Neurologic Disease after Yellow Fever Vaccination,São Paulo,Brazil, 2017–2018

Yellow fever (YF) vaccine can cause neurologic complications. We examined YF vaccine–associated neurologic disease reported from 3 tertiary referral centers in São Paulo, Brazil, during 2017–2018 and compared the performance of criteria established by the Yellow Fever Vaccine Working Group/Centers for Disease Control and Prevention and the Brighton Collaboration. Among 50 patients who met inclusion criteria, 32 had meningoencephalitis (14 with reactive YF IgM in cerebrospinal fluid), 2 died, and 1 may have transmitted infection to an infant through breast milk. Of 7 cases of autoimmune neurologic disease after YF vaccination, 2 were acute disseminated encephalomyelitis, 2 myelitis, and 3 Guillain-Barré syndrome. Neurologic disease can follow fractional vaccine doses, and novel potential vaccine-associated syndromes include autoimmune encephalitis, opsoclonus-myoclonus-ataxia syndrome, optic neuritis, and ataxia. Although the Brighton Collaboration criteria lack direct vaccine causal assessment, they are more inclusive than the Centers for Disease Control and Prevention criteria.     

Disparity of amniotic fluid volume and fetal size: problem of the stuck twin--US studies

The "stuck twin" phenomenon in monochorionic diamniotic (MCDA) pregnancies is characterized by marked disparity in both fluid volume and fetal size between the twin gestations. To determine the prevalence, sonographic characteristics, and clinical outcome of this phenomenon, discharge summaries, placental pathologic reports, and prenatal sonograms from 307 twin pregnancies were reviewed. Of 52 cases of MCDA pregnancies, 18 (35%) demonstrated marked disparity in amniotic fluid volume. In 16 of these 18 cases there was discordant twin growth, further suggesting the diagnosis of twin transfusion syndrome. All 16 cases and an additional nine cases supplied by another center demonstrated a small, morphologically normal fetus in an oligohydramniotic sac suspended anteriorly (72%) or laterally (28%) in the uterus. The amniotic membrane separating this twin from the larger twin in the polyhydramniotic sac was thin, closely applied to the smaller fetus, and difficult to detect. Perinatal morbidity was 100% for all twin pairs, and premature labor occurred in all cases. Perinatal mortality ranged from 88% for the larger/poly twin to 96% for the small/oligo twin.     

Immunologic analysis of the cloned platelet thrombin receptor activation mechanism: evidence supporting receptor cleavage, release of the N-terminal peptide, and insertion of the tethered ligand into a protected environment

The recently cloned functional thrombin receptor is thought to be activated by thrombin cleavage of the bond between R41 and S42, followed by the insertion of the new N-terminal region ("tethered ligand") into an unknown site in the receptor. Antibodies to peptides at or near the cleavage site have been reported to inhibit thrombin- induced platelet activation to varying extents, but the precise mechanism(s) of their inhibition is unknown. We have produced: (1) a polyclonal antibody in rabbits to a peptide containing amino acids 34 to 52 (anti-TR34-52); enzyme-linked immunosorbent assays (ELISA) indicate that anti-TR34-52 contains antibodies to regions on both sides of the thrombin cleavage site; (2) two murine monoclonal antibodies (MoAbs) to a peptide containing amino acids 29 to 68; one antibody reacts primarily with residues N-terminal to the thrombin cleavage site, and the other reacts primarily with residues C-terminal to the cleavage site; and (3) a polyclonal rabbit antibody to a peptide containing amino acids 83 to 94 (anti-TR83-94). Anti-TR34-52 binds to platelets as judged by flow cytometry, and pretreating platelets with a thrombin receptor peptide ligand does not lead to loss of antibody reactivity, suggesting that platelet activation does not initiate redistribution or internalization of surface thrombin receptors. In contrast, pretreating platelets with thrombin leads to complete loss of anti-TR34-52 binding. Similarly, the binding of both MoAbs to platelets is dramatically reduced by pretreatment with thrombin. However, the binding of anti-TR83-94 is not decreased by thrombin activation, confirming that the receptor is not internalized. Anti-TR34-52 profoundly inhibits low dose thrombin-induced platelet shape change and aggregation, but the inhibition can be overcome with higher thrombin doses. However, anti-TR34-52 does not inhibit platelet aggregation induced by tethered ligand peptides. The TR34-52 peptide is a thrombin substrate, with cleavage occurring at the R41-S42 bond as judged by high performance liquid chromatography (HPLC) and platelet aggregation analysis. Anti-TR34-52 prevented cleavage of the TR34-52 peptide, suggesting that the antibody prevents platelet activation, at least in part, by preventing cleavage of the thrombin receptor. These data, although indirect, provide additional support for a thrombin activation mechanism involving thrombin cleavage of the receptor; in addition, they provide new evidence indicating that receptor cleavage is followed by loss of the N-terminal peptide, and insertion of the tethered ligand into a protected domain.     

Testing the committee approach to translating measures across cultures: Translating primary communication inventory from English to Japanese

This paper presents the initial translation process and follow‐up psychometric evaluation of the Japanese version of the Primary Communication Inventory (J‐PCI). The J‐PCI was developed using the committee approach to translation and then used in a study exploring Japanese couples' communication satisfaction while separated during Satogaeri Bunben ‐ a Japanese perinatal tradition. The committee approach attends to cultural nuance and context and is especially useful when languages have dissimilar linguistic roots and cultures, such as Japanese and English. The translation process and evaluation included five steps; (i) selection of the original PCI for research; (ii) selection of translators; (iii) development of the J‐PCI using a committee approach; (iv) an initial small pilot study; and (v) a larger follow‐up study. The J‐PCI has good initial validity and reliability, although some nuances were observed in scoring.