The coronavirus disease of 2019 (COVID-19) disrupted health, economy, and food systems across the United States. This cross-sectional study examined the relationship between food access worries, food assistance use, and purchasing behaviors and food insecurity during COVID-19 among residents of New York State. New Yorkers were recruited to complete a web-based survey through Qualtrics. The survey took place in the summer and fall of 2020 and asked respondents about food access worries, food assistance use, food insecurity, and food purchasing behaviors. Chi-square analysis examined the relationships between food concerns, food assistance use, purchasing behaviors, and demographic characteristics by reported food insecurity, and significant results were analyzed in a series of logistic regression models. Results showed that higher food worries, Supplemental Nutrition Assistance Program (SNAP) use, reported food assistance and delivery as food sources, and self-reported Hispanic ethnicity were associated with a higher likelihood of experiencing food insecurity. Future research is needed to assess the ongoing impacts of the pandemic on food access and food insecurity, particularly among underserved groups. Measures that provide additional money for food and improved food access can alleviate barriers to accessing enough healthy food at this time.

Following Skelton's procedure with unilateral adrenonephrectomy, contralateral adrenal enucleation and application of 1% NaCl with the drinking fluid, genetically normotensive rats develop hypertension and a generalized arteriosclerosis, i.e. necrotizing hypertensive angiopathy. In the present study, the effect of high blood pressure was investigated in 13 Skelton hypertensive rats and 13 normotensive control rats. Systolic blood pressure was investigated by tail plethysmography over a period of 7 weeks. During the experiments, 3 of the Skelton rats died with final high blood pressure values, whereas all controls remained alive. Mean systolic blood pressure of the 10 surviving Skelton rats increased from 108 to 223 mm Hg. The control rats remained normotensive. Accordingly, heart weights of the hypertensives were higher than those of the controls (p = 0.0027). At the end of the experiment, arteriosclerosis was quantified by counting the heart arteries and arterioles with deposits of fibrinoid in the vascular wall in 10 histological cross-sections per heart. In the right ventricular wall of 6 of the 10 surviving Skelton rats, arteries and arterioles with deposits of fibrinoid in the vascular wall were detected. No such alteration was observed in the left ventricular wall or in the interventricular septum. About one third of the altered blood vessels showed fibrinoid necrosis. In contrast, the normotensive control rats had neither fibrinoid necrosis nor sclerotic arteries in corresponding sections of the hearts (p = 0.0052). The findings show that Skelton hypertension can be used as an experimental model for quantitative histological investigation of coronary arteriosclerosis in hypertensive rats. It has to be carified why coronary arteriosclerosis only develops in the right and not in the left ventricular wall or in the interventricular myocardium, and why coronary arteriosclerosis is not obligatory in all hypertensive rats.

Following Skelton's procedure with unilateral adrenonephrectomy, contralateral adrenal enucleation and application of 1% NaCl with drinking fluid, normal rats develop hypertension and generalized severe arteriosclerosis within 7 weeks, experimental group I. Thereby the mean systolic blood pressure increased from 108 +/- 10 to 223 +/- 12 mm Hg, and 90 arteriosclerotic blood vessels could be counted in 100 histological sections (10 from each animal) of the hearts. Following Skelton's procedure and admixture of flunarizine with the food (40 mg flunarizine per kg for 8 weeks, started 1 week before the operation; mean plasma flunarizine value: 336 +/- 136 ng/ml at the end of the experiment), experimental group II, all rats developed hypertension too, whereby the mean systolic blood pressure increased from 109 +/- 10 to 214 +/- 16 mm Hg, but in contrast to experimental group I, only one artery with sclerosis could be observed in 100 comparable histological sections of the hearts. The untreated control rats, experimental group III, remained normotensive, and no arteriosclerotic blood vessels could be observed. The findings presented show that the calcium-antagonist flunarizine with the dosage used does not reduce hypertension, but almost completely suppresses hypertension-induced arteriosclerosis of the myocardial blood vessels without lowering the high blood pressure.

Rats develop hypertension following Skelton’s treatment, i.e., (a) unilateral adrenalectomy and contralateral adrenal enucleation, (b) unilateral nephrectomy, and (c) administration of 1% NaCl with the drinking fluid (Skelton 1959). The pathogenesis of Skelton hypertension is still obscure. But in this hypertension model the adrenal operation (a) can be substituted by stress (Deane and McKibbin 1946) due to pantothenic acid deficiency (Schwabedal et al. 1985) and the nephrectomy (b) by means of a slight reduction in the kidney blood perfusion (Schwabedal 1987 a, 1988 a).

Schwabedal, Peter E.*; Brügging-Schmitz, G.*; Oestreich, W.†; Szathmary, S. C.† Author Information

In endemic pantothenic acid deficiency of some Japanese populations, increased occurrence of hypertension has been described. However, all attempts to produce hypertension experimentally by means of pantothenic acid deficiency have failed up to now. As a consequence, the observations made in Japan have largely been ignored. In this paper, pantothenic acid deficiency will be shown to be a factor in the experimental origin of hypertension due to adrenal regeneration.