It is recognized that, as the bladder fills, there is a corresponding increase in sensation. This awareness of the volume in the bladder is then used in a complex decision making process to determine if there is a need to void. It is also part of everyday experience that, when the bladder is full and sensations strong, these sensations can be suppressed and the desire to void postponed. The obvious explanation for such altered perceptions is that they occur centrally. However, this may not be the only mechanism. There are data to suggest that descending neural influences and local factors might regulate the sensitivity of the systems within the bladder wall generating afferent activity. Specifically, evidence is accumulating to suggest that the motor-sensory system within the bladder wall is influenced in this way. The motor-sensory system, first described over 100 years ago, appears to be a key component in the afferent outflow, the afferent “noise,” generated within the bladder wall. However, the presence and possible importance of this complex system in the generation of bladder sensation has been overlooked in recent years. As the bladder fills the motor activity increases, driven by cholinergic inputs and modulated, possibly, by sympathetic inputs. In this way information on bladder volume can be transmitted to the CNS. It can be argued that the ability to alter the sensitivity of the mechanisms generating the motor component of this motor-sensory system represents a possible indirect way to influence afferent activity and so the perception of bladder volume centrally. Furthermore, it is emerging that the apparent modulation of sensation by drugs to alleviate the symptoms of overactive bladder (OAB), the anti-cholinergics and the new generation of drugs the β3 sympathomimetics, may be the result of their ability to modulate the motor component of the motor sensory system. The possibility of controlling sensation, physiologically and pharmacologically, by influencing afferent firing at its point of origin is a “new” concept in bladder physiology. It is one that deserves careful consideration as it might have wider implications for our understanding of bladder pathology and in the development of new therapeutic drugs. In this overview, evidence for the concept peripheral modulation of bladder afferent outflow is explored.
ObjectivesThe decision-making process within health care has been widely researched, with shared decision-making, where both patients and clinicians share technical and personal information, often being cited as the ideal model. To date, much of this research has focused on systems where patients receive their care and treatment free at the point of contact (either in government-funded schemes or in insurance-based schemes). Oral health care often involves patients making direct payments for their care and treatment, and less is known about how this payment affects the decision-making process. It is clear that patient characteristics influence decision-making, but previous evidence suggests that clinicians may assume characteristics rather than eliciting them directly. The aim was to explore the influences on how dentists' engaged in the decision-making process surrounding a high-cost item of health care, dental implant treatments (DITs).MethodsA qualitative study using semi-structured interviews was undertaken using a purposive sample of primary care dentists (n = 25). Thematic analysis was undertaken to reveal emerging key themes.ResultsThere were differences in how dentists discussed and offered implants. Dentists made decisions about whether to offer implants based on business factors, professional and legal obligations and whether they perceived the patient to be motivated to have treatment and their ability to pay. There was evidence that assessment of these characteristics was often based on assumptions derived from elements such as the appearance of the patient, the state of the patient's mouth and demographic details. The data suggest that there is a conflict between three elements of acting as a healthcare professional: minimizing provision of unneeded treatment, trying to fully involve patients in shared decisions and acting as a business person with the potential for financial gain.ConclusionsIt might be expected that in the context of a high-cost healthcare intervention for which patients pay the bill themselves, that decision-making would be closer to an informed than a paternalistic model. Our research suggests that paternalistic decision-making is still practised and is influenced by assumptions about patient characteristics. Better tools and training may be required to support clinicians in this area of practice.
Bladder afferent outflow, linked to sensation, plays a critical role in bladder pathology: abnormal outflow results in altered sensation, leading to increased voiding frequency, urge and often incontinence. β3-adrenoceptor agonists have been suggested to be beneficial in treating these symptoms. However, the absence of a significant sympathetic innervation of the detrusor and only a modest relaxation of bladder muscle by β3 agonists has questioned the therapeutic site of action of β3 agonists in the bladder. The present study was done to explore the possibility that β3-adrenoceptors might be located in the pelvic plexus. Using the rat, where the pelvic plexus is located primarily within a single ganglion, the major pelvic ganglion (MPG), immuno-histochemical approaches were used to identify structures expressing β3-adrenoceptor immuno-reactivity (β3AR-IR). The only structures found to express β3AR-IR were small-diameter tyrosine hydroxylase and vesicular mono-amine transporter immuno-reactive (TH-IR and vmat-IR) neurones. These neurones, found in clusters or singly on the periphery of the ganglion, or dispersed in smaller clumps throughout the MPG, are similar to the small intensely fluorescent (SIF) cells described previously. Not all small cells expressed β3AR-IR. A population of the small cells were also immuno-reactive to the type 3 muscarinic receptor (M3R-IR) and the P2X3 purinergic receptor (P2X3-IR). Clumps of small cells were associated with calcitonin gene-related peptide immuno-reactive (CGRP-IR) nerve fibres (putative sensory fibres) and a small number were contacted by putative cholinergic nerves expressing immuno-reactivity to vesicular acetylcholine transporter (vacht-IR). These observations are consistent with the idea that small cells are interneurons and one of the components making up complex neural circuits within the MPG. The precise physiological role of these neural elements in the MPG is unknown. However, as one therapeutic action of β3-adrenoceptor agonists is to modulate sensation, it is possible that these neural circuits may be involved in the regulation of afferent outflow and sensation.
In commercial flocks of laying hens, keel bone fractures (KBFs) are prevalent and associated with behavioural indicators of pain. However, whether their impact is severe enough to induce a depressive-like state of chronic stress is unknown. As chronic stress downregulates adult hippocampal neurogenesis (AHN) in mammals and birds, we employ this measure as a neural biomarker of subjective welfare state. Radiographs obtained longitudinally from Lohmann Brown laying hens housed in a commercial multi-tier aviary were used to score the severity of naturally-occurring KBfs between the ages of 21-62 weeks. Individual birds' transitions between aviary zones were also recorded. Focal hens with severe KBFs at 3-4 weeks prior to sampling (n = 15) had lower densities of immature doublecortinpositive (DCX +) multipolar and bipolar neurons in the hippocampal formation than focal hens with minimal fractures (n = 9). KBF severity scores at this time also negatively predicted DCX + cell numbers on an individual level, while hens that acquired fractures earlier in their lives had fewer DCX + neurons in the caudal hippocampal formation. Activity levels 3-4 weeks prior to sampling were not associated with AHN. KBFs thus lead to a negative affective state lasting at least 3-4 weeks, and management steps to reduce their occurrence are likely to have significant welfare benefits. Keel bone fractures (KBFs) present a serious welfare problem for the egg production industry, given that between 20 to 96% of birds within commercial flocks in various countries are reported to have some level of damage (Belgium 1 ; Canada 2 ; Denmark 3 ; The Netherlands 4 ; Switzerland 5,6 ; and the UK 7-9). Estimates of KBF prevalence increase with age, rising from 5.5% of birds affected within a flock at onset of lay 10 to as many as 97% by the end of a production cycle 4. Many KBFs appear to arise from collisions, both with perches 11 , which hens are highly motivated to use 12 , and other equipment including drinkers and support beams. Although the presence of a KBF does not suppress perching behaviour 13 , it does reduce frequency of range access via popholes 14. Further behavioural evidence also supports the assumption that KBFs are a source of pain or discomfort for laying hens (reviewed by Riber et al. 15), with recent studies demonstrating their association with altered movement throughout the aviary 16,17. Focusing on more direct assessments of movement and pain, hens with KBFs display greater latencies to fly down from perches 100 and 150 cm above the floor to obtain a food reward than hens without fractures, whilst delays in fractured birds alone are reduced following administration of various analgesics 18-20. Furthermore, a conditioned place preference for the location in which the analgesic was administered is observed to develop only in hens with KBFs 21. While this indicates that short-term relief from pain arising from keel fractures is a reinforcing occurrence, whether their un-medicated experience is negative and/or salient enough to produ...
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