Iranian Biomedical Journal
Volume:28 Issue: 1, Jan 2024

The present study aims to provide an insight to the comprehensive efforts of Pasteur Institute of Iran (PII) regarding COVID-19 management, research, achievements, and vaccine production, though there are many challenges. The relevant literature review was investigated through national and international database and also reports from the related research departments. Six strategies were taken by PII to manage the pandemic of COVID-19. While this pandemic has been hopefully controlled, SARS-CoV-2 could still be a potential threat. Therefore, COVID-19 data management and updated studies, as well as long-term safety and efficacy of the SARS-CoV-2 vaccines are still on the agenda.

Celiac disease is a complex disorder influenced by genetic and environmental factors. When people with a genetic predisposition to CD consume gluten, an inflammatory response is triggered in the small intestine, and this reaction can be alleviated by the elimination of gluten from the diet. The clinical manifestations of CD vary greatly from person to person and begin at a young age or in adulthood. Influence of genetic factors on CD development is evident in carriers of the DQ2 and/or DQ8 allele. HLA genotypes are associated with gut colonization by bacteria, particularly in individuals suffering from CD. In addition, beneficial gut microbes are crucial for the production of DPP-4, which plays a key role in immune function, as well as metabolic and intestinal health. Therefore, probiotics have been recommended as a complementary food supplement in CD.

Simvastatin has anti-inflammatory and antioxidant properties against cardiac I/RI. However, it suffers from low bioavailability and a short half-life. Nanoniosomes are novel drug delivery systems that may increase SIM effectiveness. The present research evaluates the impact of SIM-loaded nanoniosomes on the OGD/R injury model of H9c2 cells.

Cells were seeded based on five groups: (1) control; (2) OGD/R; (3) OGD/R receiving SIM; (4) OGD/R receiving nanoniosomes; and (5) OGD/R receiving SIM‑loaded nanoniosomes. OGD/R injury of the H9c2 cells was treated with SIM or SIM‑loaded nanoniosomes. Cell viability, two inflammatory factors, necroptosis factors, along with HMGB1 and Nrf2 gene expressions were assessed.

The cells treated with SIM‑loaded nanoniosomes showed a significant elevation in the cell viability and a reduction in HMGB1, Nrf2, TNF-α, IL-1β, RIPK1, and ROCK1 expression levels compared to the OGD/R and SIM groups.

Based on our findings, nanoniosomes could safely serve as a drug delivery system to counterbalance the disadvantages of SIM, resulting in improved aqueous solubility and stability.

DDR1 signaling plays a critical role in various cellular functions. Increased DDR1 expression has been shown in different human cancers.t-DARPP is a truncated isoform of DARPP-32, and its upregulation promotes cell survival and migration. Most lung cancer patients have NSCLC, and their survival rate is low. Therefore, it is necessary to study new and effective targeted therapies. Increased t-DARPP expression in NSCLC patients is associated with patient survival and can act as a prognostic marker correlated with increasing stages of NSCLC. The current study aimed to evaluate alteration in DDR1 expression and its effects on t-DARPP expression in NSCLC.

Two human lung adenocarcinoma cell lines, A549 and Calu-3, were treated with collagen type I and transfected with DDR1 siRNA. The relative expression of DDR1 and t-DARPP was evaluated using qRT-PCR.

The results indicated that collagen type I could stimulate DDR1 expression in NSCLC cells. Also, DDR1 upregulation resulted in a significant increase in t-DARPP expression. In contrast, suppression of DDR1 expression significantly decreased t-DARPP expression.

Our findings propose that modification in the expression of DDR1, caused by collagen type I and siRNA, might influence the expression of t-DARPP in NSCLC that is linked to NSCLC progression. Moreover, this alteration could potentially serve as an innovative target for therapeutic intervention.

HERV-K env is associated with several neurological disorders, including MS. Clinical studies have demonstrated a plausible interaction between HERV-K env and other MS risk factors. The present study aimed to investigate the possible association between HERV-K18 env and TGF-β. We further assessed the in vitro effect of EBV infection on HERV-K18 env expression in the presence and absence of vitamin D in MS patients.

PBMCs from 20 MS patients and 20 healthy controls were infected with the B95.8 EBV, seeded into 24-well plates and incubated in the presence or absence of 100 nM of 1,25(OH)D3. The expression levels of HERV-K18 env and TGF-β were measured using real-time PCR.

While the expression level of HERV-K18 env was significantly higher in MS patients than the healthy controls, this trend for TGF-β was significantly reverse. Interestingly, an inverse correlation was found between HERV-K18 env and TGF-β expression in MS patients, although the in vitro stimulation of PBMCs with EBV and vitamin D showed no significant differences in terms of HERV-K18 expression.

Our findings highlight the potential role of HERV-K18 env in MS patients.

 The surface properties of dental and orthopedic implants are directly related to their osseointegration rate. Coating and/or modifying the implant surface might reduce the time of healing. In this study, we aimed to examine the effects of a hybrid surface consisting of a brushite surface coating and cross-linked water-soluble eggshell membrane protein on the osseointegration of Ti screws under in vivo conditions.

  Twenty Ti alloy screws were implanted monocortically in anteromedial regions of New Zealand rabbit tibiae. Ten screws were untreated and used as controls. The remaining 10 screws were coated with calcium phosphate and following cross-linked with ostrich eggshell membrane protein. All rabbits were sacrificed six weeks after the surgery. Peri-screw tissues were evaluated by µ-CT, histological and histomorphometrical methods. 

 The μ-CT assessments indicated that the experimental group had significantly higher mean BSA and TbN than those of the control group (p ˂ 0.05). BV, TbSp, TbTh and BMD scores of the control and experimental groups were quite similar (p > 0.05). The vascularization score of the experimental group was significantly higher than the control group (4.29 vs. 0.92%). No sign of the graft-versus-host reaction was observed.

  Our findings reveal that coating Ti alloy implants with calcium phosphate cross-linked with strich eggshell membrane protein increases the osseointegration of Ti alloy screws by increasing the bone surface area, number of trabeculae and vascularization in the implant site.

The potential anticancer effect of melittin has motivated scientists to find its exact molecular mechanism of action. There are few data on the effect of melittin on the UPR and autophagy as two critical pathways involved in tumorigenesis of colorectal and drug resistance. This study aimed to investigate the effect of melittin on these pathways in the CRC HCT116 cells.

MTT method was carried out to assess the cytotoxicity of melittin on the HCT116 cell line for 24, 48, and 72 h. After selecting the optimal concentrations and treatment times, the gene expression of autophagy flux markers (LC3-βII and P62) and UPR markers (CHOP and XBP-1s) were determined using qRT-PCR. The protein level of autophagy initiation marker (Beclin1) was also determined by Western blotting.

MTT assay showed a cytotoxic effect of melittin on the HCT116 cells. The increase in LC3-βII and decrease in P62 mRNA expression levels, along with the elevation in the Beclin1 protein level, indicated the stimulatory role of melittin on the autophagy. Melittin also significantly enhanced the CHOP and XBP-1s expressions at mRNA level, suggesting the positive role of the melittin on the UPR activation.

This study shows that UPR and autophagy can potentially be considered as two key signaling pathways in tumorigenesis, which can be targeted by the BV melittin in the HCT116 cells. Further in vivo evaluations are recommended to verify the obtained results.

MiR-34a and miR-126 mainly act as tumor suppressors and are often downregulated in various cancers, including NSCLC. We aimed to determine the methylation status of miR-34a and miR-126 in NSCLC patients.

The current study included 63 paraffin-embedded NSCLC and paired adjacent normal tissues. After DNA extraction and bisulfite treatment, the methylation status of miR-34a and miR-126 were evaluated using the MSP method.

There was no statistically significant difference between tumor and normal tissues regarding the methylation status of miR-34a and miR-126 (p > 0.05). Moreover, we found no significant correlation between the methylation status of miR-34a and miR-126 with patients’ demographic parameters, including gender, age, and pathology subtype (p > 0.05).

Considering the low expression of mir-126 and mir-34 in NSCLC, more sensitive methods are recommended to be exploited for detecting the level of methylation or underlying mechanisms other than promoter hypermethylation in silencing these genes in NSCLC.