Interleukin-23 receptor gene polymorphisms in Iranian patients with juvenile systemic lupus erythematosus

Introduction and objectives: Considering the possible roles of interleukin-23 receptor (IL-23R) gene in the pathogenesis of juvenile systemic lupus erythematosus (JSLE), the objective of this study was to elucidate whether polymorphisms of the IL23R are associated with susceptibility to JSLE in an Iranian population. Materials and methods: A case-control study on 62 patients with JSLE and 78 healthy controls was performed to investigate the associations of four single nucleotide polymorphisms (SNPs) in IL-23R gene, namely, rs7517847, rs10489629, rs11209026, and rs1343151, with susceptibility to JSLE, using real-time polymerase chain reaction Taqman genotyping technique. Results: Analysis of allele and genotype frequency of four selected SNPs revealed statistically significant positive association between homozygous variant of rs7517847 (TT) (P, 0.02) and T allele at the same position (P, 0.01) with JSLE vulnerability. There was no significant association between other evaluated SNPs and JSLE susceptibility. Conclusion: These findings suggest that particular IL-23R gene variants could affect individual susceptibility to JSLE

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Interleukin-23 receptor gene polymorphisms in Iranian patients with juvenile systemic lupus erythematosus.

INTRODUCTION AND OBJECTIVES: Considering the possible roles of interleukin-23 receptor (IL-23R) gene in the pathogenesis of juvenile systemic lupus erythematosus (JSLE), the objective of this study was to elucidate whether polymorphisms of the IL23R are associated with susceptibility to JSLE in an Iranian population. MATERIALS AND METHODS: A case-control study on 62 patients with JSLE and 78 healthy controls was performed to investigate the associations of four single nucleotide polymorphisms (SNPs) in IL-23R gene, namely, rs7517847, rs10489629, rs11209026, and rs1343151, with susceptibility to JSLE, using real-time polymerase chain reaction Taqman genotyping technique. RESULTS: Analysis of allele and genotype frequency of four selected SNPs revealed statistically significant positive association between homozygous variant of rs7517847 (TT) (P, 0.02) and T allele at the same position (P, 0.01) with JSLE vulnerability. There was no significant association between other evaluated SNPs and JSLE susceptibility. CONCLUSION: These findings suggest that particular IL-23R gene variants could affect individual susceptibility to JSLE.

Association of NLRP3 single nucleotide polymorphisms with ulcerative colitis: A case-control study.

BACKGROUND: Ulcerative colitis (UC) is inflammatory bowel disease (IBD), characterized by chronic inflammation episodes within mucosal layer of the intestine mostly affecting colon and rectum. As the role of innate immunity in pathogenesis of disease and important role of NLRP3, the aim of this study is to investigate the association of NLRP3 SNPs with UC in Iranian patients. METHODS: Blood samples from 45 UC patients and 56 healthy subjects were tested for single nucleotide polymorphisms in rs10754558, rs3806265, rs4612666, and rs35829419 of NLRP3 gene, using real-time PCR method. RESULTS: Among the investigated SNPs, "GG" genotype of rs10754558 have been 2.48 times more common among UC patients (P=0.04), while "CG" genotype has indicated protective effect against UC, as more frequently found in healthy subjects. CONCLUSION: Despite no significant association between three investigated SNPs and disease, "GG" and "CG" genotypes of rs10754558 have been significantly associated with disease.

Anomalous left brachiocephalic vein: important vascular anomaly concomitant with congenital anomalies and heart diseases.

BACKGROUND: Anomalous left brachiocephalic vein (ALBCV) is a rare and less known systemic venous anomaly. Infrequently, this vein takes an abnormal course and passes to the right behind or beneath the aortic arch to create the superior vena cava (SVC). Its incidence was reported much higher in patients with congenital heart disease especially in conotruncal and aortic arch anomalies. It could be misdiagnosed with normal or abnormal mediastinal structures. It also could make complication during surgeries or invasive strategies. Previously, this anatomical finding has been reported in case reports and there are just few studies evaluating these patients as a group to find other abnormalities MATERIALS AND METHODS: We conducted a retrospective, multicentre study between 2008 and 2014 at three institutions. We reviewed thoracic computed tomography angiography of 1372 patients referred to these centres. The diagnosis of ALBCV was confirmed by an expert radiologist and the imagings were reassessed to identify new cases and concomitant anomalies. We analysed the imagings' details and measured the prevalence of each anomaly. RESULTS: Among the 22 cases of ALBCV, 12 (54.5%) and 10 (45.4%) patients were males and females, respectively, with median age of 12.5 years. Tetralogy of Fallot (TOF) was considered as a most concomitant anomaly with ALBCV (54.5%). Two patients had associated atrial septal defect (ASD) and defined as pentalogy of Fallot. Right-sided aortic arc (RSAA) was detected in 12 (54.5%) patients; mirror image was found in 5 of them. Pure ventricular septal defect or pulmonary stenosis without TOF was recognised in 4 patients. Three cases had isolated overriding aorta (13.6%). In 3 patients, we could find patent ductus arteriosus (13.6%). In 2 (9%) patients, abdominal haemangioma was incidentally diagnosed. Aberrant left retrotracheal subclavian artery was detected in 1 (4.5%) patient. One patient only had isolated ALBCV (4.5%). CONCLUSIONS: In our study, ALBCV was frequently seen in association with other congenital anomalies. mostly TOF and RSAA. In patients with pulmonary hypoplasia or aplasia, some parts of lung's blood supply were provided by abnormal aorto-pulmonary connections. For a radiologist, it is important to differentiate this anomaly in cross-sectional imaging from persistent left SVC, partial anomalous pulmonary veins return and an enlarged lymph node. Detection of ALBCV could draw the attention to the more serious heart disease and in isolated forms prevented further evaluations.

Association of interleukin-1 family gene polymorphisms with juvenile idiopathic arthritis in Iranian population

BACKGROUND: Cytokines, including interleukin-1 (IL-1), seem to contribute towards the pathogenesis of juvenile idiopathic arthritis (JIA), so this study was designed to evaluate the associations of IL-1 gene cluster and IL-1 receptor (IL-1R) gene single nucleotide polymorphisms (SNPs) with JIA proneness in Iranian population. MATERIALS AND METHODS: Genomic DNA of 55 Iranian patients with JIA and 140 controls were extracted and typed for IL-1alpha gene at position −889, IL-1beta gene at positions −511 and +3962, IL-1R gene at position Pst-I 1970, and interleikin-1 receptor antagonist (IL-1Ra) gene at position Mspa-I 11100, using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls. RESULTS: The CC genotype of IL-1Ra at Mspa-I 11100 position was found to be more frequent in patients with JIA compared to healthy individuals (P=0.03), although the CT genotype at the same position was significantly higher in the control group in comparison with patients with JIA (P=0.02). No significant differences were observed between the two groups of case and control for IL-1alpha (−889 C/T), IL-1beta (−511 C/T and +3962 C/T) and IL-1R (Pst-1 1970 C/T). CONCLUSION: The results of the present investigation suggest that certain IL-1Ra gene variants are associated with individuals' susceptibility to JIA. Nevertheless, further studies are required to establish the results of the current study

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Association of tumour necrosis factor-alpha G/A -238 and G/A -308 single nucleotide polymorphisms with juvenile idiopathic arthritis.

Juvenile idiopathic arthritis (JIA) is a heterogeneous autoimmune disorder of unknown origin. As proinflammatory cytokines are known to contribute towards the pathogenesis of JIA, this case-control study was performed to examine the associations of certain single nucleotide polymorphisms (SNPs) of tumour necrosis factor-α (TNF-α) gene. Fifty-three patients with JIA participated in this study as patients group and compared with 137 healthy unrelated controls. Genotyping was performed for TNF-α gene at positions -308 and -238, using polymerase chain reaction with sequence-specific primers method. Results of the analysed data revealed a significant positive association for TNF-α gene at positions -308 and -238 for A allele in patients group compared with controls (P < 0.01). At the genotypic level, the frequency of TNF-α gene at positions -308 and -238 for GG genotype was discovered to be higher in the patients with JIA compared to the healthy controls (P < 0.01), while GA genotype at the same positions was observed to be less frequent in the case group than the controls (P < 0.01). At the haplotypic level, a significant positive association for TNF-α GG haplotype (positions -308, -238) together with a notable negative association for TNF-α AG and GA haplotypes at the same positions were detected in the patients group in comparison with the healthy individuals (P < 0.01). Cytokine gene polymorphisms might affect the development of JIA. Particular TNF-α gene variants could render individuals more susceptible to JIA..

Association of interleukin-1 family gene polymorphisms with juvenile idiopathic arthritis in Iranian population.

BACKGROUND: Cytokines, including interleukin-1 (IL-1), seem to contribute towards the pathogenesis of juvenile idiopathic arthritis (JIA), so this study was designed to evaluate the associations of IL-1 gene cluster and IL-1 receptor (IL-1R) gene single nucleotide polymorphisms (SNPs) with JIA proneness in Iranian population. MATERIALS AND METHODS: Genomic DNA of 55 Iranian patients with JIA and 140 controls were extracted and typed for IL-1α gene at position -889, IL-1ß gene at positions -511 and +3962, IL-1R gene at position Pst-I 1970, and interleikin-1 receptor antagonist (IL-1Ra) gene at position Mspa-I 11100, using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls. RESULTS: The CC genotype of IL-1Ra at Mspa-I 11100 position was found to be more frequent in patients with JIA compared to healthy individuals (P=0.03), although the CT genotype at the same position was significantly higher in the control group in comparison with patients with JIA (P=0.02). No significant differences were observed between the two groups of case and control for IL-1α (-889 C/T), IL-1ß (-511 C/T and +3962 C/T) and IL-1R (Pst-1 1970 C/T). CONCLUSION: The results of the present investigation suggest that certain IL-1Ra gene variants are associated with individuals' susceptibility to JIA. Nevertheless, further studies are required to establish the results of the current study.

Association of interleukin-2 and interferon-γ single nucleotide polymorphisms with Juvenile systemic lupus erythematosus

Purpose: Juvenile systemic lupus erythematosus (JSLE) is a severe and chronic autoimmune disease of unknown origin. Inflammatory cytokines can play a pivotal role in the pathogenesis of JSLE, while their secretion is under genetic control. The current investigation was performed to analyse the associations of particular single nucleotide polymorphisms (SNPs) of interleukin-2 (IL-2) and interferon-gamma (IFN-γ) genes in a case control study. Materials and methods: The allele, genotype and haplotype frequencies of the polymorphic IL-2 (G/T at −330, rs2069762, and G/T at +166, rs2069763) and IFN-γ (A/T at +874, rs2430561) genes were estimated in 59 patients with JSLE by contrast with 140 healthy controls using polymerase chain reaction with sequence-specific primers method. Results: Results of the analysed data revealed a negative allelic association for JSLE in IL-2 −330/T (P=0.02), as well as a positive allelic association for IL-2 −330/G (P=0.02). IL-2 GG genotype (−330) in the patient group was also significantly overrepresented (P<0.001), while IL-2 GT genotype (−330) was notably decreased in the patients with JSLE (P<0.001). Additionally, the frequency of IL-2 (−330, +166) GT haplotype was significantly higher in the patient group (P<0.001). Conclusion: IL-2 cytokine gene polymorphisms could affect individual susceptibility to JSLE and can take on the role of possible genetic markers for vulnerability to JSLE

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Association of interleukin 1 gene cluster and interleukin 1 receptor gene polymorphisms with ischemic heart failure.

BACKGROUND: Proinflammatory cytokines have been known to play a considerable part in the pathomechanisms of chronic heart failure (CHF). Given the importance of proinflammatory cytokines in the context of the failing heart, we assessed whether the polymorphisms of interleukin (IL)-1 gene cluster, including IL-1α, IL-1ß, and IL-1 receptor antagonist (IL-1RA) and IL-1R gene are predictors of CHF due to ischemic heart disease. METHODS: Forty- three patients with ischemic heart failure were recruited in this study as patients group and compared with 140 healthy unrelated control subjects. Using polymerase chain reaction with sequence-specific primers method, the allele and genotype frequency of 5 single nucleotide polymorphisms (SNPs) within the IL-1α (-889), IL-1ß (-511, +3962), IL-1R (psti 1970), and IL-1RA (mspa1 11100) genes were determined. RESULTS: The frequency of the IL-1ß -511/C allele was significantly higher in the patient group compared to that in the control group (p = 0.031). The IL-1ß (-511) C/C genotype was significantly overrepresented in patients compared to controls (p = 0.022). CONCLUSIONS: Particular allele and genotype in IL-1ß gene were overrepresented in patients with ischemic heart failure, possibly affecting the individual susceptibility to this disease (Tab. 1, Ref. 27).

Association of Interleukin-2, but not Interferon-Gamma, single nucleotide polymorphisms with juvenile idiopathic arthritis

BACKGROUND: Cytokines, including interleukin-2 (IL-2) and interferon-gamma (IFN-γ), seem to play a role in the pathogenesis of juvenile idiopathic arthritis (JIA). The aim of this study was to investigate the associations of IL-2 and IFN-γ single nucleotide polymorphisms (SNPs) with susceptibility to JIA in an Iranian population. METHODS: enomic DNA of 54 Iranian patients with JIA and 139 healthy unrelated controls were typed for IL-2 (G/T at −330 and +166) as well as IFN-γ gene (A/T at +874), using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls. RESULTS: A significantly higher frequency of the IL-2 −330 GG genotype (p < 0.01) was found in the JIA patients compared to the controls. However, the GT genotype at the same position was notably lower than in controls (p < 0.01). Moreover, IL-2 (−330, +166) GT haplotype was more frequent in patients with JIA in comparison with controls. No significant differences was observed between the two groups of case and control for IL-2 (G/T at +166) and IFN-γ (A/T at +874) SNPs. CONCLUSION: The results of the current study suggest that certain SNPs of IL-2 gene have association with individuals' susceptibility to JIA. However, further investigations are required to confirm the results of this study

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FLG single nucleotide polymorphisms in chronic idiopathic urticaria

BACKGROUND: Filaggrin (FLG), which is formed from profilaggrin protein during epidermal terminal differentiation, is a prerequisite to squame biogenesis and thus for perfect formation of the skin barrier. Yet, the relationship between genetic polymorphisms of FLG and chronic idiopathic urticaria (CIU) has not been investigated. METHODS: The study population consisted of 93 CIU patients and 93 healthy control subjects without a history of allergic, autoimmune or any other systemic disease. Five single nucleotide polymorphisms (SNPs) of FLG were investigated: rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299. RESULTS: For all the investigated polymorphisms, 100% of both CIU patients and control subjects exhibited one given allele and consequently one given genotype as following: A/A genotype for two SNPs, rs3126065 and rs2786680, C/C genotype for two SNPs, rs2485518 and rs3814300, and G/G genotype for one SNP rs3814299 of FLG, and hence no association was found between either allele frequencies or genotype distributions of FLG SNPs and CIU in an Iranian population. CONCLUSIONS: The present study examined the possible relationship between SNPs of FLG and CIU for the first time, and demonstrated that none of five investigated SNPs (rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299) are correlated with CIU in an Iranian population. Further investigations are required to address whether ethnicity/race impacts on relationship between SNPs of FLG and CIU

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Association of interleukin-2 and interferon-γ single nucleotide polymorphisms with Juvenile systemic lupus erythematosus.

PURPOSE: Juvenile systemic lupus erythematosus (JSLE) is a severe and chronic autoimmune disease of unknown origin. Inflammatory cytokines can play a pivotal role in the pathogenesis of JSLE, while their secretion is under genetic control. The current investigation was performed to analyse the associations of particular single nucleotide polymorphisms (SNPs) of interleukin-2 (IL-2) and interferon-gamma (IFN-γ) genes in a case control study. MATERIALS AND METHODS: The allele, genotype and haplotype frequencies of the polymorphic IL-2 (G/T at -330, rs2069762, and G/T at +166, rs2069763) and IFN-γ (A/T at +874, rs2430561) genes were estimated in 59 patients with JSLE by contrast with 140 healthy controls using polymerase chain reaction with sequence-specific primers method. RESULTS: Results of the analysed data revealed a negative allelic association for JSLE in IL-2 -330/T (P=0.02), as well as a positive allelic association for IL-2 -330/G (P=0.02). IL-2 GG genotype (-330) in the patient group was also significantly overrepresented (P<0.001), while IL-2 GT genotype (-330) was notably decreased in the patients with JSLE (P<0.001). Additionally, the frequency of IL-2 (-330, +166) GT haplotype was significantly higher in the patient group (P<0.001). CONCLUSION: IL-2 cytokine gene polymorphisms could affect individual susceptibility to JSLE and can take on the role of possible genetic markers for vulnerability to JSLE.

Interleukin 10 and transforming growth factor beta 1 gene polymorphisms in juvenile idiopathic arthritis.

OBJECTIVES: The aim of this study is to identify the associations between interleukin 10 (IL-10) and transforming growth factor beta 1 (TGF-ß1) gene polymorphisms and individual susceptibility to juvenile idiopathic arthritis (JIA) in a group of Iranian patients. BACKGROUND: Cytokine genes, including IL-10 and TGF-ß1, are known to play important roles in the pathogenesis of JIA. METHODS: Using polymerase chain reaction with sequence-specific primers method, the frequency of alleles, genotypes and haplotypes of IL-10 (positions -1082, -819, -592) and TGF-ß1 (codon 10, codon 25) single-nucleotide polymorphisms (SNPs) were investigated in 55 patients with JIA as a case group and compared with 140 healthy unrelated controls. RESULTS: The G allele was significantly less frequent at TGF-ß1 codon 25 in patients with JIA than in the controls (p < 0.01). The frequency of CT genotype at TGF-ß1 codon 10 was found to be higher in healthy individuals in comparison with that in patients group (p = 0.04). We observed no differences in the frequency of alleles, genotypes and haplotypes of IL-10 gene between the groups of patients and controls. CONCLUSIONS: Considering the low frequency of existence of TGF-ß1 G allele at codon 25 as well as TGF-ß1 CT genotype at codon 10 in patients with JIA, it seems that these cytokine gene polymorphisms could play role as the protective factors against JIA.

Association of Interleukin-2, but not Interferon-Gamma, single nucleotide polymorphisms with juvenile idiopathic arthritis.

BACKGROUND: Cytokines, including interleukin-2 (IL-2) and interferon-gamma (IFN-γ), seem to play a role in the pathogenesis of juvenile idiopathic arthritis (JIA). The aim of this study was to investigate the associations of IL-2 and IFN-γ single nucleotide polymorphisms (SNPs) with susceptibility to JIA in an Iranian population. METHODS: Genomic DNA of 54 Iranian patients with JIA and 139 healthy unrelated controls were typed for IL-2 (G/T at -330 and +166) as well as IFN-γ gene (A/T at +874), using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls. RESULTS: A significantly higher frequency of the IL-2 -330 GG genotype (p<0.01) was found in the JIA patients compared to the controls. However, the GT genotype at the same position was notably lower than in controls (p<0.01). Moreover, IL-2 (-330, +166) GT haplotype was more frequent in patients with JIA in comparison with controls. No significant differences was observed between the two groups of case and control for IL-2 (G/T at +166) and IFN-γ (A/T at +874) SNPs. CONCLUSION: The results of the current study suggest that certain SNPs of IL-2 gene have association with individuals' susceptibility to JIA. However, further investigations are required to confirm the results of this study.

FLG single nucleotide polymorphisms in chronic idiopathic urticaria.

BACKGROUND: Filaggrin (FLG), which is formed from profilaggrin protein during epidermal terminal differentiation, is a prerequisite to squame biogenesis and thus for perfect formation of the skin barrier. Yet, the relationship between genetic polymorphisms of FLG and chronic idiopathic urticaria (CIU) has not been investigated. METHODS: The study population consisted of 93 CIU patients and 93 healthy control subjects without a history of allergic, autoimmune or any other systemic disease. Five single nucleotide polymorphisms (SNPs) of FLG were investigated: rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299. RESULTS: For all the investigated polymorphisms, 100% of both CIU patients and control subjects exhibited one given allele and consequently one given genotype as following: A/A genotype for two SNPs, rs3126065 and rs2786680, C/C genotype for two SNPs, rs2485518 and rs3814300, and G/G genotype for one SNP rs3814299 of FLG, and hence no association was found between either allele frequencies or genotype distributions of FLG SNPs and CIU in an Iranian population. CONCLUSIONS: The present study examined the possible relationship between SNPs of FLG and CIU for the first time, and demonstrated that none of five investigated SNPs (rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299) are correlated with CIU in an Iranian population. Further investigations are required to address whether ethnicity/race impacts on relationship between SNPs of FLG and CIU.

Interleukin-4 single nucleotide polymorphisms in juvenile systemic lupus erythematosus.

Juvenile systemic lupus erythematosus (JSLE) is a chronic, recurrent multisystem inflammatory disease, caused by a combination of environmental events and genetic risk factors. As cytokines, including interleukin-4 (IL-4), seem to have a role in the pathogenesis of JSLE, the investigation was performed to evaluate the associations of specific single nucleotide polymorphisms (SNPs) of IL-4 and IL-4RA genes in a case-control study. Fifty-nine patients with JSLE were recruited in this study as patients' group and compared with 140 healthy volunteers. Genotyping was performed for IL-4 gene at positions -1098, -590 and -33, as well as IL-4 receptor α (IL-4RA) gene at position +1902, using polymerase chain reaction with sequence-specific primers method. Following alleles were found to be more common among patients with JSLE: C at -590 and -33 and T at -1098 of IL-4 gene (P value < 0.001; OR = 4.6, P value < 0.001; OR = 2.7 and P value < 0.001; OR = 2.1, respectively). Additionally, significant positive associations for the following genotypes were recognized in JSLE cases, compared with controls: C/C at -33, C/C at -590 and T/T at -1098 of IL-4 gene (P value < 0.001; OR = 5.3, P value < 0.001; OR = 29.5 and P value < 0.001; OR = 3.3, respectively), while following genotypes were less frequent among patients with JSLE: T/C at -33 and -590 and T/G at -1098 of IL-4 gene (P value < 0.001; OR = 0.1, P value < 0.001; OR = 0.03 and P value < 0.001; OR = 0.3, respectively). Furthermore, we noticed an astonishing negative haplotypic association for JSLE for IL-4 (positions -1098, -509 and -33) TTC, GCC and TTT haplotypes (P value < 0.001). There was also a significant relationship between TCC haplotype (IL-4 gene at positions -1098, -590 and -33) and having JSLE (P value < 0.001). On the other hand, we found no significant associations between IL-4R polymorphisms and the susceptibility to JSLE. Cytokine gene polymorphisms may influence susceptibility to JSLE. Particular IL-4 gene variants are associated with JSLE and might have a role in the pathophysiology of disease.

A small size 1-3 atm pulsed CO2 laser with series-connected spark gaps ultraviolet preionization.

A small size pulsed CO2 laser with rounded edge flat profiled electrodes and variable gas pressure in 1-3 atm range has been constructed and characterized. The perionization system consists of a pair of 16 series-connected spark gaps located along either side of the main electrodes by which, the number of required preionization capacitors is reduced to 4. Sharpening of the main discharge has been performed using a 300 pF peaking capacitor. A maximum energy of 160 mJ/pulse was obtained for CO2:N2:He≡1:1:8 gas mixture and 33 kV discharge voltage. By increasing the laser gas pressure in 1-3 atm range, the duration of spike and tail parts of the laser pulses have been reduced from 110 ns and 4 µs to 37 ns and 1 µs, respectively.

DRR regulates AKT activation to drive brain cancer invasion.

Glioblastoma (GBM) is the most common and invasive adult brain cancer. The rapid invasion of cancer cells into the normal brain is a major cause of treatment failure, yet the mechanisms that regulate this process are poorly understood. We have identified a novel mechanism of brain cancer invasion. We show that downregulated in renal cell carcinoma (DRR), which is newly expressed in invasive gliomas, recruits AKT to focal adhesions. This DRR- induced pathological relocalization of AKT bypasses commonly altered upstream signaling events and leads to AKT activation and invasion. We also developed an oligonucleotide therapeutic that reduces DRR expression and prevents glioma invasion in an in vivo preclinical model of the disease. Our findings identify DRR as a novel GBM target and show that oligonucleotides targeting DRR is a novel therapeutic approach for the treatment of DRR-positive GBMs.

Common methods to treat addiction in treatment- rehabilitation centers in tehran.

BACKGROUND: This study was to determine common methods to treat addiction used by patients checked into Outpatient Treatment and Rehabilitation Clinics in Tehran. METHODS: The study was conducted in Social Security affiliated outpatient clinics including three governmental and several private centers in 22 districts of Tehran. Demographic data, personal information, social characteristics and information regarding prevention, treatment, and follow-up records of 1,372 patients were obtained and analyzed. RESULTS: A majority of cases referring to the treatment centers were male (95.2%). Patients were 14 to 75 yr (mean 35.48 ± 10.57 yr); 61.7% were married and lived in rented homes in the city; 938/1372 (68.4%) had at least one previous attempt failure when seeking re-treatment. A majority of them (77.8%) had a history of 1 to 4 quit attempts; a number 63.1% had an abstinence period of 1 week to 6 months. CONCLUSION: The majority of our understudy subjects had a history of previous attempts to treat their addiction with a maximum abstinence period of 6 months.

DRR drives brain cancer invasion by regulating cytoskeletal-focal adhesion dynamics.

Malignant glioma invasion is a primary cause of brain cancer treatment failure, yet the molecular mechanisms underlying its regulation remain elusive. We developed a novel functional-screening strategy and identified downregulated in renal cell carcinoma (DRR) as a regulator of invasion. We show that DRR drives invasion in vitro and in vivo. We found that while DRR is not expressed in normal glial cells, it is highly expressed in the invasive component of gliomas. Exploring underlying mechanisms, we show that DRR associates with and organizes the actin and microtubular cytoskeletons and that these associations are essential for focal adhesion (FA) disassembly and cell invasion. These findings identify DRR as a new cytoskeletal crosslinker that regulates FA dynamics and cell movement.