Prenatal sonographic diagnosis of nondysraphic intramedullary lipomas: A case report

Nondysraphic intramedullary lipomas of the spinal cord are rare, and there are currently no reports of their observation in utero. Here, we present the sonographic (US) findings in such a case. Four intraspinal hyperechoic masses were observed on US on the dorsal aspect of the fetal spine in a 30‐year‐old woman at 30 weeks' gestation. Findings were consistent with those of prenatal MRI and were confirmed on autopsy after induced abortion. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 46 :278–281, 2018     

Arterial Stiffness as a Predictor of Clinical Hypertension

The association between vascular stiffening and blood pressure is likely bidirectional. The present study was designed to examine temporal relationships among vascular stiffness, blood pressure progression, and hypertension. The Asymptomatic Polyvascular Abnormalities Community study is a community‐based, prospective, long‐term follow‐up observational study. The present investigation is based on the baseline examinations (2010–2011) and the first follow‐up measurements (2012–2013) included in the study. A total of 4025 participants were followed for an average of 27 months. Of 2153 participants free of hypertension at the baseline examination, 432 (20.07%) had incident hypertension. The authors observed that brachial‐ankle pulse wave velocity (baPWV) was an independent predictor of incident hypertension. baPWV during baseline examination was positively associated with higher systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure during the first follow‐up examination. baPWV but not blood pressure during baseline examination was associated with baPWV during the first follow‐up examination. This study not only provides evidence that baPWV is an independent predictor of blood pressure progression and incident hypertension, but also provides evidence that blood pressure is not associated with baPWV after adjusting for baseline baPWV.     

Human HLA-specific T-cell clones with stable expression of a suicide gene: a possible tool to drive and control a graft-versus-host- graft- versus-leukemia reaction?

Allogeneic bone marrow transplantation is still limited by the morbidity and mortality caused by graft-versus-host disease (GVHD), resulting from host recognition by donor T lymphocytes. It is possible to drastically reduce the T-cell content of the graft. However, transplanted T cells can also have a beneficial effect by graft enhancement and the graft-versus-leukemia effect. How can we keep the beneficial GVL effect while protecting the patient from possible GVHD? A recent report proposed the ex vivo transfer of the herpes simplex thymidine kinase (HSv-tk) gene into donor T cells before their infusion with hematopoietic stem cells. This procedure is expected to allow selective donor T-cell depletion with ganciclovir should GVHD occur, but it has two major drawbacks: reinjection of a fraction of untransfected T cells cannot be avoided and heterogeneity of the transfected population results in increased risks such as HSv-tk gene instability or dysfunction of some of the transfected T cell. Alternative approaches must be considered. We demonstrate here the feasibility of generating HSv-tk transfected HLA-specific CD4+ cytotoxic T-cell clonal populations, in which 100% of the cells have the HSv-tk gene inserted at a single site within their genome. These clones retained their specificity, their function, and their sensitivity to ganciclovir treatment. Our approach is not limited to bone marrow transplantation. Indeed, this procedure represents a useful alternative to retroviral gene transduction and is applicable to every circumstance where clinical use of gene modified T-cell clones is to be considered.     

t(3;21)(q26;q22): a recurring chromosomal abnormality in therapy- related myelodysplastic syndrome and acute myeloid leukemia

We have identified an identical reciprocal translocation between the long arms of chromosomes 3 and 21 with breakpoints at bands 3q26 and 21q22, [t(3;21)(q26;q22)], in the malignant cells from five adult patients with therapy-related myelodysplastic syndrome (t-MDS) or acute myeloid leukemia (t-AML). Primary diagnoses were Hodgkin's disease in two patients and ovarian carcinoma, breast cancer, and polycythemia vera in one patient each. Patients had been treated with chemotherapy including an alkylating agent for their primary disease 1 to 18 years before the development of t-MDS or t-AML. We have not observed the t(3;21) in over 1,500 patients with a myelodysplastic syndrome or acute myeloid leukemia arising de novo or in over 1,000 patients with lymphoid malignancies. We have previously reported that the t(3;21) occurs in Philadelphia chromosome-positive chronic myelogenous leukemia (CML). Thus, the t(3;21) appears to be limited to t-MDS/t-AML and CML, both of which represent malignant disorders of an early hematopoietic precursor cell. These results provide a new focus for the study of therapy-related leukemia at the molecular level.     

Thrombin decreases von Willebrand factor binding to platelet glycoprotein Ib

Thrombin is a physiological agonist that promotes platelet aggregation and secretion. In this study we observed that thrombin can also inhibit a function of platelets related to primary hemostasis. Platelet stimulation by thrombin decreased the binding of von Willebrand factor (vWF) to glycoprotein (GP) Ib and decreased ristocetin-induced agglutination, in vitro reactions that correlate with initial platelet adhesion to the vessel wall. Binding of the monoclonal antibody API to GP Ib was also decreased. Cytoskeletal participation in the change of GP Ib was suggested because pretreatment of platelets with cytochalasin to prevent actin filament formation prevented the thrombin-induced decreases in vWF binding. API binding, and ristocetin-induced agglutination. Measurement of GP Ib in detergent extracts by electroimmunoassay demonstrated no loss after thrombin stimulation. Electroimmunoassay also demonstrated that the API epitope of GP Ib on intact thrombin-treated platelets was accessible for complete digestion by chymotrypsin. Therefore GP Ib was neither released from the platelet surface nor internalized by thrombin treatment. A previously recognized effect of thrombin is its induction of receptor sites on platelet surface GP IIb-IIIa for contact-promoting proteins, including vWF that are involved in the platelet spreading and aggregation that follow adhesion. Therefore the action on GP Ib may combine with the effect on GP IIb-IIIa to shift platelet reactivity from GP Ib-vWF-mediated initial contact with the vessel wall to GP IIb-IIIa-mediated spreading and aggregation.