Clinical Biochemistry
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- ItemPANCREATIC IMMUNE CELL ALTERATIONS IN AN ANIMAL MICE MODEL OF LIVER FIBROSIS(2023-10-19) Diana Abu ArraAbstract Background: Liver fibrosis is closely linked to the most common metabolic illnesses and developing acute pancreatitis (AP). Aims: This study aims to investigate the effects of liver fibrosis on modulating changes in pancreatic NK cells and involvement of molecular pathways in a mice model of liver injury. Methodology: Carbon-tetrachloride; CCl4 (i.p injected) of acute (2 weeks) and chronic (4 weeks) models of male C57/BL mice of liver injury was performed. At the end of experiments, mice were anaesthetized, and serum was collected for assessing liver enzymes, pancreatic injury of lipase and amylase. Annexin V examination of the pancreatic tissue for β-islet cell apoptosis, metabolic makers of C-peptide levels as well as for lipid and glucose profiles were performed. The livers were harvested for histological evaluations of inflammatory (H&E staining) and fibrotic (Sirius Red stain) profiles. Moreover, real-time polymerase chain reaction (PCR) was used for SMA and collagen III. IL-6 levels from pancreatic β-Islet cells were also evaluated. Pancreatic tissue-resident (tr)NK cells were isolated and evaluated for their activity through assessing INF- γ and IL-6 receptor by the ELISA. Results: In the chronic CCl4 induced-model histological characterization of the liver injury was deteriorated as compared to the acute model and the naïve mice. Serum ALT and AST levels, as well as metabolic evaluations of cholesterol, triglyceride, C-peptide, fasting blood sugar, and fibrotic profiles revealed a positive relationship with illness progression and severity of liver fibrosis. Pancreatic enzymes were elevated in liver fibrosis mice model and were associated with β-islet cells apoptosis. An inverse strength association between IL-6 of β-Islet cells and severities of liver fibrosis was achieved. β-Islet cells which exhibit high secretions to IL6 and caused an up-expressions of trNK IL6R, which in part, affected trNK activity and caused their inability to produce enough quantities of IFN-γ. Conclusion: Liver fibrosis induces pancreatic injury, as evidenced by elevated amylase and lipase levels and increased islet cell apoptosis. Dysregulation of lipid and glucose metabolism might have implications for pancreatic health. Antagonizing IL6 and/or IL6R could improve NK cell activity and delay progression of AP. Keywords: Pancreas; NK cells; liver fibrosis; mice model .
- ItemPREVALENCE AND MOLECULAR CHARACTERIZATION OF GROUP B STREPTOCOCCUS (GBS) FROM NABLUS AREA(2023-09-19) Alaa Ahmad Lottfy AwwadBackground: Group B streptococci (GBS) are gram-positive bacteria, normally colonize human's genital and gastrointestinal tract asymptomatically, they colonize 18% of women worldwide, they could be transmitted to 50% of newborns from their colonized mothers causing invasive diseases. Objectives: The objectives of this study are to find out GBS prevalence in Nablus, Palestine, the serotypes present, the antibiotics susceptibility and antibiotics resistance genes present on isolated GBS. Methodology: It is a descriptive cross-sectional study, conducted from September 2022 to January 2023 at Rafidia Governmental Surgical Hospital and Al-Itihad Hospital, a convenient sampling technique was used to study 184 pregnant women with gestational age of 33 weeks and above. Descriptive data of participants was collected using questionnaires. A total of 184 vaginal swabs were taken from participants. Swabs were cultured on Uriselect 4 chrom media, bale blue colonies were confirmed by CAMP test and by PCR. Susceptibility pattern was performed. Antibiotic resistance genes and capsular polysaccharide antigens were also tested using PCR. Results: GBS prevalence was 11.4%, a significant association had been found between GBS colonization and residency in city (P-value: 0.014). 100% of GBS isolates were sensitive to penicillin, ampicillin, amoxicillin, vancomycin, ceftriaxone, linezolid, cefepime, and ceftriaxone, 71.4% were resistant to tetracycline, 28.5% resistant to erythromycin, 23.8% resistance to clindamycin and 4.7% resistant to levofloxacin. ermB resistance gene presented in 19% of isolates, mefA presented in 4.7% of isolates and the majority 90% presented with the tetM gene. Serotype III accounted for 42.8% of isolates, serotype V 23.8%, 14.2% were serotype II, 9.5% were serotype Ib, 4.7% were serotype IV whereas 4.7% were non-typeable. Conclusions: This study used combined methodology comparable to the international CLSI guidelines to confirm GBS isolates, serotypes, and the antibiotics profile. GBS isolates accounted for 11.4% of screened pregnant, GBS colonization was significantly associated with living in city (P-value 0.014), 100% of isolates were sensitive to penicillin, and 71.4% were resistant to tetracycline. Most isolates possessed the tetM resistance gene. Serotype III was the predominant (42.8%). Keywords: GBS, Streptococcus agalactiae, serotypes, antibiotics resistance genes
- ItemTHE IMMUNE AND METABOLIC IMPACTE OF TESTESTERONE ON MICE MODEL OF LIVER FIBROSIS(2023-06-14) Hadeel Moneer SnoberBackground: Natural killer (NK) cells showed an anti-fibrotic effect; however, their function is thought to be impaired in advanced liver injury. The objective of this study was to evaluate the immune response and metabolic impact of testosterone on mice model of liver injury. Methods: Carbon-tetrachloride (i.p injected) of acute (2 weeks) and chronic (4 weeks) models of male mice of liver injury was performed. Testosterone (4 mg/kg mouse body weight) was injected intraperitoneal injection following the first week of acute model of CCl4 and following the second week of the chronic model of CCl4. At the end of experiments, mice were sacrificed, and serum were collected for assessing liver enzymes of ALT, AST, inflammatory marker of IL-6, metabolic makers of C-peptide levels as well as for lipid and glucose profiles. Livers were harvested and used for histological assessments for inflammation and for fibrosis. Fibrosis profile from liver extracts; SMA and Collagen III, The samples underwent assessment utilizing the real-time polymerase chain reaction (PCR) technique. Moreover, liver tissue-resident NK cells were isolated and evaluated for their activity through assessing INF- and IL-6 receptor by the ELISA and flow-cytometry respectively. Results: The serum levels of ALT, AST, and IL-6, as well as metabolic evaluations of cholesterol, triglyceride, C-peptide, fasting blood sugar, and fibrotic profiles, exhibited a linear correlation with the progression of the disease. Histological characterization of the liver was worsened in the chronic model of liver injury. Testosterone-treated mice exhibit a significant reduction in collagen depositions with less dense fibrosis tissue associated with reduced liver injury enzymes and metabolic markers in both the acute and the chronic CCl4 mice model after testosterone treatment (P<0.05). Moreover, testosterone treatments displayed significant decrease in serum IL-6 of 2.4-fold (p=0.0001) and 2.3-fold (p=0.0003) in the acute and chronic models, respectively (p=0.002) and data were associated with increase in INF-release from NK associated with a reduction in their IL-6 receptor expressions (P<0.05). Conclusion: Testosterone has an anti-inflammatory and anti-fibrotic action by storing histology for lowering SMA and Col III levels as well as decreasing ALT and AST levels. In CCl4-induced mice, testosterone improved the metabolic profile by lowering cholesterol, triglyceride, FBS, and C-peptide levels. Testosterone has an anti-inflammatory impact via decreasing inflammatory cytokine levels (lower IL-6).Testosterone treatment of CCl4-mice restored trNK cell function by increasing NK INF-g and decreasing IL-6 receptor levels. These findings emphasize testosterone's immune-modulatory effects, which are linked to its anti-inflammatory and anti-fibrotic capabilities. Our results suggest an anti-inflammatory and anti-fibrotic treatment approach of testosterone for delaying disease progressions. Keywords: Liver fibrosis; Mice Model; Testosterone; Immune And Metabolic Impact.