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Background: Recurrent respiratory papillomatosis (RRP) is caused by HPV types 6 and 11 and has a substantial papilloma growth in the airway and is recurrent. The activity of HPV neoplasms is related to the cell cycle, a complex series of processes that cause cells to grow and replicate. The p53 and Ki67 proteins, as one of the tumor gene controllers, have the function of controlling the cell cycle and assisting the apoptotic process of damage to DNA. Objective: This study aims to analyze the relationship between RRP aggressiveness and p53 and Ki67 protein expression as one of the predictive factors for aggressive disease progression. Methods: This study was an observational analytic study with a crosssectional form. The p53 and Ki67 protein examination results were obtained from immunohistochemical examination by staining monoclonal antibody rabbit Anti-Human p53 and Ki67 clone 318-6-11. Data analysis used binary logistic regression to determine the relationship between the independent and dependent variables with a significant p <0.05. Results: From 19 samples, the distribution of the sex distribution of male patients (42.10%), while for women of eleven patients (57.90%). The type of RRP that was served the most by the participants was RPP for 13 children (68.40%). Positive p53 protein expression was found in 8 (42.10%) patients, while 11 (57.90%) patients had negative p53 protein expression. Moreover, on positive Ki67 protein expression, there were 5 (26.30%) patients and 14 (73.70%) patients with negative Ki67 protein expression. Discussion: High p53 protein expression indicates that the cell cycle is not controlled, so it is regulated by the p53 protein to control the cycle through the process of apoptosis or capture. The uncontrolled cell cycle causes tumors to grow very fast. Meanwhile, high Ki67 protein expression indicates an uncontrolled cell cycle because most of them are not resting. Conclusion: There is no relationship between the aggressiveness of recurrent tract papillomas with p53 and Ki67 protein expression. [ABSTRACT FROM AUTHOR]

Fusarium culmorum (Fc) and F. graminearum (Fg) belong to the predominant causal agents of fusarium crown and root rot (FCR) in wheat. While many studies have been done to investigate crown rot, including stem base infection, root colonization and mycotoxin production associated with root rot is not well understood. In this study the impact of mycotoxins on the colonization of wheat roots and stem bases was analysed by using Fc and Fg isolates that varied in both quantity and types of trichothecenes they produce. Seedling inoculations in growth chambers with a high deoxynivalenol (DON)‐ and 3‐acetyldeoxynivalenol (3ADON)‐producing isolate led to more severe symptoms and 20‐times greater colonization of the stem base, as measured by Fc DNA accumulation, than isolates that produced less DON/3ADON. In contrast to stem base colonization, in vitro inoculations of roots with a Tri5 deletion mutant deficient in Fg trichothecene production led to three‐times higher colonization than the wildtype. Furthermore, an Fc isolate that produced low levels of zearalenone resulted in twice the level of colonization of a high DON/3ADON‐producing isolate included in the study. When root inoculation with a low DON/3ADON‐producing Fc isolate was supplemented with exogenous DON, DON production decreased by more than half per unit weight of Fc DNA, and root colonization doubled compared to the untreated control. Therefore, in contrast to its potential role as an aggressiveness factor in stem base infection, trichothecene production by Fc and Fg is detrimental to the early stages of wheat root colonization in FCR. [ABSTRACT FROM AUTHOR]

The blue mould decay of apples is caused by Penicillium expansum and is associated with contamination by patulin, a worldwide regulated mycotoxin. Recently, a cluster of 15 genes ( patA-patO) involved in patulin biosynthesis was identified in P. expansum. blast analysis revealed that patL encodes a Cys6 zinc finger regulatory factor. The deletion of patL caused a drastic decrease in the expression of all pat genes, leading to an absence of patulin production. Pathogenicity studies performed on 13 apple varieties indicated that the PeΔ patL strain could still infect apples, but the intensity of symptoms was weaker compared with the wild-type strain. A lower growth rate was observed in the PeΔ patL strain when this strain was grown on nine of the 13 apple varieties tested. In the complemented PeΔ patL: patL strain, the ability to grow normally in apple and the production of patulin were restored. Our results clearly demonstrate that patulin is not indispensable in the initiation of the disease, but acts as a cultivar-dependent aggressiveness factor for P. expansum. This conclusion was strengthened by the fact that the addition of patulin to apple infected by the PeΔ patL mutant restored the normal fungal colonization in apple. [ABSTRACT FROM AUTHOR]