Pain and disability in women with patellofemoral pain relate to kinesiophobia, but not to patellofemoral joint loading variables.

BACKGROUND: Altered patellofemoral joint (PFJ) loading and elevated kinesiophobia are commonly reported in people with patellofemoral pain (PFP). However, the relative relationship of these physical-psychological variables with pain and disability in people with PFP is unknown. AIM: To explore the relationship of PFJ loading during stair ascent and kinesiophobia, with self-reported pain and disability in women with PFP. METHODS: Fifty-seven women with PFP completed the Tampa Scale for Kinesiophobia, a Visual Analog Scale (0-100 mm) for pain during stair ascent, and the Anterior Knee Pain Scale (disability). Stair ascent mechanics were assessed via three-dimensional motion analysis while participants ascended an instrumented seven-step staircase. Peak PFJ contact force and stress, and PFJ contact force and stress loading rates were estimated using a musculoskeletal model. The relationships of PFJ kinetics during stair ascent and kinesiophobia, with the Anterior Knee Pain Scale (disability) and pain during stair ascent, were evaluated with Spearman rank correlation. Variables (kinetics and kinesiophobia) significantly correlating with the dependent variables (pain and disability) were inserted in linear regression models. RESULTS: Kinesiophobia was moderately associated with self-reported pain (rho = 0.37) and disability (rho = -0.58) in women with PFP. No PFJ loading variables were found to be associated with self-reported pain or disability (P > .05). Kinesiophobia explained 14% of the variance of participants' pain while ascending stairs and 33% of the variance of participant's self-reported disability. CONCLUSION: Addressing kinesiophobia during treatment of women with PFP may be important to reduce self-reported pain and disability.

Resurgence of Eating Disorders with Olanzapine.

BACKGROUND: Olanzapine is commonly utilized in palliative care for the treatment of nausea, and a known side effect of olanzapine is increased appetite. Olanzapine is also known to cause re-emergence of eating disorders (EDs) in patients utilizing olanzapine for its antipsychotic effects. It is unclear to what extent this may also occur in patients with serious/life-limiting illness. METHODS AND RESULTS: We present a case of a 70-year-old female with recurrent ovarian cancer and a history of bulimia nervosa (BN) that developed resurgence of her BN after initiation of olanzapine for cancer-associated nausea. Her BN resolved with reducing the dose of olanzapine. CONCLUSION: It is important to recognize that recurrence of EDs can occur when using olanzapine in the palliative care setting.

Phage-Bacterial Dynamics with Spatial Structure: Self Organization around Phage Sinks Can Promote Increased Cell Densities.

Bacteria growing on surfaces appear to be profoundly more resistant to control by lytic bacteriophages than do the same cells grown in liquid. Here, we use simulation models to investigate whether spatial structure per se can account for this increased cell density in the presence of phages. A measure is derived for comparing cell densities between growth in spatially structured environments versus well mixed environments (known as mass action). Maintenance of sensitive cells requires some form of phage death; we invoke death mechanisms that are spatially fixed, as if produced by cells. Spatially structured phage death provides cells with a means of protection that can boost cell densities an order of magnitude above that attained under mass action, although the effect is sometimes in the opposite direction. Phage and bacteria self organize into separate refuges, and spatial structure operates so that the phage progeny from a single burst do not have independent fates (as they do with mass action). Phage incur a high loss when invading protected areas that have high cell densities, resulting in greater protection for the cells. By the same metric, mass action dynamics either show no sustained bacterial elevation or oscillate between states of low and high cell densities and an elevated average. The elevated cell densities observed in models with spatial structure do not approach the empirically observed increased density of cells in structured environments with phages (which can be many orders of magnitude), so the empirical phenomenon likely requires additional mechanisms than those analyzed here.

Accelerated ageing and renal dysfunction links lower socioeconomic status and dietary phosphate intake.

BACKGROUND: We have sought to explore the impact of dietary Pi intake on human age related health in the pSoBid cohort (n=666) to explain the disparity between health and deprivation status in this cohort. As hyperphosphataemia is a driver of accelerated ageing in rodent models of progeria we tested whether variation in Pi levels in man associate with measures of biological ageing and health. RESULTS: We observed significant relationships between serum Pi levels and markers of biological age (telomere length (p=0.040) and DNA methylation content (p=0.028), gender and chronological age (p=0.032). When analyses were adjusted for socio-economic status and nutritional factors, associations were observed between accelerated biological ageing (telomere length, genomic methylation content) and dietary derived Pi levels among the most deprived males, directly related to the frequency of red meat consumption. CONCLUSIONS: Accelerated ageing is associated with high serum Pi levels and frequency of red meat consumption. Our data provide evidence for a mechanistic link between high intake of Pi and age-related morbidities tied to socio-economic status.

Type I Interferon Counters or Promotes Coxiella burnetii Replication Dependent on Tissue.

Coxiella burnetii is an intracellular pathogen and the cause of Q fever. Gamma interferon (IFN-γ) is critical for host protection from infection, but a role for type I IFN in C. burnetii infection has not been determined. Type I IFN supports host protection from a related pathogen, Legionella pneumophila, and we hypothesized that it would be similarly protective in C. burnetii infection. In contrast to our prediction, IFN-α receptor-deficient (IFNAR(-/-)) mice were protected from C. burnetii-induced infection. Therefore, the role of type I IFN in C. burnetii infection was distinct from that in L. pneumophila Mice treated with a double-stranded-RNA mimetic were protected from C. burnetii-induced weight loss through an IFNAR-independent pathway. We next treated mice with recombinant IFN-α (rIFN-α). When rIFN-α was injected by the intraperitoneal route during infection, disease-induced weight loss was exacerbated. Mice that received rIFN-α by this route had dampened interleukin 1ß (IL-1ß) expression in bronchoalveolar lavage fluids. However, when rIFN-α was delivered to the lung, bacterial replication was decreased in all tissues. Thus, the presence of type I IFN in the lung protected from infection, but when delivered to the periphery, type I IFN enhanced disease, potentially by dampening inflammatory cytokines. To better characterize the capacity for type I IFN induction by C. burnetii, we assessed expression of IFN-ß transcripts by human macrophages following stimulation with lipopolysaccharide (LPS) from C. burnetii Understanding innate responses in C. burnetii infection will support the discovery of novel therapies that may be alternative or complementary to the current antibiotic treatment.