Felicia Jefferson

Vertical Greenery Systems as a Strategy in Urban Heat Island Mitigation

Integrating vegetation into architecture has become widely recognized as a multi-beneficial practice in architecture and engineering design to combat an array of environmental issues. Urban areas have microclimates that are different than the climates of their surrounding rural areas. Patterns in these differences over the years have shown that urban microclimates tend to be significantly warmer in comparison. This phenomenon is now recognized as the urban “heat island” effect. While the associated consequences of this urban heating are far reaching, excess energy expenditure, air pollution emissions, and threats to human health are among the most critical for evaluation. The integration of vegetative green space in urban planning, coupled with highly reflective materials in place of conventional paved surfaces on roads and rooftops have proven to be effective methods of urban heat island mitigation. While as separate entities these methods are effective, innovative technology has brought forth greening roofs which allows vegetation to compensate where other roof-cooling strategies fall short. Substantially, vertical greenery systems compensate where greening roofs fall short. This paper explores both integrated vegetation as an optimal mitigation strategy for urban heat islands and vertical plant walls as an optimal design.

Endocrine-Disrupting Chemicals: Adverse Effects of Bisphenol A and Parabens to Women’s Health

Endocrine-disrupting chemicals (EDCs) have the ability to inhibit normal hormonal levels and may exert an array of inimical consequences in human health. These toxins have special adverse effects in women. This review summarizes recent literature reporting on endocrine-disrupting chemicals, specifically the effects induced by parabens from personal care products and cosmetics, and bisphenol A (BPA) found in food containers, with association to adverse effects on women’s health. Finally, the review provides recommendation on utilizing such EDCs to better meet the needs of consumers, while avoiding these chemical modifiers.

Period-amplitude analysis reveals wake-dependent changes in the electroencephalogram during sleep deprivation.

STUDY OBJECTIVES Electroencephalographic slow wave activity (SWA) during non-rapid eye movement (NREM) sleep results from the synchronous oscillation of cortical neurons and is the standard measurement of sleep homeostasis. SWA is not a direct measure of sleep pressure accumulation, but rather a measure of the NREM-sleep response to accumulated sleep pressure. Currently, no practical standard for the direct measurement of sleep pressure accumulation exists. Recently, it was demonstrated that rat cortical neurons undergo oscillations during wake that are similar to the cortical oscillations responsible for SWA. Furthermore, these oscillations increase in number as time awake increases. Here we hypothesize that period-amplitude analysis of the electroencephalogram (EEG), which treats the EEG as a series of discrete waves, can measure these cortical oscillations, and thus, is a measure of sleep-pressure accumulation during extended wake. DESIGN Mice were sleep deprived for 24 h by confinement to a slowly rotating wheel in order to assess wake-dependent changes in EEG wave incidence. MEASUREMENTS AND RESULTS Continuous period-amplitude analysis of the waking EEG across 24 h of sleep deprivation revealed that the incidence of 2 to 6 Hz waves increased exponentially over the deprivation period. This increase in wave incidence appeared to occur in two phases with exponential time constants of approximately 0.12 h and 3 h. Further analysis revealed that the changes in wave incidence were significantly correlated with two established markers of sleep pressure, SWA and NREM sleep latency. CONCLUSIONS The data suggest that wave incidence is an effective method of measuring sleep homeostasis in the waking EEG that provides better temporal resolution than spectral power analysis.

4-Aminobiphenyl Downregulation of NAT2 Acetylator Genotype–Dependent N- and O-acetylation of Aromatic and Heterocyclic Amine Carcinogens in Primary Mammary Epithelial Cell Cultures from Rapid and Slow Acetylator Rats

Aromatic and heterocyclic amine carcinogens present in the diet and in cigarette smoke induce breast tumors in rats. N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2) enzymes have important roles in their metabolic activation and deactivation. Human epidemiological studies suggest that genetic polymorphisms in NAT1 and/or NAT2 modify breast cancer risk in women exposed to these carcinogens. p-Aminobenzoic acid (selective for rat NAT2) and sulfamethazine (SMZ; selective for rat NAT1) N-acetyltransferase catalytic activities were both expressed in primary cultures of rat mammary epithelial cells. PABA, 2-aminofluorene, and 4-aminobiphenyl N-acetyltransferase and N-hydroxy-2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine and N-hydroxy-2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline O-acetyltransferase activities were two- to threefold higher in mammary epithelial cell cultures from rapid than slow acetylator rats. In contrast, SMZ (a rat NAT1-selective substrate) N-acetyltransferase activity did not differ between rapid and slow acetylators. Rat mammary cells cultured in the medium supplemented 24 h with 10muM ABP showed downregulation in the N-and O-acetylation of all substrates tested except for the NAT1-selective substrate SMZ. This downregulation was comparable in rapid and slow NAT2 acetylators. These studies clearly show NAT2 acetylator genotype-dependent N- and O-acetylation of aromatic and heterocyclic amine carcinogens in rat mammary epithelial cell cultures to be subject to downregulation by the arylamine carcinogen ABP.

A dopamine receptor d2-type agonist attenuates the ability of stress to alter sleep in mice.

Although sleep disruptions that accompany stress reduce quality of life and deteriorate health, the mechanisms through which stress alters sleep remain obscure. Psychological stress can alter sleep in a variety of ways, but it has been shown to be particularly influential on rapid eye movement (REM) sleep. Prolactin (PRL), a sexually dimorphic, stress-sensitive hormone whose basal levels are higher in females, has somnogenic effects on REM sleep. In the current study, we examined the relationship between PRL secretion and REM sleep after restraint stress to determine whether: 1) the ability of stress to increase REM sleep is PRL-dependent, and 2) fluctuating PRL levels underlie sex differences in sleep responses to stress. Because dopamine D2 receptors in the pituitary gland are the primary regulator of PRL secretion, D2 receptor agonist, 1-[(6-allylergolin-8β-yl)-carbonyl]-1-[3-(dimethylamino) propyl]-3-ethylurea (cabergoline), was used to attenuate PRL levels in mice before 1 hour of restraint stress. Mice were implanted with electroencephalographic/electromyographic recording electrodes and received an ip injection of either 0.3-mg/kg cabergoline or vehicle before a control procedure of 1 hour of sleep deprivation by gentle handling during the light phase. Six days after the control procedure, mice received cabergoline or vehicle 15 minutes before 1 hour of restraint stress. Cabergoline blocked the ability of restraint stress to increase REM sleep amount in males but did not alter REM sleep amount after stress in females even though it reduced basal REM sleep amount in female controls. These data provide evidence that the ability for restraint stress to increase REM sleep is dependent on PRL and that sex differences in REM sleep amount may be driven by PRL.

Identifying Cognitive Impairment in Hospitalized Older Adults to Prevent Readmission: Two Case Studies

ABSTRACT Objective: To describe two patient outcomes post-discharge from an acute hospital admission. Both patients underwent cognitive testing during hospitalization. Methods: A battery of cognitive tests was administered to two hospitalized older adult patients. Both patients were evaluated in their homes within 72 hours of discharge and again at 14- and 30-days by a nurse practitioner. Results: One of the patients was readmitted within 30 days of hospital discharge due to complications from an amputation. This patient did not perform well on cognitive measures which may have been related to his pain levels and/or his medication regimen. Conclusions: Not all readmissions are avoidable; however, if readmissions are related to cognitive impairment, implementing strategies tailored to this population may reduce readmission rates. Clinical Implications: Risk factors for readmission should be identified so the discharge team can develop a tailored plan of care. Including both the patient and an informal caregiver may reduce the chance of a hospital readmission in older adults with cognitive impairment regardless of the etiology.