To evaluate the impact of age and COVID-19 variant time period on morbidity and mortality among those hospitalized with COVID-19.Patients from the American Heart Association's Get With The Guidelines COVID-19 cardiovascular disease registry (January 20, 2020-February 14, 2022) were divided into groups based on whether they presented during periods of wild type/alpha, delta, or omicron predominance. They were further subdivided by age (young: 18-40 years; older: more than 40 years), and characteristics and outcomes were compared.The cohort consisted of 45,421 hospitalized COVID-19 patients (wild type/alpha period: 41,426, delta period: 3349, and omicron period: 646). Among young patients (18-40 years), presentation during delta was associated with increased odds of severe COVID-19 (OR, 1.6; 95% CI, 1.3-2.1), major adverse cardiovascular events (MACE) (OR, 1.8; 95% CI, 1.3-2.5), and in-hospital mortality (OR, 2.2; 95% CI, 1.5-3.3) when compared with presentation during wild type/alpha. Among older patients (more than 40 years), presentation during delta was associated with increased odds of severe COVID-19 (OR, 1.2; 95% CI, 1.1-1.3), MACE (OR, 1.5; 95% CI, 1.4-1.7), and in-hospital mortality (OR, 1.4; 95% CI, 1.3-1.6) when compared with wild type/alpha. Among older patients (more than 40 years), presentation during omicron associated with decreased odds of severe COVID-19 (OR, 0.7; 95% CI, 0.5-0.9) and in-hospital mortality (OR, 0.6; 95% CI, 0.5-0.9) when compared with wild type/alpha.Among hospitalized adults with COVID-19, presentation during a time of delta predominance was associated with increased odds of severe COVID-19, MACE, and in-hospital mortality compared with presentation during wild type/alpha. Among older patients (aged more than 40 years), presentation during omicron was associated with decreased odds of severe COVID-19 and in-hospital mortality compared with wild type/alpha.
Supplementary Figure from Hypophosphatemia Due to Increased Effector Cell Metabolic Activity Is Associated with Neurotoxicity Symptoms in CD19-Targeted CAR T-cell Therapy
The Puerto Rico population may be modeled as an admixed population with contributions from three continents: Sub-Saharan Africa, Ancient America, and Europe. Extending the study of the genetics of inflammatory bowel disease (IBD) to an admixed population such as Puerto Rico has the potential to shed light on IBD genes identified in studies of European populations, find new genes contributing to IBD susceptibility, and provide basic information on IBD for the care of US patients of Puerto Rican and Latino descent. In order to study the association between immune-related genes and Crohn’s disease (CD) and ulcerative colitis (UC) in Puerto Rico, we genotyped 1159 Puerto Rican cases, controls, and family members with the ImmunoChip. We also genotyped 832 subjects from the Human Genome Diversity Panel to provide data for estimation of global and local continental ancestry. Association of SNPs was tested by logistic regression corrected for global continental descent and family structure. We observed the association between Crohn’s disease and NOD2 (rs17313265, 0.28 in CD, 0.19 in controls, OR 1.5, p = 9×10−6) and IL23R (rs11209026, 0.026 in CD, 0.0.071 in controls, OR 0.4, p = 3.8×10−4). The haplotype structure of both regions resembled that reported for European populations and “local” continental ancestry of the IL23R gene was almost entirely of European descent. We also observed suggestive evidence for the association of the BAZ1A promoter SNP with CD (rs1200332, 0.45 in CD, 0.35 in controls, OR 1.5, p = 2×10−6). Our estimate of continental ancestry surrounding this SNP suggested an origin in Ancient America for this putative susceptibility region. Our observations underscored the great difference between global continental ancestry and local continental ancestry at the level of the individual gene, particularly for immune-related loci.
To evaluate single-pass loop electrosurgical excision procedure (LEEP-SP) versus LEEP with top hat (LEEP-TH) in terms of treatment failure defined as high-grade squamous intraepithelial lesion (HSIL) cytology within 2 years' follow-up.This single-institution cohort study used a prospectively collected cervical dysplasia database including all patients who underwent LEEP-SP or LEEP-TH for biopsy-proven cervical intraepithelial neoplasia between 2005 and 2019.Of 340 patients included, 178 underwent LEEP-SP and 162 LEEP-TH. The LEEP-TH patients were more likely to be older (mean age, 40.4 vs 36.5 years; p < .001) and have a positive preprocedure endocervical sampling (68.5% vs 11.8%; p < .001). Positive margins were found in 23 LEEP-SP (12.9%) and in 25 LEEP-TH (15.4%; p = .507). There was no significant difference in depth of excision between LEEP-SP (13.21 ± 23.19 mm) and LEEP-TH (17.37 ± 28.26 mm; p = .138). At 2 years, there was no difference in the rates of HSIL cytology (5.2% vs 6.3%; p = .698), any positive human papillomavirus test, or HSIL cytology (25% vs 15%; p = .284). The 57 patients undergoing repeat excision were more likely to be older (mean age, 40.95 vs 37.52 years; p = .023), have had a LEEP-TH (26.3% vs 73.7%; p < .001), and have initial cytologic HSIL (64.9% vs 35.0%; p < .001).In this single-institution study, there is no difference in the rate of recurrent HSIL in patients undergoing LEEP-SP versus LEEP-TH. A LEEP-TH may have limited additional benefit over a LEEP-SP in the treatment of cervical HSIL.
Objective Childhood‐onset depression is associated with increased risk of recurrent depression and high morbidity extending into adolescence and adulthood. This multisite randomized controlled trial evaluated two active psychosocial treatments for childhood depression: family‐focused treatment for childhood depression (FFT‐CD) and individual supportive psychotherapy (IP). Aims were to describe effects through 52 weeks postrandomization on measures of depression, functioning, nondepressive symptoms, and harm events. Methods Children meeting criteria for depressive disorders ( N = 134) were randomly assigned to 15 sessions of FFT‐CD or IP and evaluated at mid‐treatment for depressive symptoms and fully at roughly 16 weeks (after acute treatment), 32 weeks, and 52 weeks/one year. See clinicaltrials.gov: NCT01159041. Results Analyses using generalized linear mixed models confirmed the previously reported FFT‐CD advantage on rates of acute depression response (≥50% Children's Depression Rating Scale reduction). Improvements in depression and other outcomes were most rapid during the acute treatment period, and leveled off between weeks 16 and 52, with a corresponding attenuation of observed group differences, although both groups showed improved depression and functioning over 52 weeks. Survival analyses indicated that most children recovered from their index depressive episodes by week 52: estimated 76% FFT‐CD, 77% IP. However, by the week 52 assessment, one FFT‐CD child and six IP children had suffered recurrent depressive episodes. Four children attempted suicide, all in the IP group. Other indicators of possible harm were relatively evenly distributed across groups. Conclusions Results indicate a quicker depression response in FFT‐CD and hint at greater protection from recurrence and suicide attempts. However, outcomes were similar for both active treatments by week 52/one year. Although community care received after acute treatment may have influenced results, findings suggest the value of a more extended/chronic disease model that includes monitoring and guidance regarding optimal interventions when signs of depression‐risk emerge.
<p>Contribution of all assayed secreted cytokines to CD8 cytokine functional strength indices (FSI). Groups are divided by clinical response and tonic vs stimulated culture conditions. Error bars represent +/- standard error of the mean (SEM).</p>
<p>Contribution of all assayed secreted cytokines to CD4 cytokine polyfunctionality strength indices (PSI). Groups are divided by clinical response and tonic vs stimulated culture conditions. Error bars represent +/- standard error of the mean (SEM).</p>
<p>Correlation matrix between intracellular cytokine FSIs and phosphoprotein FSIs with the CD8 compartment. Values for the tonic conditions (A) and stimulated conditions (B) are shown. Heatmap and numerical values for the corresponding Pearson’s r for each correlation condition are shown.</p>