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Abstract Background Amidst the escalating loss of global biodiversity, freshwater mussels (family Unionidae) have become one of the most imperiled animal groups. Acquiring more biological and phylogenetic information on understudied taxa constitutes a pivotal aspect of conservation biology. Consequently, a comprehensive examination was conducted on Koreosolenaia, Parvasolenaia, and Sinosolenaia from China encompassing morphology, anatomy, distribution, and molecular systematics to provide theoretical support for future species endangerment assessments and biodiversity conservation. Results The shell characteristics of Koreosolenaia, Parvasolenaia, and Sinosolenaia were clearly distinct, and the soft-body morphology could also be easily distinguished from each other. The papillae of the incurrent aperture of Sinosolenaia iridinea, Sinosolenaia recognita, and Sinosolenaia oleivora, which were previously described as difficult, exhibited significant variations that could be utilized for species diagnosis. Furthermore, both incurrent and excurrent apertures of the Sinosolenaia species had small cysts on their dorsal surfaces which may be unique to this particular group. Comparative analysis of six mitochondrial genomes (Parvasolenaia rivularis, Koreosolenaia sitgyensis, Sinosolenaia iridinea, Sinosolenaia recognita, Sinosolenaia carinata, and Sinosolenaia oleivora) revealed a completely consistent gene arrangement pattern. Additionally, there was a high consistency in nucleotide base content and skewness, amino acid usage, and relative synonymous codon usage among the six complete mitochondrial genomes. Mitochondrial phylogenomics of these genomes with additional taxa within Gonideinae robustly supported the generic relationships as follows: (Inversidens + ((Microcondylaea + Sinosolenaia) + (Parvasolenaia + (Koreosolenaia + (Ptychorhynchus + (Postolata + Cosmopseudodon)))))). Conclusions The present study provided significant data on the shell morphology and soft-body anatomy of Koreosolenaia, Parvasolenaia, and Sinosolenaia, thereby clarifying the diagnostic characteristics for these challenging taxa. Additionally, we established a robust phylogenetic framework at both the generic and species levels based on mitochondrial genomics.

A new species of freshwater mussel belonging to the genus Pseudocuneopsis, namely Pseudocuneopsis yangshuoensis sp. nov., is diagnosed and described from Guangxi Province, China. This paper provides a detailed morphological description, photograph of the type specimen, and anatomical characteristics along with partial sequences of mitochondrial COI as DNA barcode data for this novel species. The new species can be distinguished from its congeners (Pseudocuneopsis sichuanensis and Pseudocuneopsis capitata) by shell shape, beak position and surface sculpture. The interspecies genetic distance based on the COI barcode between P. yangshuoensis sp. nov. and P. sichuanensis is 8%, while it reaches 9% with P. capitata. Therefore, we provide robust morphological and molecular evidence to support the validity of this new species.

The occurrence and transmission of carbapenemase-producing-Enterobacterales (CPE) on a global scale has become a major issue. Clinical reports are rarely providing information on the genomic and plasmid features of carbapenem-resistant Serratia marcescens. Our objective was to investigate the resistance and transmission dynamics of two carbapenem-resistant S. marcescens that are resistant to carbapenem and have caused bacteremia in China. Blood specimens were taken from two individuals with bacteremia. Multiplex PCR was employed to identify genes that code for carbapenemase. Antimicrobial susceptibility tests and plasmid analysis were conducted on S. marcescens isolates SM768 and SM4145. The genome of SM768 and SM4145 were completely sequenced using NovaSeq 6000-PE150 and PacBio RS II platforms. Antimicrobial resistance genes (ARGs) were predicted using the ResFinder tool. S1 nuclease pulsed-field gel electrophoresis (S1-PFGE) and southern blotting were employed to analyze plasmids. Two S. marcescens that produced KPC-2 were identified from bloodstream infections. The antimicrobial susceptibility testing demonstrated that both of the isolates had a resistance to various antibiotics. The whole-genome sequence (WGS) and plasmid analysis revealed the presence of blaKPC-2-bearing IncR plasmids and multiple plasmid-borne antimicrobial resistance genes in the isolates. Our comparative plasmid analysis suggested that the two IncR plasmids identified in this study could be derived from a common ancestor. Our findings revealed the emergence of blaKPC-2-bearing IncR plasmid in China, which could be a hindrance to the transmission of KPC-2-producing S. marcescens in clinical settings.

Objective: To evaluate the long-term consequences of COVID-19 survivors one year after recovery, and to identify the risk factors associated with abnormal patterns in chest imaging manifestations or impaired lung function. Methods: COVID-19 patients were recruited and prospectively followed up with symptoms, health-related quality of life, psychological questionnaires, 6-minute walking test, chest computed tomography (CT), pulmonary function tests, and blood tests. Multivariable logistic regression models were used to evaluate the association between the clinical characteristics and chest CT abnormalities or pulmonary function. Results: Ninety-four patients with COVID-19 were recruited between January 16 and February 6, 2021. Muscle fatigue and insomnia were the most common symptoms. Chest CT scans were abnormal in 71.28% of participants. The results of multivariable regression showed an increased odds in age. Ten patients had diffusing capacity of the lung for carbon monoxide (DLCO) impairment. Urea nitrogen concentration on admission was significantly associated with impaired DLCO. IgG levels and neutralizing activity were significantly lower compared with those in the early phase. Conclusions: One year after hospitalization for COVID-19, a cohort of survivors were mainly troubled with muscle fatigue and insomnia. Pulmonary structural abnormalities and pulmonary diffusion capacities were highly prevalent in surviving COVID-19 patients. It is necessary to intervene in the main target population for long-term recovery.

Abstract Background Argeia pugettensis is an isopod species that parasitizes other crustaceans. Its huge native geographic range spans the Pacific from China to California, but molecular data are available only for a handful of specimens from North-American populations. We sequenced and characterised the complete mitogenome of a specimen collected in the Yellow Sea. Results It exhibited a barcode (cox1) similarity level of only 87–89% with North-American populations, which is unusually low for conspecifics. Its mitogenome is among the largest in isopods (≈16.5 Kbp), mostly due to a large duplicated palindromic genomic segment (2 Kbp) comprising three genes. However, it lost a segment comprising three genes, nad4L-trnP-nad6, and many genes exhibited highly divergent sequences in comparison to isopod orthologues, including numerous mutations, deletions and insertions. Phylogenetic and selection analyses corroborated that this is one of the handful of most rapidly evolving available isopod mitogenomes, and that it evolves under highly relaxed selection constraints (as opposed to positive selection). However, its nuclear 18S gene is highly conserved, which suggests that rapid evolution is limited to its mitochondrial genome. The cox1 sequence analysis indicates that elevated mitogenomic evolutionary rates are not shared by North-American conspecifics, which suggests a breakdown of cox1 barcoding in this species. Conclusions A highly architecturally disrupted mitogenome and decoupling of mitochondrial and nuclear rates would normally be expected to have strong negative impacts on the fitness of the organism, so the existence of this lineage is a puzzling evolutionary question. Additional studies are needed to assess the phylogenetic breadth of this disrupted mitochondrial architecture and its impact on fitness.

Antiviral innate immune response triggered by nucleic acid recognition plays an extremely important role in controlling viral infections. The initiation of antiviral immune response against RNA viruses through ligand recognition of retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) was extensively studied. RLR’s role in DNA virus infection, which is less known, is increasing attention. Here, we review the research progress of the ligand recognition of RLRs during the DNA virus infection process and the viral evasion mechanism from host immune responses.

HHV-6B (human herpesvirus 6B) is well known to evade host antiviral responses and establish a lifelong latent infection. How HHV-6B evades RNA recognition is still poorly understood. Our results indicate that HHV-6 U26 plays a vital role in RLR/MAVS signaling pathway activity. Knockout of endogenous MAVS could facilitate HHV-6B replication. The findings in this study could provide new insights into host-virus interactions and help develop a new therapy against HHV-6B infection.

Human herpesvirus 6 (HHV-6) is an important immunosuppressive and immunomodulatory virus worldwide. However, whether and how HHV-6 infection influences the metabolic machinery of the host cell to provide the energy and biosynthetic resources for virus propagation remains unknown. In this study, we identified that HHV-6A infection promotes glucose metabolism in infected T cells, resulting in elevated glycolytic activity with an increase of glucose uptake, glucose consumption and lactate secretion. Furthermore, we explored the mechanisms involved in HHV-6A-mediated glycolytic activation in the infected T cells. We found increased expressions of the key glucose transporters and glycolytic enzymes in HHV-6A-infected T cells. In addition, HHV-6A infection dramatically activated AKT-mTORC1 signaling in the infected T cells and pharmacological inhibition of mTORC1 blocked HHV-6A-mediated glycolytic activation. We also found that direct inhibition of glycolysis by 2-Deoxy-D-glucose (2-DG) or inhibition of mTORC1 activity in HHV-6A-infected T cells effectively reduced HHV-6 DNA replication, protein synthesis and virion production. These results not only reveal the mechanism of how HHV-6 infection affects host cell metabolism, but also suggest that targeting the metabolic pathway could be a new avenue for HHV-6 therapy.

Abstract Background Propofol, a commonly used intravenous anesthetic, is associated with various respiratory adverse events, most notably different degrees of respiratory depression, which pose significant concerns for patient safety. Respiration is a fundamental behavior, with the initiation of breathing in mammals dependent on neuronal activity in the lower brainstem. Previous studies have suggested that propofol-induced respiratory depression might be associated with glutamatergic neurons in the pre-Bötzinger complex (preBötC), though the precise mechanisms are not well understood. In this study, we classify glutamatergic neurons in the brainstem preBötC using whole-cell patch-clamp techniques and investigate the effects of propofol on the electrophysiological properties of these neurons. Our findings aim to shed light on the mechanisms of propofol-induced respiratory depression and provide new experimental insights. Methods We first employed electrophysiological techniques to classify glutamatergic neurons within the preBötC as Type-1 or Type-2. Following this classification, we applied varying concentrations of propofol through bath application to examine its effects on the electrophysiological properties of each type of glutamatergic neuron. Results We found that Type-1 neurons exhibited a longer latency in excitation, while Type-2 neurons did not show this delayed excitation. On this basis, we further observed that bath application of propofol at concentrations of 5 μM and 10 μM shortened the latency period of Type-1 glutamatergic neurons but did not affect the latency period of Type-2 glutamatergic neurons. Conclusion Our study focuses on the glutamatergic neurons in the preBötC of adult mice. It introduces a novel method for classifying these neurons and reveals how propofol affects the activity of the two different types of glutamatergic neurons within the preBötC. These findings contribute to understanding the cellular basis of propofol-induced respiratory depression.

Human herpesviruses 6A and 6B (HHV-6A and HHV-6B, respectively) are two virus species in the betaherpesvirus subfamily that exhibit T cell tropism. CD46 and CD134 are the cellular receptors for HHV-6A and HHV-6B, respectively. Interestingly, the efficiency of HHV-6A/6B entry is different among different types of target cells despite similar receptor expression levels on these cells. Here, we found that the cellular factor gp96 (also known as glucose-regulated protein 94 [GRP94]) is expressed on the cell surface and interacts with viral glycoprotein Q1 (gQ1) during virus entry. gp96 cell surface expression levels are associated with the efficiency of HHV-6A and HHV-6B entry into target cells. Both loss-of-function and gain-of-function experiments indicated that gp96 plays an important role in HHV-6 infection. Our findings provide new insight into the HHV-6 entry process and might suggest novel therapeutic targets for HHV-6 infection. IMPORTANCE Although new clinical importance has been revealed for human herpesviruses 6A (HHV-6A) and 6B, much is still unknown about the life cycles of these viruses in target cells. We identified a novel cellular factor, gp96, that is critical for both HHV-6A and -6B entry into host cells. As gp96 can function as an adjuvant in vaccine development for both infectious agents and cancers, it can be a potential therapeutic target for infection by these two viruses. [ABSTRACT FROM AUTHOR]

Background: Sevoflurane anesthesia is widely used in pediatric patients. In this study, we investigated whether early multiple exposures to sevoflurane induced cognitive dysfunction by altering the hippocampal expression of ApoE later in development. Methods: Sprague–Dawley rats were exposed to 2.6% sevoflurane at postnatal day 7 (P7), P14, and P21 for 2 h. The ability of learning and memory was assessed using the Morris water maze at P37 and P97. The hippocampal volume was measured by magnetic resonance imaging (MRI) at P37 and P97. The hippocampal expression of ApoE was assessed by immunohistochemical analyses and real-time polymerase chain reaction (PCR). Results: Behavioral testing revealed that the ability of learning and memory in the sevoflurane-exposed rats was decreased compared with the control animals; however, there was no significant difference (P > 0.05). The MRI results showed a significant decrease in the left hippocampal volume, left maximum hippocampal length, and right maximum hippocampal length in the sevoflurane young group compared with the control young group (P 0.05). Among the adult animals, there was no significant difference between the groups in any parameter tested (P > 0.05). Conclusion: Multiple exposures to sevoflurane during the neonatal period decreased the volume of the hippocampus and increased the hippocampal expression of ApoE. The differential expression level of ApoE in different hippocampal subdivisions suggested that the expression of ApoE was regionally specific and reversible. Key Words: sevoflurane, Sprague–Dawley rat, neonatal period, behavior, apolipoprotein E, β-amyloid

Background Because etomidate induces prolonged adrenal suppression, even following a single bolus, its use as an infused anesthetic is limited. Our previous study indicated that a single administration of the novel etomidate analog methoxyethyletomidate hydrochloride (ET-26-HCl) shows little suppression of adrenocortical function. The aims of the present study were to (1) determine the minimum infusion rate of ET-26-HCl and compare it with those for etomidate and cyclopropyl-methoxycarbonylmetomidate (CPMM), a rapidly metabolized etomidate analog that is currently in clinical trials and (2) to evaluate adrenocortical function after a continuous infusion of ET-26-HCl as part of a broader study investigating whether this etomidate analog is suitable for long infusion in the maintenance of anesthesia. Method The up-and-down method was used to determine the minimum infusion rates for ET-26-HCl, etomidate and CPMM. Sprague-Dawley rats (n = 32) were then randomly divided into four groups: etomidate, ET-26-HCl, CPMM, and vehicle control. Rats in each group were infused for 60 min with one of the drugs at its predetermined minimum infusion rate. Blood samples were drawn initially and then every 30 min after drug infusion to determine the adrenocorticotropic hormone-stimulated concentration of serum corticosterone as a measure of adrenocortical function. Results The minimum infusion rates for etomidate, ET-26-HCl and CPMM were 0.29, 0.62, and 0.95 mg/kg/min, respectively. Compared with controls, etomidate decreased serum corticosterone, as expected, whereas serum corticosterone concentrations following infusion with the etomidate analogs ET-26-HCl or CPMM were not significantly different from those in the control group. Conclusion The corticosterone concentrations tended to be reduced for the first hour following ET-26-HCl infusion (as compared to vehicle infusion); however, this reduction did not reach statistical significance. Thus, further studies are warranted examining the practicability of using ET-26-HCl as an infused anesthetic.