Injury surveillance in elite Paralympic athletes with limb deficiency: a retrospective analysis of upper quadrant injuries.

BACKGROUND: Compared to injury surveillance in Olympic athletes relatively little literature exists for Paralympic athletes. Injury surveillance data underpin design and evaluation of injury prevention strategies in elite sport. The aim of this study is investigate upper quadrant injuries in elite athletes with limb deficiency. METHODS: A retrospective analysis of upper quadrant injuries in elite athletes with limb deficiency with available data (2008-2016) was conducted using medical notes extracted from English Institute of Sport (EIS) records. Eligibility criteria included funded athletes, eligible for EIS physiotherapy support with an upper and/or lower limb disability arising from full or partial limb deficiency. RESULTS: A total 162 injuries from 34 athletes were included. Participant characteristics: 20 males (59%), from 9 sports, with mean age 27 years (range 16-50 years) and 15 with congenital limb loss (44%). Athletes age 20-29 years experienced most injuries, four per athlete. The glenohumeral joint was the reported injury site (23%, n = 38). Index (first) injuries accounted for 77% (n = 128) injuries, 17% (n = 28) a recurrence and 6% (n = 10) an exacerbation. More than half of injuries occurred in training (58%, n = 94), this being slightly higher in those with traumatic limb loss. Athletes with quadruple levels of limb deficiency had double the number of recurrent injuries as those with single or double limb deficiency. CONCLUSION: Elite athletes with limb deficiency experience upper quadrant injuries, with glenohumeral joint the most frequently reported. The quality and consistency of data reported limits definitive conclusions, although findings highlight the importance of precision and accuracy in recording injury surveillance to enable implementation of effective injury prevention strategies.

Perceived cancer-related pain and fatigue, information needs, and fear of cancer recurrence among adult survivors of childhood cancer.

OBJECTIVE: Pain and fatigue are under-researched late effects of childhood cancer and its treatment, and may be interpreted by survivors as indicating cancer recurrence. Moreover, unmet information needs for managing pain and fatigue may be related to fear of cancer recurrence. We investigated the complex relationships between perceived cancer-related pain and fatigue, unmet information needs for managing pain and fatigue, and fear of cancer recurrence. METHODS: We surveyed 404 adult survivors of any form of childhood cancer (M = 16.82 years since treatment completion). RESULTS: Many survivors reported perceived cancer-related pain (28.7%) and fatigue (40.3%), and anticipated future pain (19.3%) and fatigue (26.2%). These symptomologies were all related to unmet information needs for managing pain (18.8%) and fatigue (32.2%; all p's<.001). Survivors reporting unmet information needs for managing pain (B = .48, 95% CI = 0.19-0.76, p = .001) and fatigue (B = .32, 95% CI = 0.06-0.52, p = .015) reported higher fear of cancer recurrence than survivors reporting no information needs. CONCLUSION: Survivors often have unmet information needs for managing pain and fatigue, and these unmet needs are related to fear of cancer recurrence. PRACTICE IMPLICATIONS: Long-term follow-up clinics should assess pain and fatigue. Information provision about pain and fatigue may be an important tool to help manage fear of cancer recurrence.

Biased interpretations of ambiguous bodily threat information in adolescents with chronic pain.

Adult patients with chronic pain are consistently shown to interpret ambiguous health and bodily information in a pain-related and threatening way. This interpretation bias may play a role in the development and maintenance of pain and disability. However, no studies have yet investigated the role of interpretation bias in adolescent patients with pain, despite that pain often first becomes chronic in youth. We administered the Adolescent Interpretations of Bodily Threat (AIBT) task to adolescents with chronic pain (N = 66) and adolescents without chronic pain (N = 74). Adolescents were 10 to 18 years old and completed the study procedures either at the clinic (patient group) or at school (control group). We found that adolescents with chronic pain were less likely to endorse benign interpretations of ambiguous pain and bodily threat information than adolescents without chronic pain, particularly when reporting on the strength of belief in those interpretations being true. These differences between patients and controls were not evident for ambiguous social situations, and they could not be explained by differences in anxious or depressive symptoms. Furthermore, this interpretation pattern was associated with increased levels of disability among adolescent patients, even after controlling for severity of chronic pain and pain catastrophizing. The current findings extend our understanding of the role and nature of cognition in adolescent pain, and provide justification for using the AIBT task in longitudinal and training studies to further investigate causal associations between interpretation bias and chronic pain.

Child attention to pain and pain tolerance are dependent upon anxiety and attention control: An eye-tracking study.

BACKGROUND: Pain is common and can be debilitating in childhood. Theoretical models propose that attention to pain plays a key role in pain outcomes, however, very little research has investigated this in youth. This study examined how anxiety-related variables and attention control interacted to predict children's attention to pain cues using eye-tracking methodology, and their pain tolerance on the cold pressor test (CPT). METHODS: Children aged 8-17 years had their eye-gaze tracked whilst they viewed photographs of other children displaying painful facial expressions during the CPT, before completing the CPT themselves. Children also completed self-report measures of anxiety and attention control. RESULTS: Findings indicated that anxiety and attention control did not impact children's initial fixations on pain or neutral faces, but did impact how long they dwelled on pain versus neutral faces. For children reporting low levels of attention control, higher anxiety was associated with less dwell time on pain faces as opposed to neutral faces, and the opposite pattern was observed for children with high attention control. Anxiety and attention control also interacted to predict pain outcomes. For children with low attention control, increasing anxiety was associated with anticipating more pain and tolerating pain for less time. CONCLUSIONS: This is the first study to examine children's attention to pain cues using eye-tracking technology in the context of a salient painful experience. Data suggest that attention control is an important moderator of anxiety on multiple outcomes relevant to young people's pain experiences. SIGNIFICANCE: This study uses eye tracking to study attention to pain cues in children. Attention control is an important moderator of anxiety on attention bias to pain and tolerance of cold pressor pain in youth.

Aberrant expression of regulators of cell-fate found in eutopic endometrium is found in matched ectopic endometrium among women and in a baboon model of endometriosis.

BACKGROUND: We have recently shown that women with endometriosis express an increased amount of telomerase and nucleolin, with concomitant loss of γ-H2AX in eutopic endometrium. To further examine these selected factors that regulate cell fate, in the pathogenesis of endometriosis, we studied the expression of telomerase, nucleolin, proliferating cell nuclear antigen and γ-H2AX in ectopic endometriotic deposits from women, and in matched eutopic and ectopic endometrial tissue from a baboon model of endometriosis. METHODS: Ectopic active peritoneal endometriotic lesions were collected from seven symptomatic women. Endometriosis was induced in six baboons by intra-peritoneal autologous inoculation of menstrual endometrium. Eutopic and matched ectopic endometrial tissues were collected prior to and 6, 12 and 15 months after the induction of endometriosis as previously described. Eutopic endometrium was also obtained from eight healthy fertile control baboons. Immunohistochemistry was performed as previously described, and telomerase activity was confirmed using the telomeric repeat amplification protocol assay. RESULTS: All active human endometriotic lesions expressed the proliferative markers but showed weak or absent staining for γ-H2AX. A similar expression pattern of these markers was seen in the ectopic lesions of the baboons with induced disease. In these baboons, the eutopic endometrium also showed intense immunoreactivity for all proliferative markers 6-12 months after induction with a parallel loss of γ-H2AX. The opposite staining pattern was seen in eutopic endometrium of healthy animals and in pre-induction endometrium of animals with induced disease. CONCLUSIONS: Endometriotic lesions have excess proliferative potential; in baboons, these were present within 12 months of the initiation of the disease. In eutopic tissue, these changes appear to be induced by the development of endometriosis.

Compromised chorionic villous vascularization in idiopathic second trimester fetal loss.

BACKGROUND: For normal fetal growth and development a well-developed chorionic villous vascularization is essential. AIM: The aim of this study is to investigate whether idiopathic second trimester fetal loss is associated with an underdeveloped chorionic villous vascularization. METHODS: 38 placentas after late miscarriage, classified as idiopathic fetal loss (IFL, n=16) or as fetal loss due to intrauterine infection (IUI, n=22) were collected. After CD34 immunohistochemical staining the villous stromal area, number of villous vessels, vascular area and vascular area density (central, peripheral and total) were measured in randomly selected immature intermediate villi. RESULTS: The mean gestational age was 19+4 weeks for the IFL group and 20+6 weeks for the IUI group. After controlling for gestational age, we found no differences in fetal weight, placental weight, villous stromal area, number of vessels and central vascular features. The mean peripheral vascular area and peripheral vascular area density were, after adjusting for gestational age, reduced in the IFL group. CONCLUSION: Idiopathic second trimester fetal loss is associated with a reduced peripheral chorionic villous vascularization. We hypothesize that in these cases, placentation is already disturbed in first trimester of pregnancy, leading to a reduced materno-fetal interface in second trimester, thus to early postplacental fetal hypoxia and fetal death.

Pathobiology of epiretinal and subretinal membranes: possible roles for the matricellular proteins thrombospondin 1 and osteonectin (SPARC).

Epiretinal and subretinal membranes are fibrocellular proliferations which form on the surfaces of the neuroretina as a sequel to a variety of ocular diseases. When these proliferations complicate rhegmatogenous retinal detachment (a condition known as proliferative vitreoretinopathy or PVR), the membranes often contain numerous retinal pigment epithelial (RPE) cells and a variety of extracellular proteins. The extracellular proteins include adhesive proteins like collagen, laminin and fibronectin. In addition, several matricellular proteins with potential counter-adhesive functions are present in the membranes. Two such matricellular proteins, thrombospondin 1 and osteonectin (or SPARC: Secreted Protein Acidic and Rich in Cysteine), tend to be co-distributed with the RPE cells in PVR membranes. By virtue of their counter-adhesive properties, thrombospondin 1 and SPARC may reduce RPE cell-matrix adhesion and so permit key RPE cellular activities (for example, migration or shape change) in periretinal membrane development. Furthermore, within a 'cocktail' containing other proteins such as the metalloproteinases and growth factors like the scatter factor/hepatocyte growth factor family, matricellular proteins may play a role in the RPE cell dissociation from Bruch's membrane, which characterises early PVR.

Hepatocyte growth factor/scatter factor in the eye.

Hepatocyte growth factor, also known as scatter factor (HGF/SF) is a multipotential cytokine which can produce a range of responses in target cells and its influence in the eye in health and disease is just beginning to be appreciated. Usually HGF/SF is synthesised by mesenchymally derived cells and targets and signals epithelial cells in a paracrine manner via their c-Met surface receptor. However, there is growing evidence for the existence of autocrine loops in a number of cell systems prominent among which are ocular cells such as the corneal endothelium, the lens epithelium, the retinal pigment epithelium (RPE) and others. Marked cellular proliferation is stimulated when activated HGF/SF is exposed to hepatocytes, renal epithelium, melanocytes and vascular endothelial cells but it is often a poor mitogen for other cell types. In target cells the cytokine promotes other bioactions such as junctional breakdown, shape change, cell scattering, directional and nondirectional migration, cell survival, invasive behaviour and/or tubule formation. These activities seem to depend on HGF/SF linking with the c-Met receptor and pathways to stimulate the various types of cytokine/receptor response are being unravelled at the present time. In corneal wound healing, HGF/SF is produced by stromal keratocytes and targets the repairing epithelium. HGF/SF is a constituent of tears, aqueous humour and vitreous humour at levels above that found in plasma although it is not clear how much is activated. Aqueous HGF/SF may well influence lens epithelial, corneal endothelial and trabecular meshwork cell survival. Vitreous levels of HGF/SF are elevated in proliferative vitreoretinopathy (PVR), where a target cell is the RPE and in proliferative diabetic retinopathy (PDR) where HGF/SF has been shown to be a major angiogenesis factor. Finally HGF/SF may be involved in the metastatic spread of tumour cells from uveal melanomata and in the formation of vascular channels in these tumours.