On the Three-Parameter Burr Type XII Distribution and its Application to Heavy Tailed Lifetime Data

This paper identifies the characteristics of three-parameter Burr Type XII distribution and discusses its utility in survivorship applications. It addresses the problem of estimating the three-parameter Burr XII distribution and its doubly truncated version. The results are applied on a real dataset by fitting the distribution to the survival time of breast cancer patients in the Gaza Strip. These data are known to have a heavy tailed distribution since patients in this area received different protocols of treatments in different levels of hospitals locally and abroad. The findings indicated that the estimates of the parameters of the truncated distribution are more efficient than those obtained from the original distribution since the distribution is heavy tailed and involves many highly extreme observations

Asymmetric magnetic bubble expansion under in-plane field in Pt/Co/Pt: effect of interface engineering

We analyse the impact of growth conditions on asymmetric magnetic bubble expansion under in-plane field in ultrathin Pt / Co / Pt films. Specifically, using sputter deposition we vary the Ar pressure during the growth of the top Pt layer. This induces a large change in the interfacial structure as evidenced by a factor three change in the effective perpendicular magnetic anisotropy. Strikingly, a discrepancy between the current theory for domain-wall propagation based on a simple domain-wall energy density and our experimental results is found. This calls for further theoretical development of domain-wall creep under in-plane fields and varying structural asymmetry.Comment: 16 pages, 3 figure

Re-Hardening of Hadron Transverse Mass Spectra in Relativistic Heavy-Ion Collisions

We analyze the spectra of pions and protons in heavy-ion collisions at relativistic energies from 2 A GeV to 65+65 A GeV by using a jet-implemented hadron-string cascade model. In this energy region, hadron transverse mass spectra first show softening until SPS energies, and re-hardening may emerge at RHIC energies. Since hadronic matter is expected to show only softening at higher energy densities, this re-hardening of spectra can be interpreted as a good signature of the quark-gluon plasma formation.Comment: 10 pages, 3 figures, 1 table, Poster presentation at QM2001, Revised to correct latex error in citation on April 6, 200

Mid-gut ACTH-secreting neuroendocrine tumor unmasked with (18)F-dihydroxyphenylalanine-positron emission tomography.

Ectopic ACTH Cushing's syndrome (EAS) is often caused by neuroendocrine tumors (NETs) of lungs, pancreas, thymus, and other less frequent locations. Localizing the source of ACTH can be challenging. A 64-year-old man presented with rapidly progressing fatigue, muscular weakness, and dyspnea. He was in poor condition and showed facial redness, proximal amyotrophy, and bruises. Laboratory disclosed hypokalemia, metabolic alkalosis, and markedly elevated ACTH and cortisol levels. Pituitary was normal on magnetic resonance imaging (MRI), and bilateral inferior petrosal sinus blood sampling with corticotropin-releasing hormone stimulation showed no significant central-to-periphery gradient of ACTH. Head and neck, thoracic and abdominal computerized tomography (CT), MRI, somatostatin receptor scintigraphy (SSRS), and (18)F-deoxyglucose-positron emission tomography (FDG-PET) failed to identify the primary tumor. (18)F-dihydroxyphenylalanine (F-DOPA)-PET/CT unveiled a 20-mm nodule in the jejunum and a metastatic lymph node. Segmental jejunum resection showed two adjacent NETs, measuring 2.0 and 0.5 cm with a peritoneal metastasis. The largest tumor expressed ACTH in 30% of cells. Following surgery, after a transient adrenal insufficiency, ACTH and cortisol levels returned to normal values and remain normal over a follow-up of 26 months. Small mid-gut NETs are difficult to localize on CT or MRI, and require metabolic imaging. Owing to low mitotic activity, NETs are generally poor candidates for FDG-PET, whereas SSRS shows poor sensitivity in EAS due to intrinsically low tumor concentration of type-2 somatostatin receptors (SST2) or to receptor down regulation by excess cortisol. However, F-DOPA-PET, which is related to amine precursor uptake by NETs, has been reported to have high positive predictive value for occult EAS despite low sensitivity, and constitutes a useful alternative to more conventional methods of tumor localization. LEARNING POINTS: Uncontrolled high cortisol levels in EAS can be lethal if untreated.Surgical excision is the keystone of NETs treatment, thus tumor localization is crucial.Most cases of EAS are caused by NETs, which are located mainly in the lungs. However, small gut NETs are elusive to conventional imaging and require metabolic imaging for detection.FDG-PET, based on tumor high metabolic rate, may not detect NETs that have low mitotic activity. SSRS may also fail, due to absent or low concentration of SST2, which may be down regulated by excess cortisol.F-DOPA-PET, based on amine-precursor uptake, can be a useful method to localize the occult source of ACTH in EAS when other methods have failed

Crushing singularities in spacetimes with spherical, plane and hyperbolic symmetry

It is shown that the initial singularities in spatially compact spacetimes with spherical, plane or hyperbolic symmetry admitting a compact constant mean curvature hypersurface are crushing singularities when the matter content of spacetime is described by the Vlasov equation (collisionless matter) or the wave equation (massless scalar field). In the spherically symmetric case it is further shown that if the spacetime admits a maximal slice then there are crushing singularities both in the past and in the future. The essential properties of the matter models chosen are that their energy-momentum tensors satisfy certain inequalities and that they do not develop singularities in a given regular background spacetime.Comment: 19 page

Deletion of Sirt3 does not affect atherosclerosis but accelerates weight gain and impairs rapid metabolic adaptation in LDL receptor knockout mice: implications for cardiovascular risk factor development.

Sirt3 is a mitochondrial NAD(+)-dependent deacetylase that governs mitochondrial metabolism and reactive oxygen species homeostasis. Sirt3 deficiency has been reported to accelerate the development of the metabolic syndrome. However, the role of Sirt3 in atherosclerosis remains enigmatic. We aimed to investigate whether Sirt3 deficiency affects atherosclerosis, plaque vulnerability, and metabolic homeostasis. Low-density lipoprotein receptor knockout (LDLR(-/-)) and LDLR/Sirt3 double-knockout (Sirt3(-/-)LDLR(-/-)) mice were fed a high-cholesterol diet (1.25 % w/w) for 12 weeks. Atherosclerosis was assessed en face in thoraco-abdominal aortae and in cross sections of aortic roots. Sirt3 deletion led to hepatic mitochondrial protein hyperacetylation. Unexpectedly, though plasma malondialdehyde levels were elevated in Sirt3-deficient mice, Sirt3 deletion affected neither plaque burden nor features of plaque vulnerability (i.e., fibrous cap thickness and necrotic core diameter). Likewise, plaque macrophage and T cell infiltration as well as endothelial activation remained unaltered. Electron microscopy of aortic walls revealed no difference in mitochondrial microarchitecture between both groups. Interestingly, loss of Sirt3 was associated with accelerated weight gain and an impaired capacity to cope with rapid changes in nutrient supply as assessed by indirect calorimetry. Serum lipid levels and glucose tolerance were unaffected by Sirt3 deletion in LDLR(-/-) mice. Sirt3 deficiency does not affect atherosclerosis in LDLR(-/-) mice. However, Sirt3 controls systemic levels of oxidative stress, limits expedited weight gain, and allows rapid metabolic adaptation. Thus, Sirt3 may contribute to postponing cardiovascular risk factor development

Unusual presentations of functional parathyroid cysts: a case series and review of the literature.

Cysts of parathyroid origin are sometimes encountered and can easily be mistaken as thyroidal cysts. Functional parathyroid cysts, with symptoms and signs of hyperparathyroidism, are rare and may be a diagnostic challenge to clinicians. We report here on three cases of functional parathyroid cysts that illustrate diagnosis difficulties related to unusual clinical presentations in three Caucasian women, including negative parathyroid scintigraphy. Patient 1, an 87-year-old Caucasian woman presented with confusion and dysphagia. She had hypercalcemia and elevated parathyroid hormone levels suggesting primary hyperparathyroidism. Parathyroid scintigraphy did not reveal any focal uptake, but a computed tomography scan of her neck identified a large cyst in the upper right thyroid region. At cervicotomy, a parathyroid cystic adenoma was removed. Patient 2, a 31-year-old Caucasian woman was investigated after a hypertensive crisis related to primary hyperparathyroidism. Cervical ultrasound identified a large cystic lesion in the lower left thyroid lobe that was removed by minimally invasive cervicotomy. Patient 3, a 34-year-old Caucasian woman presented with an indolent growing mass of the neck and a past medical history of kidney stones. Primary hyperparathyroidism was diagnosed. Ultrasound showed a cystic mass, but parathyroid scintigraphy was negative. Cervical exploration revealed a large cystic adenoma, containing high parathyroid hormone levels. Diagnosis of functional parathyroid cysts can be challenging due to various clinical presentations and negative parathyroid scintigraphy. Surgery, but not fine-needle sclerotherapy, appears to be the safest treatment option. Despite its rarity, differential diagnosis of cystic lesion of the neck should include primary hyperparathyroidism due to functional parathyroid cysts

Electromagnetically Actuated Ball Valve Micropumps

We present two types of oscillating diaphragm micropumps configured with passive ball valves and using electromagnetic actuation. One type is made out of poly(methyl methacrylate) (PMMA), while the other one is made out of borosilicate glass. Both were produced using the powder blasting microfabrication method. The pumping resonant frequency was measured to be within the range of 20 – 30 Hz for both prototypes. At the resonance, a maximum back-pressure of 280 mbar and a maximum water flow rate of about 5 mL/min were obtained. The experimental results can be well described by a simple hydrodynamic model of the system

Infections with Avian Pathogenic and Fecal Escherichia coli Strains Display Similar Lung Histopathology and Macrophage Apoptosis

The purpose of this study was to compare histopathological changes in the lungs of chickens infected with avian pathogenic (APEC) and avian fecal (Afecal) Escherichia coli strains, and to analyze how the interaction of the bacteria with avian macrophages relates to the outcome of the infection. Chickens were infected intratracheally with three APEC strains, MT78, IMT5155, and UEL17, and one non-pathogenic Afecal strain, IMT5104. The pathogenicity of the strains was assessed by isolating bacteria from lungs, kidneys, and spleens at 24 h post-infection (p.i.). Lungs were examined for histopathological changes at 12, 18, and 24 h p.i. Serial lung sections were stained with hematoxylin and eosin (HE), terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) for detection of apoptotic cells, and an anti-O2 antibody for detection of MT78 and IMT5155. UEL17 and IMT5104 did not cause systemic infections and the extents of lung colonization were two orders of magnitude lower than for the septicemic strains MT78 and IMT5155, yet all four strains caused the same extent of inflammation in the lungs. The inflammation was localized; there were some congested areas next to unaffected areas. Only the inflamed regions became labeled with anti-O2 antibody. TUNEL labeling revealed the presence of apoptotic cells at 12 h p.i in the inflamed regions only, and before any necrotic foci could be seen. The TUNEL-positive cells were very likely dying heterophils, as evidenced by the purulent inflammation. Some of the dying cells observed in avian lungs in situ may also be macrophages, since all four avian E. coli induced caspase 3/7 activation in monolayers of HD11 avian macrophages. In summary, both pathogenic and non-pathogenic fecal strains of avian E. coli produce focal infections in the avian lung, and these are accompanied by inflammation and cell death in the infected areas