Mozambican Midwives' Views on Barriers to Quality Perinatal Care

Our purpose in this study was to explore the midwives' perception of factors obstructing or facilitating their ability to provide quality perinatal care at a central labor ward in Maputo. In-depth interviews were undertaken with 16 midwives and were analyzed according to grounded theory technique. Barriers to provision of quality perinatal care were identified as follows: (i) the unsupportive environment, (ii) nonempowering and limited interaction with women in labor, (iii) a sense of professional inadequacy and inferiority, and (iv) nonappliance of best caring practices. A model based on the midwives' reflections on barriers to quality perinatal care and responses to these were developed. Actions aimed at overcoming the barriers were improvising and identifying areas in need of change. Identified evading actions were holding others accountable and yielding to dysfunction and structural control. In order to improve perinatal care, the midwives need to see themselves as change agents and not as victims of external and internal causal relationships over which they have no influence. It is moreover essential that the midwives chose actions aiming at overcoming barriers to quality perinatal care instead of choosing evading actions, which might jeopardize the health of the unborn and newborn infant. We suggest that local as well as national education programs need to correspond with existing reality, even if they provide knowledge that surpasses the present possibilities in practice. Quality of intrapartum and the immediate newborn care requires a supportive environment, however, which in the context of this study presented such serious obstacles that they need to be addressed on the national level. Structural and administrative changes are difficult to target as these depend on national organization of maternal health care (MHC) services and national health expenditures.     

Antioxidative Potential of Duranta Repens (Linn.) Fruits Against H2O2 Induced Cell Death In Vitro

The effects of Duranta repens fruits were investigated on H₂O₂ induced oxidative cell death to evaluate its antioxidative potential in vitro. HEK293T cells were treated with different concentrations [0–1000 µg/ ml] of ethanol extract (E-Ex) and methanol extract (M-Ex) of D. repens for 24h, and then treated with 100 µM H₂O₂ for 24h. Cell viability, antioxidant parameters of cells, and antioxidant constituents of the extracts were determined. Treatment with limited dose of E-Ex or M-Ex increased the survival rate of H₂O₂-treated HEK293T cells, however the extra-high dose showed growth inhibitory effect. Treatment with E-Ex or M-Ex protected cellular lipid per-oxidation. In vitro analyses showed the 2,2-diphenyl-1-picrylhydrazyl and H₂O₂ scavenging activities as well as reducing potential of the extracts. We report here that the limited dose of E-Ex and M-Ex possess antioxidative potential, which can protect H₂O₂-induced oxidative cell damage.     

Chronic Mild Hyperhomocysteinemia Alters Inflammatory and Oxidative/Nitrative Status and Causes Protein/DNA Damage,as well as Ultrastructural Changes in Cerebral Cortex: Is Acetylsalicylic Acid Neuroprotective?

Homocysteine is a sulfur-containing amino acid derived from methionine metabolism. When plasma homocysteine levels exceed 10–15 μM, there is a condition known as hyperhomocysteinemia, which occur as a result of an inborn error of methionine metabolism or by non-genetic causes. Mild hyperhomocysteinemia is considered a risk factor for development of neurodegenerative diseases. The objective of the present study was to evaluate whether acetylsalicylic acid has neuroprotective role on the effect of homocysteine on inflammatory, oxidative/nitrative stress, and morphological parameters in cerebral cortex of rats subjected to chronic mild hyperhomocysteinemia. Wistar male rats received homocysteine (0.03 μmol/g of body weight) by subcutaneous injections twice a day and acetylsalicylic acid (25 mg/Kg of body weight) by intraperitoneal injections once a day from the 30th to the 60th postpartum day. Control rats received vehicle solution in the same volume. Results showed that rats subjected to chronic mild hyperhomocysteinemia significantly increased IL-1β, IL-6, and acetylcholinesterase activity and reduced nitrite levels. Homocysteine decreased catalase activity and immunocontent and superoxide dismutase activity, caused protein and DNA damage, and altered neurons ultrastructure. Acetylsalicylic acid totally prevented the effect of homocysteine on acetylcholinesterase activity and catalase activity and immunocontent, as well as the ultrastructural changes, and partially prevented alterations on IL-1β levels, superoxide dismutase activity, sulfhydryl content, and comet assay. Acetylsalicylic acid per se increased DNA damage index. In summary, our findings showed that chronic chemically induced model of mild hyperhomocysteinemia altered some parameters and acetylsalicylic acid administration seemed to be neuroprotective, at least in part, on neurotoxicity of homocysteine.     

Histopathology of familial and early-onset gastric cancer

Early-onset gastric cancer (EOGC) is defined as gastric cancer presenting at the age of 45 or younger. Approximately 10% of gastric cancer patients fall into the EOGC category. Furthermore, 10% of young gastric cancer patients have a positive family history, some of which are accounted for by inherited gastric cancer predisposition syndromes. Although the underlying genetic events are not always known, it can involve CDH1 germline mutations, encoding an aberrant form of E-cadherin, resulting in Hereditary diffuse gastric cancer (HDGC) and this occurs in 25–40% of tested families. Management options for asymptomatic mutation carriers are fraught, since endoscopic surveillance can miss cancer foci and prophylactic gastrectomy has profound clinical sequelae. This review serves to bring us up-to-date with the latest findings in EOGC and HDGC including implications for the clinician, geneticist and pathologist.     

Congenital Cytomegalovirus Infection in Children with Autism Spectrum Disorder: Systematic Review and Meta-Analysis

Association of congenital cytomegalovirus (CMV) infection with autism spectral disorder (ASD) has been suggested since 1980s. Despite the observed association, its role as a risk factor for ASD remains to be defined. In the present review, we systematically evaluated the available evidence associating congenital CMV infection with ASD using PubMed, Web of Science, Cochrane Library, and Embase databases. Any studies on children with CMV infection and ASD were evaluated for eligibility and three observational studies were included in meta-analysis. Although a high prevalence of congenital CMV infection in ASD cases (OR 11.31, 95% CI 3.07–41.66) was indicated, too few events (0–2 events) in all included studies imposed serious limitations. There is urgent need for further studies to clarify this issue.