Predictors of major adverse cardiac and cerebrovascular events after percutaneous coronary intervention in older adults: a systematic review and meta-analysis.

AIM: We systematically reviewed and meta-analyzed the predictors of major adverse cardiac and cerebrovascular events (MACE/MACCE) in older adults who underwent PCI. METHODS: Three databases, PubMed, Embase, and Scopus, were searched for observational studies considering the out-of-hospital MACE/MACCE in adults ≥ 60 years old with coronary artery disease (acute or chronic) who underwent PCI. Studies were eligible if they had determined at least two statistically significant predictors of MACE/MACCE by multivariable analysis. We used the QUIPS tool to evaluate the risk of bias in the studies. Random-effects meta-analysis was utilized to pool the hazard ratios (HRs) of the most reported predictors. RESULTS: A total of 34 studies were included in the review. Older age (HR = 1.04, 95% Confidence Interval (CI): 1.03-1.06, P-value < 0.001), diabetes (HR = 1.36, 95% CI: 1.22-1.53, P < 0.001), history of myocardial infarction (MI) (HR = 1.88, 95% CI: 1.37-2.57, P < 0.001), ST-elevation MI (STEMI) at presentation (HR = 1.72, 95% CI: 1.37-2.18, P < 0.001), reduced left ventricular ejection fraction (LVEF) (HR = 2.01, 95% CI: 1.52-2.65, P < 0.001), successful PCI (HR = 0.35, 95% CI: 0.27-0.47, P < 0.001), eGFR (HR = 0.99, 95% CI: 0.97-1.00; P-value = 0.04) and left main coronary artery (LMCA) disease (HR = 2.07, 95% CI: 1.52-2.84, P < 0.001) were identified as predictors of MACE. CONCLUSION: We identified older age, diabetes, history of MI, STEMI presentation, lower LVEF, and LMCA disease increased the risk of MACE/MACCE after PCI in older adults. Meanwhile, higher eGFR and successful PCI predicted lower adverse events risk. Future studies should focus on a more robust methodology and a precise definition of MACE. REGISTRATION: PROSPERO (CRD42023480332).

Non-coding RNAs are correlated to TGF-ß receptor type 2 in patients with colorectal cancer.

BACKGROUND: Multiple molecular expression alterations, particularly in non-coding RNAs, play fundamental roles in the regulations of cellular processes and may relate to the occurrence and progression of colorectal cancer (CRC). In the present study, we investigated the associations between TGFBR2, miR20a-5p and long non-coding RNA (lncRNA) LAMTOR5-AS1 in CRC patients. METHODS: Colorectal cancer and adjacent normal tissue samples (n = 34) were prepared from CRC patients. The associations between TGFBR2, miR20a-5p and lncRNA LAMTOR5-AS1 were predicted using bioinformatics tools. The expression levels of TGFBR2, miR20a-5p and lncRNA LAMTOR5-AS1 were measured using a quantitative real-time polymerase chain reaction technique. The TGFBR2 protein values were measured by western blotting. The clinical importance of lncRNA LAMTOR5-AS1 was assessed using receiver operating characteristic curve. RESULTS: The up-regulated levels of TGFBR2 (p = 0.02), TGFBR2 protein (p = 0.008) and lncRNA LAMTOR5-AS1 (p = 0.02) were significantly observed in CRC tissues compared to the adjacent normal tissues. The miR20a-5p expression level (p = 0.009) was downregulated in CRC tissues. In addition, the miR20a-5p expression level was inversely correlated to the TGFBR2 gene (r2  = 0.88, p < 0.0001), protein (r2  = 0.95, p < 0.0001) and lncRNA LAMTOR5-AS1 gene (r2  = 0.93, p < 0.0001) expression levels. Based on the area under curve, the increase of lncRNA LAMTOR5-AS1 expression level with a sensitivity of 64.52% and specificity of 65.52% was considered in CRC patients. CONCLUSIONS: We propose that miR20a-5p is inversely related to long non-coding RNA (lncRNA) LAMTOR5-AS, such that it may be involved in the regulation of TGFBR2 expression level in CRC patients.

Cellular crosstalk in atherosclerotic plaque microenvironment.

Atherosclerosis is an underlying pathology of many vascular diseases as a result of cellular, structural and molecular dysfunctions within the sub-endothelial space. This review deals with the events involved in the formation, growth and remodeling of plaque, including the cell recruitment, cell polarization, and cell fat droplets. It also describes cross talking between endothelial cells, macrophages, and vascular smooth muscle cells, as well as the cellular pathways involved in plaque development in the plaque microenvironment. Finally, it describes the plaque structural components and the role of factors involved in the rupture and erosion of plaques in the vessel. Video Abstract.

Ferulic acid exerts a protective effect against cyclosporine-induced liver injury in rats via activation of the Nrf2/HO-1 signaling, suppression of oxidative stress, inflammatory response, and halting the apoptotic cell death.

Drug-induced liver injury is one of the main challenges that leads to the withdrawal of several drugs in the clinical setting. Cyclosporine is one of the drugs that its long-term administration exerts devastating effects on the hepatocytes. In the present study, we aimed to evaluate the effect of ferulic acid, a natural compound found in plants, on cyclosporine-mediated hepatotoxicity. Forty-eight male Wistar rats were treated with cyclosporine and/or ferulic acid to evaluate the function as well as the morphology of liver cells. We found that ferulic acid dose-dependently recovered the functional as well as histopathological parameters of liver cells, as revealed by the improvement of hepatocellular vacuolation, portal fibroplasia, and necrosis. Moreover, this phenolic compound was able to restore the balance of the redox system in cyclosporine-treated rats by activating the nuclear factor (NF) erythroid 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling axis. Of note, the protective effects of ferulic acid against cyclosporine-mediated liver toxicity were not restricted only to induction of the potential antioxidant property, as in the presence of this agent, the expression of pro-inflammatory cytokines such as NF-κB, tumor necrosis factor (TNF)-α, and interleukin-1ß was also diminished. Ferulic acid also shifted the equilibrium between the expression levels of proapoptotic to antiapoptotic proteins and thereby prevented the development of cyclosporine-induced liver injury. Overall, these findings highlighted that ferulic acid can reduce cyclosporine-induced liver injury due to its antioxidant properties.

Payment systems for dialysis and their effects: a scoping review.

BACKGROUND: End stage renal disease (ESRD) is a major health concern and a large drain on healthcare resources. A wide range of payment methods are used for management of ESRD. The main aim of this study is to identify current payment methods for dialysis and their effects. METHOD: In this scoping review Pubmed, Scopus, and Google Scholar were searched from 2000 until 2021 using appropriate search strategies. Retrieved articles were screened according to predefined inclusion criteria. Data about the study characteristics and study results were extracted by a pre-structured data extraction form; and were analyzed by a thematic analysis approach. RESULTS: Fifty-nine articles were included, the majority of them were published after 2011 (66%); all of them were from high and upper middle-income countries, especially USA (64% of papers). Fee for services, global budget, capitation (bundled) payments, and pay for performance (P4P) were the main reimbursement methods for dialysis centers; and FFS, salary, and capitation were the main methods to reimburse the nephrologists. Countries have usually used a combination of methods depending on their situations; and their methods have been further developed over time specially from the retrospective payment systems (RPS) towards the prospective payment systems (PPS) and pay for performance methods. The main effects of the RPS were undertreatment of unpaid and inexpensive services, and over treatment of payable services. The main effects of the PPS were cost saving, shifting the service cost outside the bundle, change in quality of care, risk of provider, and modality choice. CONCLUSION: This study provides useful insights about the current payment systems for dialysis and the effects of each payment system; that might be helpful for improving the quality and efficiency of healthcare.

Effects of myo-inositol plus folic acid on ovarian morphology and oocyte quality in PCOS mouse model.

Although the role of myo-inositol (MYO) in promoting the oocyte quality of PCOS patients has been documented in human studies; the cellular effects of this supplement on oocytes have not been directly examined due to ethical limitations. In the first phase of this study, MYO dosimetry was carried out simultaneously with the PCOS model development. An effective dose was obtained following the assessment of fasting insulin and testosterone levels using ELISA and ovarian morphology appraisal by histopathology. In the second phase, following the continuous administration of the effective dose of MYO and dehydroepiandrosterone (DHEA), cellular evaluation was performed. The quality of oocytes from superovulation was analyzed by examining maturity and normal morphology percentage using a stereomicroscope, intracellular reactive oxygen species (ROS) and glutathione (GSH) levels using fluorometry, and ATP count evaluation using ELISA. The results revealed that, among the four different MYO concentrations, the 0.36 mg/g dose compared with the DHEA group reduced testosterone levels and large atretic antral follicles (LAtAnF) diameter. This dose also increased the corpus luteum count and the granulosa:theca (G/T)layer thickness ratio in antral follicles. Furthermore, this dose increased mature oocytes and normal morphology percentage, ATP count, and GSH levels; however, it decreased ROS levels in mature oocytes. Our findings provide the grounds for further cellular and molecular studies on the PCOS mouse model, suggesting that the improvement in mitochondrial function and its antioxidant properties is probably one of the mechanisms by which MYO increases oocyte quality.

GABBR2 as a Downstream Effector of the Androgen Receptor Induces Cisplatin Resistance in Bladder Cancer.

The precise molecular mechanisms responsible for resistance to cisplatin-based chemotherapy in patients with bladder cancer remain elusive, while we have indicated that androgen receptor (AR) activity in urothelial cancer is associated with its sensitivity. Our DNA microarray analysis in control vs. AR-knockdown bladder cancer sublines suggested that the expression of a GABA B receptor GABBR2 and AR was correlated. The present study aimed to determine the functional role of GABBR2 in modulating cisplatin sensitivity in bladder cancer. AR knockdown and dihydrotestosterone treatment considerably reduced and induced, respectively, GABBR2 expression, and the effect of dihydrotestosterone was at least partially restored by an antiandrogen hydroxyflutamide. A chromatin immunoprecipitation assay further revealed the binding of AR to the promoter region of GABBR2 in bladder cancer cells. Meanwhile, GABBR2 expression was significantly elevated in a cisplatin-resistant bladder cancer subline, compared with control cells. In AR-positive bladder cancer cells, knockdown of GABBR2 or treatment with a selective GABA B receptor antagonist, CGP46381, considerably enhanced the cytotoxic activity of cisplatin. However, no additional effect of CGP46381 on cisplatin-induced growth suppression was seen in GABBR2-knockdown cells. Moreover, in the absence of cisplatin, CGP46381 treatment and GABBR2 knockdown showed no significant changes in cell proliferation or migration. These findings suggest that GABBR2 represents a key downstream effector of AR signaling in inducing resistance to cisplatin treatment. Accordingly, inhibition of GABBR2 has the potential of being a means of chemosensitization, especially in patients with AR/GABBR2-positive bladder cancer.

Is the severity of alopecia areata associated with arterial stiffness?

Background: This study aimed to evaluate the severity of alopecia areata (AA) associations with metabolic syndrome, body composition evaluated by bioimpedance techniques, and arterial stiffness based on pulse-wave velocity analysis. Materials and Methods: This cross-sectional study was conducted on patients referred to AA Clinic at Razi Hospital in 2021 and 2022. Patients with AA with the Severity of Alopecia Tool (SALT) score above 20% and receiving no systemic therapy were included. Patient demographic and clinical information, symptoms of metabolic syndrome, and bioimpedance factors were collected, and the relationship between disease severity, metabolic syndrome, and bioimpedance indicators was evaluated. Results: In this study, 59 patients were examined, with 26 (44.07%) being female and 33 (55.93%) being male. The mean age of the patients was 37.42 years (standard deviation [SD] =11.28). The severity of the disease was assessed using the SALT score, with the mean severity in terms of the percentage being 69.83% (SD = 28.57%). In the regression model, SALT score was independently related to the severity of vascular stiffness after adjusting for the effect of other variables (beta = 0.033, 95% CI = 0.009-0.057, P = 0.046). Moreover, SALT score was significantly related to metabolic syndrome after adjusting for the effect of other variables (OR = 1.035, 95% CI = 1.012-1.059, P = 0.002). Conclusion: This study found that AA severity is associated with a higher chance of having metabolic syndrome and arterial stiffness which may lead to cardiovascular diseases in patients with AA, and screening patients regarding cardiometabolic diseases is mandated.

Upregulation of TGF-ß type II receptor in high glucose-induced vascular smooth muscle cells.

BACKGROUND: Mortality in patients with diabetes mellitus is estimated above 65% due to cardiovascular diseases. The aim of study was to investigate the effects of high-glucose conditions on TGF-ß type II receptor (TGFBR2) expression levels, cell viability, and migration rate in vascular smooth muscle cells (VSMCs). METHODS: VSMCs were incubated in 30 mM and 50 mM of glucose for 24 h, 48 h, and 72 h periods. The gene and protein expression levels were investigated by Real-time qRT-PCR and western blotting techniques, respectively. The cell viability was evaluated by MTT assay. VSMC migration rate was also studied by wound healing assay. RESULTS: The TGFBR2 gene and protein expression levels were significantly upregulated in all the groups treated with glucose in 24 h, 48 h, and 72 h periods. The cell viability was not significantly affected in values of 30 mM and 50 mM of glucose. The increase of migration rate of VSMCs was not significant. CONCLUSION: The results suggested the increased expression levels of TGFBR2 in the response to high glucose conditions may modulate the cellular events through the signaling pathway network in VSMCs.

New-onset acute ischemic stroke following COVID-19: A case-control study.

Background: Neurological manifestations of coronavirus disease 2019 (COVID-19) have been highlighted. COVID-19 potentially increases the risk of thromboembolism. We aimed to compare patients with COVID-19 with and without new-onset acute ischemic stroke (AIS). Materials and Methods: In this single-center retrospective case-control study, demographics, clinical characteristics, laboratory findings, and clinical outcomes were compared between 51 patients with both COVID-19 and AIS (group A) and 160 patients with COVID-19 and without AIS (group B). Results: Patients in group A were significantly older, more likely to present with critical COVID-19 (P = 0.004), had higher rates of admission in the intensive care unit (P < 0.001), more duration of hospitalization (P < 0.001), and higher in-hospital mortality (P < 0.001). At the time of hospitalization, O2 saturation (P = 0.011), PH (P = 0.04), and HCO3 (P = 0.005) were lower in group A. White blood cell count (P = 0.002), neutrophil count (P < 0.001), neutrophil-lymphocyte ratio (P = 0.001), D-Dimer (P < 0.001), blood urea nitrogen (BUN) (P < 0.001), and BUN/Cr ratio (P < 0.001) were significantly higher in patients with AIS. Conclusion: Stroke in COVID-19 is multifactorial. In addition to conventional risk factors of ischemic stroke (age and cardiovascular risk factors), we found that patients with more severe COVID-19 are more prone to ischemic stroke. Furthermore, leukocyte count, neutrophil count, neutrophil-lymphocyte ratio, D-Dimer, BUN, and BUN/Cr ratio were higher in patients with AIS following COVID-19 infection.

Comparison of Optic Nerve Sheath Diameter (ONSD) in Low-Pressure Versus Normal Pressure Pneumoperitoneum in Laparoscopic Cholecystectomy: A Randomized Clinical Study.

Background: Low pressure laparoscopic cholecystectomy has been advocated due to reduction in postoperative pain, ventilation problems, hemodynamic complications, and potential for reduction in surgical events. No reported data have been found focusing on the effects of low-pressure laparoscopic cholecystectomy on intracranial pressure (ICP). The aim of this study was to investigate the effect of low-pressure laparoscopic cholecystectomy on intracranial pressure measured by optic nerve sheath diameter (ONSD) in Imam Hossein Medical Center, Tehran, Iran. Methods: The patients classified as American Society of Anesthesiologists physical status I or II undergoing elective laparoscopic cholecystectomy due to benign gallbladder disease were randomly assigned to low-pressure laparoscopy (LPL) group or normal pressure laparoscopy group (NPL). ONSD was measured at 3 different times: (1) before induction of anesthesia; (2) after initiation of gas insufflation; and (3) after the termination of gas insufflation. The collected data were entered into SPSS software (V 24). Data were demonstrated with frequency (percentage) or mean ± standard deviation. We used the Mann-Whitney test to compare the means of continuous variables. The Friedman test was used to compare the mean of variables over time in each of the 2 groups. The significance level in all analyses was considered at ˂0.05. Results: ONSD after the termination of gas insufflation was significantly lower in the LPL group with the mean of 4.97±0.83 mm than the NPL group with the mean of 5.62±1.32 mm (p=0.018). ONSD before induction of anesthesia or immediately after gas insufflation did not differ significantly between LPL and NPL groups. Duration of anesthesia and surgery, mean arterial pressure, the total dose of propofol (p=0.600), and fentanyl (p=0.201) did not show significant differences between the 2 groups. Conclusion: ONSD was lower with low-pressure laparoscopic cholecystectomy after the termination of gas insufflation, which emphasized the neural protective effect of low intraperitoneal pressure. Further studies are needed to evaluate this diagnostic tool in different populations, especially in patients with increased ICP undergoing laparoscopic interventions.

miR-181b and miR-204 suppress the VSMC proliferation and migration by downregulation of HCK.

BACKGROUND: VSMC proliferation and migration pathways play important roles in plaque formation in the vessel stenosis and re-stenosis processes. The microRNAs affect the expression of many genes that regulate these cellular processes. The aim of this study was to investigate the effects of miR-181b, miR-204, and miR-599 on the gene and protein expression levels of hematopoietic cell kinase (HCK) in VSMCs. METHODS: miR-181b, miR-204 were predicted for the suppression of HCK in the chemokine signaling pathway using bioinformatics tools. Then, the VSMCs were transfected by PEI-containing microRNAs. The HCK gene and protein expression levels were evaluated using RT-qPCR and Western blotting techniques, respectively. Moreover, the cellular proliferation and migration were evaluated by MTT and scratch assay methods. RESULTS: The miR-181b and miR-204 decreased significantly the HCK gene and (total and phosphorylated) protein expression levels. Also, the miR-599 did not show any significant effects on the HCK gene and protein levels. The data also showed that miR-181b, miR-204, and miR-599 prevent significantly the proliferation and migration of VSMCs. CONCLUSION: The downregulation of HCK by miR-181b and miR-204 suppressed the VSMC proliferation and migration.

Overexpression of DDIT4 and TPTEP1 are associated with metastasis and advanced stages in colorectal cancer patients: a study utilizing bioinformatics prediction and experimental validation.

BACKGROUND: Various diagnostic and prognostic tools exist in colorectal cancer (CRC) due to multiple genetic and epigenetic alterations causing the disease. Today, the expression of RNAs is being used as prognostic markers for cancer. METHODS: In the current study, various dysregulated RNAs in CRC were identified via bioinformatics prediction. Expression of several of these RNAs were measured by RT-qPCR in 48 tissues from CRC patients as well as in colorectal cancer stem cell-enriched spheroids derived from the HT-29 cell line. The relationships between the expression levels of these RNAs and clinicopathological features were analyzed. RESULTS: Our bioinformatics analysis determined 11 key mRNAs, 9 hub miRNAs, and 18 lncRNAs which among them 2 coding RNA genes including DDIT4 and SULF1 as well as 3 non-coding RNA genes including TPTEP1, miR-181d-5p, and miR-148b-3p were selected for the further investigations. Expression of DDIT4, TPTEP1, and miR-181d-5p showed significantly increased levels while SULF1 and miR-148b-3p showed decreased levels in CRC tissues compared to the adjacent normal tissues. Positive relationships between DDIT4, SULF1, and TPTEP1 expression and metastasis and advanced stages of CRC were observed. Additionally, our results showed significant correlations between expression of TPTEP1 with DDIT4 and SULF1. CONCLUSIONS: Our findings demonstrated increased expression levels of DDIT4 and TPTEP1 in CRC were associated with more aggressive tumor behavior and more advanced stages of the disease. The positive correlations between TPTEP1 as non-coding RNA and both DDIT4 and SULF1 suggest a regulatory effect of TPTEP1 on these genes.

Correlations between vitronectin, miR-520, and miR-34 in patients with stenosis of coronary arteries.

BACKGROUND: In-stent restenosis usually occurs by platelet activation, neointima formation, VSMC migration, and proliferation in the position of the vessel stent. The monocytes have a magnificent role in neointimal hyperplasia since these cells recruit to the site of vessel injury through chemokines and other secretion proteins. This study is focused on the investigation of vitronectin, miR-193, miR-34, and miR-520 expression levels in PBMCs isolated from stenosed patients. METHODS: A total of sixty subjects undergoing coronary artery angiography containing patients with stent no restenosis (n = 20), in-stent restenosis (n = 20), and healthy participants (n = 20) participated in the study. The vitronectin, miR-193, miR-34, and miR-520 expression levels were measured by the RT-qPCR technique. Data were analyzed by SPSS software. RESULTS: The vitronectin, miR-34, and miR-520 expression levels changed significantly in patients with vessel in-stent restenosis (p = 0.02, p = 0.02, and p = 0.01, respectively). Furthermore, there were inverse correlations between the expression levels of vitronectin gene and miR-34 (r = - 0.44, p = 0.04) as well as miR-520 (r = - 0.5, p=0.01). CONCLUSIONS: The molecular events in the vessel stenosis may be affected by targeting vitronectin with miR-520 and miR-34.

Adhesion of monocytes and endothelial cells isolated from the human aorta suppresses by miRNA-PEI particles.

BACKGROUND: Knowledge of stenosis in coronary arteries requires an understanding of the cellular and molecular processes that occur throughout the leukocyte rolling process. In this study, the roles of miR-125a-5p and miR-495-3p were investigated on the adhesion of endothelial cells (ECs) isolated from the human aorta. METHODS: Human primary endothelial cells were obtained from the aorta of people who had died of brain death. Whole blood was used to isolate the monocytes. The miR-125 and miR-495 were predicted and transfected into ECs using Poly Ethylene Imine (PEI). The expression levels of adhesion molecules and monocyte recruitment were identified by the RT-qPCR technique and Leukocyte-Endothelial Adhesion Assay kit, respectively. RESULTS: The ICAM-1, ICAM-2 and VCAM-1 expression levels decreased significantly in the miR-495/PEI-transfected ECs (P < 0.05) while in the miR-125/PEI-transfected ECs only the ICAM-2 and ITGB-2 expression levels decreased significantly (P < 0.05) as compared to the miR-synthetic/PEI-transfected ECs. Furthermore, the monocyte adhesion was decreased in the miR-125 and miR-mix/PEI-transfected ECs as compared to the miR-synthetic/PEI-transfected ECs (P = 0.01 and P = 0.04, respectively). CONCLUSION: According to the findings, the efficient relations between miR-125 and adhesion molecules may be responsible for the inhibition of monocyte rolling.

Design and synthesis of novel quinazolinone-pyrazole derivatives as potential α-glucosidase inhibitors: Structure-activity relationship, molecular modeling and kinetic study.

In this study, a new series of quinazolinone-pyrazole hybrids were designed, synthesized and screened for their α-glucosidase inhibitory activity. The results of the in vitro screening indicated that all the molecular hybrids exhibited more inhibitory activity (IC50 values ranging from 60.5 ± 0.3 µM-186.6 ± 20 µM) in comparison to standard acarbose (IC50 = 750.0 ± 10.0 µM). Limited structure-activity relationship suggested that the variation in the inhibitory activities of the compounds affected by different substitutions on phenyl rings of diphenyl pyrazole moiety. The enzyme kinetic studies of the most potent compound 9i revealed that it inhibited α-glucosidase in a competitive mode with a Ki of 56 µM. Molecular docking study was performed to predict the putative binding interaction. As expected, all pharmacophoric moieties used in the initial structure design playing a pivotal role in the interaction with the binding site of the enzyme. In addition, by performing molecular dynamic investigation and MM-GBSA calculation, we investigated the difference in structural perturbation and dynamic behavior that is observed over α-glycosidase in complex with the most active compound and acarbose relative to unbound α-glycosidase enzyme.

In vitro degradation of low-density polyethylene by new bacteria from larvae of the greater wax moth, Galleria mellonella.

Three bacterial species isolated from whole body extracts of the greater wax moth larvae, Galleria mellonella, were evaluated for their ability to utilize low-density polyethylene (LDPE) as a sole carbon source in vitro. These bacteria were identified as Lysinibacillus fusiformis, Bacillus aryabhattai, and Microbacterium oxydans. Their ability to biodegrade LDPE was assessed by growth curves, cell biomass production, polyethylene (PE) weight loss, and the presence of LDPE hydrolysis products in the growth media. Consortia of these bacteria with three other bacteria previously shown to degrade LDPE (Cupriavidus necator H16, Pseudomonas putida LS46, and Pseudomonas putida IRN22) were also tested. Growth curves of the bacteria utilizing LDPE as a sole carbon source revealed a peak in cell density after 24 h. Cell densities declined by 48 h but slowly increased again to different extents, depending on the bacteria. Incubation of LDPE with bacteria isolated from greater wax moth larvae had significant effects on bacterial cell mass production and weight loss of LDPE in PE-containing media. The bacterial consortia were better able to degrade LDPE than were the individual species alone. Gas chromatographic analyses revealed the presence of linear alkanes and other unknown putative LDPE hydrolysis products in some of bacterial culture media.

Optimization of decellularized human placental macroporous scaffolds for spermatogonial stem cells homing.

Decellularized scaffolds have been found to be excellent platforms for tissue engineering applications. The attempts are still being made to optimize a decellularization protocol with successful removal of the cells with minimal damages to extracellular matrix components. We examined twelve decellularization procedures using different concentrations of Sodium dodecyl sulfate and Triton X-100 (alone or in combination), and incubation time points of 15 or 30 min. Then, the potential of the decellularized scaffold as a three-dimensional substrate for colony formation capacity of mouse spermatogonial stem cells was determined. The morphological, degradation, biocompatibility, and swelling properties of the samples were fully characterized. The 0.5%/30 SDS/Triton showed optimal decellularization with minimal negative effects on ECM (P ≤ 0.05). The swelling ratios increased with the increase of SDS and Triton concentration and incubation time. Only 0.5%/15 and 30 SDS showed a significant decrease in the SSCs viability compared with other groups (P < 0.05). The SSCs colony formation was clearly observed under SEM and H&E stained slides. The cells infiltrated into the subcutaneously implanted scaffold at days 7 and 30 post-implantation with no sign of graft rejection. Our data suggest the %0.5/30 SDS/Triton as an excellent platform for tissue engineering and reproductive biology applications.

Effect of Portulaca Oleracea (purslane) extract on liver enzymes, lipid profile, and glycemic status in nonalcoholic fatty liver disease: A randomized, double-blind clinical trial.

Purslane (Portulaca oleracea L.) is the richest green leafy vegetable source of omega-3, especially alpha linolenic acid (ALA). Experimental studies have shown beneficial effects of purslane extract on liver enzymes. The aim of the present study was to examine the effect of purslane hydroalcohoic extract in patients with non-alcoholic fatty liver disease (NAFLD). In a randomized double-blinded clinical trial, 74 patients were randomly assigned to receive either 300 mg purslane extract or placebo capsules for 12 weeks. Compared with baseline, alanine aminotransferase (ALT) (-9 [-17, 0.50] mg/dl; p = .007), aspartate aminotransferase (AST) (-4 [-10, -0.50] mg/dl; p = .001), gamma glutamyltransferase (GGT) (-6.21 ± 9.85 mg/dL; p < .001), fasting blood glucose (FBG) (-8 [-11, -1.50] mg/dl; p < .001) insulin resistance (-0.95 ± 2.23; p = .020), triglyceride (-20 [-67.50, 3.50] mg/dl; p = .010), and low-density lipoprotein cholesterol (LDL-C) (-5 [-12, -1] mg/dl; p < .001) decreased significantly in the purslane group. At the end of study, no significant changes were observed in liver steatosis grade, insulin, liver enzymes, total bilirubin, lipid profile, and blood pressure between the two groups. The findings of our study show that purslane extract at the dose of 300 mg/day for 12 weeks has no significant effects on liver enzymes, lipid profile, and glycemic indices in patients with NAFLD.

Ophthalmic manifestations of COVID-19; a less-appreciated yet significant challenge.

AIM: The current world has changed in all shapes since the emergence of the novel coronavirus (nCoV-2) also known as COVID-19. Among the extra-pulmonary manifestations of nCoV-2, ophthalmic symptoms have less been systematically studied. The so far existing body of evidence indicates that nCoV-2 has the potential to affect both anterior and posterior chambers of the eye. Albeit, the exact mechanisms which underlie ophthalmic manifestations of nCoV-2 are yet to be elucidated. METHODS: The present brief review is an attempt to put together and highlight the significant yet limited number of studies which have spotlighted ophthalmic issues in nCoV-2 patients using a systematic literature search strategy. RESULTS: All case series or reports (including both published and preprint articles) which described ocular manifestations of patients with COVID-19 and/or documented testing of SARS-COV-2 in ocular secretions via various sampling or detection methods were sought to be included. CONCLUSION: The ophthalmic presentations in SARS-COV-2 are often found to be salient. Raising awareness in this respect may help defining evidencebased protective measures in today's practice of ophthalmology and allied disciplines.