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Articles by Beni-Suef University

Predominance of fetal malformations among pregnant women: A multi-centric observational study

Published on: 28th April, 2021

OCLC Number/Unique Identifier: 9022388562

Objective: To observe the predominance of fetal anomalies in pregnant women in a multi-centric setting. Methods: This prospective observational study included 20225 pregnant women who came for antenatal care in University Hospital and fetal medicine units from 2016 to 2019. Fetal anatomical scanning was done for all participants. Results: One hundred eighty-three cases had fetal congenital anomalies, yielding a prevalence of around 0.9%. Third of cases had positive consanguinity, this increased in cases of skeletal and thoracic anomalies. The presence of past history of anomalies was evident in 8.2% mostly with skeletal and heart anomalies. History of drug intake was only verified in 1.6% of cases. Sixty-three women out of 183 (34.4%) were diagnosed to have anomalies in fetal nervous system. Conclusion: Prenatal diagnosis are recommended for early detection of congenital anomalies and counselling.
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Perinuclear halo indicate Trichomonas vaginalis in Pap smear

Published on: 11th January, 2019

OCLC Number/Unique Identifier: 7986007615

Trichomonas vaginalis could be seen in Pap smears where it is reported, but because main concerned is placed on malignant cells in Pap smears, not much effort is done to search for this parasite in smears. In this study, 100 cervical and vaginal specimens were examined microscopically by the conventional Papanicolaou method and liquid base cytology (LBC) for the presence of Trichomonas vaginalis (T.vaginalis). 16% were infected with T.vaginalis while 10% of diagnosis based on both perinuclear halo and T. vaginalis presence although the association between perinuclear halo and T, vaginalis is statistically insignificant it is recommended to increase the number of the cases to prove or disprove the association
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Maternal thyroid dysfunction and neonatal cardiac disorders

Published on: 27th December, 2017

OCLC Number/Unique Identifier: 7355941189

The normal levels of thyroid hormones (THs; thyroxine, T4 & 3,5,3′-triiodo-L-thyronine, T3) are necessary for the normal development [1-48], particularly the fetal and neonatal cardiac growth and development [49]. The actions of THs are facilitated genomically by thyroid receptors (TRs, α and β) and non-genomically at the plasma membrane, in the cytoplasm and in cellular organelles [4,49-55], by stimulation of Na+, K+, Ca2+ and glucose transport, activation of protein kinase C (PKC), protein kinase A (PKA) and mitogen activated and protein kinase (ERK/MAPK) [4]. In addition, the transport of T4 and T3 in and out of cells is controlled by several classes of transmembrane TH-transporters (THTs) [56], including members of the organic anion transporter family (OATP), L-type amino acid transporters (LATs), Na+/Taurocholate cotransporting polypeptide (NTCP), and monocarboxylate transporters (MCTs) [4,49,57,58]. Adding additional complexity, the metabolism of T4 and T3 is regulated by 3 selenoenzyme iodothyronine deiodinases (Ds: D1, D2 and D3) [59-61]. On the other hand, the congenital hypothyroidism can cause the following [49,62-64], (1) congenital heart diseases; (2) diastolic hypertension; (3) reduced cardiac output, stroke volume and a narrow pulse pressure; (4) dilatation and overt heart failure; (5) elevation in the systemic vascular resistance [65-68]. Similarly, the chronic hyperthyroidism can cause the following [49,64]: (1) cardiac hypertrophy; (2) increase in the cardiomyocyte (CM) length rather than width; (3) noticeable diminution in systemic vascular resistance; (4) elevation in the cardiac contractility; (5) systolic hypertension; (6) increase in the cardiac output, venous volume return, blood volume and pulse pressure; and (7) reduction in the systemic vascular resistance [49,69]. T3-therapy can induce DNA synthesis and cardiomyocyte proliferation, and improve the cardiac contractility; though, this action is as still unidentified [49,70-74].
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