Post infectious sequelae such as sepsis and septic shock are poorly understood and annually take the lives of millions over the world. Severe microbial infections caused by Gram Positive and Gram Negative bacteria and by fungi are the main causes, which are aggravated by the rapid development of antibiotic resistance. It is unfortunate that today all the clinical trials of sepsis which tested the efficacy of single antagonists failed. Sepsis was recently redefined as a synergistic multifactorial episode where no unique alarmin had been identified, which if inhibited could control the deleterious biochemical and immune immunological events characteristic of sepsis. An apparent “breakthrough “in our understanding of sepsis pathogenicity was published in 2009 in Nature Medicine arguing that the main cause of mortality in sepsis is the release from neutrophils (PMNs) nets of highly toxic nuclear histone. This caused endothelial cell dysregulation leading to organ failure. However, this concept downplays the concept that concomitantly with the activation of PMNs, a plethora of additional proinflammatory agents is also released. These can act in synergy with histone to injure cells. Furthermore, since many additional clinical disorders not related to sepsis also reported high levels of circulating histones, this toxic agent may be considered just another marker of cell damage. The failure to treat sepsis by the administration of only single antagonists should be replaced by cocktails of appropriate anti inflammatory agents.

The aim of this study was to examine the structure of the placental villi associated with Zika virus at 28 weeks of pregnancy without another antecedent of illness and to be evaluated with light microscopy. Two groups of population of placental villi were taken of placenta study and placenta normal. The group studies proceed of placenta obtained at 37 weeks by caesarian delivery with fetal suffering. The placenta normal was obtained at 38 weeks with an increase of weight of woman pregnancy of 10 Kg both being processed according to previous works realized. The decidual region and stem villi showed infiltration of mononuclear cells. Stem villi were observed with thrombotic vessels, fibrinoid deposition, vascular obliteration, throphoblast necrosis and fibrosis. Zones of immature intermediate villi were seen suffering degenerative changes. Clear zones appeared in the stromal region of the placental villi. Mature intermediate villi have not bends and are absent of terminal villi. Numerous syncytial nodules are showed in zones of microinfarcts. Bad development of the ramifications of the placental villi is noted. These results indicate a destructive and generalized effect on the structure of the placental tree as also it has been affected by others viruses which damage the placenta contributing with fetal suffering or fetal death.

The Zika virus is a mosquito-borne flavivirus (Aedes) first identified in Uganda in 1947. Here we tried to collect scattered data and present a synthesis of the history and the current status of the disease. Its major epidemic in the world was presented and effective prevention techniques were cited. WHO estimated that 3 to 4 million people were expected to be infected with the Zika virus in 2017. Strategies for the prevention and control of Zika virus disease should include the use of insect repellent and mosquito vector eradication since there is currently no vaccine available.

Placental villi in a case of fetal death associate to complications of pregnancy as preeclampsia severe, megaloblastic macrocitic anemia, infection by Zika virus and marginal insertion of umbilical cord were showed in woman pregnancy of 26 years old at 22 weeks of pregnancy causing severe degenerative changes. Is our objective to explore the cell surface of the trophoblast identifying the changes observed with scanning electron microscopy. Samples of normal trophoblast were compared with samples of the case with the four complications. This case was correlated besides with the features found with light microscopy according with a preliminary study previously published. Groups of villi were seen not following their normal morphological pattern. Immature globular terminal villi rush out of mesenchymal villi in irregular aspect. These presented depressions or prolongations of syncytial plasma membrane. Mesenchymal villi are originating mature intermediate villi without to present terminal villi in their trajectory. Immature villi are covered by fibrinoid deposition as others placental villi. Many villi exhibit deep cracks. With frequency curvilinear mature intermediate villi were observed with proliferation of terminal villi in their extremity. These results indicate morphological bad development of the villous tree to the 22 weeks of pregnancy with deficiency of terminal villi and high risk of normal interchange of gases or nutrients contributing with the fetal death.

Periodontal disease or periodontitis is a chronic inflammatory disease which involves a group interactions between the pathogen and cellular host response. It is found to be the most prevalent bacterial diseases in humans. Ubiquitination is the mechanism in which the polypeptide ubiquitin is covalently attached to the obsolete proteins and degrades them with the help of three enzymes namely E1 (ubiquitin-activating enzyme), E2 (Ubiquitinconjugating enzyme), and E3 (Ubiquitin ligase). Any misfolding or malfunction of these proteins results in the overall destability leading to metabolic disorders in humans. It was studied that some E3 enzymes help in activating the E2 enzymes. The study was aimed mainly to see the role of E2 in the ubiquitination process and to screen the expression levels in the absence of E3. In this study the protein of interest was extracted from the recombinant bacterial clones and purified using the affinity, ion exchange and gel exclusion chromatography. The protein was then studied for the ubiquitination and deubiquitination assays and confirmation was done using SDS PAGE. E3 is normally required for the substrate complex formation, but in contrast we found that in the absence of E3, conjugating activity was found. Our results showed that E2 alone was responsible for the polyubiquitination which was confirmed on the western blot in both the assays. This peculiar feature of E2 can unravel many questions of genetic disorders too in humans.