Compared to the HCs, the TLE group showed significantly weaker functional connectivity among EEGs in the executive control network. Moreover, in the TLE group, we found that the functional connectivity was significantly positively correlated with accuracy and negatively correlated with EC_effect. In addition, the functional connectivity of the executive control network was significantly higher than that of the resting state network in the HCs. In the TLE group, however, there was no significant change in functional connectivity strengths between the executive control network and resting state network. CONCLUSION Our results indicate that the decreased functional connectivity in theta band may provide a potential mechanism for executive control deficits in TLE patients.BACKGROUND Changes in gene regulation are widely recognized as an important driver of adaptive phenotypic evolution. However, the specific molecular mechanisms that underpin such changes are still poorly understood. Chromatin state plays an essential role in gene regulation, by influencing the accessibility of coding loci to the transcriptional machinery. Changes in the function of chromatin remodellers are therefore strong candidates to drive changes in gene expression associated with phenotypic adaptation. Here, we identify amino acid homoplasies in the chromatin remodeller CHD9, shared between the extinct marsupial thylacine and eutherian wolf which show remarkable skull convergence. CHD9 is involved in osteogenesis, though its role in the process is still poorly understood. We examine whether CHD9 is able to regulate the expression of osteogenic target genes and examine the function of a key substitution in the CHD9 DNA binding domain. RESULTS We examined whether CHD9 was able to upregulate its osteogenicof protein homoplasy and its role in developmental processes. Mutations in coding genes may be a mechanism for driving adaptive changes in gene expression, and their validation is essential towards determining the functional consequences of evolutionary homoplasy.BACKGROUND Sick neonates can be early readmitted if and only if their mothers have good knowledge of the key neonatal danger signs at first discharge. P7C3 Thus, it was aimed to assess the level and determinants of maternal knowledge on these signs at first discharge from NICU. METHODS A hospital based cross sectional study design was employed at Debre Tabor General Hospital, South Gondar Zone. A sample of 363 participants was included to the study from September 2018 to February 2019 through systematic selection of every other eligible mother baby pair. Data were collected through face to face interview at time of discharge from NICU. Knowledge score of neonatal danger signs was computed by adding the total number of correct spontaneous responses to 9 key danger signs with a minimum score of 0 and maximum of 9 [0 when a mother named none of the key danger signs and 9 when the mother named all the signs]. Mothers who scored ≥3 points were considered to have good knowledge whereas those scoring less than 3 points had poor knowledge. RESULTS 224(61.70%) mothers had good knowledge of neonatal danger signs at discharge from NICU. Secondary and above level of education [AOR = 4.62], receiving danger sign information during stay at NICU [AOR = 3.64], four and above antenatal visits [AOR = 3.04], well preparedness of birth [AOR = 13.70], institutional delivery [AOR = 6.46] and good knowledge of essential newborn care [AOR = 4.41] were significant factors. CONCLUSIONS At discharge time, maternal knowledge of neonatal danger signs wasn't comparable to their exposure of NICU environment. Therefore, danger sign education should be routinely given during maternal stay at NICU. Moreover, existing efforts should be enhanced to improve number of antenatal visits, institutional delivery rate and postnatal services along the continuum of maternal and child health care in South Gondar Zone.BACKGROUND Neisseria meningitidis serogroups W and Y are the most common serogroups causing invasive meningococcal disease in Sweden. The majority of cases are caused by the serogroup W UK 2013 strain of clonal complex (cc) 11, and subtype 1 of the serogroup Y, YI strain of cc23. In this study, virulence factors of several lineages within cc11 and cc23 were investigated in transgenic BALB/c mice expressing human transferrin. Transgenic mice were infected intraperitoneally with serogroup W and Y isolates. Levels of bacteria and the proinflammatory cytokine CXCL1 were determined in blood collected 3 h and 24 h post-infection. Apoptosis was investigated in immune cells from peritoneal washes of infected mice. Adhesion and induction of apoptosis in human epithelial cells were also scored. RESULTS The levels of bacteraemia, CXCL1, and apoptosis were higher in serogroup W infected mice than in serogroup Y infected mice. Serogroup W isolates also induced higher levels of apoptosis and adhesion in human epithelial cells. No significant differences were observed between different lineages within cc11 and cc23. CONCLUSIONS N. meningitidis Serogroup W displayed a higher virulence in vivo in transgenic mice, compared to serogroup Y. This was reflected by higher bacteremia, proinflammatory activity, and ability to induce apoptosis in mouse immune cells and human epithelial cells.BACKGROUND Mycobacterium tuberculosis resides inside host macrophages during infection and adapts to resilient stresses generated by the host immune system. As a response, M. tuberculosis codes for short-chain dehydrogenases/reductases (SDRs). These SDRs are nicotinamide adenine dinucleotide-reliant oxidoreductases involved in cell homeostasis. The precise function of oxidoreductases in bacteria especially M. tuberculosis were not fully explored. This study aimed to know the detail functional role of one of the oxidoreductase Rv0148 in M. tuberculosis. RESULTS In silico analysis revealed that Rv0148 interacts with Htdy (Rv3389) and the protein interactions were confirmed using far western blot. Gene knockout mutant of Rv0148 in M. tuberculosis was constructed by specialized transduction. Macrophage cell line infection with this knockout mutant showed increased expression of pro-inflammatory cytokines. This knockout mutant is sensitive to oxidative, nitrogen, redox and electron transport inhibitor stress agents.