Risk factors of low birth weight at three hospitals in Khartoum State, Sudan.

The aim of this study was to determine the percentage of women who give birth to low birth weight (LBW) children and to study the association of the different risk factors with LBW in three of large hospitals in Khartoum State, Sudan. This was a cross sectional study of 381 women. Three groups: 151, 130 and 100 women, who gave birth to live children, were selected from Alsuadi Teaching Hospital, Khartoum Teaching Hospital and Alribat University Hospital, respectively. Data were collected through structured interviews and the birth weights were recorded as measured by midwives. Uni-Multi variate analysis of the data was performed using SPSS 19. Permissions were taken from hospital administration and the participants before the conduction of the research. 13% of live born children were of low birth weight. The main risk factors for low birth weight in the study were the lack of adequate education (OR= 1.9) gestational age (OR= 5.5), type of pregnancy (OR= 9.6), presence of hypertension (OR= 3.6), renal disease (OR= 2.1), bleeding during pregnancy (OR= 6.1) and presence of moderate or severe anemia (OR= 3.19). While Adequacy of antenatal care (ANC) visits, presence of diabetes mellitus during pregnancy, smoking and malaria in the first three trimesters, presence of previous children and spacing were all found to be statistically not significant risk factors. Many of the risk factors are modifiable and can be prevented by improvement of the health care during pregnancy.

Angiotensin II-induced JNK activation is mediated by NAD(P)H oxidase in isolated rat pancreatic islets.

Angiotensin II (AII), the active component of the renin angiotensin system (RAS), plays a vital role in the regulation of physiological processes of the cardiovascular system, but also has autocrine and paracrine actions in various tissues and organs. Many studies have shown the existence of RAS in the pancreas of humans and rodents. The aim of this study was to evaluate potential signaling pathways mediated by AII in isolated pancreatic islets of rats. Phosphorylation of MAPKs (ERK1/2, JNK and p38MAPK), and the interaction between proteins JAK/STAT were evaluated. AII increased JAK2/STAT1 (42%) and JAK2/STAT3 (100%) interaction without altering the total content of JAK2. Analyzing the activation of MAPKs (ERK1/2, JNK and p38MAPK) in isolated pancreatic islets from rats we observed that AII rapidly (3 min) promoted a significant increase in the phosphorylation degree of these proteins after incubation with the hormone. Curiously JNK protein phosphorylation was inhibited by DPI, suggesting the involvement of NAD(P)H oxidase in the activation of protein.

TLR2 and TLR4 expression after kidney ischemia and reperfusion injury in mice treated with FTY720.

Ischemia and reperfusion injury (IR) is an antigen independent inflammatory process that causes tissue damage. After IR, kidneys up-regulate leukocyte adhesion molecules and toll-like receptors (TLRs). Moreover, injured kidneys can also secrete factors (i.e. heat shock protein) which bind to TLRs and trigger intracellular events culminating with the increase in the gene expression of inflammatory cytokines. FTY720 is an immunomodulatory compound and protects at least in part kidneys submitted to IR. The mechanisms associated with FTY720's beneficial effects on kidneys after IR remain elusive. We investigated whether FTY720 administration in mice submitted to kidney IR is associated with modulation of TLR2 and TLR4 expression. C57BL/6 mice submitted to 30min of renal pedicles clamp were evaluated for serum parameters (creatinine, urea and nitric oxide), kidney histology, spleen and kidney infiltrating cells expression of TLR2 and TLR4, resident kidney cells expression of TLR2 and TLR4 and IL-6 protein expression in kidney. FTY720-treated mice presented decrease in serum creatinine, urea and nitric oxide, diminished expression of TLR2 and TLR4 both in spleen and kidney infiltrating cells, and reduced kidney IL-6 protein expression in comparison with IR non-treated mice. However, acute tubular necrosis was present both in IR non-treated and IR+FTY720-treated groups. Also, FTY720 did not prevent TLR2 and TLR4 expression in kidney resident cells. In conclusion, FTY720 can promote kidney function recovery after IR by reducing the inflammatory process. Further studies are needed in order to establish whether TLR2 and TLR4 down regulation should be therapeutically addressed as protective targets of renal function and structure after IR.