An Update on the Use of Wearable Devices in Men's Health.

Men's health represents an often-overlooked aspect of public health. Men have higher mortality rates worldwide and are more negatively affected by chronic conditions such as obesity and heart disease, as well as addiction to alcohol and tobacco. Men also have health issues such as prostate cancer and male sexual dysfunction which only affect them. Because of the skewed burden of morbidity and mortality on men, it is imperative from a public health perspective to make a concerted effort to specifically improve men's health. The use of wearable devices in medical practice presents a novel avenue to invest in men's health in a safe, easily scalable, and economic fashion. Wearable devices are now ubiquitous in society, and their use in the healthcare setting is only increasing with time. There are commercially available devices such as smart watches which are available to lay people and healthcare professionals alike to improve overall health and wellness, and there are also purpose-built wearable devices which are used to track or treat a specific disease. In our review of the literature, we found that while research in the field of wearable devices is still in its early stages, there is ample evidence that wearable devices can greatly improve men's health in the long-term.

Derivation and Characterization of Murine and Amphibian Müller Glia Cell Lines.

Purpose: Müller glia (MG) in the retina of Xenopus laevis (African clawed frog) reprogram to a transiently amplifying retinal progenitor state after an injury. These progenitors then give rise to new retinal neurons. In contrast, mammalian MG have a restricted neurogenic capacity and undergo reactive gliosis after injury. This study sought to establish MG cell lines from the regeneration-competent frog and the regeneration-deficient mouse. Methods: MG were isolated from postnatal day 5 GLAST-CreERT; Rbfl/fl mice and from adult (3-5 years post-metamorphic) X laevis. Serial adherent subculture resulted in spontaneously immortalized cells and the establishment of two MG cell lines: murine retinal glia 17 (RG17) and Xenopus glia 69 (XG69). They were characterized for MG gene and protein expression by qPCR, immunostaining, and Western blot. Purinergic signaling was assessed with calcium imaging. Pharmacological perturbations with 2'-3'-O-(4-benzoylbenzoyl) adenosine 5'-triphosphate (BzATP) and KN-62 were performed on RG17 cells. Results: RG17 and XG69 cells express several MG markers and retain purinergic signaling. Pharmacological perturbations of intracellular calcium responses with BzATP and KN-62 suggest that the ionotropic purinergic receptor P2X7 is present and functional in RG17 cells. Stimulation of XG69 cells with adenosine triphosphate-induced calcium responses in a dose-dependent manner. Conclusions: We report the characterization of RG17 and XG69, two novel MG cell lines from species with significantly disparate retinal regenerative capabilities. Translational Relevance: RG17 and XG69 cell line models will aid comparative studies between species endowed with varied regenerative capacity and will facilitate the development of new cell-based strategies for treating retinal degenerative diseases.

Secretory Functions of Macrophages in the Human Pancreatic Islet Are Regulated by Endogenous Purinergic Signaling.

Endocrine cells of the pancreatic islet interact with their microenvironment to maintain tissue homeostasis. Communication with local macrophages is particularly important in this context, but the homeostatic functions of human islet macrophages are not known. In this study, we show that the human islet contains macrophages in perivascular regions that are the main local source of the anti-inflammatory cytokine interleukin-10 (IL-10) and the metalloproteinase MMP9. Macrophage production and secretion of these homeostatic factors are controlled by endogenous purinergic signals. In obese and diabetic states, macrophage expression of purinergic receptors MMP9 and IL-10 is reduced. We propose that in those states, exacerbated ß-cell activity due to increased insulin demand and increased cell death produce high levels of ATP that downregulate purinergic receptor expression. Loss of ATP sensing in macrophages may reduce their secretory capacity.

Disrupting the blood-brain barrier by focused ultrasound induces sterile inflammation.

MRI-guided pulsed focused ultrasound (pFUS) combined with systemic infusion of ultrasound contrast agent microbubbles (MB) causes localized blood-brain barrier (BBB) disruption that is currently being advocated for increasing drug or gene delivery in neurological diseases. The mechanical acoustic cavitation effects of opening the BBB by low-intensity pFUS+MB, as evidenced by contrast-enhanced MRI, resulted in an immediate damage-associated molecular pattern (DAMP) response including elevations in heat-shock protein 70, IL-1, IL-18, and TNFα indicative of a sterile inflammatory response (SIR) in the parenchyma. Concurrent with DAMP presentation, significant elevations in proinflammatory, antiinflammatory, and trophic factors along with neurotrophic and neurogenesis factors were detected; these elevations lasted 24 h. Transcriptomic analysis of sonicated brain supported the proteomic findings and indicated that the SIR was facilitated through the induction of the NFκB pathway. Histological evaluation demonstrated increased albumin in the parenchyma that cleared by 24 h along with TUNEL+ neurons, activated astrocytes, microglia, and increased cell adhesion molecules in the vasculature. Infusion of fluorescent beads 3 d before pFUS+MB revealed the infiltration of CD68+ macrophages at 6 d postsonication, as is consistent with an innate immune response. pFUS+MB is being considered as part of a noninvasive adjuvant treatment for malignancy or neurodegenerative diseases. These results demonstrate that pFUS+MB induces an SIR compatible with ischemia or mild traumatic brain injury. Further investigation will be required before this approach can be widely implemented in clinical trials.

Iatrogenic foreign body in the urinary bladder.

A 60 years old man presented with a history of suprapubic pain, painful micturition, perineal pain, and acute retention of urine followed by catheterization. On abdominal ultrasound, there was a metallic needle found in the urinary bladder which was confirmed on pelvis X-ray. The needle was found to be a metallic piece of a resectoscope cutting loop which was removed through cystourethroscopy.

Periocular Scleromyxedema.

Scleromyxedema is characterized by cutaneous mucinosis and rarely presents to oculoplastic surgeons with bilateral upper and lower eyelid swelling. The authors present 2 case reports with a review of the literature and discuss the ophthalmic manifestations of scleromyxedema and the management of these cases. Both patients were in their early 50s and were fit and well prior to the presentation. They both presented with eyelid swelling and underlying nodularity of the subcutaneous tissue. The skin biopsy confirmed cutaneous manifestations of scleromyxedema. The systemic manifestations responded to intravenous and oral steroids and intravenous infusions of immunoglobulin. The ophthalmic manifestations were managed conservatively. Scleromyxedema is a rare connective tissue disease characterized by cutaneous mucinosis, extracutaneous manifestations, and monoclonal gammopathy. It rarely affects the eyelids and cornea. The authors would like to present 2 cases of periocular scleromyxedema.

Reflux of drug during intra-vitreal anti-VEGF therapies.

PURPOSE: To report reflux of anti-VEGF drug during intravitreal injections. METHOD: Review of electronic case notes of patients undergoing intra-vitreal anti-VEGF treatments. Prospective data collection was performed with a specific emphasis on presence or absence of reflux. RESULTS: 152 records of 102 eyes were available from an 8-month period. 119 Ranibizumab injections and 33 bevazicumab injections were considered. Reflux was noted in 48 injections (31%). For eyes with first injection of anti-VEGF agent, reflux was noted in 9/23 eyes. Eyes with at least one previous injection were observed to have reflux in 24/79 eyes. Presence of reflux was statistically tested against posterior vitreous detachment and phakic status and was found to be statistically insignificant. CONCLUSION: Intra-vitreal anti-VEGF injections with volumes of 0.05 ml appears to produce displacement of the conjunctiva with a transient fluid-filled bleb immediately after the injection in approximately 1/3 of eyes.

Macular infarction after inadvertent intracameral cefuroxime.

UNLABELLED: We present the case of a 70-year-old patient who had uneventful cataract surgery. Because of a procedural mishap, the patient received an excess dose of intracameral cefuroxime of approximately 62.5 mg. Two weeks postoperatively, evidence of macular infarction with cystoid macular edema was seen on fundus fluorescein angiography. The patient was treated with 4.0 mg of intravitreal triamcinolone, but the visual acuity failed to improve; the final pinhole acuity was 3/60. Based on the postoperative progress, we speculate that a delayed mechanism of vascular toxicity is implicated. The importance of systematic procedures to reduce the risk for mistakes is emphasized, especially for a procedure such as cataract surgery where efficiency is increasingly important. FINANCIAL DISCLOSURE: Neither author has a financial or proprietary interest in any material or method mentioned.

Primary intravitreal ranibizumab for myopic choroidial neovascularisation.

Myopic chorodial neovascularisation (mCNV) is an important cause of visual loss in high myopia with almost 10% of eyes with pathological myopia developing mCNV. Intravitreal anti-VEGF agents have recently been documented to be effective in mCNV. However, controversy exists regarding the optimal drug, its dose, and the frequency of administration. We performed a retrospective case review examining patients who had myopia of less than -6D and a chorodial neovascular membrane diagnosed on fundus fluorescein angiography (FFA) that were treated with 3 injections of ranibizumab (Lucentis) 5mg/0.05ml given at monthly intervals. The course was repeated if the ocular coherence tomography (OCT) continued to show intra-retinal oedema at review. We recorded logMAR visual acuities and central foveal thickness (CFT) at baseline and final review. Improvement in visual acuity was significantly improved (p = 0.049) by a mean of 0.24 logMAR (range 0 to 0.74). Every patient achieved at least visual stability. Mean CFT reduction was also significantly improved (p = 0.02) by a mean of 109 microns (range -8 to 198). Our series and current literature seem to support as primary treatment a standard dose of an anti-VEGF agent. Further, larger studies are required to clarify whether any particular injection strategy is clearly superior.

Effect of reflux of drug during intravitreal anti-VEGF therapies on foveal thickness.

PURPOSE: To report any variation in foveal thickness in eyes with and without reflux during anti-VEGF injection. METHOD: Review of electronic case notes and scans. RESULTS: 18 patients receiving bevazicumab were identified as having reflux (n = 3) or no reflux (n = 15). Pre-injection average central foveal thickness (CFT) was 439 microns (µ) and post-injection average CFT was 417µ. The change in mean CFT was -22 µ (range -330 to 336 µ). 70 patients receiving ranibizumab (lucentis) were identified as having reflux (n = 22) or no reflux (n = 48). Average pre-injection CFT was 336 µ and post-injection average CFT was 289 µ. The change in mean CFT was -48 µ (range -163 to 443 µ). The change in CFT between the group with reflux and no reflux in bevazicumab and ranibizumab injections was statistically insignificant. CONCLUSION: Reflux following injection of anti-VEGF agents does not appear to cause a sub-therapeutic effect.

Assessment of delays in presentation of patients with retinal detachment to a tertiary referral centre.

The referral pathway of patients with retinal detachment from primary care providers to a tertiary care ophthalmic unit was examined, in order to determine the length and source of any delays between the onset of symptoms and arrival at the hospital. A prospective survey of all symptomatic patients (n = 60) admitted for primary rhegmatogenous retinal detachment surgery was carried out over an 8 week period. Twenty-one patients were referred by their optometrists and 18 by their general practitioners. The remainder were referred by local accident and emergency and ophthalmic departments or presented directly to the tertiary referral centre. Patients who presented to their optometrists were symptomatic for an average of four times longer. More than half the patients thought that the time to initial presentation was the most significant delay. Referral from optometrists via general practitioners and local ophthalmic clinics was considerably longer. Increased awareness of symptoms, necessity of urgent referral and knowledge of available services locally may reduce delay for those who require emergency sight-saving surgery.