Increased pulmonary embolism in patients with COVID-19: a case series and literature review.

There is some recent evidence that the coronavirus disease 2019 (COVID-19) increases the risk of venous thromboembolism by creating a prothrombotic state. COVID-19 and pulmonary embolism (PE) are both associated with tachypnoea, hypoxemia, dyspnoea, and increased D-dimer. Diagnosis of pulmonary embolism in a patient with COVID-19 compared to an individual without it, using the conventional clinical and biochemical evidence is challenging and somehow impossible. In this study, we reported four male cases affected by COVID-19 and admitted to hospitals in Sanandaj, Iran. The patients were all older adults (ranging between 56 and 95 years of age). Fever, chills, muscle pain, and cough were evident in all the cases. Red blood cell levels were low, and pulmonary embolism was clearly detected on spiral computed tomographic (CT) angiography of the pulmonary circulation of all patients. These cases demonstrated that COVID-19 may lead to pulmonary embolism by causing blood coagulation problems. As COVID-19 continues to cause considerable mortality, more information is emerging which reveals its complicated pathogenicity. In the meantime, venous thromboembolism remains an uncommon finding in patients with COVID-19. It is essential that health care providers perform the necessary diagnostic evaluations and provide appropriate treatment for patients.

A case report of greater saphenous vein thrombosis in a patient with coronavirus (COVID-19) infection.

In December 2019, the World Health Organization (WHO) announced a series of pneumonia cases caused by an unknown origin, discovered in Wuhan, China. A dangerous virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a disease named acute respiratory syndrome, which was later popularly called coronavirus infection (COVID-19). Patients with acute COVID-19 are at high risk of thrombosis in various blood vessels due to hypercoagulability, blood stasis, and endothelial damage. In this study, we present a case report of a patient with COVID-19, who was hospitalized in one of the hospitals in Sanandaj, Iran. There were symptoms of fever, chills, muscle aches, cough, and tachycardia. Laboratory tests showed high levels of CRP, ESR, Ferritin CLIA, LDH and D-Dimer in this patient. Doppler ultrasound of the patient also revealed an abnormal finding, thrombosis in the right greater saphenous vein. This suggests that COVID-19 may lead to other negative effects through damage to blood vessels.

miR223-3p, HAND2, and LIF expression regulated by calcitonin in the ERK1/2-mTOR pathway during the implantation window in the endometrium of mice.

PROBLEM: Approximately one-third of infertility cases are related to the female partner, and implantation failure is the primary reason for female infertility. The current research was established to assess the impact of calcitonin on endometrial receptivity. METHODS OF STUDY: 64 female BALB/c mice were assigned to 2 groups as follows: mice with regular ovarian cycle and mice with stimulated ovarian cycle. The two groups were further divided into four subgroups as follows: control (Ctrl), calcitonin (CT), pp242, and CT + pp242 groups. Calcitonin and pp242 were injected on days 3, 4, and 5 of pregnancy. On day 5 of gestation, all of the animals were sacrificed, and their uterine was removed for the morphological analysis, as well as the expression assessment genes and proteins. RESULTS: The results demonstrated that ovarian stimulation increased the rate of phosphorylation of ERK1/2 and mTOR proteins, and resulted in the upregulation of miR-223-3p. The administration of calcitonin also elevated the expression levels of LIF and HAND2 gene in both regular ovarian and ovarian-stimulated cycles. In ovarian-stimulated groups, the administration of calcitonin led to a decrease in the expression of miR-223-3p. Calcitonin administration also markedly increased the phosphorylation of 4EBP1 and ERK1/2 in the regular ovarian cycle. CONCLUSION: It seems that calcitonin is capable of enhancing the endometrial receptivity of the uterine, thereby the overexpression of HAND2 and LIF and downregulation of miR-223-3p through the ERK1/2-mTOR signaling pathway.

Acute Ischemic and Hemorrhagic Stroke and COVID-19: Case Series.

The coronavirus COVID-19 pandemic is the defining global health crisis of our time and the greatest challenge we have faced since the World Wars; it can attack several systems in the body and has high complications and mortality. COVID-19 can cause venous and arterial thromboembolism due to immobility, high inflammation, extensive intravascular blood coagulation, and hypoxia. In this study, we report 5 cases of adults with COVID-19, hospitalized in Tohid Hospital, Sanandaj, Iran. Three patients were male and two were female. The youngest patient was 20 years old and the oldest was 55 years old. All patients had at least one family member with coronavirus. Fever, chills, muscular pain, cough, and tachypnea were present in all patients. Red blood cell (RBC) was observed in all patients at a low level. Computed tomography (CT) scans of all patients showed abnormal findings in different areas of the brain. These cases indicate that COVID-19 may damage blood vessels in the brain and lead to stroke.

Ovarian vein thrombosis after coronavirus disease (COVID-19) infection in a pregnant woman: case report.

Corona virus outbreak started in December 2019, and the disease has been defined by the World Health Organization as a public health emergency. Coronavirus is a source of deep venous thrombosis (DVT) due to complications such as over-coagulation, blood stasis, and endothelial damage. In this study, we report a 26-year-old pregnant woman with coronavirus who was hospitalized with a right ovarian vein thrombosis at Besat Hospital in Sanandaj. Risk classification for deep vein thrombosis (DVT) disease is of crucial importance for the forecast of coronavirus.

The effect of fludrocortisone on the uterine receptivity partially mediated by ERK1/2-mTOR pathway.

Implantation of embryos needs endometrial receptivity. Mineralocorticoids is one of the causes influencing the implantation window. This study targeted to evaluation fludrocortisone different properties on endometrial receptivity. The objective of this study was to assess whether treatment with fludrocortisone could impact the expression of diverse genes and proteins that are involved in uterine receptivity in mice. In this study, 40 female adult BALB/c mice were used. The samples were allocated to four groups of ten. Control group (C) received: vehicle; fludrocortisone group (FCA): received 1.5 mg/kg fludrocortisone; PP242 group (PP242): received 30 mg/kg PP242; fludrocortisone+PP242 group (FCA+PP242): received fludrocortisone and PP242. Mice were killed on window implantation day after mating and confirmed pregnancy. The endometrial epithelium of mouse was collected to assess mRNA expression of leukemia inhibitory factor (LIF), mucin-1 (MUC1), heparin-binding epidermal growth factor (HB-EGF), (Msx.1), miRNA Let-7a, and miRNA 223-3p as well as protein expression of extracellular signal-regulated kinase 1/2 (ERK1/2), mammalian target of rapamycin (mTOR), and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) in the uterine using real-time PCR and western blot, respectively. In comparison with the control group, fludrocortisone administration upregulated the expression of LIF, HB-EGF, Msx.1, miRNA Let-7a, ERK1/2, and mTOR in the epithelial endometrium. The PP242-treated group demonstrated a significant rise in the expression of MUC1, miRNA 223-3p and a remarkable decline in ERK1/2 and p-4E-BP1 levels in comparison with the control group. Combination therapy of (FCA+PP242) resulted in a remarkable rise in LIF, Msx-1, HB-EGF, ERK1/2, and mTOR levels, in comparison with the PP242 group. Furthermore, combination therapy of (FCA+PP242) downregulated the expression of MUC1 in comparison with the PP242-treated group. According to the results, fludrocortisone affected uterine receptivity possibly by means of modulating the expression of genes involved in the uterine receptivity and activation of the ERK1/2-mTOR pathway.