Nerve conduction studies help delineate the extent and distribution of the neural lesion. The nerve conduction was studied on upper (median, ulnar and radial nerves) and lower (personal, posterior tibial and sural nerves) extremities in 83 healthy subjects 23 to 66 years of age, and normal values were established (Table 1). The mean motor terminal latency (TL): median, 3.6 (±0.6) milliseconds; ulnar, 2.9 (±0.5) milliseconds; radial nerve, 2.3 (±0.4) milliseconds. Mean motor nerve conduction velocity (MNCV) along distal and proximal segments: median, 61.2 (±9.1) (W-E) and 57.8 (±13.2) (E-Ax) meters per second; ulnar, 63.7 (±9.1) (W-E) and 50.6 (±10.0) meters per second. Mean sensory nerve conduction velocity (SNCV): median, 34.7 (±6.7) (F-W), 63.7 (±7.1) (W-E) and 62.8 (±12.3) (E-Ax) meters per second; ulnar, 38.0 (±6.7) (F-W), 63.4 (±7.5) (W-E) and 57.0 (±10.1) (E-Ax) meters per second; radial, 45.3 (±6.8) (F-W) and 64.2 (±11.0) (W-E) meters per second; sural nerve, 43.4 (±6.1) meters per second. The amplitudes of action potential and H-reflex were also standardized. Mean H latency was 28.4 (±3.2) milliseconds. And, the fundamental principles, several factors altering the rate of nerve conduction and clinical application of nerve stimulation techniques were reviewed.
Action Potentials ; Adult* ; Extremities ; H-Reflex ; Healthy Volunteers ; Humans ; Neural Conduction* ; Radial Nerve ; Reference Values ; Sural Nerve

Dyslipidemia is a potentially modifiable cardiovascular risk factor. Whereas the recommendations for the treatment target of dyslipidemia in the general population are being more and more rigorous, the 2013 Kidney Disease: Improving Global Outcomes clinical practice guideline for lipid management in chronic kidney disease (CKD) presented a relatively conservative approach with respect to the indication of lipid lowering therapy and therapeutic monitoring among the patients with CKD. This may be largely attributed to the lack of high-quality evidence derived from CKD population, among whom the overall feature of dyslipidemia is considerably distinctive to that of general population. In this review article, we cover the characteristic features of dyslipidemia and impact of dyslipidemia on cardiovascular outcomes in patients with CKD. We also review the current evidence on lipid lowering therapy to modify the risk of cardiovascular events in this population. We finally discuss the association between dyslipidemia and CKD progression and the potential strategy to delay the progression of CKD in relation to lipid lowering therapy.

Authors recorded standard electroretinogram in two groups of diabetic patients. Group A, consisted of 60 eyes with no visible diabetic retinopathy and Group B, 30 eyes with mild nonproliferative diabetic retinopathy. The electroretinogram was recorded according to the standard electroretinogram procedure recommanded by the ISCEV. In rod and cone response, the amplitude of b wave were 329.0+/-46.9 microvoltin Group A and 308.8+/-37.8 microvoltin Group B. The implicit time of b wave were 40.5+/-3. 0microvoltin Group A and 45.8+/-5.4microvolti n Group B. The summed amplitude of oscillatory potentials were 125.7+/-38.7microvolt in Group A and 112.0+/-17.7microvoltin Group B. Above results indicate that for the disgnostic criteria for diabetic retinopathy, the amplitude and implict time of b wave, and the summed amplitude of oscillatory potentials in maximal combined response were useful. On receiver operating characteristic(ROC) curves in maximal combined response, cut off value for the amplitude and implicit time of b wave were 315 microvoltand 42ms espectively. Cut off value for the summed amplitude of oscillatory potentia-als was 118 microvolt. In results, on ROC curve, the implicit time of b wave in maximal combined response was most accurate, and the summed amplitude of oscillary potentials was the next, followed by the amplitude of b wave in the maximal combined response.
Diabetic Retinopathy* ; Early Diagnosis* ; Humans ; ROC Curve

Food allergy (FA) and atopic dermatitis (AD) are representative allergic diseases that begin early in life and result in considerable socioeconomic burden. While the pathophysiology and the optimal treatment modalities of these diseases are largely unknown, the role of microbes in health and disease are being highlighted. Recent advances in analyzing microbiome have enabled us to expand our research on impacts of the microbiome on the onset and course of FA and AD. Risk factors that are presumed to affect intestinal microbiome also modulate the onset of allergic diseases, which is more evident in AD than in FA. Considering animal studies, intestinal microbiota interacts with FA and the influence is bi-directional. The activation of regulatory T cell and the innate immune system is supposed to mediate the interaction. Regarding human studies, there exists the difference in the composition of microbiome between subjects with FA or AD and matched normal controls, which can further play as a predictive marker for later development of FA or AD. Probiotics are now investigated as a primary therapeutic agent or as an adjuvant tool for conventional therapies in preventing or modulating FA or AD. Currently, several reports on favorable outcomes become available, which should be replicated and backed up by large-scale studies with more detailed protocols.
Animals ; Dermatitis, Atopic* ; Food Hypersensitivity* ; Gastrointestinal Microbiome ; Humans ; Immune System ; Microbiota* ; Probiotics ; Risk Factors

No abstract available.
Behcet Syndrome* ; Renal Insufficiency*

The prevalence of allergic diseases has been increasing rapidly, especially in developing countries. Various adverse health outcomes such as allergic disease can be attributed to rapidly increasing air pollution levels. Rapid urbanization and increased energy consumption worldwide have exposed the human body to not only increased quantities of ambient air pollution, but also a greater variety of pollutants. Many studies clearly demonstrate that air pollutants potently trigger asthma exacerbation. Evidence that transportation-related pollutants contribute to the development of allergies is also emerging. Moreover, exposure to particulate matter, ozone, and nitrogen dioxide contributes to the increased susceptibility to respiratory infections. This article focuses on the current understanding of the detrimental effects of air pollutants on allergic disease including exacerbation to the development of asthma, allergic rhinitis, and eczema as well as epigenetic regulation.
Air Pollutants ; Air Pollution ; Asthma ; Developing Countries ; Eczema ; Environmental Exposure ; Epigenomics ; Human Body ; Hypersensitivity ; Nitrogen Dioxide ; Ozone ; Particulate Matter ; Prevalence ; Respiratory Tract Infections ; Rhinitis, Allergic ; Tobacco Smoke Pollution ; Urbanization

No abstract available.
Aluminum* ; Onychomycosis* ; Yttrium*

In the decades since the discovery of angiotensin-converting enzyme 2 (ACE2), its protective role in terms of antagonizing activation of the classical renin-angiotensin system (RAS) axis has been recognized in clinical and experimental studies on kidney and cardiovascular diseases. The effects of ACE inhibitor/angiotensin type 1 receptor blockers (ACEi/ARBs) on ACE2-angiotensin-(1-7) (Ang- (1-7))-Mas receptor (MasR) axis activation has encouraged the use of such blockers in patients with kidney and cardiovascular diseases, until the emergence of coronavirus disease 2019 (COVID-19). The previously unchallenged functions of the ACE2-Ang-(1-7)-MasR axis and ACEi/ARBs are being re-evaluated in the era of COVID-19; the hypothesis is that ACEi/ARBs may increase the risk of severe acute respiratory syndrome coronavirus 2 infection by upregulating the human ACE2 receptor expression level. In this review, we examine ACE2 molecular structure, function (as an enzyme of the RAS), and distribution. We explore the roles played by ACE2 in kidney, cardiovascular, and pulmonary diseases, highlighting studies that defined the benefits imparted when ACEi/ARBs activated the local ACE2- Ang-(1-7)-MasR axis. Finally, the question of whether ACEi/ARBs therapies should be stopped in COVID-19-infected patients will be reviewed by reference to the available evidence.