671 research outputs found

    Author Reading: Amy Haddad, PhD

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    Dr. Haddad read from her poetry collection, An Otherwise Healthy Woman. Dr. Haddad is a poet, nurse, and educator at Creighton University where she now holds the rank of Professor Emerita. Her poetry and short stories have been published in the American Journal of Nursing, Janus Head, Journal of Medical Humanities, Touch, Bellevue Literary Review, Pulse, Persimmon Tree, Annals of Internal Medicine, Aji Magazine, DASH, Oberon Poetry Magazine, and the anthologies Between the Heart Beats and Intensive Care: More Poetry and Prose by Nurses from University of Iowa Press, and Stories of Illness and Healing: Women Write Their Bodies from Kent State University Press. Her poetry chapbook, The Geography of Kitchens, was published by Finishing Line Press in 2021. The University of Nebraska Press is publishing her first poetry collection, An Otherwise Healthy Woman, in 2022. She is also an alumna of the University of Nebraska Medical Center’s College of Nursing.https://digitalcommons.unmc.edu/mcgoogan_lectures/1003/thumbnail.jp

    On the closed form of the covariance matrix and its inverse of the causal arma process

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    Derivation of the theoretical autocovariance function of a causal autoregressive moving-average process of order (p, q), ARMA(p, q), when q ≥ 1 is considered. A recursive relationship is established between the covariance matrices of an ARMA(p, q) process and its associated ARMA(p, q-1) process. The obtained recursion is shown to produce the inverse of the covariance matrix and its determinant. Moreover, the introduced method can be easily implemented in any programming environment.ANDERSON TW, 1977, J MULTIVARIATE ANAL, V7, P584, DOI 10.1016-0047-259X(77)90069-0; Box GEP, 1976, TIME SERIES ANAL; Brockwell P. J., 1987, TIME SERIES THEORY M; Choi BS, 1992, ARMA MODEL IDENTIFIC; Durbin J., 1960, REV INT STATIST I, V28, P233, DOI DOI 10.2307-1401322; HADDAD JN, 1995, J TIME SER ANAL, V16, P551, DOI 10.1111-j.1467-9892.1995.tb00254.x; Haddad JN, 1998, COMMUN STAT-SIMUL C, V27, P617, DOI 10.1080-03610919808813499; VANDERLEEUW J, 1994, J ECONOMETRICS, V63, P397, DOI 10.1016-0304-4076(94)90032-9910

    Redox and oxidant-mediated regulation of apoptosis signaling pathways: immuno-pharmaco-redox conception of oxidative siege versus cell death commitment

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    The mechanisms controlling apoptosis remain largely obscure. Because apoptosis is an integral part of the developmental program and is frequently the end-result of a temporal course of cellular events, it is referred to as programmed cell death. While there is considerable variation in the signals and requisite cellular metabolic events necessary to induce apoptosis in diverse cell types, the morphological features associated with apoptosis are highly conserved. Free radicals, particularly reactive oxygen species (ROS), have been proposed as common mediators for apoptosis. Many agents that induce apoptosis are either oxidants or stimulators of cellular oxidative metabolism. Conversely, many inhibitors of apoptosis have antioxidant activities or enhance cellular antioxidant defenses. Mammalian cells, therefore, exist in a state of oxidative siege in which survival requires an optimum balance of oxidants and antioxidants. The respiratory tract is subjected to a variety of environmental stresses, including oxidizing agents, particulates and airborne microorganisms that, together, may injure structural and functional lung components and thereby jeopardize the primary lung function of gas exchange. To cope with this challenge, the lung has developed elaborate defense mechanisms that include inflammatory-immune pathways as well as efficient antioxidant defense systems. In the absence of adequate antioxidant defenses, the damage produced is detected by the cell leading to the activation of genes responsible for the regulation of apoptosis, conceivably through stress-responsive transcription factors. Oxidative stress, in addition, may cause a shift in cellular redox state, which thereby modifies the nature of the stimulatory signal and which results in cell death as opposed to proliferation. 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    Hydatid Disease of the Central Nervous System

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    Although hydatid disease is rare, it may come to the attention of neurosurgeons in nonendemic areas either by Internet consultations or by patients traveling to advanced centers for further management. Thus all neurosurgeons should be well informed about this condition. We reviewed our experience and consulted literature to come up with a consensus concerning the pathogenesis, the pathology, diagnosis, and management of hydatid disease of the central nervous system. We provide a comparison of this disease in the brain and the spine. In the brain, it is a disease of childhood and in the spine, of adulthood. The diagnosis in both locations is best made by being aware of the possibility of their occurrence and by imagery. The route of spread to the brain is different from that in the spine. The management of hydatid of the brain may be curative if the principles of management are well applied and adhered to. In the spine, the condition is a very protracted one and may require several surgeries.ABADA M, 1977, NEUROCHIRURGIE, V23, P195; ABOU-DAOUD K T, 1965, J Med Liban, V18, P159; ACQUAVIV.R, 1964, NEURO-CHIR, V10, P649; ALVAREZ F, 1982, SURG NEUROL, V17, P163, DOI 10.1016-0090-3019(82)90267-1; APT WL, 1976, J NEUROSURG, V44, P72, DOI 10.3171-jns.1976.44.1.0072; ARAJ GF, 1977, Z PARASITENKD, V52, P31, DOI 10.1007-BF00380556; ARASIL E, 1978, SURG NEUROL, V9, P9; BAASSIRI A, 1984, AM J NEURORADIOL, V5, P474; BETTAIEB A, 1978, NEUROCHIRURGIE, V24, P205; Boudawara MZ, 1999, NEUROCHIRURGIE, V45, P321; Dew H.R., 1928, HYDATID DIS ITS PATH; ELKHAMLICHI A, 1990, NEUROCHIRURGIE, V36, P312; ERSAHIN Y, 1995, CLIN NEUROL NEUROSUR, V97, P321, DOI 10.1016-0303-8467(95)00052-L; Evliyaoglu C, 1998, NEURORADIOLOGY, V40, P387; FAHL M, 1994, CLIN IMAG, V18, P179, DOI 10.1016-0899-7071(94)90078-7; FRAYHA GJ, 1981, T ROY SOC TROP MED H, V75, P447, DOI 10.1016-0035-9203(81)90118-8; GRISEL P, 1929, REV CHIR ORTHOP REPA, V67, P376; HADDAD FS, 2003, PAN ARAB J NEUROSURG, V7, P33; HADDAD FS, 1997, PAN ARAB J NEUROSURG, V1, P46; HADDAD FS, 1957, ARCH INT HYDATID, V16, P445; HADDAD GF, 2000, CONT NEUROSURG, V22, P1; HERNIGOU P, 1992, REV RHUM, V59, P131; KALAITZOGLOU I, 1997, AM J NEURORADIOL, V18, P1586; KAOUTZANIS M, 1989, ACTA NEUROCHIR WIEN, V98, P660; KARRAY S, 1990, J BONE JOINT SURG BR, V72, P84; KIDDELL RJ, 1969, PATHOLOGY, V11, P129; MICHELI F, 1987, EUR NEUROL, V27, P1, DOI 10.1159-000116120; MILLS TJ, 1956, J BONE JOINT SURG BR, V38, P884; MORSHED AA, 1977, NEUROCHIRURGIA, V20, P211; MURRAY RO, 1959, J BONE JOINT SURG BR, V41, P499; NURCHI G, 1992, NEUROSURGERY, V30, P436; OZEK MM, 1994, PEDIATR NEUROSURG, V20, P84, DOI 10.1159-000120770; PAU A, 1987, SURG NEUROL, V27, P365, DOI 10.1016-0090-3019(87)90014-0; PETER JC, 1994, PEDIATR NEUROSURG, V20, P78, DOI 10.1159-000120769; PORAT S, 1984, SPINE, V9, P648, DOI 10.1097-00007632-198409000-00018; RAO S, 1991, CLIN ORTHOP RELAT R, P164; RAYPORT M, 1964, J NEUROSURG, V21, P647, DOI 10.3171-jns.1964.21.8.0647; RONG SH, 1985, CLIN RADIOL, V36, P301; SCHROEDER AH, 1952, J NERV MENT DIS, V116, P1025, DOI 10.1097-00005053-195212000-00050; Sener RN, 1996, COMPUT MED IMAG GRAP, V20, P395, DOI 10.1016-S0895-6111(96)00055-9; SLIM MS, 1971, J PEDIATR SURG, V6, P440, DOI 10.1016-S0022-3468(71)80005-2; Tizniti S, 2000, J NEURORADIOLOGY, V27, P200; Turgut M, 1997, J NEUROSURG, V86, P714, DOI 10.3171-jns.1997.86.4.071444

    Pseudopapillary Granulosa Cell Tumor: A Case of This Rare Subtype

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    Background: The pseudopapillary pattern of granulosa cell tumor is rare. Case:We describe a the case of a 35-year-old woman who presented with an initial diagnosis of papillary serous cystadenocarcinoma Results: Evaluation, including immunohistochemistry, led to the diagnosis of pseudopapillary granulosa cell tumor. Conclusion: The pseudopapillary pattern of granulosa cell tumor is rare, and must be suspected in order to utilize appropriate immunohistochemistry and reach the correct diagnosis. Inhibin positivity is particularly helpful.Peer reviewe

    L-γ-glutamyl-L-cysteinyl-glycine (glutathione; GSH) and GSH-related enzymes in the regulation of pro- and anti-inflammatory cytokines: A signaling transcriptional scenario for redox(y) immunologic sensor(s)?

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    Of the antioxidant-prooxidant mechanisms mediating the regulation of inflammatory mediators, particularly cytokines, oxidative stress-related pathways remain a cornerstone. It is conspicuous that there is a strong association between free radical accumulation (ROS-RNS; oxidative stress) and the evolution of inflammation and inflammatory-related responses. The scenario that upholds a consensus on the aforementioned is still evolving to unravel, from an immunologic perspective, the molecular mechanisms associated with ROS-RNS-dependent inflammation. Cytokines are keynote players when it comes to defining an intimate relationship among reduction-oxidation (redox) signals, oxidative stress and inflammation. How close we are to identifying the molecular basis of this intricate association should be weighed against the involvement of specific signaling molecules and, potentially, transcription factors. l-γ-Glutamyl-l-cysteinyl-glycine, or glutathione (GSH), an antioxidant thiol, has shaped, and still is refining, the face of oxidative signaling in terms of regulating the milieu of inflammatory mediators, ostensibly via the modulation (expression-repression) of oxygen- and redox-responsive transcription factors, hence termed redox(y)-sensitive cofactors. When it comes to the arena of oxygen sensing, oxidative stress and inflammation, nuclear factor-κB (NF-κB) and hypoxia-inducible factor-1α (HIF-1α) are key players that determine antioxidant-prooxidant responses with oxidative challenge. It is the theme therein to underlie current understanding of the molecular association hanging between oxidative stress and the evolution of inflammation, walked through an elaborate discussion on the role of transcription factors and cofactors. 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    Vendaphaea lajuma Haddad 2009, sp. n.

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    Vendaphaea lajuma sp. n. Figs 1–27 Etymology: The species name is a noun in apposition taken from the type locality. Description: Male. Measurements: CL 3.40–3.45, CW 2.73–2.80, AL 3.18–3.50, AW 2.05–2.55, TL 6.03– 6.68, FL 0.37–0.39, SL 1.39–1.43, SW 1.30–1.36. Distances between eyes:AME–AME 0.11, AME–ALE 0.07, ALE–ALE 0.56, PME–PME 0.06, PME–PLE 0.19, PLE–PLE 0.79. MOQAW 0.43, MOQPW 0.41, MOQL 0.51, PERW 1.02. Length of leg segments (sequence from femur to tarsus, and total): I 2.48+1.25+2.35+ 2.05+0.60=8.73; II 2.25+1.17+1.85+1.85+0.58=7.70; III 1.73+0.98+1.25+1.35+0.55= 5.86; IV 2.40+1.05+1.93+2.20+0.71=8.29. General appearance as in Fig. 1. Carapace somewhat flattened, elevating slightly from eye region, highest at 3/4 carapace length; eye region distinctly narrowed and bulging; surface covered in short straight white setae medially and short black setae laterally; fovea long, distinct, at 2/3 carapace length; carapace uniform deep red, with slightly darker striae radiating from fovea (Fig. 1). All eyes with brown rings, lateral eyes on slightly raised tubercles;AER procurved, laterals slightly larger than medians;AME separated by distance slightly larger than their diameter;AME separated from ALE by 2/3AME diameter; clypeus height equal to 1.5×AME diameter; PER slightly procurved, nearly straight, medians slightly larger than laterals; PME separated by distance equal to 2/3 their diameter; PME separated from PLE by distance approximately equal to 1.5× PME diameter; CW:PERW = 2.75:1. Chelicerae orange-red, with scattered long black setae on anterior surface; three teeth on promargin, proximal tooth smallest, median tooth largest; median and distal teeth closer to each other than to proximal tooth; retromargin with two widely separated teeth, distal tooth close to fang base, slightly smaller than proximal tooth; endites rounded on anterior prolateral margin, straight laterally and truncated posteriorly; labium 1.5 times broader than long; sternum shield-shaped, narrowed anteriorly, as broad as long, dark orange-red, brown along lateral margins. Legs stoutly built, particularly anterior pairs; all legs densely covered in short straight grey setae, particularly dorsum of patellae, tibiae and metatarsi; anterior tibiae and metatarsi strongly spined ventrally; coxae brown; femora I uniform dark red-orange, slightly darker distally; femora II dark orange-red, with grey distal band; femora III and IV yellow-orange, with narrow proximal and broad distal bands; patellae orange, with grey bands medially; tibiae I and II dark orange dorsally, grey ventrally; tibiae III and IV orange with grey markings dorsally and ventrally; metatarsi I–III orange dorsally with grey distal band; metatarsi IV yellow-orange dorsally with median and distal grey bands, grey ventrally; all tarsi dark brown; leg spination: femora: I plv 2 rlv 2; patellae: spineless; tibiae: I plv 8– 9 rlv 7–8, II plv 7–8 rlv 6, IV rl 1 plv 1 vt 1; metatarsi: I plv 5 rlv 5, II plv 5 rlv 5, III pl 2 plv 1 rlv 1 vt 2, IV plv 2 vt 3. Abdomen oval, dorsal scutum absent; dorsum grey-brown, densely covered with short straight black and grey setae; five short paired black chevron markings slightly lateral of midline in posterior half of abdomen, each ending in small cream spot; single median cream spot above spinnerets; venter unsclerotised, pale grey with darker grey mottling, densely covered in short straight grey setae. Male palp bright orange, without spines; cymbium broad, with dense setal mat medially and modified clavate setae along prolateral and distal margins (Figs 18, 19, 22, 25); palpal tibiae with rounded ventral-retrolateral bump, curved dorsal-retrolateral apophysis (proximal position, at approximately 60° to dorsal position), directed dorsally, and dorsal lobe (Figs 22, 25); tip of apophysis with three distinctive denticles (Figs 18, 23, 25); tegulum broad, pale orange, with thick embolus originating prolaterally, curving anticlockwise towards distal margin, with translucent conductor situated retrolaterally of embolus (Fig. 23); median apophysis spike-like, situated medially on tegulum within membranous section with a proximallydirected lobe (Figs 20, 22–24). Female. Measurements: CL 3.35–3.73, CW 2.60–2.83, AL 4.05–4.80, AW 3.10–3.90, TL 6.85– 7.85, FL 0.35–0.45, SL 1.38–1.50, SW 1.30–1.45. Distances between eyes:AME–AME 0.11, AME–ALE 0.06, ALE–ALE 0.59, PME–PME 0.10, PME–PLE 0.19, PLE–PLE 0.84. MOQAW 0.48, MOQPW 0.44, MOQL 0.59, PERW 1.08. Length of leg segments (sequence from femur to tarsus, and total): I 2.63+1.39+2.44+ 2.15+0.60=9.21; II 2.35+1.25+1.90+1.88+0.57=6.95; III 1.82+1.08+1.30+1.44+0.55= 6.19; IV 2.45+1.30+2.20+2.40+0.70=9.05. General appearance, morphology, colouration and markings as for male (Fig. 2); anterior eye row procurved, laterals very slightly larger than medians;AME separated by distance slightly larger than their diameter; AME separated from ALE by 3/4 AME diameter; clypeus height slightly larger than AME diameter; PER slightly procurved, nearly straight, medians slightly larger than laterals; PME separated by distance equal to 2/3 their diameter; PME separated from PLE by distance approximately equal to 1.5× PME diameter; CW:PERW = 2.62:1. Chelicerae with three teeth on promargin, proximal tooth smallest, median tooth largest; median and distal teeth closer to each other than to proximal tooth; retromargin with two subequal teeth, distal tooth close to fang base. Leg spination: femora: I plv 2 rlv 2; patellae: spineless; tibiae: I plv 9 rlv 8–9, II plv 7–8 rlv 6–7; metatarsi: I plv 5 rlv 5, II plv 4–5 rlv 5, III pl 2 plv 1 rlv 1 vt 2, IV plv 3 rlv 1 vt 2. Epigyne with broad posterior lobe, with diamond-shaped median septum; copulatory openings situated laterally of septum (Fig. 26); spermathecae curved, projecting into body (Fig. 27), distinctly visible through integument (Fig. 26). Holotype: ơ SOUTH AFRICA: Limpopo: Soutpansberg Mountains, Lajuma Mountain Retreat, Woodland, 23°02.528'S: 29°26.866'E, 3.xi.2004, M. Mafadza, sifting leaf litter (NCA 2008/562). Paratypes: all from the same locality as holotype: Island 2, 23°01.921'S: 29°26.193'E, 23.xi.2004, M. Mafadza, active searching, 2ơ (NCA 2005/2016), 1ơ 2^(NCA 2008/563); Island 3, 23°01.890'S: 29°26.167'E, 23.xi.2004, M. Mafadza, active searching,1ơ 1^(NCA 2005/2015);Grassland patch, 23°02.414'S: 29°26.687'E, 6.ii.2008, C. Haddad, base of grass tussocks, 1ơ 7^(NCA 2008/514); same locality, 3–11.ii.2008, C. Haddad, base of grass tussocks, 2^(MPEG 15441). Distribution:Apparently endemic to the western Soutpansberg Mountains in the Limpopo Province, South Africa. It was not collected during published surveys of the Kruger National Park (Dippenaar-Schoeman & Leroy 2003), Makalali Game Reserve (Whitmore et al. 2001), Nylsvley Nature Reserve (Dippenaar-Schoeman et al. 2009), Polokwane Nature Reserve (Dippenaar et al. 2008), or the Sovenga Hill inselberg near Polokwane (Modiba et al. 2005); all of these conserved areas fall within the Limpopo Province. It was also not collected at any of ten sites sampled as part of the South African National Survey of Arachnida in the Limpopo Province (S. Foord & A.S. Dippenaar-Schoeman, pers. comm): Bewaarkloof, Blouberg, Entabeni, Lekgalameetse, Leopard Creek Private Conservation Reserve, Marakele, Mogalakwena, Pafuri, Tshulu, and Wonderkop. This strongly suggests that V. lajuma sp. n. is a Soutpansberg endemic. Habitat preferences: V. lajuma sp. n. was initially collected by Foord et al. (2008) from leaf litter of mixed woodland habitats in the Soutpansberg, where subsequent samples were also collected from montane savannah. The material collected by the author (NCA 2008/514), including 20 additional specimens that were sent to various colleagues for morphological and genetic studies, were all collected from the bases of grass tussocks in montane savannah.Published as part of Haddad, Charles R., 2009, Vendaphaea, a new dark sac spider genus apparently endemic to the Soutpansberg Mountains, South Africa (Araneae: Corinnidae), pp. 269 in African Invertebrates 50 (2) on pages 272-275, DOI: 10.5733/afin.050.0204, http://zenodo.org/record/791047

    The distortionary effects of tariff exemptions in Argentina

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    Tariff exemptions for exporters are widely used by many countries as aninstrument for providing export incentives. This author argues that when tariff exemptions are granted as a means of industrial regional promotion to an industry independently of its export performance, the tariff exemptions lose their potential as an export promotion instrument. The case of Argentina is of interest because it exemplifies the practice of many developing countries. A simple model is used to show that the indiscriminate use of duty exemptions has several undesirable effects : 1) duty exemptions deprive the government of revenues; 2) the more widespread the exemption, the less effective they become as an instrument for export promotion; 3) exemptions widen the variability of effective protection rates of industries in relation to their capital intensity; and 4) exemptions increase the demand for imports more than an export subsidy does, because output in the competing input industry contracts.Environmental Economics&Policies,TF054105-DONOR FUNDED OPERATION ADMINISTRATION FEE INCOME AND EXPENSE ACCOUNT,Economic Theory&Research,Consumption,Export Competitiveness

    Writings of Western Reserve Women

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    Gladys Haddad explores the status of women in Ohio’s Western Reserve through a collection of letters and journal entries. The author focuses on the “nineteenth century definition of the female role”, women’s perception of this role, and the sense of accomplishment they felt within this defined place. Conference paper; originally published in Western Reserve Studies Symposium (2nd:1987 : Cleveland, Ohio
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