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Summer pruning effects in apple have generally been attributed to improved light penetration and to reduced carbohydrate supply. However, the common basis to most of these effects seems to be the retardation of senescence, a process under hormonal control. Summer pruning causes a temporary loss of apical dominance except when thinning cuts are used. It also causes a temporary increase in cytokinin supply, presumably mainly by increased export from the roots. Both effects presumably result from reduced auxin availability.

Depending on its timing, the resulting rejuvenation may consist of mobilization and redistribution of nutrients and phytohormones, breaking of axillary buds, inhibition of flower induction, delayed fruit development and later induction of dormancy. The extent of pruning responses increases with the vigour of the tree, the earliness of pruning and its severity. Heading and stubbing are more effective in provoking these responses than thinning of shoots. In areas with a short season, summer pruning may not only delay, but also prevent, the onset of dormancy, with adverse effects on winter hardiness. The mostly positive influence of summer pruning on fruit colour by factors in addition to better light penetration is discussed. Summer pruning, where considered necessary, needs to be adjusted to local conditions and coordinated with other cultural practices.  相似文献   

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Almost half of all clinical cases of mastitis are caused by Gram-negative bacteria. Among these bacteria, intramammary infection by Pseudomonas aeruginosa remains one of the most refractory to antibiotic therapy. The ability to recognize potentially harmful pathogens whether previously encountered or not, as well as the induction of an initial pro-inflammatory response to these pathogens, are critical components of host innate immunity. Although the innate immune response to another Gram-negative mastitis-causing pathogen, Escherichia coli, has been well-characterized, little is known about the response to other Gram-negative bacteria, including P. aeruginosa. The objective of the current study was to characterize the systemic and localized bovine innate immune response to intramammary infection with P. aeruginosa. The contralateral quarters of ten mid-lactating Holstein cows were challenged with either saline or P. aeruginosa. Following the establishment of infection, milk samples were collected and assayed for changes in cytokine and growth factor concentrations, complement activation, and changes in the levels of soluble CD14 (sCD14) and lipopolysaccharide (LPS)-binding protein (LBP), two accessory molecules involved in host recognition of Gram-negative bacteria. Initial increases in milk somatic cell counts were evident within 12h of experimental challenge and remained elevated for >or=3 weeks. Increased permeability of the mammary gland vasculature, as evidenced by elevated milk levels of BSA, was initially observed 20 h post-infection and persisted for 2 weeks. Within 32 h of challenge, increased levels of IL-8, TNF-alpha, IL-10, and IL-12 were detected, however, the elevated levels of these cytokines were not sustained for longer than a 24h period. In contrast, elevations in IL-1beta, IFN-gamma, TGF-alpha, TGF-beta1, TGF-beta2, sCD14, LBP, and activated complement factor 5 (C5a) were sustained for periods of >48 h. Systemic changes were characterized by elevated body temperature, induction of the acute phase protein synthesis of serum amyloid A and LBP, and a transient decrease in circulating neutrophils and lymphocytes. Together, these data demonstrate the capability of the mammary gland to mount a robust innate immune response to P. aeruginosa that is characterized by the induction of pro-inflammatory cytokines, complement activation, and increased levels of accessory molecules involved in Gram-negative bacterial recognition.  相似文献   
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