A review of the pathogenicity mechanism of Verticillium dahliae in cotton

Verticillium wilt,caused by the notorious fungal pathogen Verticillium dahliae,is one of the main limiting factors for cotton production.Due to the stable dormant structure microsclerotia,long-term variability and co-evolution with host plant,its pathogenicity mechanism is very complicated,and the interaction mechanism between pathogen and host plant is also unclear.So identification and functional analysis of the genes involved in the pathogenicity or virulence of this fungus will benefit to uncover the molecular pathogenic mechanism of V.dahliae.In this review,many multifunction genes covering microsclerotia development,pathogen infection,effector proteins,transcription factors,horizontal gene transfer and trans-kingdom RNA silencing have been summarized to provide a theoretical basis to deep understand the molecular pathogenicity mechanism of V.dahliae and promote to effectively control Verticillium wilt.Furtherly,these pathogenicity-related genes may be considered as targets for effective control of Verticillium wilt in cotton.

Pathogenesis and drug resistance mechanism of Burkholderia pseudomallei

Burkholderia pseudomallei is the pathogen that causes melioidosis.Melioidosis has a long duration of chronic infection,atypical clinical manifestations at acute onset,and is prone to life-threatening complications and poor prognosis.Understanding the pathogenesis and drug resistance mechanism of Burkholderia pseudomallei will effectively help the diagnosis and treatment of the disease and improve the prognosis.This review focuses on the extracellular movement of Burkholderia pseudomallei in host cells,the way of infecting host cells,virulence factors,and drug resistance mechanisms(efflux pumps,changes in target sites,etc.).This study provides a possible direction for the early diagnosis,treatment and control of melioidosis caused by this bacterium.

Pathogenicity of Serratia marcescens to hazelnut weevil(Curculio dieckmanni)

The hazelnut weevil(Curculio dieckmanni Faust.)is a major pest of Asian hazel(Corylus heterophylla Fisch.)in China.Dead hazelnut weevil larvae were examined and the associated pathogenic bacterium was identifi ed as Serratia marcescens Bizio.This signifi cantly shortened the lifespan of hazelnut weevil.Larval weight was reduced as a function of S.marcescens concentration and exposure time.The structure of infected midgut cells was altered,with necrosis of the wall tissues and many cells becoming dislodged,creating cavities.The S.marcencens strain inhibited digestive enzyme activity and protective enzymes in the midgut of adult hazelnut weevil.Inhibition on S.marcencens strain increased with treatment time.S.marcescens directly destroyed the midgut cells and interfered with digestive and protective enzymes.This decreased the food intake and increased mortality of hazelnut weevil.S.marcescens appears to be an eff ective bacterium for the control of hazelnut weevil but requires further study,including biological formulation development and fi eld application.

A Review on the Pathogenicity of Cucumber Mosaic Virus

Cucumber mosaic virus （CMV）, a positive-sense single-stranded RNA virus, has a very wide host range and a worldwide distribution, and is considered as one of the most virulent plant viruses in the world. The CMV gene sequences, gene products, and their interaction with hosts have been extensively reported since it was discovered in 1916. With the development of high-throughput sequencing and proteomics, great progress has been made in the molecular mechanism of CMV pathogenesis in recent years. In this review, we introduce CMV-encoded proteins, CMV-related satellite RNAs and the roles of host factors in the pathogenesis of CMV, to provide a theoretical basis for future study of CMV.

A Preliminary Study on Principle of Etiology Mechanism

Based on the inspiration from Hetu and Luoshu,a principle diagram of pathogenicity of pathogenic factors was established.Accordingly,the inner correlations between pathogenic factor type and biological factors,and between pathogenic factors and host were analyzed.Mechanism of pathogenesis was discussed with five representative cases.The result indicated that effect of biological factors on host could be proved only with the performance of internalization conditions of biological factor and host.The reciprocal transformation between biological factors and pathogenic factors was decided by interaction and state of co-existed factors and host.The results suggested that it is a better and attractive choice to regulate and optimize the host’s state in practice than direct elimination of pathogens with antibiotics.

Ion Channel Genes and Epilepsy:Functional Alteration,Pathogenic Potential,and Mechanism of Epilepsy

Ion channels are crucial in the generation and modulation of excitability in the nervous system and have been implicated in human epilepsy. Forty-one epilepsyassociated ion channel genes and their mutations are systematically reviewed. In this paper, we analyzed the genotypes, functional alterations（funotypes）, and phenotypes of these mutations. Eleven genes featured loss-offunction mutations and six had gain-of-function mutations.Nine genes displayed diversified funotypes, among which a distinct funotype-phenotype correlation was found in SCN1A. These data suggest that the funotype is an essential consideration in evaluating the pathogenicity of mutations and a distinct funotype or funotype-phenotype correlation helps to define the pathogenic potential of a gene.

Expression of transforming growth factor beta-1 in fibrosis of transplanted kidney

Objective: In order to study the role and significance of transforming growth factor beta-1 (TGF-β1 )mRNA in transplanted renal fibrosis(TRF). Methods: Renal pathologic changes and expression of TGF-β1 mRNA were observed using in situ hybridization technique. The normal renal tissue as a. control group. Results: Expression of TGF-β1, mRNA in the renal fibrosis increased, compared with that in the control group. The expression rate were co-related to the stage of TRF. Conclusion: TGF-β1 is related to the pathogenesis and development of TRF.

Research Advances of Exotoxin Gene and Related Vaccines of Clostridium perfringens

Clostridium peringens, also called clostridium westergren, mainly causes diseases in ruminants, such as gas gangrene, enterotoxaemia, hemorrhagic enteritis of cattle and sheep. The bacteria are divided into five subtypes including A, B, C, D and E subtype, which can secrete more than 10 kinds of exotoxin,In these toxins, a, β, ε and ζ play a key pathogenic role. At present, the disease is prevented mainly by univalent vaccine, combined vaccine and muhivalent inactivated vaccine. And the genetic engineering subunit vaccine and nucleic acid vaccine has wide develop- ment prospects. In order to provide some reference for comprehensive prevention and deep research of C. pe^ringens, the etiological characteristics of C. perfrin- germ, pathogenic mechanism of exotoxin and research progress of related vaccines were reviewed, and the genetic engineering subunit vaccine and nucleic acid vac- cine development prospects were also discussed in this paper.

The generation and use of animal models of osteosarcoma in cancer research

Osteosarcoma is the most common malignant bone tumor affecting children and adolescents.Currently,the most common treatment is surgery combined with neoadjuvant chemotherapy.Although the survival rate of patients with osteosarcoma has improved in recent years,it remains poor when the tumor(s)progress and distant metastases develop.Therefore,better animal models that more accurately replicate the natural progression of the disease are needed to develop improved prognostic and diagnostic markers,as well as targeted therapies for both primary and metastatic osteosarcoma.The present review described animal models currently being used in research investigating osteosarcoma,and their characteristics,advantages,and disadvantages.These models may help elucidate the pathogenic mechanism(s)of osteosarcoma and provide evidence to support and develop clinical treatment strategies.

Animal models of mpox virus infection and disease

Mpox(monkeypox)virus(MPXV),which causes a mild smallpox-like disease,has been endemic in Africa for several decades,with sporadic cases occurring in other parts of the world.However,the most recent outbreak of mpox mainly among men that have sex with men has affected several continents,posing serious global public health concerns.The infections exhibit a wide spectrum of clinical presentation,ranging from asymptomatic infection to mild,severe disease,especially in immunocompromised individuals,young children,and pregnant women.Some therapeutics and vaccines developed for smallpox have partial protective and therapeutic effects against MPXV historic isolates in animal models.However,the continued evolution of MPXV has produced multi-ple lineages,leading to significant gaps in the knowledge of their pathogenesis that constrain the development of targeted antiviral therapies and vaccines.MPXV infections in various animal models have provided a central plat-form for identification and comparison of diseased pathogenesis between the contemporary and historic isolates.In this review,we discuss the susceptibility of various animals to MPXV,and describe the key pathologic features of rodent,rabbit and nonhuman primate models.We also provide application examples of animal models in elu-cidating viral pathogenesis and evaluating effectiveness of vaccine and antiviral drugs.These animal models are essential to understand the biology of MPXV contemporary isolates and to rapidly test potential countermeasures.Finally,we list some remaining scientific questions of MPXV that can be resolved by animal models.

The key mechanisms of multi-system responses triggered by central nervous system damage in hand,foot,and mouth disease severity

Hand,foot,and mouth disease(HFMD)is a prevalent infectious affliction primarily affecting children,with a small portion of cases progressing to neurological complications.Notably,in a subset of severe HFMD cases,neurological manifestations may result in significant sequelae and pose a risk of mortality.We systematically conducted literature retrieval from the databases PubMed(1957–2023),Embase(1957–2023),and Web of Science(1957–2023),in addition to consulting authoritative guidelines.Subsequently,we rigorously selected the most relevant articles within the scope of this review for comprehensive analysis.It is widely recognized that the severity of HFMD is attributed to a multifaceted array of pathophysiological mechanisms.The implication of multi-system dysfunction appears to be perturbances of the human defense system;therefore,it contributes to the severity of HFMD.In this review,we provide an overview and analysis of recent insights into the molecular mechanisms contributing to the severity of HFMD,with a particular focus on cytokine release syndrome,the involvement of the renin-angiotensin system,regional immunity,endothelial dysfunction,catecholamine storm,viral invasion,and the molecular mechanisms of neurological damage.We speculate that the domino effect of diverse physiological systems,initiated by damage to the central nervous system,serve as the primary mechanisms governing the severity of HFMD.Simultaneously,we emphasize the knowledge gaps and research urgently required to delineate a quick roadmap for ongoing and essential studies on HFMD.

Mycoplasma lipoproteins and Toll-like receptors

Mycoplasmas, the smallest free-living, self-replicating bacteria with diameters of 200 to 800 nm, have been reported to be associated with human diseases. It is well known that the mycoplasma lipoprotein/peptide is able to modulate the host immune system, whose N-terminal structure is an important factor in inducing immunity and distinguishing Toll-like receptors (TLRs). However, there is still no clear elucidation about the pathogenic mechanism of mycoplasma lipoprotein/peptide and the signaling pathway. Some researchers have focused on understanding the structures of these proteins and the relationships between their structure and biological function. This review provides an update on the research in this field.