A low anaerobic power has been proposed as a factor that may be limiting the achievement of a plateau in VO2 of children who perform maximal aerobic power tests. This study examined the frequency of plateau achievement in pre-pubertal children and compared VO2max, peak (PP) and mean (MP) anaerobic power in subjects who either achieved a plateau (PLAT) or did not (NO PLAT). Eighteen healthy pre-pubertal (Tanner Stage, pubic hair = 1) males (age = 9.1 1.6 yrs, ht = 134.4 +/- 9.7cm, wt = 33.3 +/- 9.2kg, VO2max = 40.0 +/- 6.7 ml x kg(-1) min(-1)) were tested. All subjects completed a 30 sec Wingate Anaerobic Test and a McMaster aerobic protocol to volitional fatigue on a cycle ergometer. Only 33% of the subjects met the PLAT criterion. No differences were found for PP or MP between those who achieved a plateau and those who did not (PLAT: PP= 6.3 +/- 0.8W/kg and MP = 5.2 +/- 0.7W/kg; NO PLAT: PP= 6.3 +/- 1.2 W/kg and MP = 5.2 +/- 1.3 W/kg). We conclude that anaerobic power is not a factor limiting the achievement of a plateau in VO2 of pre-pubertal boys who perform maximal aerobic power tests.

The variation in the reported rates of KCS can be attributed to factors such as: limited sample size, age of patients sampled, gender, subjective versus objective determination of DED. The association between RA and KCS is well established and contributes to morbidity [4][5][6]. Features and pathogenesisSymptoms of KCS include: burning, gritty sensation and dryness. A recent meta-analysis demonstrated a link between dry eye disease and depression and anxiety [7]. If left untreated, KCS may lead to a lidwiper epitheliopathy (analogous to that found in long-term contact lens wearer), keratitis, and possibly even opacification of the cornea [8]. In severe cases, one can see paracentral corneal melts which can cause permanent visual loss, and even perforation.Inflammation has been postulated as the underlying cause for KCS [9]. The pathogenesis of RA involves an inappropriate attack on the

To determine serum levels of IgE and sCD23 and lymphocyte subpopulations, we studied 37 control subjects and 84 patients (27 with allergic rhinitis, 27 with extrinsic asthma, and 30 with intrinsic asthma). A rise in surface CD23 on B and monocyte cells and sCD23 serum levels was exhibited by patients with rhinitis and extrinsic asthma. Unexpectedly, in intrinsic asthmatic patients, high CD23 expression on monocytes and high sCD23 levels were seen that did not result in IgE production. It appears that CD23, in its soluble form, could be a good disease marker, especially in asthma. Atopic patients yielded a significantly lower proportion of CD4+ T cells than intrinsic asthmatic patients and normal persons. Otherwise, CD4+CD29+CD45RA- and CD4+CD29-CD45RA T-cell subsets were significantly decreased in all patient groups.

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The advent of hydroxyurea and advanced medical care, including immunizations has led to improved survival among patients with Sickle Cell Disease (SCD). This prolonged survival however, introduces a chronic inflammatory disorder, Rheumatoid Arthritis (RA), which presents at a relatively older age and is rarely reported among SCD patients. In this review, we highlight the epidemiological association of SCD-RA and discuss the underlying common pathogenetic mechanisms, such as endothelial dysfunction, the role of inflammatory cytokines and oxidative stress. We also point to the difficulties in ascertaining the clinical diagnosis of RA in SCD patients. Finally, we provide rationale for therapeutic options available for RA and the challenges in the management of these patients with agents that are known to increase the risk of infection and immunosuppression such as steroids, disease modifying anti-rheumatic drugs and biologics.

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Background The association of Neuromyelitis Optica Spectrum Disorders (NMOSD) with autoimmune disorders including Sjögren’s syndrome (SS), is well recognized. Epstein Barr virus (EBV) has been associated to various neurological entities. We describe a case where EBV infection likely preceded NMOSD in a patient with unrecognized SS. The clinical features, work up and management are described. Case presentation A 40-year woman with history of stroke and Guillain-Barre Syndrome (GBS) two years prior, presented with progressive lower extremity weakness and pain. Brain MRI revealed hyperintensities in the cerebellar and parietal lobes consistent with old infarcts, high intensity signal in the white matter and enhancing intramedullary lesion at the level of T2 and the conus medullaris. Cerebrospinal fluid (CSF) revealed no oligoclonal bands. Next day, the patient developed right ankle weakness and urinary incontinence. NMOSD was suspected and pulse steroids initiated. Patient’s weakness resolved. Antinuclear antibodies (ANA), anti-SSA/SSB and Aquaporin 4 antibodies (AQP4Ab) were positive. CSF was positive for EBV. Parotid gland ultrasound revealed non-homogeneous tissue. Ganciclovir and plasmapheresis were started. The patient’s sensation and motor deficits improved and one month after, she had regained motor power and sphincter control. The patient was discharged on oral prednisone and plans for rituximab infusions. On follow-up imaging, Spinal MRI showed areas of myelomalacia and complete resolution at the level of T2 and conus medularis lesions respectively. The patient had no additional flares, but did complain of chronic neuropathic pain. Conclusion NMOSD commonly coexist with other autoimmune diseases. The association of SS and NMOSD is well recognized. EBV infections can present with neurological manifestations however, EBV has also been linked to the development of autoimmunity. In our case, EBV was detected in CSF and antiviral therapy was initiated in addition to the treatment modalities for NMOSD which led to a full recovery in our patient.

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