Occupational Carpal Tunnel Syndrome: a scoping review of causes, mechanisms, diagnosis, and intervention strategies.

Carpal Tunnel Syndrome (CTS) has traditionally been viewed as a specialized medical condition. However, its escalating prevalence among professionals across a multitude of industries has sparked substantial interest in recent years. This review aims to delve into CTS as an occupational disease, focusing on its epidemiological patterns, risk factors, symptoms, and management options, particularly emphasizing its relevance in professional environments. The complex interaction of anatomical, biomechanical, and pathophysiological factors that contribute to the development of CTS in different work settings underlines the critical role of ergonomic measures, prompt clinical identification, and tailored treatment plans in reducing its effects. Nevertheless, the challenges presented by existing research, including diverse methodologies and definitions, highlight the need for more unified protocols to thoroughly understand and tackle this issue. There's a pressing demand for more in-depth research into the epidemiology of CTS, its injury mechanisms, and the potential role of targeted medicine. Moreover, recognizing CTS's wider ramifications beyond personal health is essential. The economic burden associated with CTS-related healthcare costs, productivity losses, and compensation claims can significantly impact both businesses and the broader society. Therefore, initiatives aimed at preventing CTS through workplace interventions, education, and early intervention programs not only benefit the affected individuals but also contribute to the overall well-being of the workforce and economic productivity. By fostering a collaborative approach among healthcare professionals, employers, policymakers, and other stakeholders, we can strive towards creating safer and healthier work environments while effectively managing the challenges posed by CTS in occupational settings.

The Analysis of Blood Inflammation Markers as Prognostic Factors in Parkinson's Disease.

Parkinson's disease is a chronic, progressive, and neurodegenerative disease, and yet with an imprecise etiopathogenesis. Although neuroinflammation was initially thought to be a secondary condition, it is now believed that microglia-induced inflammation could also contribute to the degeneration of the nigrostriatal pathway. Here, we aimed to establish the feasibility of basic inflammatory biomarkers as prognostic factors in PD. The study was based on retrospective analyses of blood samples taken from patients diagnosed with PD, as well as from healthy subjects. Complete medical records, total leukocyte count with subpopulations, and erythrocyte sedimentation rate (ESR) were analyzed. We calculated the serum neutrophils-to-lymphocytes ratio (NLR) and platelet-to lymphocytes ratio (PLR), and also compared the laboratory data between the PD group and the control group. Only PLR and NLR showed statistically significant differences (p < 0.001 and 0.04, respectively). In our study, ESR did not show statistically significant correlations with motor score or with disability. In our research, ESR was correlated with the disease duration (p = 0.04), and PLR showed a significant correlation with disease stage (p = 0.027) and disease duration (p = 0.001), but not with motor state. These biomarkers could prove to be effective tools for a primary evaluation of inflammation in PD, but further tests are required to properly investigate the neuroinflammatory status of these patients.

Analysis of Some Behavioral Risk Factors in Relation to Acute Coronary Events.

The association of acute coronary events and behavioral risk factors is already known. Of these, smoking and alcohol consumption are the behavioral risk factors with the most intense impact in the occurrence of these events. The correct knowledge of the dynamics and their involvement in the evolution of acute coronary events remains of overwhelming importance in the light of current data. To achieve the purpose of this study data from three family medicine practices from the period November 2018 to May 2019 were corroborated. Anonymous questionnaires were applyed to the subjects. For this study, questions related to the habit of smoking and consuming alcohol were selected. The study aimed to analyze the associative relationships between acute coronary events and two of the most common behavioral risk factors, smoking and alcohol consumption. The highest prevalence of acute coronary events was observed in current smokers and in former smokers. The period of exposure to smoking showed that this is one of the variables most strongly associated with an increased risk of acute coronary events. Moderate consumption of wine or beer seems to have a weak association with acute coronary events, even weaker than those who do not consume at all suggesting a protective effect.

The Impact of the Associated Pathology in Acute Coronary Events.

Acute coronary events (ACE) are one of the main concerns for both clinical medicine and prophylaxis. The study aims to follow the frequency of the pathology associated with ACE and to establish its association with the occurrence of ACE. The study included 865 adult participants between the ages of 19-86. Subjects completed a complex questionnaire that included questions about health status. The study was conducted by applying the subjects to an anonymous questionnaire, in three family medicine practices between November 2018 to May 2019 and targeted healthy people. The frequencies of the following types of associated pathologies were evaluated: high blood pressure (HBP), hypercholesterolemia, stroke, diabetes, depression, stress. In hypertensive patients the prevalence of ACE was 6,99% (N=11) and in those not diagnosed with HBP of only 0,29% (N=2). The risk of ACE was 20 times higher than in those without HBP (RR=20,93; p<0.001). The prevalence of ACE was high among subjects with high cholesterol levels (21,43%) compared with those with normal values (3,03%; N=22), the risk of ACE being 7 times higher (RR=7,06; p<0.001). The prevalence of diabetes was more than four times higher in subjects with ACE (17,3%; N=9) compared with those without ACE (3,9%; N=32). Among those affected by diabetes, the prevalence of ACE was 21,95% (9/41), and risk of ACE in people with diabetes was four times higher (RR=4,21; p<0.001). Although cardiovascular disease is the most common pathology in the contemporary world, a number of comorbidities arise as ACE generators (hypertension, hypercholesterolemia, diabetes), along with psycho-emotional disorders such as depression, anxiety or stress, which outline, ensures, contributes or accelerates the progression to ACE.

Phosphodiesterase-5 inhibitors ameliorate structural kidney damage in a rat model of contrast-induced nephropathy.

The aim of the study was to investigate the potential of sildenafil and tadalafil to ameliorate structural kidney damage in contrast-induced nephropathy (CIN). A rat model of CIN was developed by dehydration, administration of a nitric oxide inhibitor and a prostaglandin synthesis inhibitor (L-NAME/indomethacin) and contrast media exposure to iopromide. The effect of pre-treatment with sildenafil, tadalafil or N-acetyl cysteine (NAC) for 7 days prior to CIN induction was investigated. All animals were sacrificed at 24 h after CIN induction and both kidneys were collected. Histopathological examination was performed under light microscopy in serial tissue sections stained with hematoxylin and eosin. CIN group showed hydropic changes of the renal tubules (proximal and distal convoluted tubules and Henle's loop), an increased Bowman space with lobulated glomerulus and alteration of macula densa region of distal convolute tubules. The groups pretreated with sildenafil and tadalafil showed nearly normal histological aspects of renal tissue. The group pretreated with NAC showed similar but less intense histopathologic changes compared to CIN group. Sildenafil and tadalafil pre-treatment ameliorates CIN-related structural kidney damage and the protective potential of these agents is superior to NAC.

Sildenafil and tadalafil reduce the risk of contrast-induced nephropathy by modulating the oxidant/antioxidant balance in a murine model.

The aim of the study was to evaluate the potential protective role of sildenafil and tadalafil in contrast-induced nephropathy (CIN) by modulating oxidative stress. Thirty Wistar male rats were equally assigned into five groups: sham, CIN, CIN + sildenafil (10 mg/kg bw/day), CIN + tadalafil (5 mg/kg bw/day) and CIN + N-Acetyl Cysteine (NAC) (100 mg/kg bw/day) as a positive control. CIN was induced by 12 h dehydration and administration of indomethacin (10 mg/kg bw), N-ω- nitro-L-arginine methyl ester (10 mg/kg bw), and iopromide (3 g/kg bw iodine). Blood was drawn prior to and 24 h after CIN induction for evaluating renal function and oxidative stress. In the CIN group, total antioxidant capacity (TAC), reduced glutathione (GSH) and catalase (CAT) levels were significantly decreased; and protein carbonyl (PROTC) and thiobarbituric reactive species (TBARS) were significantly increased compared to the sham group. Pre- Sildenafil and tadalafil pre-treatment reduced CIN risk and reversed oxidative stress almost to the sham group levels. These results suggest that PDE5Is can be good candidates for preventing CIN based on their ability to modulate the oxidant/antioxidant balance.