Washing with sodium bisulfite solution removed ~90% of acetaldehyde and prevented oxazolidine formation. The study indicated that ephedrines reacted with aldehydes in ethyl acetate to produce oxazolidines and washing with sodium bisulfite solution prevented it. It is necessary to exercise caution when using ethyl acetate to extract ephedrines.Burns are one of the most severe traumas, causing coagulative destruction of the skin. The use of various products that accelerate wound healing in patients with burns may affect rates of patient survival and reduce complications. We studied the effects of subcutaneous ozone injection on second-degree burn wounds in animal model. For this study, 72 Sprague-Dawley male rats were divided randomly into the following three groups control group , silver sulfadiazine group, and ozone group; each group was then divided randomly into two subgroups (day 7 or day 14 examination and sacrifice). Superficial partial thickness burns were created on the lower back. In the control group, subcutaneous 0.9% serum saline was injected daily into the burn area. In the silver sulfadiazine group, burns were dressed daily with silver sulfadiazine. In the ozone group, subcutaneous ozone was injected daily into the burn area. We performed tissue hydroxyproline level measurements and histopathological evaluations. When groups were compared in terms of weight change, no significant difference was found between day 7 and day 14. With regard to tissue hydroxyproline levels the ozone group had significantly higher levels on both day 7 and day 14 (P less then .001). In histopathological evaluations, we determined that wound healing in the ozone group was significantly higher than in the other groups. We found that subcutaneous ozone therapy was more effective than silver sulfadiazine in the healing process of second-degree burn wounds and could be safely used in the treatment of burn wounds.
Growth hormone insensitivity (GHI) in children is characterized by short stature, functional IGF-I deficiency and normal or elevated serum GH concentrations. The clinical and genetic etiology of GHI is expanding. We undertook genetic characterization of short stature patients referred with suspected GHI and features which overlapped with known GH-IGF-I axis defects.

Between 2008 and 2020, our center received 149 GHI referrals for genetic testing. Genetic analysis utilized a combination of candidate gene sequencing (CGS), whole exome sequencing (WES), array comparative genomic hybridization (aCGH) and a targeted whole genome short stature gene panel.

Genetic diagnoses were identified in 80/149 subjects (54%) with 45/80 (56%) having known GH-IGF-I axis defects (GHR n=40, IGFALS n=4, IGFIR n=1). The remaining 35/80 (44%) had diagnoses of 3M syndrome (n=10) (OBSL1 n=7, CUL7 n=2 and CCDC8 n=1), Noonan syndrome (n=4) (PTPN11 n=2, SOS1 n=1 and SOS2 n=1), Silver-Russell syndrome (n=2) (Loss of methylation on chromosome 11p15 and uniparental disomy for chromosome 7), Class 3-5 copy number variations (n=10) and disorders not previously associated with GHI (n=9) (Barth syndrome, Autoimmune lymphoproliferative syndrome, Microcephalic osteodysplastic primordial dwarfism Type II, Achondroplasia, Glycogen storage disease Type IXb, Lysinuric protein intolerance, Multiminicore Disease, MACS syndrome and Bloom syndrome).

We report the wide range of diagnoses in 149 patients referred with suspected GHI, which emphasizes the need to recognize GHI as a spectrum of clinical entities in undiagnosed short stature patients. Detailed clinical and genetic assessment may identify a diagnosis and inform clinical management.
We report the wide range of diagnoses in 149 patients referred with suspected GHI, which emphasizes the need to recognize GHI as a spectrum of clinical entities in undiagnosed short stature patients. Detailed clinical and genetic assessment may identify a diagnosis and inform clinical management.
Atrial fibrillation (AF) is associated with a high risk of cardiovascular and non-cardiovascular death, even on anticoagulation. It is controversial, which conditions-including concomitant diseases and AF itself-contribute to this mortality. To further clarify these questions, major determinants of long-term mortality and their contribution to death were quantified in an unselected cohort of AF patients.

We established a large nationwide registry comprising 8833 AF-patients with a median follow-up of 6.5 years (45 345 patient-years) and central adjudication of adverse events. Baseline characteristics of the patients were evaluated as predictors of mortality using Cox regression and C-indices for determination of predictive power. Annualized mortality was highest in the first year (6.2%) and remained high thereafter (5.2% in men and 5.5% in women). Thirty-eight percent of all deaths were cardiovascular, mainly due to heart failure or sudden death. Sex-specific age was the strongest predictor of mortality, endent impact on long-term mortality in our representative cohort.
Burns on the face pose unique management challenges because they are in a place that is constantly visible, so scars are hard to hide. The goal of this study was to review our experience of adult patients who had face burns.

We performed a retrospective review of adult patients (≥ 18 years old) who were admitted to a regional burn center from July 2015 - June 2019 with face burns. Sex, age, ethnicity, burn etiology, burn size, and discharge status were collected from electronic medical records of the patients who met study criteria. Descriptive statistics, student's t-tests, and chi-square tests were performed in Stata/SE 16.1. Significance was defined as a p-value <0.05.

In four years, 595/1705 patients (~35% of admissions) were admitted with face burns. The mean age was 44.9 ± 17.0 (mean ± SD) years, with the majority being men (475, 80%). The mean burn size was 19.8 ± 20.9% total body surface area (TBSA) with 10.1 ± 19.8% TBSA being third degree. The mean head burn size for any face burn was 2.8 ±e span we studied, but only a small fraction (5%) had face grafts. The patients who needed grafting for their head burns had significantly larger total body and face burns, and had a 2.4-fold higher mortality rate compared to patients who did not need grafting. Most face burns were caused by flame, especially the use of accelerants or flammable gases. Prevention efforts should focus on avoiding the use of accelerants and being careful with flammable gases.
Overall, head burns in adults were common within the four-year time span we studied, but only a small fraction (5%) had face grafts. The patients who needed grafting for their head burns had significantly larger total body and face burns, and had a 2.4-fold higher mortality rate compared to patients who did not need grafting. Most face burns were caused by flame, especially the use of accelerants or flammable gases. selleck Prevention efforts should focus on avoiding the use of accelerants and being careful with flammable gases.selleck