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Nutritional deprivation during gestation may result in specific abnormalities in lung development, such as a decreased ratio of lung size to body size. Other studies have found associations between maternal malnutrition during pregnancy and adverse asthma-related immune responses19. Pathways from Poverty to Asthma Physical environmental toxicants Indoor allergens/air pollution: Within developed countries, residential exposures to home allergens. Indeed, numerous studies have found that poor individuals are more likely to consume polluted air and water, to reside in noisier, lower-quality and more-crowded homes, and to live in neighbourhoods with greater physical deterioration all characteristics that may increase exposure to known risk factors for asthma. For lower-income countries, including Mexico, China, and India, the effects of indoor and outdoor pollution on asthma are perhaps even more pronounced5,15. Many residents in these countries rely on biomass fuels (wood, dung, crop residue) for cooking and heating which, when burned, emit high concentrations of particulate emissions that may exacerbate asthma. Cigarette smoke: the respiratory health effects of smoking have also been well documented. Maternal pre-natal cigarette smoking and post-natal environmental tobacco smoke exposure have been associated with higher risk of asthma in early childhood and greater asthma morbidity, wheeze and respiratory infections in children of all ages. As with other physical exposures, smoking behaviours are socially patterned within populations, low-income individuals are both more likely to engage in tobacco use and less likely to quit than their higher-income counterparts. Smoking can be viewed as a strategy to cope with negative affect or stress and smoking has been associated with a variety of stressors disproportionately afflicting the poor, including unemployment, minority group status, family disorder, and violence. Social Environmental Toxicants Psychosocial Stress: the social environment may contribute to asthma risk through upstream social factors that determine differential exposures to relevant asthma pathogens and toxicants and through the differential experiencing of psychological stress which is increasingly linked to the expression of asthma and other allergic disorders21. While a number of theoretical models explaining health disparities have been proposed, the psychosocial stress model may be particularly relevant for allergic disorders involving immunomodulation. In developing countries, the situation is even starker, as illustrated in Figure 5. In China, for instance, provider resistance to inhaled medication prescriptions, inadequate patient knowledge and lack of affordability has left large segments of the population untreated, resulting in some of the highest case fatality rates in the world5. Likewise, the proportion of Brazilian asthmatics using inhaled corticosteroids ranges from 6-9%, largely due to the cost30. These barriers to care in effect create a "double jeopardy" situation where those most at risk of having more severe asthma, the economically disadvantaged, are also the least likely to receive appropriate treatment. Social capital is strongly correlated with violent crime rates which impact community resilience by undermining social cohesion. Thus, crime and violence (or the lack of it) can be used as an indicator of collective well-being, social relations, or social cohesion within a community and society. Moreover, studies are beginning to explore the health effects of living in a violent environment, with a chronic pervasive atmosphere of fear and the perceived threat of violence conceptualized as chronic stress. Pharmacies may resist operating 24 hours per day due to safety concerns in poorer neighbourhoods. The pervasive trauma, stress and psychological impact associated with war-impacted regions may induce psycho-physiological sequelae that contribute to adverse health consequences which may include asthma23. For example, Wright and colleagues24 documented an association between exposure to war-related stressors and incident asthma in older Kuwaitis, following the Iraqi invasion and occupation (199091). Further research should explore the relative role of political instability and/or terrorism in explaining disparities in the global burden of disease, including allergic disorders. World Map of the Proportion of the Population with Access to Essential Drugs Copyright 2013 World Allergy Organization 102 Pawankar, Canonica, Holgate, Lockey and Blaiss Conclusions While physical characteristics of neighbourhood and housing environments such as air pollution, dampness, dust and the presence of pests are contributors to variations in the risk of allergic disorders including asthma within and across populations, these factors do not fully account for the excess asthma burden; particularly among the very poor. Rather, the data discussed above suggest that the social patterning of asthma reflects differential exposure to pathogenic factors in both the physical and social environment. Implementing anti-smoking policies and public health interventions in developing countries targeted by the tobacco industry is critical. There is a need for research in other parts of the world to more fully elucidate pathways linking social structure, economics, and disparities in allergic disease. Research Needs · Future research needs to pay increased attention to the social, political and economic forces that result in marginalization of certain populations in disadvantaged regions of the world which may increase exposure to known environmental risk factors. It is unlikely that the health problems of these disadvantaged populations can be solved without understanding the potential role of such social determinants of health and intervening on these more distal influences31. Affordability of inhaled corticosteroids as a potential barrier to treatment of asthma in some developing countries.

Effects of alfuzosin 10 mg once daily on sexual function in men treated for symptomatic benign prostatic hyperplasia. Page 201 108840 161540 102460 119050 138260 165330 153230 101630 101470 132030 124000 154220 130720 102950 127850 109070 155500 September 2010 Appendix 3: Master Bibliography American Urological Association, Inc. A practical guide to the evaluation and treatment of male lower urinary tract symptoms in the primary care setting. Curvilinear transurethral ultrasound applicator for selective prostate thermal therapy. Longterm impact of superinfection by hepatitis G virus in hepatitis C virus-positive renal transplant patients. A study on the outcome of percutaneous transluminal renal angioplasty in patients with renal failure. Decision aids for benign prostatic hyperplasia: applicability across race and education. Immunoexpressions of p21, Rb, mcl-1 and bad gene products in normal, hyperplastic and carcinomatous human prostates. Regulation of proliferation/apoptosis equilibrium by mitogen-activated protein kinases in normal, hyperplastic, and carcinomatous human prostate. Estrogen receptors alpha and beta in the normal, hyperplastic and carcinomatous human prostate. Comparison in human normal prostate, benign prostatic hyperplasia, and prostatic carcinoma. Interferon-gamma and its functional receptors overexpression in benign prostatic hyperplasia and prostatic carcinoma: parallelism with c-myc and p53 expression. Effect of angiotensin converting enzyme inhibitor or beta blocker on glomerular structural changes in young microalbuminuric patients with Type I (insulin-dependent) diabetes mellitus. Combined use of alpha-adrenergic and muscarinic antagonists for the treatment of voiding dysfunction. Activator protein 2alpha transcription factor expression is associated with luminal differentiation and is lost in prostate cancer. Longitudinal changes in post-void residual and voided volume among community dwelling men. Neuroendocrine differentiation of human prostatic primary epithelial cells in vitro. Trans-differentiation of prostatic stromal cells leads to decreased glycoprotein hormone alpha production. The development of benign prostatic hyperplasia by trans-differentiation of prostatic stromal cells. Interdigitating dendritic cell sarcoma of urinary bladder mimicking large intravesical calculus. Effect of an outcomes-managed approach to care of neuroscience patients by acute care nurse practitioners. Lower urinary tract symptoms and erectile dysfunction: epidemiology and treatment in the aging man. Systemic stress responses in patients undergoing surgery for benign prostatic hyperplasia. Urtica dioica for treatment of benign prostatic hyperplasia: a prospective, randomized, double-blind, placebo-controlled, crossover study. Overexpression of E-cadherin and beta-catenin proteins in metastatic prostate cancer cells in bone. Ultrastructure of the secretion of prostasomes from benign and malignant epithelial cells in the prostate. Economic evaluation of treatment strategies for benign prostatic hyperplasia-is medical therapy more costly in the long run. Prostate specific antigen complexed to alpha-1-antichymotrypsin in patients with intermediate prostate specific antigen levels. Effectiveness of an anti-inflammatory drug, loxoprofen, for patients with nocturia.

With the exception of one patient, there were no associated adverse clinical sequelae, no related secondary interventions, no type I endoleaks, and at five-year follow-up, the aneurysm size was stable or decreased. In these 14 patients with > 5 mm but 10 mm migration, the aneurysm size had decreased more than 10 mm in 64. Conversion the Kaplan-Meier analysis below demonstrates that standard risk, roll-in, and high risk patients have 5-year freedom from conversion rates of 97. In total, there were 6 reports of conversion to open surgical repair, including 5 within the original study follow-up period of 2 years, and 1 during the extended study follow-up period of 2 to 5 years, for which not all patients participated. Freedom from Conversion to Open Surgical Repair (Inclusive of Intra-operative, Peri-operative, Post-operative, and Late) A summary of the Kaplan Meier Curves is presented in Table 15. Summary of Kaplan-Meier Curves (Freedom from Conversion1) Treatment 30 days 1 year to 2 years to 3 years to 4 years to Study Arm Parameter to 30 days to 1 year 2 years 3 years 4 years 5 years 2 199 198 190 173 108 105 # at risk 0 2 1 0 0 1 # of events 1 6 16 65 3 32 # censored3 Standard 7 23 88 91 123 Cumulative censored4 1 Risk Kaplan-Meier 1. Standard Persistent, proximal, type I endoleak due to undersized proximal graft 248 Risk diameter. High Risk High Risk 222 543 Rupture1 due to insufficient length of iliac landing zone. Graft infection2 33 Standard 543 Graft infection2 Risk Standard Aortic neck dilatation with proximal type I endoleak and subsequent 1468 Risk aneurysm growth. No conversions to open repair were required intra-operatively or peri-operatively, and they were infrequent post-operatively. Prior to one year, conversions to open repair were related to rupture due to insufficient length of iliac landing zone (0. The lessons learned from these cases were the importance of careful planning and sizing to obtain adequate diameters and lengths of components for the patient anatomy, and selection of patients with good proximal anatomy. Between one and five years, conversions to open repair were related only to graft infection (0. In addition, the study examined aneurysm size change, device migration, endoleak, patency, and device integrity. The long-term results from those patients who agreed to participate continue to support the safety and effectiveness of the device and the need for annual clinical and imaging follow-up for detection of progression of disease, aneurysm growth, endoleak, loss of patency and device integrity. A requirement of approval was that follow-up data from patients implanted with the 36 mm diameter device from the Australian clinical study and U. This summary provides updated follow-up data received through August 29, 2011, for the Australian clinical study and the U. There were thirteen deaths beyond 12 months, and ten of these deaths were judged by the treating physician to be related to pre-existing conditions or not device- or procedure-related. There continues to be only one reported rupture, but of a common iliac artery (presumably due to excessive over-sizing of the iliac leg component), and no reports of conversion to open repair (reference Table 17). One case of aneurysm growth showed no detectable endoleak, but possible growth due to endotension resulting from unsuitable proximal neck characteristics. There were no reports of device migration (> 10 mm), confirming both the barbs and stent-to-graft attachment are adequate to withstand migration forces acting on the 36 mm diameter device. Endoleak, Aneurysm Change from Baseline, Migration, Graft Patency, and Secondary Interventions at Each Follow-up Exam Period Percent of patients Pre-discharge Australian clinical study Endoleak (all types) Aneurysm Change Shrinkage No change Growth2,3 Migration Intact devices Graft patency Any secondary intervention Endoleak (all types) Aneurysm Change3 50% (1/21) 1-month 13. Cook evaluates product performance from this commercial experience based on adverse event reporting systems throughout the world. One of these cases was associated with partial detachment of a suprarenal stent (manufactured prior to the strengthened suprarenal stent attachment implemented for U. Annual clinical and radiographic follow-up is recommended to assess progressive disease and aortic neck dilation. Prior to availability of this device, treatment for inadequate proximal fixation or seal was limited. Adjunctive primary stenting of Zenith endograft limbs during endovascular abdominal aortic aneurysm repair: Implications for limb patency. It is available in two configurations: 1) a converter configuration to treat short-bodied pre-existing grafts and 2) a main body configuration to treat longer-bodied pre-existing grafts. In one case, the patient presented to the hospital with a ruptured aneurysm, and the physicians decided to treat the patient with a Renu converter because they thought it would be faster than placing a bifurcated device. The remaining four patients with aortic rupture included three patients where difficulty removing the top cap was encountered, and one patient with inadvertent covering of the renal arteries that did not survive the conversion.

A curious feature is the manifestation of pain in body regions that are not associated with local or spinal injury. These painful regions exhibit very high rates of pathologically evoked pain (allodynia and hyperpathia). The most frequently reported painful body regions are the knee area, shoulders, and feet. Neuronal hyperexcitability has been suggested as a contributing factor to the chronic pain. Treatment of central pain in patients with traumatic brain injury is challenging, because most of these patients are also suffering from cognitive deficits and emotional distress, and neuropathic pain may overlap with pain of psychogenic origin. It was previously called thalamic pain according to the typical location of the lesion, but it can also be due to cortical (parietal cortex), subcortical, internal capsule (posterior limb), or brainstem lesion. In the majority of patients, central poststroke pain is a contralateral hemi-pain, not always including the face, but it may also be restricted to part of the upper or lower extremity. The most common pain quality is Central Neuropathic Pain 193 hematomas usually present with headache and progressive neurological symptoms, but central neuropathic pain is an uncommon symptom in these cases. The cornerstones of the diagnosis are a detailed history of development of symptoms and relieving and aggravating factors, and a careful neurological examination including sensory testing to touch, pinprick, cold, warmth, and vibration. Abnormal sensory findings suggest the possibility of neuropathic pain, and other neurological findings help to localize the site of the lesion. It is important to keep in mind that the region of sensory abnormalities may be larger than the painful region (Case 2). Typical neurological findings referring to a central neurological lesion are a positive Babinski sign, accelerated tendon reflexes, and spasticity. Careful clinical examination is usually sufficient for this process, such as diagnosing musculoskeletal pain or pain due to local infection. Diagnostic studies, such as neuroimaging and cerebrospinal fluid analysis, may provide useful information in reaching an accurate diagnosis, but they may not be available. In such conditions, recognition of the clinical features of the causative diseases is very useful. The decision as to the use of limited resources and selection of patients for referral is based on the possibilities of treatment of the causative disease, such as with neurosurgery. Spinal and cerebral abscesses, spinal traumas with partial cord lesion, and spinal tumors are examples of conditions with radically improved prognosis with active surgical treatment. Cerebral abscess should be suspected if a patient has fever and progressive neurological symptoms (in cerebral abscess contralateral symptoms, and in spinal abscess sensory and motor deterioration below the level of the abscess). History of trauma before the onset of weakness of the limbs and sensory changes, including central pain, is suggestive of partial cord lesion. If there is an unstable lesion of the vertebral column, quick stabilizing surgery may prevent complete paralysis, and the same is true with laminectomies in spinal contusion with partial paresis. Slowly progressive paraparesis and sensory changes may be caused by a spinal tumor. The final prognosis depends on the histology of the tumour and the severity of the symptoms before surgery. The first line of therapy, after a thorough assessment, is information and education, for both the patient and the family. The character of the pain, the disease causing it, and the possibilities for pain relief need to be explained to the patient and the family. As symptomatic treatment of central neuropathic pain is less successful than treatment of peripheral neuropathic pain, giving thorough information may be the best way to help the patient. Similarly to peripheral neuropathic pain, antidepressants and anticonvulsants are used for symptomatic treatment of central neuropathic pain. It is started with 10­25 mg in the evening, and the dose is escalated by 10­25 mg steps to 50­150 mg/day depending on the extent of side effects. Difficulties in urination, constipation, dry mouth, and dizziness are typical side effects, which may prevent further dose escalation.