abasalt hosseinzadeh colagar

Hyaluronan-mediated motility receptor (HMMR) and Stabilin-2 (STAB2), known as extracellular matrix cell surface protein’s receptors, bind to hyaluronic acid and lead to various cell functions.

The study aims to investigate the relationship between the HMMR-rs299295 (C>T/ A485V) and STAB2-rs2271637 (C>G/ L2401V) gene variants and the risk of prostate neoplasms in the Mazandaran population, North of Iran.

This study was conducted based on a case-control and in silico approach. Genomic DNA was extracted from 598 intravenous blood samples, collected from 250 benign prostatic hyperplasia (case group I) and 250 malignant prostate (case group II) neoplasms as cases, and 98 healthy men as control. The HMMR-rs299295 and STAB2-rs2271637 genotypes were identified using the polymerase chain reaction-restriction fragment length polymorphism method. Bioinformatics analyses were conducted using PolyPhen-2, GOR IV, and GeneMANIA free web tools.

The study found that the mutant T allele in HMMR-rs299295 and the G allele in STAB2-rs2271637 are associated with an increased risk of prostate neoplasm, including benign prostatic hyperplasia and prostate cancer (p < 0.001). Bioinformatic analyses revealed structural changes and potential damage from these variants. The HMMR-A485V variant might impair interaction with family with sequence similarity 83 member D, and the STAB2-L2401V variant could disrupt domain 7 of FAS1, together they may affect the protein's physical interactions, especially with mitogen-activated protein kinase 1.

The mutant alleles of T in HMMR-rs299295 and the G in STAB2-rs2271637 may disrupt protein structures and probably contribute to prostate neoplasm progression.

Today evaluation of polymorphisms of the antioxidant enzyme-encoding genes, which affect the activity of antioxidant enzymes, could be used as risk prediction models for male infertility. This study aims to evaluate coloration of serum paraoxonase (PON1) activity levels in the semen and its L55M gene variants with risk male infertility. In a case-control study, semen samples were collected from 80 healthy controls and 128 infertile men at Fatemeh Al-Zahra IVF and Pastor Laboratory (Babol, Mazandaran, Iran). PON1 activity of semen samples was measured by spectrophotometric methods. Genotyping of all individuals based on PON1-L55M loci performed by PCR-RFLP and PCR-sequencing and molecular effects of leucine (L) to methionine (M) substitution were investigated by bioinformatics tools. Results showed a significant difference in genotype frequencies of PON1-L55M polymorphism between patient and control groups, and c.163T>A transition effect on the structure and function of PON1 protein. Also, TA genotype (OR=1.754, 95%CI=0.971 to 3.166, P= 0.062) and AA genotype (OR=5.067, 95%CI=1.366 to 18.789, P= 0.015) were associated with male infertility. Men with mutant allele (AA+TA) are exposed to be at the risk of male infertility (OR= 1.990, 95%CI= 1.118 to 3.54, P= 0.019). Also, the allelic analysis showed that the A allele was associated with the increased risk of idiopathic male infertility (OR= 1.749, 95%CI= 1.143 to 2.676, P= 0.010). Additionally, PON1 activity was higher in the TT (LL) individuals compared to the TA (LM) and AA (MM) men in both groups (LL> LM> MM). Since, the PON1-L55M gene variants are related to PON1 activity levels in the semen and serum paraoxonase is known as an important antioxidant calcium-dependent enzyme, it could be implicated in male infertility. Based on these findings, the presence of mutant allele (A) and or decreasing semen’s PON1 level may be an indicator/ prediction factor for male infertility.

CD44, a cell-surface receptor and a key player in cellular signaling, can act as both tumor suppressor and promoter. This study aimed to investigate the association of CD44 rs13347C>T variants with prostate neoplasms, including both benign prostatic hyperplasia (BPH) and prostate cancers using a case-control and bioinformatics approach. Genomic DNA was extracted from 545 blood samples (225 BPH, 225 prostate cancers, and 95 control) and the CD44 rs13347C>T genotypes were identified using PCR-RFLP. We explored miRNA interactions using the miRNASNP-v3 database and GeneMANIA for co-expression networks. Results showed cancer patients had significantly higher PSA levels compared to both controls (p= 0.03) and BPH (p= 0.01). Additionally, digital rectal examination-positive and smoker BPH patients showed significantly the increased cancer risk (p= 0.004, p= 0.046). Prostate cancer group indicated significantly higher frequency of CD44 rs13347C>T mutant allele compared to control and BPH groups, particularly in TT and CT+TT genotypes (p < 0.05). miRNA SNP-v3 database predicted the mutant allele of CD44 rs13347C>T could lose 1 and gain 6 miRNAs for a new site created. Co-expression analysis revealed a direct interaction between CD44 and aryl hydrocarbon receptor (AHR), a gene known to be dysregulated in smokers. Furthermore, these genes alone display co-expression interactions with integrin subunit alpha 4 (ITGA4), protein plays a paradoxical role, both suppressing and promoting tumors. Based on the findings, the mutant allele of CD44 rs13347C>T may disrupt miRNA binding, which may potentially impact CD44, AHR, and ITGA4 expression in smokers, possibly contributing to prostate cancer progression.

Today, the geographical distribution of a species based on maximum entropy using spatial data from geographical information system, remote sensing data and statistical techniques have a great contribution on conservation management of species. The aim of this study is evaluate the effects of environmental variable on distribution and habitat suitability of great gerbil (Rhombomys opimus) and predicting its habitat in Golestan province, Iran.

For this purpose, 272 presence-only data and 13 environment variables as independent variables were selected for this species. Then, geographic distribution and habitat suitability modeling were performed by maximum entropy approach in MaxEnt software, using to these presence data and variables.

Our results showed that, some of the habitat variables including: altitude, NDVI, soil type and climate had the greatest plays for habitat suitability and geographical distribution of R. opimus in this area. While that, aspect had less effects than other variables.

Based on our findings, habitats of R. opimus was continues and about 10.1% of Golestan province pereidicted as a suitable habitat for the great gerbil.

Diabetic retinopathy is the most severe diabetic microvascular complication that causes changes in the vessel wall. One of the genes involved in this disease is PON1, which encodes paraoxanase1 protein in liver and kidney. It might regulate inflammatory and microvascular responses to the disease. The rs662 T>C is one of the single nucleotide polymorphisms of this gene that changes glutamine to arginine at position 192.

In this study, 300 samples were collected, including 100 healthy and 100 diabetics without retinopathy, and 100 diabetics retinopathies were studied and their age range was from 30 to 80 years. Then 2.5 ml of blood was collected from all relevant individuals in tubes containing EDTANa2</sub>. This polymorphism was examined by tetra-ARMS PCR.

Results showed that there is no significant correlation between genotypes and alleles related to PON1 and Diabetes (CC genotype: p=0.609; C allele: p=0.228). On the other hand, an association was observed between PON1 and diabetic retinopathy (CT+CC genotype: p<0.001; CT allele: p<0.001). Considering that the Polyphen database examined the changes caused by replacing the amino acid arginine instead of glutamine at position 129 on the protein, it does not consider these changes dangerous and has introduced this polymorphism as benign.

Based on the findings of this study, the rs662 locus could be considered as one of the molecular markers in future research.

Today, numerous antimicrobial and anticancer properties have been reported for plant lectins due to theirability to bind to carbohydrates. The Urtica dioica agglutinin (UDA lectin) is a monomeric, small, and low molecularweight glycoprotein. It has attracted the attention of many researchers for identification, treatment, and other clinicalpurposes.

The aim of this study is the optimization of the chitin affinity chromatography based on Sepharose 4B (CNBractivated Sepharose 4B) for the rapid purification of UDA lectin from Urtica dioica rhizome.

The chitin ligands were dissolved in 40% Trichloroacetic acid and attached to Sepharose4B according to the Amersham-Biosciences instructions. The attachment of the ligand to the Sepharose 4B beads wasinvestigated by Fourier transform infrared (FTIR) spectroscopy. An acidic crude extract of nettle rhizome passes fromchromatographic columns in two sizes with dimensions: 24 x 0.51 cm and 8.44 x 0.86 cm. Quantity and quality of purifiedlectin were calculated by the Bradford microplate method SDS-PAGE gel electrophoresis and human erythrocyte cell(RBC) hemagglutination, respectively.

The analysis of FTIR spectrograms showed that major changes were observed in the fingerprint regions. Besides,due to the dissolution of Sepharose 4B and chitin in the aqueous phase, this difference was not significant in the Imineand Nitrile regions. On the other hand, the comparative results of purification chromatograms showed that increasingthe column length causes a smaller half-width and increases the length of the purified peak. Also, it leads to high-qualitypurified UDA lectin, with a molecular weight of almost 12.5 kDa in gel electrophoresis. Hemagglutination activityon trypsinized red blood cells was displayed, and agglutination of purified UDA lectin started at least at 300 μg.mL-1concentration.

According to our findings, we suggested that dissolving chitin in the polar solvent of Trichloroacetic acid,using Sepharose 4B as the beads of a matrix, and increasing the column length might lead to a decrease in the half-widthof the peak. These can increase the purity and concentration of purified UDA lectin, and speed up the purification process. These findings could be used by researchers to accelerate the purification of UDA lectin in other studies, dealing with drug delivery systems, ELISA techniques, and cell growth.

Myopic regression is a major complication of photorefractive keratectomy (PRK). The rates and causes vary considerably among different studies. This study aimed to investigate myopic regression at six months after myopic PRK.

In this retrospective cohort study, we included all eligible patients with myopia ranging from - 0.75 to - 9 D, aged 18 to 50 years, who underwent PRK by a single surgeon with the availability of preoperative and postoperative data at six months after the initial procedure. All participants underwent comprehensive ophthalmic examinations preoperatively and at six months post-PRK. Overcorrection was planned based on the participant’s age range to achieve the desired refractive result after PRK. All patients received the same postoperative antibiotic and steroid eye drops in a similar dosage regimen, and the contact lenses were removed after complete corneal epithelial healing. Based on the spherical equivalent of refraction six months after PRK, eyes without and with myopic regression were allocated into groups 1 and 2, respectively.

We included 254 eyes of 132 patients who underwent myopic PRK with a mean (standard deviation) age of 30.12 (7.48) years; 82 (62.12%) were women and 50 (37.88%) were men. The frequency of myopic regression was significantly lower in patients with younger age, lower preoperative cylindrical refraction, and lower ablation depth (all P < 0.05). Overcorrection was more successful in eyes with low myopia than in eyes with high myopia (P < 0.05). The highest frequency of myopic regression occurred in eyes with moderate myopia (25.68%), followed by eyes with high myopia (20.0%) and low myopia (6.54%). Among different age groups, patients aged ≤ 30 years had a lower frequency of myopic regression. The frequency of myopic regression in the different age groups was 5.0% at 18 – 20 years, 7.46% at 26 – 30 years, 12.28% at 21 – 25 years, 21.31% at 31 – 35 years, and 26.53% at 36 – 50 years.

Overcorrection was more successful in eyes with low myopia than in eyes with high myopia. The success rate was higher in younger patients with lower astigmatism and ablation depths. Myopic regression was most frequent in eyes with moderate myopia, followed by those with high and low myopia. Further studies should replicate our findings over a longer follow-up period with a larger sample size before generalization is warranted.

Colorectal cancer is one of the most common cancers in the world. Various factors are involved in the development and progression of this disease. One of these agents is cyclooxygenase-2 (COX-2). COX-2 is a product of the PTGS2 gene and converts free arachidonic acid to prostaglandins. COX-2 is not naturally expressed in most normal cells. Noticeably, the increased expression of COX-2 has been observed in chronic inflammatory diseases and various cancers. COX-2 promotes colorectal cancer through various signaling pathways. COX-2 plays its role in colorectal cancer by induction of Bcl-2 expression, and β-catenin pathway activation, and leads to translocate of the NF-κB from the cytoplasm to the nucleus. NF-κB transcription factor plays an important role in physiological processes such as cell proliferation, cell death, and inflammation. Deregulation of NF-κB and its impact on the signaling pathway play a critical role in the development and progression of colorectal cancer. Another factor that plays a role in the development and progression of colorectal cancer is the β-catenin gene. Mutations in the β-catenin gene have been found in more than half of colorectal cancer patients. Bcl-2 is also known as an anti-apoptotic factor in all types of cancers. COX-2 controls all these pathways. Therefore, targeting COX-2 can be proposed as a therapeutic strategy for the treatment of colorectal cancer. The purpose of this review is to investigate the signaling pathways related to COX-2 in colorectal cancer

Recurrent spontaneous abortion (RSA) is one of the causes of infertility following fetus creation. This can lead to the reduction of the fertility rate in various populations. Collagens’ structure, their ratios to each other, and their connections to various receptors are some of the key players in successful fetus implantation. Among them, COL12A1 has a special role because of its very high expression in the uterus. Also, the CD44 protein as a cell adhesion molecule which is a receptor for some of the collagens plays a significant role in RSA. The aim of the study is to investigate the association of CD44-rs13347 and CoL12A1-rs970547 with RSA in a case-control base, and the impacts of COL12A1-rs970547 on protein structure. To genotype single nucleotide polymorphisms (SNPs) of the genes, the PCR-RFLP method was performed on the 124 RSA and 124 control samples. The results were analyzed by the binary-logistic regression method (p-value≤0.05). The SNPs’ effect on the proteins’ structure was analyzed by PSIPRED, HOPE, LOMET, and chimera-USF. Proteins signaling pathway and physical interaction between COL12A1 and CD44 were investigated by KEGG-pathway and GeneMANIA, respectively. Results showed that TT (P= 0.032) genotype of CD44-rs13347 increased the risk of RSA while the CT (P= 0.027) genotype of CD44-rs13347, TT (P= 0.044) genotype, and T (P= 0.019) mutant allele of COL12A1-rs970547 decreased the risk of RSA. Moreover, 3D structures investigation indicated that COL12A1-rs970547 may affect the structure of COL12A1 and its interaction with Integrins. The analysis of the signaling pathway and proteins’ physical interaction network also revealed the interaction of COL12A1 and CD44 with MMP2 and MMP9. On this base, we recommend that T allele of COL12A1-rs970547 has a protective feature against RSA, especially in homozygous form by improving their interaction with Integrins and probably MMPs, too. On the other hand, the CD44-rs13347 probably has an indirect influence on the attachment of the fetus to the extracellular matrix by affecting the MMPs and finally leading to a greater risk of RSA.

Expression of CD44 variant 6 (CD44v6) as a homing-associated cell adhesion molecule (HCAM),hasproved to change most cancer cells. Aim of the study is the effect of mutant allele of CD44 (rs8193C>T),Pum2regulatory element as a prognosis factor of prostate neoplasms: a case-control,in silico studies in the Mazandaranprovince-Iran.

In a case-control study,CD44-rs8193C>T genotyping of the 420 prostate neoplasms (210benign prostatic hyperplasia (BPH) patients,210 prostate cancer patients),150 healthy samples are performedby the touchdown polymerase chain reaction with confronting two-pair primers (PCR-CTPP) method. The T mutantallele effects on the mRNA structure,cell pathways were also investigated in silico methods.

Our results showed that the increase of T mutant allele frequency was significantly associated with BPHcompared with prostate cancer. Furthermore,results showed TT genotype was significantly associated with BPH[odds ratio (OR),0.572,P,0.015],and also influenced the CD44v6 transcript secondary structure,miRNA binding,and regulatory element-binding site for Pum2 protein. Attachment of Pum2 to standard CD44 transcript may lead totranscript isoform-switching,shift-expression to a variety of CD44 isoforms,which can trigger some of the cellsignaling pathways,such as Nanog-Stat,PKC-Nanog,and PKC-Twist.

Based on this,the presence of the T mutant allele of CD44 (rs8193C>T) in the populations may createa regulatory element-binding site for Pum2. So,it could be known as a prognosis factor,prediction of prostateneoplasms. However,more comprehensive studies in different populations (with various ethnicities,large populationsizes),and also CD44v6 gene expression studies in protein,transcript levels are required to confirm our data.

Plantago major L.  is one of the most important medicinal plants used in traditional medicine worldwide. This study was conducted to investigate the effect of ecological and edaphic factors on the active ingredients of this plant. For this purpose, the Plantago major was collected from different regions of Mazandaran province, namely Shorab, Pain Kola, and Panbeh Zar Koti. Phenol and flavonoid levels from acidic methanol extract of plant samples were calculated using standard curve of Gallic acid and Quercetin, respectively. Antioxidant activity of the samples were investigated by three methods of DPPH, Nitric oxide and Reducing power. Our results showed that all of the Plantago major not only have a total phenol, flavonoid content, and antioxidant activity but also they have a biological activity of the extract depends on its phenol and flavonoid content. On the other hand, the antioxidant function of Plantago major species is affected by weather conditions as well as habitat characteristics and edaphic factors. On the basis of these findings, it is suggested that the identification of the potential of the Plantago major extract and selection of optimal phenological habitat and phases is essential and enables the extraction of effective ingredients in the applied of the products and the ability to enhance the medicinal yield of the plants.

Cyclooxygenase-2 (COX-2) main product is Prostaglandin E2 (PGE2) which cause mitogenesis and inflammation. COX-2 is the product of prostaglandin-endoperoxide synthase 2 (PTGS2) gene expression. COX-2 dysregulation can cause angiogenesis, differentiation, and promotion of cancer and its suppression related to control of the tumorchr('39')s size, number, and cell shape. This study focused on the association of COX-2 expression with colorectal carcinoma (CRC) among Iranian patients on mRNA level and in the Cancer Genome Atlas Program (TCGA) colon and rectum RNAseq dataset, and its relation with pathological features.

PTGS2 expression was assayed by quantitative-PCR method from 90 tissue samples collected from 45 participants. The control samples come from the non-tumor area of the same patients. The data analyzed based on ΔΔCq. The PTGS2-RNAseq data extracted and analyzed by UCSC Xena browser, and its association assessed the occurrence of CRC and invasive-features.

PTGS2 showed very significant over-expression in tumor tissues (p< 0.0001) with an N-fold expression of 2.25. But, there was not any significant association between PTGS2 and CRC invasive-pathological features such as Lymphatic, vascular and perineural invasion, the Grades of cancer, and Pathologic-M in both parts of this study.

The increase in PTGS2 is related to the occurrence of CRC among patient samples. But in both part of this study, PTGS2 is not an invasive factor, and it does not affect the cell differentiation of tumors and metastasis. Based on the high N-fold for patient samples, it can be a strong candidate as a CRC initiator biomarker.

In this study, putative interactions between all of the retinoic acid (RA) ligands (all-trans (At), 9-cis (9c), and 13-cis (13c)), and VEGF receptors (VEGFR-1, -2 and -3) were investigated. It was performed considering the glycosylation status of the receptors to achieve a more reliable mode of interactions based on glycomics. We found that RAs may have a higher affinity for ligand-binding domains in VEGFRs. Furthermore, all RA isomers can strongly attach to VEGFR-3 receptor in comparison to other ones. It was also demonstrated that receptor dimerization of RAs may be less targeted. Moreover, regarding post-translational modifications, glycosylated structures showed conflicting binding energies. RAs may target the human vasculature, specifically lymph vessels, through VEGFR-3. In addition, the ligand binding-mediated activation of VEGFRs may be affected by these agents. Also, the glycosylation status of the receptors can interfere with these manners. Furthermore, our results confirmed that the consideration of carbohydrates in crystal structures is essential for a better interpretation of ligand/receptor interactions during drug discovery studies. Even though these observations improved our understanding of the binding patterns of RAs to VEGFRs, validation of these results needs further analysis to introduce these biomolecules as anti-VEGF remedies.