Trends and Burden of Firearm-Related Injuries Among Children and Adolescents: A National Perspective.

INTRODUCTION: Firearm-related injuries in America have been under increasing scrutiny over the last several years. Few studies have examined the burden of these injuries in the pediatric population. The objective of this study was to describe the incidence of firearm-related injuries in hospitalized pediatric patients in the United States and identify the risk factors associated with readmission in this young population. METHODS: The Nationwide Readmission Database was examined from 2010 to 2017. Pediatric patients (aged ≤18 y) who survived their index hospitalization for any firearm injury were analyzed to determine incidence rate, case fatality rate, risk factors for 30-d readmission, and financial health care burden. RESULTS: There were 35,753 pediatric firearm injuries (86.8% male) with an overall incidence rate of 10.49 (95% confidence interval [CI]: 9.26-11.71) per 100,000 pediatric hospitalizations. Adolescents aged >12 y had the highest incidence rate (60.51, 95% CI: 55.19-65.84). In-hospital mortality occurred in 1948 cases (5.5%), with higher case fatality rates in males. There were 1616 (5.7%) unplanned 30-d readmissions. Multivariate analysis showed abdominal firearm injuries (hazard ratio: 1.13, 95% CI: 1.03-1.24; P = 0.006) and longer length of stay (hazard ratio: 1.27, 95% CI: 1.04-1.55; P = 0.016) were associated with a greater risk of 30-d readmission. The median health care cost for firearm-related injuries was $36,535 (interquartile range: $19,802-$66,443), 22% of which was due to readmissions. Cost associated with 30-d readmissions was $7978 (interquartile range: $4305-$15,202). CONCLUSIONS: Firearm-related injury is a major contributor to pediatric morbidity, mortality, and health care costs. Males are disproportionately affected by firearm injury, but females are more likely to require unplanned 30-d readmissions. Interventions should target female sex, injuries of suicidal intent, psychiatric comorbidities, prolonged index hospitalization, and abdominal injuries.

Association of Rs231775 Genetic Variant of Cytotoxic T-lymphocyte Associated Protein 4 with Alopecia Areata Disease in Males: A Case-Control Study.

BACKGROUND: Alopecia Areata (AA) is a common inflammatory immune-mediated non-scarring hair loss; however, the exact genetic susceptibility remains to be clarified. Cytotoxic T-lymphocyte Associated Protein 4 (CTLA4) has emerged as a central and critically important modulator of immune responses and is believed to play a crucial rule in AA pathogenesis. OBJECTIVES: To investigate the association of CTLA4 variant (rs231775) within codon 17 with AA risk and outcomes. METHODS: Genetic analyses of the rs231775 SNP of CTLA4 gene were performed in 186 males (93 AA patients and 93 controls). RESULTS: The rs231775 CTLA4 variant was significantly higher in AA patients in comparison with control subjects especially among heterozygous and dominant model. This association varied significantly with disease severity. CONCLUSIONS: Individuals with homozygosity of rs231775 CTLA4 variant represented AA disease risk and increased severity than their counterparts.Abbreviations: AA: Alopecia areata; CTLA4: Cytotoxic T-lymphocyte Associated Protein 4; SNP: Single nucleotide polymorphism; LADA: Latent autoimmune diabetes in adults; SLE: Systemic lupus erythematosus; SCU: Suez Canal University; SALT: Severity of Alopecia Tool; DNA: Deoxyribonucleic acid; RT-PCR: Real-time polymerase chain reaction, HWE: Hardy-Weinberg equation; RA: rheumatoid arthritis.

Cancer and COVID-19: analysis of patient outcomes.

Background: We sought to investigate the outcomes associated with COVID-19 disease in cancer patients. Methods: We conducted a retrospective cohort study of laboratory-confirmed COVID-19 patients. Results: Of the 206 patients included, 57 had at least one preexisting malignancy. Cancer patients were older than noncancer patients. Of the 185 discharged cases, cancer patients had a significantly higher frequency of unplanned reintubation (7.1% vs 0.9%, p < 0.049), and required longer hospital stay (8.58 ± 6.50 days versus 12.83 ± 11.44 days, p < 0.002). Regression analysis revealed that obesity and active smoking were associated with an increased risk of mortality. Conclusion: Outcomes in COVID-19 appear to be driven by obesity as well as active smoking, with no difference in mortality between cancer and noncancer patients.

In this study, we aimed to investigate how COVID-19 affected cancer patients and whether this altered their survival outcomes. To do this, we examined data from a database of patients who have passed through our institution ­ a retrospective cohort analysis. Of the 206 patients we included in the study from this database, 57 had at least one preexisting cancer. Cancer patients tended to be older than noncancer patients. Of the 185 discharged patients, cancer patients required longer hospital stays, but there was no difference in mortality. Disease complications and intensive care unit admission with obesity and active smoking put patients in our cohort at increased risk of death. To conclude, outcomes in COVID-19 patients appear to be driven by obesity as well as active smoking, with no difference in mortality between cancer and noncancer patients.

MicroRNA-target cross-talks: Key players in glioblastoma multiforme.

The role of microRNAs in brain cancer is still naive. Some act as oncogene and others as tumor suppressors. Discovery of efficient biomarkers is mandatory to debate that aggressive disease. Bioinformatically selected microRNAs and their targets were investigated to evaluate their putative signature as diagnostic and prognostic biomarkers in primary glioblastoma multiforme. Expression of a panel of seven microRNAs (hsa-miR-34a, hsa-miR-16, hsa-miR-17, hsa-miR-21, hsa-miR-221, hsa-miR-326, and hsa-miR-375) and seven target genes ( E2F3, PI3KCA, TOM34, WNT5A, PDCD4, DFFA, and EGFR) in 43 glioblastoma multiforme specimens were profiled compared to non-cancer tissues via quantitative reverse transcription-polymerase chain reaction. Immunohistochemistry staining for three proteins (VEGFA, BAX, and BCL2) was performed. Gene enrichment analysis identified the biological regulatory functions of the gene panel in glioma pathway. MGMT ( O-6-methylguanine-DNA methyltransferase) promoter methylation was analyzed for molecular subtyping of tumor specimens. Our data demonstrated a significant upregulation of five microRNAs (hsa-miR-16, hsa-miR-17, hsa-miR-21, hsa-miR-221, and hsa-miR-375), three genes ( E2F3, PI3KCA, and Wnt5a), two proteins (VEGFA and BCL2), and downregulation of hsa-miR-34a and three other genes ( DFFA, PDCD4, and EGFR) in brain cancer tissues. Receiver operating characteristic analysis revealed that miR-34a (area under the curve = 0.927) and miR-17 (area under the curve = 0.900) had the highest diagnostic performance, followed by miR-221 (area under the curve = 0.845), miR-21 (area under the curve = 0.836), WNT5A (area under the curve = 0.809), PDCD4 (area under the curve = 0.809), and PI3KCA (area under the curve = 0.800). MGMT promoter methylation status was associated with high miR-221 levels. Moreover, patients with VEGFA overexpression and downregulation of TOM34 and BAX had poor overall survival. Nevertheless, miR-17, miR-221, and miR-326 downregulation were significantly associated with high recurrence rate. Multivariate analysis by hierarchical clustering classified patients into four distinct groups based on gene panel signature. In conclusion, the explored microRNA-target dysregulation could pave the road toward developing potential therapeutic strategies for glioblastoma multiforme. Future translational and functional studies are highly recommended to better understand the complex bio-molecular signature of this difficult-to-treat tumor.

Preoperative diabetes complicates postsurgical recovery but does not amplify readmission risk following pancreatic surgery.

Background: Diabetes is a significant and prevalent medical condition associated with increased comorbidities, longer hospital length of stay, and higher healthcare costs. We aimed to assess the association between diabetes mellitus and postoperative outcomes following pancreatic surgeries. Methods: Records for patients with major elective pancreatic surgeries were retrieved retrospectively from the Nationwide Readmission Database (2010-2014). Association of diabetic status with postoperative complications, in-hospital mortality, length of stay (LOS), readmission rate, and hospital costs were investigated. Logistic regression and decision tree analyses were employed to predict adverse outcomes. Results: A total of 8,401 patients who had pancreatic surgery were included. They were categorized according to their diabetic diagnosis. Results showed that diabetic patients had a higher risk of postoperative complications compared to non-diabetics (OR: 1.27, 95% CI: 1.08-1.49, P=0.003). Bleeding and renal complications were the most significant. Uncontrolled diabetes significantly required a longer hospital stay (9.17±4.28 vs. 8.03±4.96 days, P=0.001), and incurred higher hospital costs ($34,171.04±$20,846.61 vs. $28,182.21±$24,070.27, P=0.001). After multivariate regression, no association was found with in-hospital mortality or readmission rates; however, diabetic patients' length of stay during readmission was increased at 30- and 90-day readmissions (P=0.004 and 0.007, respectively). Conclusions: Among patients who underwent pancreatic surgery, those with diabetes had a higher rate of postoperative complications compared to non-diabetics. Additionally, diabetic patients had higher hospital charges and costs during primary admission. Initial analysis of patients with diabetes showed they had higher rates of 30- and 90-day readmissions, though this did not maintain significance after regression analysis. Exploring the mechanisms underlying this finding would aid in preventing postoperative complications and reducing healthcare costs.

New Insights into the Link between Melanoma and Thyroid Cancer: Role of Nucleocytoplasmic Trafficking.

Cancer remains a major public health concern, mainly because of the incompletely understood dynamics of molecular mechanisms for progression and resistance to treatments. The link between melanoma and thyroid cancer (TC) has been noted in numerous patients. Nucleocytoplasmic transport of oncogenes and tumor suppressor proteins is a common mechanism in melanoma and TC that promotes tumorigenesis and tumor aggressiveness. However, this mechanism remains poorly understood. Papillary TC (PTC) patients have a 1.8-fold higher risk for developing cutaneous malignant melanoma than healthy patients. Our group and others showed that patients with melanoma have a 2.15 to 2.3-fold increased risk of being diagnosed with PTC. The BRAF V600E mutation has been reported as a biological marker for aggressiveness and a potential genetic link between malignant melanoma and TC. The main mechanistic factor in the connection between these two cancer types is the alteration of the RAS-RAF-MEK-ERK signaling pathway activation and translocation. The mechanisms of nucleocytoplasmic trafficking associated with RAS, RAF, and Wnt signaling pathways in melanoma and TC are reviewed. In addition, we discuss the roles of tumor suppressor proteins such as p53, p27, forkhead O transcription factors (FOXO), and NF-KB within the nuclear and cytoplasmic cellular compartments and their association with tumor aggressiveness. A meticulous English-language literature analysis was performed using the PubMed Central database. Search parameters included articles published up to 2021 with keyword search terms melanoma and thyroid cancer, BRAF mutation, and nucleocytoplasmic transport in cancer.

Interleukin 17 receptor A haplotype analysis in chronic spontaneous urticaria: A preliminary study.

BACKGROUND: Chronic spontaneous urticaria (CSU) is a distressing skin disease. Family clustering and heterogeneity in the onset and progression indicate that susceptibility to CSU is a complex trait. In this study, we performed haplotype analysis for one of the key player gene, IL17RA, for CSU to test the association with disease susceptibility and severity. METHODOLOGY: The study included 70 CSU patients and 30 healthy controls. The severity of the disease was evaluated by autologous serum skin test (ASST) and urticaria activity score (UAS). ASST test was done and quality of life was assessed using a questionnaire. Allelic discrimination analysis for rs4819554 and rs879577 was performed using real-time polymerase chain reaction technology. RESULTS: Carriers of rs4819554*G were more prone to develop CSU than its counterpart (P = .039), while rs4819554*A allele displayed more severe phenotype in the form of more prolonged disease duration (P = .040), concurrent angioedema (P < .001), higher level of treatment (P < .001), and higher score of quality of life (P < .001). Additionally, homozygote patients with rs879577*CC were associated with angioedema (P < .001). Haplotype analysis revealed that cohorts with both rs4819554*A and rs879577*T conferred protection against developing CSU (OR = 0.07, 95% CI = 0.01-0.32, P = .001). CONCLUSION: Our results showed that IL17RA gene polymorphisms might contribute to the increased susceptibility to CSU.

Obesity and the prevention of thyroid cancer: Impact of body mass index and weight change on developing thyroid cancer - Pooled results of 24 million cohorts.

BACKGROUND: Body weight may be a modifiable risk factor predisposing to different cancers. To establish a potential impact of weight change on thyroid cancer risk, we conducted a meta-analysis to evaluate the effect of body mass index (BMI) and weight change over time as a risk of developing thyroid cancer (TC). METHODS: A systematic search was performed up to February 25, 2020. Pooled relative risk (RR) were estimated using fixed and random models. Heterogeneity between articles was examined using Q-test and I2 index. Evaluation of publication bias was conducted with Egger's regression test. RESULTS: A total of 31 studies including 24,489,477 cohorts were eligible. Pooled analysis revealed that normal and underweight cohorts were associated with a decreased risk of TC (RR = 0.68, 95%CI = 0.65-0.71, p < 0.001) and (RR = 0.92, 95%CI = 0.91-0.93, p < 0.001), respectively. In contrast, overweight and obese cohorts were more likely to develop TC (RR = 1.26, 95%CI = 1.24-1.28, p < 0.001 and RR = 1.50, 95%CI = 1.45-1.55, p < 0.001, respectively). Obesity was associated with higher risk of developing TC among women (RR = 1.29, 95%CI = 1.14-1.46, p < 0.001), but not men (RR = 1.25, 95%CI = 0.97-1.62, p = 0.08). Furthermore, weight gain increased the risk of developing TC (RR = 1.18, 95%CI = 1.14-1.22, p < 0.001), while weight loss decreased the risk (RR = 0.89, 95%CI = 0.85-0.93, p < 0.001). Results showed similar trends of weight change effect in both males and females. CONCLUSIONS: Obesity is associated with higher risk of developing TC in women. However, maintaining a healthy weight is associated with reduced risk of TC in both women and men. Shifting our practice to include weight control strategies will help lead to cancer prevention.