The effect of placenta previa on fetal weight and feto-maternal blood flow: a prospective cohort study

Background: The current study aims to evaluate the effect of placenta previa on the fetal weight and to explore its effect on the uterine and umbilical arteries blood flow.Methods: The current study was a prospective cohort study conducted at Assiut Women’s Health Hospital, Egypt from 1st of October 2016 to 30th of September 2017 including placenta previa and non-placenta previa women. They were followed up by two-dimensional ultrasound and Doppler blood flow in the uterine and umbilical arteries. The main study outcome was the number of low birth weight (LBW) babies delivered at or beyond 37 weeks and blood flow changes in uterine and umbilical arteries.Results: Two hundred twelve women were divided into two groups; group I included 106 placenta previa women (PP group) and 106 non-placenta previa women (NPP group). The number of LBW babies were comparable in both groups without statistically significant difference (P value= 0.555). Neither; uterine artery nor umbilical artery blood flow had any significant differences between the groups.  Preterm delivery was significantly higher in the PP group (p value=0.000).Conclusions: Although there is no agreement, in the literature, on the association between placenta previa and LBW, authors suggest that placenta previa is not a reason for LBW babies. In addition, placenta previa shows no effect on uterine artery or umbilical artery blood flow

The FGFR4-G388R Polymorphism Promotes Mitochondrial STAT3 Serine Phosphorylation to Facilitate Pituitary Growth Hormone Cell Tumorigenesis

Pituitary tumors are common intracranial neoplasms, yet few germline abnormalities have been implicated in their pathogenesis. Here we show that a single nucleotide germline polymorphism (SNP) substituting an arginine (R) for glycine (G) in the FGFR4 transmembrane domain can alter pituitary cell growth and hormone production. Compared with FGFR4-G388 mammosomatotroph cells that support prolactin (PRL) production, FGFR4-R388 cells express predominantly growth hormone (GH). Growth promoting effects of FGFR4-R388 as evidenced by enhanced colony formation was ascribed to Src activation and mitochondrial serine phosphorylation of STAT3 (pS-STAT3). In contrast, diminished pY-STAT3 mediated by FGFR4-R388 relieved GH inhibition leading to hormone excess. Using a knock-in mouse model, we demonstrate the ability of FGFR4-R385 to promote GH pituitary tumorigenesis. In patients with acromegaly, pituitary tumor size correlated with hormone excess in the presence of the FGFR4-R388 but not the FGFR4-G388 allele. Our findings establish a new role for the FGFR4-G388R polymorphism in pituitary oncogenesis, providing a rationale for targeting Src and STAT3 in the personalized treatment of associated disorders

Rewiring coral: Anthropogenic nutrients shift diverse coral–symbiont nutrient and carbon interactions toward symbiotic algal dominance

Improving coral reef conservation requires heightened understanding of the mechanisms by which coral cope with changing environmental conditions to maintain optimal health. We used a long‐term (10 month) in situ experiment with two phylogenetically diverse scleractinians (Acropora palmata and Porites porites) to test how coral–symbiotic algal interactions changed under real‐world conditions that were a priori expected to be beneficial (fish‐mediated nutrients) and to be harmful, but non‐lethal, for coral (fish + anthropogenic nutrients). Analyzing nine response variables of nutrient stoichiometry and stable isotopes per coral fragment, we found that nutrients from fish positively affected coral growth, and moderate doses of anthropogenic nutrients had no additional effects. While growing, coral maintained homeostasis in their nutrient pools, showing tolerance to the different nutrient regimes. Nonetheless, structural equation models revealed more nuanced relationships, showing that anthropogenic nutrients reduced the diversity of coral–symbiotic algal interactions and caused nutrient and carbon flow to be dominated by the symbiont. Our findings show that nutrient and carbon pathways are fundamentally “rewired” under anthropogenic nutrient regimes in ways that could increase corals’ susceptibility to further stressors. We hypothesize that our experiment captured coral in a previously unrecognized transition state between mutualism and antagonism. These findings highlight a notable parallel between how anthropogenic nutrients promote symbiont dominance with the holobiont, and how they promote macroalgal dominance at the coral reef scale. Our findings suggest more realistic experimental conditions, including studies across gradients of anthropogenic nutrient enrichment as well as the incorporation of varied nutrient and energy pathways, may facilitate conservation efforts to mitigate coral loss.We provide a long‐term field experiment to test the implications of different nutrient sources, fish excretion and moderate levels of anthropogenic nutrients, for coral health and coral–symbiont interactions. Our study identifies a potentially novel "transition state" whereby despite maintaining high growth rates and creating no apparent negative external effects, anthropogenic nutrient enrichment drives coral–algal interactions to be dominated by the algal symbiont—that is, increased prominence of energy and nutrient flow from the algal symbiont under conditions of Fish + anthropogenic nutrients (NPK) in the figure. We hypothesize that this “rewiring” of the coral–symbiont interactions may render the coral more vulnerable to additional stressors.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162733/2/gcb15230_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162733/1/gcb15230.pd

Identification and characterization of an inhibitory fibroblast growth factor receptor 2 (FGFR2) molecule, up-regulated in an Apert Syndrome mouse model

AS (Apert syndrome) is a congenital disease composed of skeletal, visceral and neural abnormalities, caused by dominant-acting mutations in FGFR2 [FGF (fibroblast growth factor) receptor 2]. Multiple FGFR2 splice variants are generated through alternative splicing, including PTC (premature termination codon)-containing transcripts that are normally eliminated via the NMD (nonsense-mediated decay) pathway. We have discovered that a soluble truncated FGFR2 molecule encoded by a PTC-containing transcript is up-regulated and persists in tissues of an AS mouse model. We have termed this IIIa–TM as it arises from aberrant splicing of FGFR2 exon 7 (IIIa) into exon 10 [TM (transmembrane domain)]. IIIa–TM is glycosylated and can modulate the binding of FGF1 to FGFR2 molecules in BIAcore-binding assays. We also show that IIIa–TM can negatively regulate FGF signalling in vitro and in vivo. AS phenotypes are thought to result from gain-of-FGFR2 signalling, but our findings suggest that IIIa–TM can contribute to these through a loss-of-FGFR2 function mechanism. Moreover, our findings raise the interesting possibility that FGFR2 signalling may be a regulator of the NMD pathway

Transseptal puncture for left atrial ablation: Risk factors for cardiac tamponade and a proposed causative classification system

AIMS: Cardiac tamponade is a high morbidity complication of transseptal puncture (TSP). We examined the associations of TSP‐related cardiac tamponade (TRCT) for all patients undergoing left atrial ablation at our center from 2016 to 2020. METHODS AND RESULTS: Patient and procedural variables were extracted retrospectively. Cases of cardiac tamponade were scrutinized to adjudicate TSP culpability. Adjusted multivariate analysis examined predictors of TRCT. A total of 3239 consecutive TSPs were performed; cardiac tamponade occurred in 51 patients (incidence: 1.6%) and was adjudicated as TSP‐related in 35 (incidence: 1.1%; 68.6% of all tamponades). Patients of above‐median age [odds ratio (OR): 2.4 (1.19–4.2), p = .006] and those undergoing re‐do procedures [OR: 1.95 (1.29–3.43, p = .042] were at higher risk of TRCT. Of the operator‐dependent variables, choice of transseptal needle (Endrys vs. Brockenbrough, p > .1) or puncture sheath (Swartz vs. Mullins vs. Agilis vs. Vizigo vs. Cryosheath, all p > .1) did not predict TRCT. Adjusting for operator, equipment and demographics, failure to cross the septum first pass increased TRCT risk [OR: 4.42 (2.45–8.2), p = .001], whilst top quartile operator experience [OR: 0.4 (0.17–0.85), p = .002], transoesophageal echocardiogram [TOE prevalence: 26%, OR: 0.51 (0.11–0.94), p = .023], and use of the SafeSept transseptal guidewire [OR: 0.22 (0.08–0.62), p = .001] reduced TRCT risk. An increase in transseptal guidewire use over time (2016: 15.6%, 2020: 60.2%) correlated with an annual reduction in TRCT (R (2) = 0.72, p < .001) and was associated with a relative risk reduction of 70%. CONCLUSIONS: During left atrial ablation, the risk of TRCT was reduced by operator experience, TOE‐guidance, and use of a transseptal guidewire, and was increased by patient age, re‐do procedures, and failure to cross the septum first pass

Bullets over ballots: Islamist groups, the state and electoral violence in Egypt and Morocco

This article is concerned with state-sponsored electoral violence in liberalized autocracies. The first section of the paper identifies a number of variables that can help explain the decision calculus of authoritarian incumbents to deploy force against strong electoral challengers. The second section then examines these propositions with reference to Egypt and Morocco. Drawing on recent parliamentary elections in both countries the article questions why, despite facing the challenge of political Islam, the two regimes differed so markedly in their willingness to manipulate the polls by recourse to violence. Whilst the Egyptian authorities decided to abrogate all pretence of peaceful elections in favour of violent repression against the Muslim Brotherhood candidates and sympathizers, no such tactics were deployed by the ruling elite in Morocco. We suggest that three principal factors influenced the regimes' response to this electoral challenge: (1) the centrality of the elected institution to authoritarian survival; (2) the availability of alternative electioneering tools; and (3) the anticipated response of the international community. The article concludes by suggesting that in order to understand better when and how states deploy violence in elections, we need to focus on a more complex set of factors rather than simply on the electoral potency of key opposition challengers or the authoritarian nature of the state

Internet-based search of randomised trials relevant to mental health originating in the Arab world

BACKGROUND: The internet is becoming a widely used source of accessing medical research through various on-line databases. This instant access to information is of benefit to busy clinicians and service users around the world. The population of the Arab World is comparable to that of the United States, yet it is widely believed to have a greatly contrasting output of randomised controlled trials related to mental health. This study was designed to investigate the existence of such research in the Arab World and also to investigate the availability of this research on-line. METHODS: Survey of findings from three internet-based potential sources of randomised trials originating from the Arab world and relevant to mental health care. RESULTS: A manual search of an Arabic online current contents service identified 3 studies, MEDLINE, EMBASE, and PsycINFO searches identified only 1 study, and a manual search of a specifically indexed, study-based mental health database, PsiTri, revealed 27 trials. CONCLUSION: There genuinely seem to be few trials from the Arab world and accessing these on-line was problematic. Replication of some studies that guide psychiatric/psychological practice in the Arab world would seem prudent

Reverse engineering synthetic antiviral amyloids

Human amyloids have been shown to interact with viruses and interfere with viral replication. Based on this observation, we employed a synthetic biology approach in which we engineered virus-specific amyloids against influenza A and Zika proteins. Each amyloid shares a homologous aggregation-prone fragment with a specific viral target protein. For influenza we demonstrate that a designer amyloid against PB2 accumulates in influenza A-infected tissue in vivo. Moreover, this amyloid acts specifically against influenza A and its common PB2 polymorphisms, but not influenza B, which lacks the homologous fragment. Our model amyloid demonstrates that the sequence specificity of amyloid interactions has the capacity to tune amyloid-virus interactions while allowing for the flexibility to maintain activity on evolutionary diverging variants. Some human amyloid proteins have been shown to interact with viral proteins, suggesting that they may have potential as therapeutic agents. Here the authors design synthetic amyloids specific for influenza A and Zika virus proteins, respectively, and show that they can inhibit viral replication

Pathology of the human pituitary adenomas

This article describes pertinent aspects of histochemical and molecular changes of the human pituitary adenomas. The article outlines individual tumor groups with general, specific and molecular findings. The discussion further extends to the unusual adenomas or carcinomas. The description in this article are pertinent not only for the practicing pathologists who are in the position of making proper diagnosis, but also for the pituitary research scientists who engage in solving basic problems in pituitary neoplasms by histochemistry and molecular biology