The Health Status of Hispanic Agricultural Workers in Georgia and Florida

To examine the health status of Hispanic agricultural workers in Florida and Georgia. Health data from agricultural workers in the Farm Worker Family Health Program (June 2019) and research studies in Florida (May 2015 and May 2019) were examined. Data from 728 agricultural workers were collected through sociodemographic questionnaire and clinical data. In the Florida sample, 83% were overweight or obese, 70% elevated blood pressure, 60% met the definition of prediabetes. In Georgia, 64% were overweight or obese and 67% had elevated blood pressure. Weak correlations were observed between BMI and systolic blood pressure (unadjusted r?=?0.20), diastolic blood pressure (unadjusted r?=?0.19), and glucose (unadjusted r?=?0.14). Adjusting for age and gender did not show statistically significant correlation between BMI and systolic and diastolic blood pressure or glucose. While BMI has been shown to be strongly associated with high blood pressure and impaired glucose, we found a weak correlation among agricultural workers. Given the common and high use of pesticides and elevated rates of hypertension, impaired glucose, and adiposity in agricultural workers, the public health impact of this relationship may require and lead to occupational reform that protects the health of agricultural workers. Future studies should assess occupational and environmental factors and lifestyle differences between agricultural workers and the general population to better understand these discrepancies in health status.

     

The Achilles’ heel of cancer survivors: fundamentals of accelerated cellular senescence

Recent improvements in cancer treatment have increased the lifespan of pediatric and adult cancer survivors. However, cancer treatments accelerate aging in survivors, which manifests clinically as the premature onset of chronic diseases, such as endocrinopathies, osteoporosis, cardiac dysfunction, subsequent cancers, and geriatric syndromes of frailty, among others. Therefore, cancer treatment–induced early aging accounts for significant morbidity, mortality, and health expenditures among cancer survivors. One major mechanism driving this accelerated aging is cellular senescence; cancer treatments induce cellular senescence in tumor cells and in normal, nontumor tissue, thereby helping mediate the onset of several chronic diseases. Studies on clinical monitoring and therapeutic targeting of cellular senescence have made considerable progress in recent years. Large-scale clinical trials are currently evaluating senotherapeutic drugs, which inhibit or eliminate senescent cells to ameliorate cancer treatment–related aging. In this article, we survey the recent literature on phenotypes and mechanisms of aging in cancer survivors and provide an up-to-date review of the major preclinical and translational evidence on cellular senescence as a mechanism of accelerated aging in cancer survivors, as well as insight into the potential of senotherapeutic drugs. However, only with time will the clinical effect of senotherapies on cancer survivors be visible.

Cancer survival times have increased annually owing to advances in early detection and treatment that prolong patient survival. However, increasing survivorship has underscored the observation that cancer survivors develop age-related diseases prematurely, which cause significant morbidity, health expenditures, and mortality. Many cancer survivors have been exposed to chemotherapy, radiotherapy, or both; despite eradicating cancer cells, these therapies also damage normal cells to accelerate biologic aging, such that a discrepancy exists between their biologic and chronologic age (1). Considerable data exist regarding the phenotypes of accelerated aging. However, mechanical and molecular uncertainties have limited the study of these manifestations in a clinical context. Our Review discusses accelerated aging phenotypes in cancer survivors and the cellular mechanisms underpinning these phenomena. We then discuss the translational evidence on how accelerated aging phenotypes, mainly related to senescence, are being targeted while highlighting areas of uncertainty for future research to address.     

COVID-19 and Agricultural Workers: A Descriptive Study

Journal of Immigrant and Minority Health - Agricultural workers, designated as “essential” at the start of the COVID-19 pandemic, work in harsh labor conditions, and now have the added...     

STRENGTH & FUNCTIONAL ASSESSMENT OF HEALTHY HIGH SCHOOL FOOTBALL PLAYERS: ANALYSIS OF SKILLED AND NON‐SKILLED POSITIONS

Background/Purpose

Identifying an athlete''s functional capacity is an important consideration in determining when to allow an athlete to return to competition following injury. Establishing normative data for lower extremity functional assessment is valuable for comparison when making decisions regarding the high school athlete returning to play after injury. Therefore, the purpose of this study was to compare functional performance and strength between American high school football players of both skilled and non‐skilled positions.

Methods

Forty‐nine high school football players (30 skilled; 19 non‐skilled) completed a single‐session of testing consisting of a Figure of 8 test (F‐8), single‐leg vertical jump (SLVJ), single‐leg broad jump (SLBJ), and isokinetic knee strength assessment. Pearson correlation coefficients were used to determine the relationships between the results of functional testing and isokinetic strength measures. Paired t‐tests were used to determine the differences in functional performance and isokinetic muscle strength between skilled and non‐skilled athletes.

Results

Knee extension peak torque/body weight (BW) was moderately correlated (p < .01) with SLBJ (r = .54‐.61), SLVJ (r = .39‐.48), and F‐8 run times (r = ‐.50) for all athletes. Similar relationships were observed between knee flexion peak torque/BW and SLBJ (r = .48‐.49), SLVJ (r = .28‐.46), and the F‐8 run times (r = .41‐.52) for all subjects. No differences were observed between groups when examining raw peak torque values for knee flexion and extension (p > .05), however, skilled players did demonstrate greater peak torque/BW ratios (p < .05) for both knee extension and knee flexion at 60 and 240 degrees/sec. Skilled players also displayed faster F‐8 times (9.4 sec ± .3; p < .01) and greater SLBJ (p < .05) on both the dominant (81.0 in ± 9.3) and non‐dominant (83.0 in ± 7.6) limbs (p < .01) when compared to non‐skilled players.

Conclusions

Overall, skilled football players displayed greater peak torque/BW ratios and functional performance when compared to non‐skilled players. Furthermore, isokinetic peak torque/BW appears to be related to functional performance. This relationship is affected by position, with skilled players showing a stronger association. Limb dominance did not influence these functional and strength metrics. It is recommended that clinicians and coaches consider the positional differences in strength and functional performance when managing patients and athletes.

Level of Evidence

4 – Cross‐sectional Case Series     

A modified technique for craniospinal irradiation in children designed to reduce acute and late radiation toxicity

Craniospinal irradiation is an important technique for the treatment of a number of paediatric malignancies. The conventional technique uses photons for all fields and does not exploit the benefits of CT and computer planning systems. The present paper describes a modification of the conventional technique in which both photons and electrons are used for the spinal field (mixed‐beam technique). Computed tomography images and a planning computer are used for the selection of field junctions, electron beam energy and dosimetry. The intention of the technique is to reduce radiotherapy toxicity. A discussion of the potential benefits is presented.     

Partial characterization of Maize rayado fino virus isolates from Ecuador: phylogenetic analysis supports a Central American origin of the virus

Maize rayado fino virus (MRFV) infects maize and appears to be restricted to, yet widespread in, the Americas. MRFV was previously unreported from Ecuador. Maize plants exhibiting symptoms of MRFV infection were collected at the Santa Catalina experiment station in Quito, Ecuador. RT-PCR reactions were performed on total RNA extracted from the symptomatic leaves using primers specific for the capsid protein (CP) gene and 3' non-translated region of MRFV and first strand cDNA as a template. Nucleotide sequence comparisons to previously sequenced MRFV isolates from other geographic regions revealed 88-91% sequence identity. Phylogenetic trees constructed using Maximum Likelihood, UPGMA, Minimal Evolution, Neighbor Joining, and Maximum Parsimony methods separated the MRFV isolates into four groups. These groups may represent geographic isolation generated by the mountainous chains of the American continent. Analysis of the sequences and the genetic distances among the different isolates suggests that MRFV may have originated in Mexico and/or Guatemala and from there it dispersed to the rest of the Americas.     

H3K4 demethylation by Jarid1a and Jarid1b contributes to retinoblastoma-mediated gene silencing during cellular senescence

Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. Here we combine quantitative mass spectrometry, ChIP deep-sequencing, and functional studies to determine the role of histone modifications on chromatin structure and gene-expression alterations associated with senescence in primary human cells. We uncover distinct senescence-associated changes in histone-modification patterns consistent with a repressive chromatin environment and link the establishment of one of these patterns--loss of H3K4 methylation--to the retinoblastoma tumor suppressor and the H3K4 demethylases Jarid1a and Jarid1b. Our results show that Jarid1a/b-mediated H3K4 demethylation contributes to silencing of retinoblastoma target genes in senescent cells, suggesting a mechanism by which retinoblastoma triggers gene silencing. Therefore, we link the Jarid1a and Jarid1b demethylases to a tumor-suppressor network controlling cellular senescence.