1.Human Umbilical Cord Blood CD34-Positive Cells as Predictors of the Incidence and Short-Term Outcome of Neonatal Hypoxic-Ischemic Encephalopathy: A Pilot Study.
Sahar M A HASSANEIN ; Mohamed Hassan NASR ELDIN ; Hanaa A AMER ; Adel E ABDELHAMID ; Moustafa EL HOUSSINIE ; Abir IBRAHIM
Journal of Clinical Neurology 2017;13(1):84-90
BACKGROUND AND PURPOSE: Neonatal hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of neurological handicap in developing countries. Human umbilical cord blood (hUCB) CD34-positive (CD34⁺) stem cells exhibit the potential for neural repair. We tested the hypothesis that hUCB CD34⁺ stem cells and other cell types [leukocytes and nucleated red blood cells (NRBCs)] that are up-regulated during the acute stage of perinatal asphyxia (PA) could play a role in the early prediction of the occurrence, severity, and mortality of HIE. METHODS: This case-control pilot study investigated consecutive neonates exposed to PA. The hUCB CD34⁺ cell count in mononuclear layers was assayed using a flow cytometer. Twenty full-term neonates with PA and 25 healthy neonates were enrolled in the study. RESULTS: The absolute CD34⁺ cell count (p=0.02) and the relative CD34⁺ cell count (CD34+%) (p<0.001) in hUCB were higher in the HIE patients (n=20) than the healthy controls. The hUCB absolute CD34⁺ cell count (p=0.04), CD34⁺% (p<0.01), and Hobel risk scores (p=0.04) were higher in patients with moderate-to-severe HIE (n=9) than in those with mild HIE (n=11). The absolute CD34⁺ cell count was strongly correlated with CD34⁺% (p<0.001), Hobel risk score (p=0.04), total leukocyte count (TLC) (p<0.001), and NRBC count (p=0.01). CD34+% was correlated with TLC (p=0.02). CONCLUSIONS: hUCB CD34⁺ cells can be used to predict the occurrence, severity, and mortality of neonatal HIE after PA.
Asphyxia
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Case-Control Studies
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Cell Count
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Developing Countries
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Erythrocytes
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Fetal Blood*
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Humans*
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Hypoxia-Ischemia, Brain*
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Incidence*
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Infant, Newborn
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Leukocyte Count
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Mortality
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Pilot Projects*
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Stem Cells
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Umbilical Cord*
2.Eltroxin and Hesperidin mitigate testicular and renal damage in hypothyroid rats:amelioration of oxidative stress through PPARγ and Nrf2/HO-1 signaling pathway
Hadeel M. OSAMA ; Sally M. KHADRAWY ; EL-Shaymaa EL-NAHASS ; Sarah I. OTHMAN ; Hanaa M. MOHAMED
Laboratory Animal Research 2024;40(2):197-212
Background:
Thyroid hormones (THs) regulate growth, development and function of different tissues. Hypothyroidism is a common clinical disorder characterized by deficiency in THs and adversely affects the development and functions of several organs. This work aimed to investigate the ameliorative effect of eltroxin (ELT), a hypothyroidism medication, and hesperidin (HSP), a flavonoid, against testicular and renal toxicity in hypothyroid rats. Twenty-four rats were divided into four groups and treated orally for 12 weeks. Group I (control), group II (hypothyroidism) received 20 mg/kg carbimazole (CBZ), group III received CBZ and 0.045 mg/kg ELT, and group IV received CBZ and 200 mg/kg HSP.
Results:
CBZ administration induced biochemical and histopathological changes in testis and kidney. Co-administration of ELT or HSP significantly (P < 0.05) ameliorated THs, reduced urea and creatinine while raised follicle stimulating hormone (FSH), Luteinizing hormone (LH), and testosterone in serum. Testicular and renal malondialdehyde level as a lipid peroxidation indicator, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were significantly (P < 0.05) decreased while glutathione content, glutathione peroxidase, and glutathione-s-transferase activities were significantly (P < 0.05) increased. The histopathological changes were also diminished. Decreased mRNA and protein expressions of nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and peroxisome proliferator-activated receptor gamma(PPARγ) in hypothyroid rats were up-regulated after ELT or HSP treatment.
Conclusions
ELT and HSP showed antioxidant and anti-inflammatory effects against CBZ-induced testicular and renal toxicity, and these effects may be promoted via activating Nrf2/HO-1 and PPARγ signaling pathways.