ObjectivesTo report our institutional experience, management, and outcomes of cutaneous periauricular squamous cell carcinoma (SCC).Study DesignRetrospective chart review.SettingTertiary academic center.SubjectsPatients undergoing treatment of cutaneous periauricular SCC from 2000 to 2016.ResultsA total of 112 patients had a median follow-up of 24.5 months, a mean ± SD age of 75.7 ± 10.6 years, and a strong male predominance (93.8%). Site distribution shows 87 (77.7%) auricular, 26 (23.2%) preauricular, and 10 (8.8%) postauricular lesions. Of auricular lesions, tumors involved the tragus (n = 3, 3.4%), helix/antihelix (n = 47, 54.0%), conchal bowl (n = 31, 35.6%), external auditory canal (n = 18, 16.1%), and lobule (n = 3, 3.4%). Most patients presented at stage I (52.7%) versus stages II (28.6%), III (6.3%), and IV (12.5%). Patients were largely treated surgically with primary tumor resection ranging from wide local excision to lateral temporal bone resection (± parotidectomy and neck dissection), with 17.0% and 5.4% receiving adjuvant radiation and chemoradiation, respectively. Metastatic spread was seen to the parotid (25.9%) and neck (26.8%), with most common cervical spread to level II. Overall survival, disease-specific survival, and disease-free survival at 3 years were 62%, 89%, and 56%, respectively. Nodal disease was associated with worse disease-specific survival (P < .001) and disease-free survival (P = .042). Pre- and postauricular sites were associated with worse overall survival (P = .007) relative to auricular sites.ConclusionAmong cutaneous SCC, periauricular subsites pose treatment challenges related to surrounding anatomy and represent a unique tumor population. The reported propensity toward recurrence and patterns of metastasis may better guide treatment of aggressive tumors to include regional nodal dissection.

BackgroundMaternal opioid exposure during pregnancy has various effects on neonatal health. Buprenorphine/naloxone and methadone are examples of medications for opioid use disorder (MOUD) used for the treatment of opioid use disorder (OUD). Research comparing the impacts of these MOUD modalities on neonatal outcomes when used to treat pregnant people with OUD remains limited. We evaluated the differences in outcomes between neonates with in-utero exposure to buprenorphine/naloxone versus methadone. MethodologyWe performed a retrospective cohort chart review between October 15, 2008, and October 15, 2019, evaluating mother/neonate dyads at two medical centers in Michigan. The charts of female patients, aged 18+, with OUD and buprenorphine/naloxone or methadone treatment, were examined. The charts of the corresponding neonates were also examined. Multiple regression analysis was performed. ResultsIn total, 343 mother/infant dyads were included: 99 patients were treated with buprenorphine/naloxone and 232 patients were treated with methadone. The buprenorphine/naloxone group had significant differences in maternal age, hepatitis status, asthma, gestational age in weeks, neonatal intensive care unit (NICU) length of stay (LOS), neonatal opioid withdrawal syndrome (NOWS) peak score, birth head circumference, and birth weight compared to the methadone group at baseline. Adjusted multivariable regression analysis demonstrated neonates with exposure to buprenorphine/naloxone had a NOWS peak score 3.079 points less (95% confidence interval (CI): -4.525, 1.633; p = 0.001) and NICU LOS 8.955 days less (95% CI: -14.399, -3.511; p = 0.001) than neonates exposed to methadone. ConclusionsNeonates with in-utero exposure to buprenorphine/naloxone had significantly lower NOWS scores and shorter NICU LOS compared to neonates with in-utero exposure to methadone. These findings demonstrate that buprenorphine/naloxone is potentially a more favorable treatment for the reduction in metrics representing adverse neonatal outcomes in pregnant people with OUD than methadone.

Previously, a teaching model was developed to encompass cardiovascular concepts, including but not limited to venous capacitance, filling pressure (preload), and control of arterial and venous tone (1). The model was designed to articulate integrated cardiovascular responses in multiple physiologic and pathophysiologic conditions. From personal experience, students often assume that since sympathetic stimulation increases during exercise, total peripheral resistance (TPR) must also increase. This reflects a misunderstanding of the magnitude of the role of autoregulatory vasodilation in increasing muscle blood flow during exercise (2). It also reflects a lack of appreciation in the interplay of metabolic demand and the baroreceptor reflex as key factors controlling cardiac output. We use the model to show the following: the initial response to exercise is muscular autoregulatory vasodilation, leading to a decrease in TPR; decreases in TPR may initially decrease mean arterial pressure (MAP) (3); reduction in MAP reduces baroreceptor action potentials, resulting in increased sympathetic activity, including non‐muscular vasoconstriction and venoconstriction; venoconstriction mobilizes the blood stored in the venous system (capacitance); blood mobilized by venoconstriction helps to maintain filling pressure (preload) and also satisfies the increased demand for blood by the exercising muscles; increases in sympathetic tone increase the inotropic, chronotropic, and lusitropic states of the heart, and; the consequent increase in cardiac output chiefly results from the interaction of systemic vasodilation in response to metabolic demand and the response of the baroreceptor reflex. This teaching model helps emphasize the importance of autoregulation to meet metabolic needs. It also illustrates the importance of sympathetic venoconstriction in maintaining filling pressure in diverse physiological and pathophysiologic conditions. Finally, it helps students understand that cardiac output is primarily regulated in response to tissue demand, as well as how this may occur. Understanding the normal response to exercise helps the student to recognize abnormal responses in pathophysiologic conditions, such as hypertension (4). References Jawad R., McCabe R. FASEB J 34(Supp1):1 (2020) Laughlin MH. Am J. Physiol 277 (Adv Physiol Educ 22): S244–S259 (1999) Guyton A. Circulation.64 1079‐1088 (1981) Kim D., Ha JW. Clin Hypertens 22, 17 (2016)

convulsant, antiulcer, analgesics, hepatoprotective, and anti-oxidants activities in vitro and in vivo. [11][12][13][14] As a powerful antioxidant, flaxseed has a role in protecting the liver and kidneys from strong oxidants, 15 and prevent oxidative stress-induced diseases such as renal failure, liver failure, hyperlipidemia, and diabetes. 16 Monosodium glutamate (MSG) was used in Japan as a flavour enhancer in many types of food, producing a flavour called umami meaning savory. 17,18 It is also used in disguised forms, such as in flavoured natural flavours, yeast extract, hydrogenated protein, and in soy protein. Each of these substances contains a percentage of free glutamate, a harmful component of monosodium glutamate. 19 Although it is widely used as a food flavour and catalyst for taste and appetite, studies have indicated that MSG is toxic to humans and laboratory animals especially at high doses. [20][21][22] Therefore, the present study is aimed at evaluating the hepatic effect of aqueous extract of flaxseed alone and in ameliorating MSG-induced hepatotoxicity in rats. Materials and Methods Plant seeds collection and extractionDry seeds of Linum usitatisimium were obtained from the Kerbala market, Iraq. The seeds were identified and authenticated by assists Prof. Nibal M. Tarrad at the Biology Department, University of Kerbala, Iraq. The seeds were cleaned and dried for 48 hours at room temperature. The dried seeds were milled to a fine powder using a mechanical grinder. A 100-gram portion of the powdered seeds sample was suspended in 500 mL of distilled water for 24 hours at room temperature and filtered. The filtrate was then poured into a stainless plate and the