Sequencing analysis and efficient biodiesel production by lipase from Pseudomonas aeruginosa.

BACKGROUND: Recently, lipase processing for biodiesel production has shown a global increase as it is considered a potential alternative clean-fuel source. The current study's objective is to investigate of lipolytic activity of lipase produced from different strains of Pseudomonas aeruginosa (P. aeruginosa) in biodiesel production using edible plant oils. The goal is to develop an efficient and cost-effective method for producing inexpensive and environmentally friendly biodiesel. METHODS AND RESULTS: Four P. aeruginosa isolates were obtained from different environmental sources (soil), phenotypically identified, and it was confirmed by the PCR detection of the 16SrRNA gene. The isolated P. aeruginosa strains were screened for lipase production, and the recovered lipase was purified. Besides, the lipase (lip) gene was detected by PCR, and the purified PCR products were sequenced and analyzed. The production of biofuel was conducted using gas chromatography among tested oils. It was found that castor oil was the best one that enhances lipase production in-vitro.

Potential role of human umbilical cord stem cells-derived exosomes as novel molecular inhibitors of hepatocellular carcinoma growth.

Hepatocellular carcinoma (HCC) is one of the most critical cancers; thus, novel therapeutical regimens are of great need. In this study, we investigated the effects of umbilical cord mesenchymal stem cells (UC-MSCs) derived exosomes on HepG2 cell line, and the underlying mechanism to control HCC proliferation, to identify the potential clinical role of exosomes as a novel molecular therapeutic target. Proliferation, apoptosis, and angiogenesis effects were assessed together with the cell viability evaluation by MTT assay in HepG2 cells at 24/48 h. with or without UC-MSCs-derived exosomes. Gene expressions of TNF-α, caspase-3, VEGF, stromal cell-derived factor-1 (SDF-1), and CX chemokine receptor-4 (CXCR-4) were measured by quantitative real-time PCR technique. Expression of sirtuin-1 (SIRT-1) protein was detected by western blot. Treatment of HepG2 cells with UC-MSCs-derived exosomes for 24 and 48 h. demonstrated a significant reduction of cells survival compared to the control group (p < 0.05). The SIRT-1 protein, and VEGF, SDF-1, CXCR-4 expression levels were significantly lower, TNF-α and caspase-3 expression levels were significantly higher in exosomal-treated HepG2 cells for 24 and 48 h. than those in the control group. Moreover, our findings documented that the anti-proliferative, apoptotic, and anti-angiogenic effects were achieved in a time-dependent manner in which more effects were determined after 48 h supplementation compared to 24 h (p < 0.05). UC-MSCs-derived exosomes exert anticarcinogenic molecular effects on HepG2 cells through the involvement of SIRT-1, SDF-1, and CXCR-4. Hence, exosomes would be a potential novel therapy regimen against HCC. Large-scale studies are recommended to verify this conclusion.

Lectin-Like OLR1 3'UTR Rs1050286 Gene Polymorphism and Plasma Oxidized-LDL in Coronary Artery Disease and Their Relation to Cardiovascular Risk and Outcomes.

Background: Oxidized low-density lipoprotein (ox-LDL) has an important role in the genesis of coronary atherosclerosis. Lectin-like ox-LDL receptor 1 (OLR1) contributes to the uptake and internalization of ox-LDL. Genetic polymorphisms have been associated with coronary artery disease (CAD). Here we explore the association of plasma levels of ox-LDL and 3' UTR OLR1 (rs1050286) SNP with CAD risk and in-hospital adverse outcomes. Methods: A case-control study enrolled 192 patients with ST-segment elevation myocardial infarction (STEMI), 100 patients with unstable angina, and 100 healthy controls. Baseline, clinical characteristics, and risk scores of the patients were determined. Plasma ox-LDL and other biochemical variables were measured. All subjects are genotyped for OLR1 (rs1050286) by RT-PCR with TaqMan SNP genotyping assay. Results: Plasma ox-LDL was higher with enhanced sensitivity and specificity in identifying patients with STEMI and was found as a significant independent risk factor for CAD in those two groups. Levels of ox-LDL were increased with increasing poor prognostic factors in STEMI patients that are associated with an increased incidence of some adverse events and in-hospital mortality. Elevated STEMI risk was associated with T allele of OLR1 (rs1050286) (odds ratio of 4.9, 95% CI: 2.6-9.4, p< 0.001). STEMI patients who have T allele exhibited higher risk scores, coronary multivessel narrowing, and elevated incidence of in-hospital major adverse clinical events. Conclusion: These results suggest that plasma ox-LDL, as well as T allele of ORL-1 (rs1050286), is associated with the increased risk for developing STEMI and the associated adverse clinical outcomes.

Effect of Nicotine on STAT1 Pathway and Oxidative Stress in Rat Lungs.

BACKGROUND: Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The transcription factor STAT1 induces the expression of many proinflammatory genes and has been suggested to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on STAT1 pathway and oxidative stress in rat lung tissue. METHODS: Thirty rats were divided into 3 groups; group I considered as control, group II; its rats were daily injected with Nicotine at a dose of 0.4 mg/100 gm body for 8 successive weeks and group III; its rats were daily injected with Nicotine as group II, but the injection was stopped for another 4 weeks. STAT1α protein was assessed by immunohistochemistry, COX-2 and iNOS genes expression were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols were measured using spectrophotometric methods in the lung tissues of the rats. RESULTS: The results of the study revealed that group II rats had the highest expression of STAT1α protein and COX-2 and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for 4 weeks caused a marked reduction in the expression of STAT1α protein, COX-2 and iNOS genes and oxidative stress. CONCLUSION: Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.

Protective Effect of Oxytocin Against Bone Loss in a Female Rat Model of Osteoporosis.

BACKGROUND: Introduction: Oxytocin (OT) has been proposed to assist in the regulation of bone remodeling and to exert an antiosteoporotic effect. We evaluated the possible protective effect of OT against bone degeneration in ovariectomized (OVX) rats. METHODS: The study was performed on three groups of adult female rats; group I was subjected to sham operation, group II was subjected to ovariectomy, and group III was subjected to ovariectomy and intraperitoneal injection with OT for eight successive weeks. At the end of the study, bone mass density (BMD) was measured; then the rats were euthanized and their blood and bone tissues were examined. RESULTS: The group II rats had significantly less BMD and greater serum bone-specific alkaline phosphatase (bALP), osteocalcin (OC), and tartrate-resistant acid phosphatase (TRAP) levels than the group I rats. Furthermore, group II rats had fewer osteocytes and osteoblasts, and less OPG/RANKL mRNA expression than group I rats. The groups I and III and rats showed no significant differences in BMD, bALP, OC, TRAP, OPG/RANKL mRNA expression, or osteocyte and osteoblast numbers. CONCLUSION: Oxytocin may have an antiosteoporotic effect in OVX rats.

Survival outcomes of CD34+CD38-LSCs and their expression of CD123 in adult AML patients.

BACKGROUND AND AIM: Acute myeloid leukemia (AML) is one of the most common leukemias in adults. AML is generally regarded as a stem cell disease characterized by an accumulation of undifferentiated and functionally heterogeneous populations of cells, The aim of the present study was to identify leukemia stem cells in patients with AML and their correlations with treatment outcomes namely remission status, disease free survival, and overall survival. RESULTS: The mean percentages of CD34+CD38- and CD34+CD38low/-CD123+ LSCs were 2.2± 0.4and 22.3± 2.6, respectively. The percentages of CD34+cells, CD34+CD38- and CD34+CD38low/-CD123+ LSCs were significantly lower in AML patients with complete remission than those without complete response (P<0.001, P<0.004, P<0.001 respectively). The mean OS of all study patients was 20.03±1.2 months while the median OS was 21 months (95% CI=18.32-21.48). The mean DFS was 16.96±1.02 months and the median was 18 months (95% CI=8.9-11.4). DFS and OS were significantly higher among those who achieved CR than those without CR. In addition, there were significant negative effects of WBCs, CD34+cells, CD34+CD38- and CD34+CD38-CD123+LSCs on DFS and OS. PATIENTS AND METHODS: We investigated 30 patients with newly diagnosed AML; all patients underwent complete history taking, and thorough physical and clinical examination, complete blood count. Peripheral smears and bone marrow aspirates were also examined. Cytochemistry and immunophenotyping of leukemic cells were performed routinely in bone marrow using monoclonal antibodies. Flow cytometry was used to analyze leukemia stem cells and their expression of CD123. CONCLUSION: Our study elucidated that CD34+CD38-LSCs, with or without CD123+LSCs phenotype was present in a significant proportion of AML patients and it could be responsible for resistance to traditional treatments, and high percentage of MRD that was translated into significantly high number of non CR, poor DFS, and OS.

Tissue Indices of Telomere Length and p53 in Patients with Different Gastrointestinal Tumors: Correlation with Clinicopathological Status.

Telomere length dysfunction is involved in the generation of genomic rearrangements that drive progression to malignancy. A set of serological markers for telomere dysfunction, namely chitinase and N-acetylglucosaminidase (NAG), DNA damage, and tissue alteration of p53 have been identified. The probability that genomic damage, accumulation of reactive oxygen species, and shorter telomeres may be related to the onset and advancement of gastrointestinal (GI) tumors. A total of 40 patients with GI tumors and 20 healthy controls with matched age and sex were included. Estimation of serum chitinase, NAG, lipid peroxide (LPER), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase by colorimetric methods, and p53 by ELISA were assessed. Related clinicopathological features were determined. Serological chitinase, NO, LPER, and p53 were significantly increased, SOD was significantly decreased (p Ë‚ 0.001 for each) in GI tumor patients compared with controls and correlated significantly with age. There was a significant correlation between telomere dysfunction indices, p53, oxidative stress indices, and malignant stages of GI cancer patients. Moreover, a significant difference in the mean serum levels of indices between control, malignant, and benign subjects was found. Accordingly, these biomarkers play an important role in the pathogenesis of GI cancer and their estimation may predict the GI tumor behavior.

Visfatin Serum Levels in Obese Type 2 Diabetic Patients: Relation to Proinflammatory Cytokines and Insulin Resistance.

Visfatin, an adipocytokine with insulin-mimetic activity, has been previously reported to associate with obesity. Herein, we aimed to investigate the serum level of visfatin and association with proinflammatory markers and insulin resistance in obese type 2 diabetic patients. A case control study was carried out among 80 diabetics and 40 non-diabetic healthy controls, after obtaining Anthropometric measurements and blood pressure. Serum level of visfatin and C-reactive protein (CRP) were measured by Enzyme Immunoassay. Interleukin 6 (IL6), tumor necrosis factor α (TNF-) were measured by ELISA and the homeostasis model assessment for insulin resistance was calculated as a marker of insulin resistance. Compared to healthy controls, diabetic patients showed a significant high serum levels of visfatin (40.33±9.98 vs 19.03±8.22), (P= 0.001), IL6 (12.06±2.69 vs 6.02±3.03), (P < 0.0001), TNF- (13.53±2.54 vs 8.70±3.40), P < 0.0001) and CRP (7.77±1.61 vs 6.01±1.99), (P=0.003). Also there was a strong positive correlation between serum level of visfatin, IL6, TNF- and CRP and some anthropometric characteristics including (WC,BMI and insulin resistance). Furthermore, among 80 diabetic patients, serum level of visfatin was positively correlated with IL6 (r=0.47, P < 0.0001), TNF- (r=0.62, P < 0.0001), CRP (r=0.4, P=0.002) respectively. In conclusion, there is a strong positive correlation between visfatin serum level and the inflammatory markers IL6, TNF- and CRP in type 2 diabetic patients. There is also a positive correlation with insulin resistance and BMI which indicates association of visfatin with obesity and type 2 diabetes mellitus.

Obesity risk prediction among women of Upper Egypt: The impact of serum vaspin and vaspin rs2236242 gene polymorphism.

BACKGROUND: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. AIM: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. SUBJECTS AND METHODS: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using tetra-amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. RESULTS: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P=0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA+AA, P=0.004 and TT+TA vs AA, P=0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P<0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P<0.001 each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMA-IR, insulin, and ALT values (P<0.05 each) and a negative correlation with HDL-C (P<0.01). CONCLUSION: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.