Search

Background Atelectasis can occur in many clinical practices. One way to prevent this complication is through the alveolar recruitment maneuver (ARM). However, hemodynamic compromise can accompany ARM. This study aims to predict ARM-induced hypotension using a non-invasive method. Methods 94 American Society of Anesthesiologists physical status I–II patients aged 19 to 75 with scheduled spinal surgery were enrolled. After anesthesia, we performed a stepwise ARM. Data on perfusion index, mean arterial pressure, heart rate, pleth variability index, cardiac index, and stroke volume variation was collected before induction of anesthesia (T0), just before ARM (T1), at the start of ARM (T2), 0.5 min (T3), 1 min (T4), 1.5 min (T5, end of ARM), and 2 min after the beginning of ARM (T6). Hypotension was defined as when the mean arterial pressure at T5 decreased by 20% or more compared to the baseline. The primary endpoint is that the perfusion index measuring before induction of anesthesia, which reflects the patients’ own vascular tone, was correlated with hypotension during ARM. Results Seventy-five patients (79.8%) patients developed hypotension during ARM. The pre-induction persufion index (Pi) (95% confidence interval) was 1.7(1.4–3.1) in the non-hypotension group and 3.4(2.4–3.9) in the hypotension group. (p p p = 0.004), and the threshold value of the Pi was 2.4. Conclusion A higher perfusion index value measuring before induction of anesthesia can be used to predict the development of hypotension during ARM. Prophylactic management of the following hypotension during ARM could be considered in high baseline Pi patients.

Grape ripe rot is a fungal disease, which is almost inextinguishable particularly before and after harvest in most vineyards. The management of this disease largely depends on the breeding of resistant varieties. Thus, the search for resistant varieties should parallel the molecular analysis of the markers associated with disease resistance. Here, we tested the leaf inoculation assay of Colletotrichum acutatum and C. gloeosporioides by inoculating them into 350 grapevine varieties. As a result of the phenotypes common to both species, 119 varieties (34%) were classified as resistant. Consequently, we discovered the locus with nucleotide-binding sites and carboxyterminal leucine-rich repeat regions (NBS-LRR) associated with grape ripe rot resistance through genotyping-by-sequencing and genome-wide association study. Ultimately, we identified the Vitis vinifera Colletotrichum resistance protein (VvCRP) markers from chromosome 3, which belongs to the CC-NBS-LRR type, as disease-resistant proteins. These markers were verified as the melting peak, and their chromatograms of nucleotide sequences were visualized in each single nucleotide polymorphism (SNP) loci. All the SNP markers differentiated successfully the resistant from the susceptible cultivars. Interestingly, we also found that a resistant cultivar named Bailey Alicante A has a heterozygous genotype, substantiating its potential usefulness for crops such as grapevine with many hybrids. Altogether, our results indicate that VvCRP markers can be utilized to distinguish grape ripe rot-resistant cultivars, particularly in crossbreeding populations.

Postural change from a steep Trendelenburg position to a supine position (T-off) during robot-assisted laparoscopic prostatectomy (RALP) induces a considerable abrupt decrease in the mean arterial pressure (MAP). We investigated the variables for predicting postural hypotension induced by T-off using esophageal Doppler monitoring (EDM). One hundred and twenty-five patients undergoing RALP were enrolled. Data on the MAP, heart rate, stroke volume index (SVI), cardiac index, peak velocity, corrected flow time, stroke volume variation, pulse pressure variation, arterial elastance (Ea), and dynamic arterial elastance were collected before T-off and at 1, 3, 5, 7, and 10 min after T-off using EDM. MAP P P P 2, and ≤ 1.08 mmHg/mL, respectively. If patients have MAP 2 or Ea ≤ 1.08 mmHg/mL before postural change from T-off during RALP, prompt management for ensuing hypotension should be considered.Trial registration: NCT03882697 (ClinicalTrial.gov, March 20, 2019).

Influenza viruses exploit host factors to successfully replicate in infected cells. Using small interfering RNA (siRNA) technology, we identified six human genes required for influenza A virus (IAV) replication. Here we focused on the role of acid phosphatase 2 (ACP2), as its knockdown showed the greatest inhibition of IAV replication. In IAV-infected cells, depletion of ACP2 resulted in a significant reduction in the expression of viral proteins and mRNA, and led to the attenuation of virus multi-cycle growth. ACP2 knockdown also decreased replication of seasonal influenza A and B viruses and avian IAVs of the H7 subtype. Interestingly, ACP2 depletion had no effect on the replication of Ebola or hepatitis C virus. Because ACP2 is known to be a lysosomal acid phosphatase, we assessed the role of ACP2 in influenza virus entry. While neither binding of the viral particle to the cell surface nor endosomal acidification was affected in ACP2-depleted cells, fusion of the endosomal and viral membranes was impaired. As a result, downstream steps in viral entry were blocked, including nucleocapsid uncoating and nuclear import of viral ribonucleoproteins. Our results established ACP2 as a necessary host factor for regulating the fusion step of influenza virus entry.

Hepatitis B virus (HBV) genome replication requires the packaging of viral factors (pregenomic RNA and polymerase) as well as host factors, including heat shock proteins and protein kinase C. Previous reports have suggested that there are several unidentified host factors that affect this encapsidation step. In this study, we identified a new host factor, nucleophosmin (B23) that interacts with the HBV core protein 149 (Cpl49). We analyzed this factor using NHS-activated sepharose resin and MALDI-TOF MS. Using the BIAcore analysis system, we were also able to deduce that the B23.1 residues 259-294 were required for the interaction between Cpl49 and B23.1 in vitro.

Background The molecular and biological mechanisms by which many antidepressants function are based on the monoamine depletion hypothesis. However, the entire cascade of mechanisms responsible for the therapeutic effect of antidepressants has not yet been elucidated. Results We used a genome-wide microarray system containing 30,000 clones to evaluate total RNA that had been isolated from the brains of treated rats to identify the genes involved in the therapeutic mechanisms of various antidepressants, a tricyclic antidepressant (imipramine). a selective serotonin reuptake inhibitor (fluoxetine), a monoamine oxidase inhibitor (phenelzine) and psychoactive herbal extracts of Nelumbinis Semen (NS). To confirm the differential expression of the identified genes, we analyzed the amount of mRNA that was isolated from the hippocampus of rats that had been treated with antidepressants by real-time RT-PCR using primers specific for selected genes of interest. These data demonstrate that antidepressants interfere with the expression of a large array of genes involved in signaling, survival and protein metabolism, suggesting that the therapeutic effect of these antidepressants is very complex. Surprisingly, unlike other antidepressants, we found that the standardized herbal medicine, Nelumbinis Semen, is free of factors that can induce neurodegenerative diseases such as caspase 8, α-synuclein, and amyloid precursor protein. In addition, the production of the inflammatory cytokine, IFNγ, was significantly decreased in rat hippocampus in response to treatment with antidepressants, while the inhibitory cytokine, TGFβ, was significantly enhanced. Conclusions These results suggest that antidepressants function by regulating neurotransmission as well as suppressing immunoreactivity in the central nervous system.

High-throughput RNAi screens in human cells suggest new approaches to curb influenza virus infection.