Correlation between maternal and cord blood leptin and fetal growth

Leptin is a protein secreted mainly by the adipocyte in proportion to fat mass. The serum leptin concentration reflects the amount of adipose tissue in the body and has potential role on the fat deposition in the fetus. In the present study, we investigated whether umbilical and maternal serum leptin concentrations correlate with fetal growth. In addition, we determined the relationship between leptin concentration in the maternal and cord blood. We studied 100 newborn infants (48 female and 52 male; gestational age, 34 - 40 weeks) and their mothers at Alzahra hospital in Tabriz city. Serum leptin concentrations were measured by ELISA and linear regression analysis was used to evaluate correlation. In the results, there was no significant correlation between umbilical and maternal leptin concentrations (r = 0.011; p = 0.459) in all study groups. There was a correlation between umbilicalleptin concentration and birth weight of newborns (r = 0.278; p = 0.003) and correlation with body mass index (BMI) of the newborns (r = 0.249; p = 0.006). Maternal leptin concentrations correlated withmaternal weight and BMI (r = 0.277; p = 0.003, r = 0.290; p = 0.002, respectively). There was no correlation between maternal leptin concentrations and birth weight (r = - 0.162; p = 0.054) and with BMIof the newborns (r = - 0.158; p = 0.058). There was gender difference in leptin concentrations in the newborns (r = 0.331; p = 0.00025) with greater level in females. In conclusion, we have shown that theassociation between umbilical serum leptin and birth weight in this and other studies suggests a pivotal role of fetal leptin in regulating fetal growth and development

Inflammatory cytokines in bladder cancer

The presence of inflammatory cells and their products in the tumor microenvironment plays a crucial role in the pathogenesis of a tumor. Releasing the cytokines from a host in response to infection and inflammation can inhibit tumor growth and progression. However, tumor cells can also respond to the host cytokines with increasing the growth/invasion/metastasis. Bladder cancer (BC) is one of the most common cancers in the world. The microenvironment of a bladder tumor has been indicated to be rich in growth factors/inflammatory cytokines that can induce the tumor growth/progression and also suppress the immune system. On the contrary, modulate of the cancer progression has been shown following upregulation of the cytokines-related pathways that suggested the cytokines as potential therapeutic targets. In this study, we provide a summary of cytokines that are involved in BC formation/regression with both inflammatory and anti-inflammatory properties. A more accurate understanding of tumor microenvironment creates favorable conditions for cytokines targeting to treat BC. © 2019 Wiley Periodicals, Inc

Cancer stem cells as a therapeutic target in bladder cancer

Bladder cancer is one of the most prevalent genitourinary cancers responsible for about 150,000 deaths per year worldwide. Currently, several treatments, such as endoscopic and open surgery, appended by local or systemic immunotherapy, chemotherapy, and radiotherapy are used to treat this malignancy. However, the differences in treatment outcome among patients suffering from bladder cancer are considered as one of the important challenges. In recent years, cancer stem cells, representing a population of undifferentiated cells with stem-cell like properties, have been eyed as a major culprit for the high recurrence rate in superficial papillary bladder cancer. Cancer stem cells have been reported to be resistant to conventional treatments, such as chemotherapy, radiation, and immunotherapy, which induce selective pressure on tumoral populations resulting in selection and growth of the resistant cells. Therefore, targeting the therapeutic aspects of cancer stem cells in bladder cancer may be promising. In this study, we briefly discuss the biology of bladder cancer and then address the possible relationship between molecular biology of bladder cancer and cancer stem cells. Subsequently, the mechanisms of resistance applied by cancer stem cells against the conventional therapeutic tools, especially chemotherapy, are discussed. Moreover, by emphasizing the biomarkers described for cancer stem cells in bladder cancer, we have provided, described, and proposed targets on cancer stem cells for therapeutic interventions and, finally, reviewed some immunotargeting strategies against bladder cancer stem cells. © 2018 Wiley Periodicals, Inc

"APO(a) isoforms and LP(a) concentration in predicting risk for coronary artery disease: A study in men <55 years of age "

Lipoprotein (a) [Lp (a) is formed by assembly of LDL-particles and the carbohydrate rich protein, apolipoprotein (a) [apo (a)]. Elevated plasma Lp (a) levels are an independent predictor of the development of premature coronary artery disease (CAD), but is not clear whether the apo (a) isoform plays on additional and independent role or not. To investigate the possible effect of apo (a) isoform on premature CAD (in patients < 55 years of age), we have analyzed apo (a) isoforms, Lp (a) level and their relation with many recognized CAD risk factors, in 60 male patients with angiographically defined CAD and in 60 male control with no angiographic evidence of CAD. The results show elevated Lp (a) concentration (29.4±16.1, vs. 16.5±9.9 P<0.01) and frequency of S2 isoform (31.7%, vs. 6.7% P<0.01) and B isoform (10% vs. 1.7% P<0.01) in patients with premature CAD. Patients with S2 isoform exhibited significantly higher plasma Lp(a) concentration than control subject with the same isoform (39.8±15.9 vs. 20.5±6.9, P<0.05), but patient with B isoform exhibited no significant Lp(a) concentration as compared to the controls (49.5±9.46 vs. 45). In addition, all patients had a low frequency of S4 and null isoforms. The distribution of apo (a) lsoforms was significantly shifted towards small isoform size (band S2) in the CAD as compared to the controls. This study provides evidence that CAD patient < 55 years of age have a different pattern of apo (a) isoforms than controls, and therefore apo (a) isoform may play an important role in predicting premature CAD

Assessment of oxidative stress in acute myeloid leukemia

"nBackground: Many chemotherapeutic regimens used in the treatment of cancer generate free radicals that may be a part of their beneficial effects. The aim of this study was to assess the oxidative status in patients undergoing chemotherapy for acute myeloid leukemia (AML)."n "nMethods: Thirty-eight patients with AML (17 female and 21 male patients) with a mean age 34.05±12.49 years were included in the study. All the patients received cytarabine and daunorubicin as their standard induction therapy. Serum levels of malondialdehyde (MDA), total antioxidant capacity (TAC), and also the erythrocyte superoxide dismutase and glutathione peroxidase activities were measured before and 14 days after chemotherapy."n "nResults: Plasma malondialdehyde concentrations increased significantly (from a former 2.68±0.89 nmol/ml to 3.14±1.29 nmol/ml) 14 days post chemotherapy (p=0.04). Moreover, the total plasma antioxidant capacity changed from 1.09±0.15 mmol/L to 1.02±0.14 mmol/L (p=0.005). Erythrocyte superoxide dismutase and glutathione peroxidase activity decreased over time from 1157.24±543.61 U/gHb to 984.01±419.09 U/gHb (p=0.04) and 46.96±13.70 U/gHb to 41.40±6.44 U/gHb (p=0.02), respectively."n "nConclusion: In this study, an increase in malondialdehyde levels and a decrease in the levels of antioxidant enzymes and total antioxidant capacity were observed. It seems that chemotherapy by cytarabine and daunorubicin generates enormous amounts of free radicals in patients undergoing the treatment for AML. Use of antioxidant supplementation during chemotherapy i is discouraged as it may interfere with the generation of free radicals that may be a part of the therapeutic efficacy of these drugs