Background: Patients experience moderate to high level of anxiety before surgery. Many strategies such as sedative-hypnotic agents are developed to improve anxiety.
There is association between lung contusion (lC) and a progressive inflammatory response. The protective effect of vitamin C and vitamin E, as strong free radical scavengers on favourite outcome of (LC) in animal models, has been confirmed.Designto evaluate the effect of vitamins, E and C on arterial blood gas (ABG) and ICU stay, in (LC), with injury severity score (ISS) 18 ± 2, due to blunt chest trauma.MethodsThis study was a randomized, double-blind, placebo-controlled clinical trial. Patients with (ISS) 18 ± 2 blunt chest trauma, who meet criteria, participated in the study. A total of 80 patients from Feb 2015 to Jun2018and were randomly divided into 4 groups. Patients received intravenous vitamin E (1000IU mg), was (group I); intravenous vitamin C (500) (group II). Vitamin C + vitamin E = (group III), and intravenous distilled water = (control group) or (group IV). ABG, serum cortisol, and CRP levels were determined at baseline, 24 h and 48 h after the intervention.Resultsa significant decrease in ICU stay in group III compared to other groups (p < 0.001). Co-administration of vitamin C and vitamin E showed significant increases pH (values to reference range from acidemia”), oxygen pressure, and oxygen saturation in group III compared to other groups (p < 0.001). A significant decrease in carbon dioxide pressure was also detected after receiving vitamin C and vitamin E in group III, compared to other groups (p < 0.001). There was no significant difference cortisol and CRP levels between groups after the intervention.ConclusionCo-administration of vitamin C and vitamin E, improve the ABG parameters and reduce ICU stay.
Introduction
Trauma is one of the most common causes of morbidity and mortality worldwide. Since the definition of preventable death has been described many studies like current one were conducted to evaluate this issue.
Methods
This cohort retrospective study investigated archived medical files of trauma victims from 2017 to 2020 in a referral single-center trauma hospital. Registered demographic data, vital signs, Glasgow coma scale (GCS), timing of trauma and death, executed interventions, type and mechanism of trauma in addition to time errors, clinical mismanagements, and missed injuries were extracted. Injury severity score, revised trauma score, and probability of survival based on TRISS method for each case were calculated. Eventually preventable and non-preventable death were defined and compared.
Results
Finally from the all 413 trauma deaths 246(54.9 %) files were enrolled. Dead persons were from 18 to 95 years. Of all 189(76.8 %) were males. Analysis manifested 135(54.9 %) of all deaths were potentially preventable and the rest 49.1 % was non-preventable for expiration(p = 0.001). Data showed that from all variables systolic blood pressure ≥80 mmHg, respiratory rate >19 per minute, GCS>8, higher RTS, road traffic accidents and control of external bleeding were contributed to prediction of preventable trauma related mortality.
Conclusion
This study implied on that frequency of trauma related preventable death was regionally high and associating factors that could influence the number of these mortalities included systolic blood pressure, respiratory rate, GCS, revised trauma score, mechanism of trauma, and external bleeding of trauma patients.
Polymorphisms of genes can cause a decrease in DNA repair capacity and disease susceptibility, as well (1, 2). The XRCC genes play a momentous role in comprehension processes of DNA repair in mammals, especially in doublestrand break (DSB) repair (3). Therefore, normal activity of XRCC genes is a major factor for cancer prevention. On the other hand, approximately, 84400 new patients of renal cell carcinoma (RCC) are recognized by the Union of Europe. In addition, 34700 kidney cancer-related deaths happened in 2012 (4). The present study aimed to review the correlation between some XRCC1 and XRCC6 genes polymorphism and RCC. In a case control study assessing the relationship between XRCC6 C-1310G (rs2267437) polymorphism and RCC susceptibility, the results indicated that the polymorphism of XRCC6 C-1310G is involved in the etiology of RCC and it can be as a marker in the susceptibility to RCC (5). Furthermore, in a hospital-based case-control study, the association between XRCC6 T-991C (rs5751129) polymorphisms and RCC risk in a Taiwanese population was evaluated. Results of this investigation showed that the XRCC6 T-991C polymorphism is associated with RCC. This polymorphism can lead to the different mRNA expression levels, which can affect expression of the XRCC6 protein and capacity of DSB repair (6). Moreover, Wang et al. in their paper stated that the XRCC6 A-31G polymorphism (rs132770) is associated with the RCC risk and they also suggested that the XRCC6 A-31G polymorphism is an important subject in the RCC etiology (7). On the other hand, regarding the correlation between XRCC1 gene polymorphism and RCC, Hirata et al. (8) declared that XRCC1 399Gln polymorphism can be a risk factor for RCC and their results suggested that the XRCC1 399Gln allele may be linked to RCC susceptibility. In another study, Akhmadishina et al. (9) detected an association between allele A of the c.839G > A locus of the XRCC1 gene and the RCC occurrence and also they declared that polymorphism of c.839G > A in the XRCC1 gene can be contributed in RCC progress at the advanced and early stages of this disease. According to the results, we can understand that polymorphisms of XRCC1 and XRCC6 may greatly be associated with RCC, so that, XRCC6 may be a marker in genetic susceptibility to RCC and a significant subject in its etiology. In addition, XRCC1 can be linked to RCC progress at the advanced and early stages of it or susceptibility to RCC. Finally, it is advised to conduct more studies in order to obtain the comprehensive results regarding RCC and the genes.
References
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