Iranian Biomedical Journal
Volume:24 Issue: 4, Jul 2020

Biobank, defined as a functional unit for facilitating and improving research by storing biospecimen and their accompanying data, is a key resource for advancement in life science. The history of biobanking goes back to the time of archiving pathology samples. Nowadays, biobanks have considerably improved and are classified into two categories: diseased-oriented and population-based biobanks. UK biobank as a population-based biobank with about half a million samples, Biobank Graz as one of the largest biobanks in terms of sample size, and IARC biobank as a specialized WHO cancer agency are few examples of successful biobanks worldwide. The present review provides a history of biobanking, and after presenting different biobanks, we discuss in detail the challenges in the field of biobanking and its future, as well. In the end, ICR biobank, as the first Cancer biobank in Iran established in 1998, is thoroughly described.

TGF-β has long been considered as the main inducer of Tregs in tumor microenvironment and is the reason for the aberrant number of Tregs in tumor-bearing individuals. Recently, it has been suggested that the enzyme arginase I is able to mediate the induction of Tregs in a TGF-β independent fashion. The recombinant WW2/WW3 domains from Smurf2 molecule was demonstrated to increase TGF-β signaling while reducing arginase I gene expression. In this study, we aimed to examine the effects of this recombinant protein on CD4+CD25+/CD4+ proportion in the spleen of 4T1 mammary carcinoma-bearing BALB/c mice.

Flow cytometry was used to evaluate CD4+CD25+ spleen cell populations of the tumor-bearing mice that received WW2/WW3 protein treatment and those of the control group. :

The results indicated a significant rise in CD4+CD25+/CD4+ ratio, along with an average increase in tumor mass of the subjects that underwent protein treatment.

It can be inferred that the heightened CD4+CD25+/CD4+ proportion in the spleen of  protein treated  tumor-bearing mice can be the result of the increased TGF-β signaling despite the reduced arginase I expression.

The most important cause of neurodegeneration in AD is associated with inflammation and oxidative stress. Probiotics are microorganisms that are believed to be beneficial to human and animals. Probiotics reduce oxidative stress and inflammation in some cases. Therefore, this study determined the effects of probiotics mixture on the biomarkers of oxidative stress and inflammation in an AD model of rats.

In this study, 50 rats were allocated to five groups, namely control, sham, and AD groups with Aβ1-40 intra-hippocampal injection, as well as AD + rivastigmine and  AD + probiotics groups with Aβ1-40 intra-hippocampal injection and 2 ml (1010 CFU) of probiotics (Lactobacillus reuteri, Lactobacillus rhamnosus, and Bifidobacterium infantis) orally once a day for 10 weeks. MWM was used to assess memory and learning. To detect Aβ plaque, Congo red staining was used. Oxidative stress was monitored by measuring the MDA level and SOD activity, and to assess inflammation markers (IL-1β and TNF-α) in the hippocampus, ELISA method was employed.

Spatial memory improved significantly in treatment group as measured by MWM. Probiotics administration reduced Aβ plaques in AD rats. MDA decreased and SOD increased in the treatment group. Besides, probiotics reduced IL-1β and TNF-α as inflammation markers in the AD model of rats.

Our data revealed that probiotics are helpful in attenuating inflammation and oxidative stress in AD.

Numerous studies confirmed significant decrease in tissue DCN expression is associated to tumor progression and metastasis in certain types of cancer including PC. However, the potential prognostic value of tissue DCN in PC has not yet been investigated.

A total number of 40 PC and 42 patients with BPH were investigated for the expression levels of DCN in their prostatic tissues using real-rime qPCR and immunohistochemical analyses. Urinary and plasma DCN levels were also measured by ELISA.

Despite no significant changes in the mean of urine and plasma DCN concentrations between the two study groups, tissue DCN mRNA was found to be 5.5fold lower in cancer than BPH (p = 0.0001). Similarly, the stained DCN levels appeared significantly lower in cancer patients with higher Gleason Scores (8 and 9, n = 6) than those with lower Gleason Scores (6 and 7, n = 26), with a p value of 0.049.

Here, we report, for the first time, that urine and plasma DCN does not seem to have a diagnostic value in PC, while tissue DCN could potentially be used as a prognostic marker in PC.

Through combining two synthetic and natural polymers, scaffolds can be developed for tissue engineering and regenerative medicine purposes.

In this work, CMC (20%) was grafted to PCL nanofibers using the cold atmospheric plasma of helium. The PCL scaffolds were exposed to CAP, and functional groups were developed on the PCL surface.

The results of FTIR confirmed CMC (20%) graft on PCL scaffold. The MTT assay showed a significant enhancement (p < 0.05) in the cell affinity and proliferation of ADSCs to CMC20%-graft-PCL scaffolds. After 14 days, bone differentiation was affirmed through alizarin red and calcium depositions.

Based on the results, the CMC20%-graft-PCL can support the proliferation of ADSCs and induce the differentiation into bone with longer culture time.

Our previous findings indicated that carvacrol and thymol alleviate cognitive impairments caused by Aβ in rodent models of AD. In this study, the neuroprotective effects of carvacrol and thymol against Aβ25-35-induced cytotoxicity were evaluated, and the potential mechanisms were determined.

PC12 cells were pretreated with Aβ25-35 for 2 h, followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by MTT method. A flurospectrophotometer was employed to observe the intracellular ROS production. PKC activity was analyzed using ELISA.

Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Aβ25-35-induced cytotoxicity. Furthermore, Aβ25-35 could induce intracellular ROS production, while carvacrol and thymol could reverse this effect. Moreover, our findings showed that carvacrol and thymol elevate PKC activity similar to Bryostatin-1, as a PKC activator.

This study provided the evidence regarding the protective effects of carvacrol and thymol against Aβ25–35-induced cytotoxicity in PC12 cells. The results suggested that the neuroprotective effects of these compounds against Aβ25-35 might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein. Thus, carvacrol and thymol were found to have therapeutic potential in preventing or modulating AD.

The present study aimed to evaluate the effects of different concentrations of CONPs on the OS status in kidney, lung, and serum of rats.

 Male Wistar Rats were treated intraperitoneally with 15, 30,  and 60 mg/kg/day of CONPs. The biochemical parameters, including TAC, TTG, MDA, SOD, and CAT were assayed in serum, kidney, and lung tissues.

MDA decreased, but TTG and CAT increased in serum by the administration of CONPs at 15 mg/kg. In kidney homogenate obtained from the group treated with CONPs at 15 mg/kg, TAC, TTG, and CAT significantly increased compared to the control group. However, CONPs at 15, 30, and 60 mg/kg significantly decreased MDA level compared to the control group. In lung tissue, CONPs in doses of 15, 30 and 60 mg/kg significantly decreased CAT activity, TTG and TAC compared to the control group, while in kidney tissue, CONPs at the concentrations of 30 and 60 mg/kg significantly increased MDA compared to the control group.

Our findings suggest that CONPs attenuate OS in the kidney and affect the serum levels of OS-related markers but induce OS in the lung tissue in a dose-dependent manner.

The clinical phenotyping of patients with achromatopsia harboring variants in PDE6C has poorly been described in the literature. PDE6C encodes the catalytic subunit of the cone phosphodiesterase, which hydrolyzes the cGMP that proceeds with the hyperpolarization of photoreceptor cell membranes, as the final step of the phototransduction cascade.

In the current study, two patients from a consanguineous family underwent full ophthalmologic examination and molecular investigations including WES. The impact of the variant on the functionality of the protein has been analyzed using in silico molecular modeling.

The patients identified with achromatopsia segregated a homozygous missense variant (c.C1775A:p.A592D) in PDE6C gene located on chromosome 10q23. Molecular modeling demonstrated that the variant would cause a protein conformational change and result in reduced phosphodiesterase activity.

Our data extended the phenotypic spectrum of retinal disorders caused by PDE6C variants and provided new clinical and genetic information on achromatopsia.