Fruitlet core rot (FCR) is a worldwide fungal disease of pineapple, which occasionally occurs on susceptible cultivars in Taiwan. This study describes the fungal pathogens of FCR and their occurrence in Taiwan for the first time. A total of 51 fungal isolates were obtained from diseased fruitlets and blossom cups of ‘TN20’, a susceptible cultivar planted in Taiwan. These isolates were identified as the Talaromyces species T. amestolkiae, T. funiculosus, and T. stollii and Fusarium species F. ananatum, F. oxysporum, and F. annulatum based on phylogenetic analyses. All of them have been described as FCR pathogens in other countries, if considering that F. annulatum has often been misidentified as F. proliferatum. To facilitate identification, four pairs of species-specific primers were developed, which enabled rapid identification of T. amestolkiae, T. funiculosus, and T. stollii by multiplex polymerase chain reaction (PCR) and F. ananatum by PCR. Two types of diseased fruitlets, “wet” and “dry”, were observed on ‘TN20’, and T. amestolkiae, T. funiculosus, T. stollii, and F. ananatum could be isolated from both types. In addition, Talaromyces and Fusarium species were isolated from blossom cups at high frequencies, but few fungi were isolated from healthy tissues. The specific primers designed in this study could provide a useful tool to study FCR in the future, and the findings could provide a better understanding of the ecology and epidemiology of FCR.

The authors reported the clinical course of a 58-year-old female suffering from cerebral venous sinus thrombosis associated with hemorrhage after the ChAdOx1 nCov-19 vaccination. Emergent decompressive craniectomy was performed, and aggressive blood transfusion was given. Nevertheless, progressive intracerebral hemorrhage and thrombocytopenia developed. A delayed diagnosis was made on a rare complication of vaccine-induced immune thrombotic thrombocytopenia (VITT) with a positive result of anti-platelet factor 4 antibodies (PF4 Ab). The patient died 4 days postoperative due to brainstem failure.

Background In patients with heart failure, interleukin-18 (IL-18) levels increase in the circulatory system and injured myocardial tissue. Serotonin (5-hydroxytryptamine) receptors subtype 2B (HTR2B) play an essential role in cardiac function and development, and their overexpression in rats leads to myocardial hypertrophy. Epigallocatechin gallate (EGCG) is cardioprotective in myocardial ischemia–reperfusion injury in rats and can prevent pressure overload-mediated cardiac hypertrophy in vivo. Mice deficient in peroxisome proliferator-activated receptor delta (PPARδ) can have cardiac dysfunction, myocardial hypertrophy, and heart failure. Matrix metalloproteinases (MMPs) are possibly involved in cardiac remodeling. However, the relationship between IL-18 signaling, cardiac hypertrophy, and the molecular mechanisms involved remain to be fully elucidated. Objectives To elucidate the relationship between HTR2B and IL-18-induced myocardial hypertrophy and examine the antihypertrophic effects of EGCG and PPARδ. Methods We induced H9c2 cardiomyoblast hypertrophy with IL-18 in vitro and investigated the downstream signaling by real-time polymerase chain reaction (PCR) and western blotting. Hypertrophy was assessed by flow cytometry. We determined the effects of EGCG and PPARδ on IL-18-induced hypertrophic signaling via HTR2B-dependent mechanisms. Results IL-18-induced H9c2 hypertrophy upregulated brain natriuretic peptide (BNP) protein and mRNA expression by inducing the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and the hypertrophy was attenuated by pretreatment with EGCG (20 μM) and L-165,041 (2 μM), a PPARδ agonist. IL-18 upregulated the expression of HTR2B, which was inhibited by pretreatment with EGCG and L-165,041. SB215505 (0.1 μM), a HTR2B antagonist and siRNA for HTR2B, attenuated H9c2 hypertrophy significantly. Inhibition of HTR2B also downregulated the expression of MMP-3 and MMP-9. Conclusions IL-18 and HTR2B play critical roles in cardiomyoblast hypertrophy. EGCG and L-165,041 inhibit the expression of HTR2B and augment remodeling of H9c2 cardiomyoblasts, possibly mediated by MMP-3 and MMP-9.