.K.), following bilateral damage to the medial frontal and temporal lobes. Despite being able to repeat the instructions, F.K. often responded to an item in the search display that matched the cue rather than the target. This effect was reduced under certain conditions: (a) when the cue–search interval increased, (b) when F.K. paid less attention to the cue, and (c) when the target discrimination task was made more difficult. On the other hand, the effect arose even when the cue was always invalid. We suggest that information from the cue competed with the top-down set to determine search. F.K.'s lesion makes it difficult for him to impose top-down knowledge rapidly, leading to responses automatically being based on attended, but irrelevant, cues under short cue–display intervals.     

Monepantel antitumor activity is mediated through inhibition of major cell cycle and tumor growth signaling pathways

In women, epithelial ovarian cancer is the leading cause of gynaecological malignancy-related deaths. Development of resistance to standard platinum and taxane based chemotherapy and recurrence of the disease necessitate development of novel drugs to halt disease progression. An established concept is to target molecular and signaling pathways that substantially contribute to development of drug resistance and disease progression. We have previously shown that, monepantel (MPL) a novel small molecule acetonitrile derivative is highly effective in suppressing growth, proliferation and colony formation of ovarian cancer cells. These effects are achieved through inhibition of the mTOR/p70S6K pathway in cancer cells. The present study was conducted to find in vivo corroboration and explore the effect of MPL om other growth stimulating putative signaling pathways. Here, female nude mice with subcutaneous OVCAR-3 xenografts were treated with 25 and 50 mg/kg doses of MPL administered (IP) three times weekly for 2 weeks. At the doses employed, MPL was modestly effective at suppressing tumor growth, but highly effective in inhibiting, mTOR, P70S6K and 4EBP1. There were also modest reductions in tumor cyclin D1 and retinoblastoma protein expression. Furthermore, it was found that MPL treatment causes down-regulation of IGF-1R, and c-MYC thus unveiling new dimensions to the growing antitumor actions of this potential anticancer drug. MPL treatment led to reduced tumor volume and weights without causing any detectable side effects. Coupled with the recent human safety data published on this molecule, expanded future trials are highly anticipated.