Miracle-dz/UniFAR-FTUs huggingface dataset:
Inhibiting Renin-Angiotensin in the Brain: the Possible Therapeutic Implications

The renin-angiotensin system (RAS) within the brain is involved in central blood pressure regulation. Biochemical and neurophysiological studies suggest that the brain system is regulated independently of the peripheral RAS and that the system may also contribute to blood pressure control and body fluid homeostasis. In addition, circulating angiotensin II can exert some of its actions through the stimulation of angiotensin subtype 1 (AT 1 ) and subtype 2 (AT 2 ) receptors within the brain. As in peripheral tissues, the AT 1 receptor mediates the central actions of angiotensin II on osmotic control and blood pressure regulation. The AT 2 receptor appears to be involved in brain development and neuronal regeneration, but may also modulate some effects of central AT 1 receptor stimulation. Selective non-peptide antagonists of the AT 1 receptor have been shown to inhibit not only peripheral, but also central AT 1 receptors after systemic application. In animal models, treatment with AT 1 receptor antagonists proved to be beneficial with respect to stroke incidence and outcome. Other animal studies have shown that the AT 1 receptor antagonists enable endogenous angiotensin II to stimulate nerve generation via AT 2 receptors.
Comparing Android Applications to Find Copying

The Android smartphone operating system includes a Java mobile development platform that provides for rapid development and deployment of a wide variety of applications. The open nature of the platform means that reverse engineering of applications is relatively easy, and many developers are concerned as applications similar to their own show up in the Android marketplace and want to know if these applications are pirated. Fortunately, the same characteristics that make an Android application easy to reverse engineer and copy also provide opportunities for Android developers to compare downloaded applications to their own. This paper describes the process for comparing a developerâ€™s application with a downloaded application and defines an identifiability metric to quantify the degree to which an application can be identified by its bytecode.
Retinal vessel narrowing: an early predictor of future arteriosclerosis?

F or several decades, fundoscopy was one of the most reliable clinical tools for assessing the vascular impact of major cardiovascular risk factors such as diabetes mellitus and hypertension. However, in most European countries, this examination is no longer part of medical routine because of the subjectivity of the evaluation and the fact that other methodological approaches have since been developed such as carotid echography, aortic pulse wave velocity (PWV), and so forth, providing more accurate information on structural and functional vascular alterations. Interestingly, in these last years, and owing to technological advances, several devices have been proposed to measure retinal vessel calibre with accuracy and in a noninvasive manner. Using these methods, several cohort studies have shown that retinal artery narrowing (RAN) is a marker of microvascular dysfunction and is associated with chronic hypertension [1–3] and arterial stiffness [4]. In addition, narrowing of the retinal vessel lumen has been associated with a higher incidence of cardiovascular events [5] independently of blood pressure levels [6]. The study by Kawashima-Kumagai et al. [7] with RAN exhibit, over a period of 5 years, a more pronounced increase in aortic pulse wave velocity. Compared with previous published reports on this topic, this study presents two major interests:
Effects of the in vivo supply of butyrate on histone acetylation of cecum in piglets.

BACKGROUND In vitro, butyrate inhibits histone deacetylase and down-regulates expression of cyclin D1. We hypothesized that an increased entry rate of butyrate into the cecal lumen would have similar effects in vivo. METHODS We used frozen cecal tissue and data from previous studies, one showing that lactulose supplementation caused an increased rate of cecal synthesis of butyrate and decreased cecal cell proliferation and density of clostridia and the other showing that cecal cell proliferation was increased by an exogenous cecal butyrate infusion at a comparable rate. The ratio of acetylated to total histones (AH ratio) and cyclin D1 mRNA expression were measured in cecal tissue. RESULTS Lactulose supplementation caused a 189% increase in the AH ratio (p = .004), which inversely correlated with cecal cell proliferation (r = -0.782; p = .008). With cecal butyrate infusion, we observed a significant decrease in histone acetylation (p = .02), which also inversely correlated with cecal cell proliferation (r = -0.797; p = .002). Cyclin D1 expression was increased 6.5-fold by lactulose feeding (p = .02) but decreased 50% with cecal butyrate infusion (p = .004). CONCLUSIONS The effects on histone acetylation of increased "endogenous" butyrate production produced by lactulose feeding, but not exogenous cecal infusion of butyrate, mirror those in vitro. Thus, bacterial production and exogenous infusion of butyrate have opposite effects on histone acetylation and cyclin D1 expression, suggesting that the composition of bacterial flora may play a role in butyrate's in vivo effects on the cell cycle.
A Resonant Micromachined Magnetic Field Sensor

The design, modeling, and simulation of a novel micromachined magnetic field sensor are discussed. The sensor uses an electrostatic resonator whose fundamental resonant frequency is modified by a Lorentz force generated from the interaction of the sensor structure and the present magnetic field. The sensor was fabricated in a standard bulk micromachining process without the need for any additional processing steps. Since the sensor does not employ any magnetic materials, it does not exhibit hysteresis. A comprehensive model of the sensor behavior is derived which encompasses the interactions of the involved physical domains. Validity of the modeling results was verified by finite-element simulations, and later, through experiments. The sensitivities of the fabricated sensors are in the range of 48-87 Hz/T, depending on sensor structure and dimensions. The design of the sensor allows for its fabrication in many standard microelectromechanical system processes and is compatible with CMOS processes. The theoretical minimum detectable signal with current devices is on the order of 217 nT. Methods to improve the sensitivity of the current sensors are suggested. A linear response to a wide range of magnetic fields makes this design suitable for applications where large fields need to be measured with high resolution.
Effect of Near-orthogonality on Random Indexing Based Extractive Text Summarization

Application of Random Indexing (RI) to extractive text summarization has already been proposed in literature. RI is an approximating technique to deal with high-dimensionality problem of Word Space Models (WSMs). However, the distinguishing feature of RI from other WSMs (e.g. Latent Semantic Analysis (LSA)) is the near-orthogonality of the word vectors (index vectors). The near-orthogonality property of the index vectors helps in reducing the dimension of the underlying Word Space. The present work focuses on studying in detail the near-orthogonality property of random index vectors, and its effect on extractive text summarization. A probabilistic definition of near-orthogonality of RI-based Word Space is presented, and a thorough discussion on the subject is conducted in this paper. Our experiments on DUC 2002 data show that while quality of summaries produced by RI with Euclidean distance measure is almost invariant to near-orthogonality of the underlying Word Space; the quality of summaries produced by RI with cosine dissimilarity measure is strongly affected by near-orthogonality. Also, it is found that RI with Euclidean distance measure performs much better than many LSA-based summarization techniques. This improved performance of RI-based summarizer over LSA-based summarizer is significant because RI is computationally inexpensive as compared to LSA which uses Singular Value Decomposition (SVD) - a computationally complex algebraic technique for dimension reduction of the underlying Word Space.
Ultra-wideband range measurement model with Gaussian processes

This paper presents an ultra-wideband range measurement model based on Gaussian processes. An analysis of the range measurement error with off-the-shelf ultra-wideband radio modules reveals a strong correlation between the reported error and the relative pose of the two ranging modules. A Gaussian process is trained for capturing this correlation and is included in the measurement model. Its effectiveness and real-time applicability are experimentally demonstrated on a quadrocopter platform.
Reproductive and hormonal risk factors for postmenopausal luminal, HER‐2‐overexpressing, and triple‐negative breast cancer

We read with great interest the article by Phipps et al, in which they examined the risk factors for different subtypes of postmenopausal breast cancer. They found that certain reproductive factors have a greater effect on the risk of certain molecular subtypes of disease compared with others. However, the authors did not analyze oral contraceptive use as a risk factor. Oral contraceptive use has been associated with an increased risk of breast cancer in young women. Narod et al demonstrated that among BRCA1 mutation carriers, women who first used oral contraceptives before 1975, who used them before age 30 years, or who used them for 5 years may have an increased risk of developing breast cancer. Sporadic triple-negative breast cancers and tumors that are noted in carriers of the BRCA1 mutation share similar features, including estrogen receptor negativity, high nuclear grade, high Ki-67 staining, cytokeratin 5/6 expression, and epidermal growth factor receptor expression. Furthermore, BRCA1 is rarely mutated in sporadic breast cancers. However, the pathologic similarities suggest that BRCA1 or associated pathways can become inactivated in triple-negative tumors via other mechanisms, such as gene promoter methylation. We previously reported a positive association between oral contraceptive use and triple-negative breast cancer. Although we did not take into consideration the menopausal status of the patients, the frequency of oral contraceptive use in our small cohort was found to be higher in patients with the triple-negative subtype compared with patients with other subtypes of breast cancer (35.3% vs 12.2%; P1⁄4 .02). Taken together, we propose that oral contraceptive use may be associated with an increased risk of developing triple-negative breast cancer. However, to identify the exact role of oral contraceptive use in the development of breast cancer, more preclinical and clinical studies are warranted.
The Clinical Noncompliance of Oral Sotalol/Magnesium for Prophylactic Treatment of Atrial Fibrillation After Coronary Artery Bypass Grafting

Abstract Background: Postoperative atrial fibrillation has been refractory to many attempted pharmacologic prevention methods and, when effective, side effects have been described. The present aim was to study the clinical compliance of a suggested prophylactic treatment, oral sotalol, and magnesium. Methods: Coronary‐bypass patients without clinical contraindications to receive oral sotalol (80 mg twice daily) and magnesium supplementation were enrolled (n = 49) with an intention‐to‐treat strategy and being compared with a matched control group (n = 844). A protocol listed exclusion criteria of clinical compliance that was postoperatively evaluated prior to and during treatment. Results: Twenty‐seven of the 49 enrolled patients (55%) were compliant to sustain the treatment according to the protocol. The remaining patients were postoperatively excluded, mainly because of hemodynamic reasons, of whom 14 were noncompliant to initiate any treatment. The AF occurrence in the compliant group was 7% versus 36% in noncompliant patients (p = 0.035), and 24% in the control group (p = 0.076). However, with an intention‐to‐treat policy the overall AF incidence became 18%. The subgroups of enrolled patients demonstrated skewing phenomena. The noncompliant group had higher requirement for inotropic support (p = 0.029) and longer aortic cross‐clamp time (p = 0.048) compared to compliant patients. Further, the body weight of noncompliant patients was markedly lower than in the compliant counterpart (p = 0.015). Conclusions: The tested treatment protocol showed limited compliance among routine cardiac‐surgery patients, and further, introduced a biased selection of patients that skewed the results and may have partly explained the treatment effect.
Hospitalizations after the Gulf War¯Reply to K.M. Leisure et al.

2. Knoke JD, Gray GC. Hospitalizations for unexplained illnesses among U.S. veterans of the Persian Gulf War. Emerg Infect Dis 1998;4:211-19. 3. Haley RW. Bias from the healthy warrior effect and unequal follow-up in three government studies of health effects of the Gulf War. Am J Epidemiol 1998;148:315-23. 4. Murray-Leisure KA, Sees J, Zangwill B, Suguitan E, Legaspi C, Bagheri S, Mucha P, Brinser E, Kimber R, Kurban R, Greene W. Mucocutaneous-intestinalrheumatic Desert Syndrome (MIRDS): Incubation & histopathology findings. Abstract K 48, American Society for Microbiology, ICAAC, Sept. 18, 1995. 5. U.S. General Accounting Office. Gulf War Illnesses: Improved Monitoring of Clinical Progress and Reexamination of Research Emphasis are Needed. GAO/NSIAD-97-163. June 1997. 6. Sostek MB, Jackson S, Linevsky JK, Schimmel EM, Fincke BG. High prevalence of chronic gastrointestinal syndromes in a National Guard unit of Persian Gulf Veterans. Am J Gastroenterol 1996;91:2494-7. 7. Centers for Disease Control. Unexplained illness among Persian Gulf War veterans in an Air National Guard unit: Preliminary report, Aug 1990-March 1995. Morb Mortal Week Rep 1995;44:443-7 8. Fukada K, Nisenbaum R, Stewart G, Thompson WW, Robin L, Washko R, et al. Chronic multisystem illnesses affecting Air Force veterans of the Gulf War. JAMA 1998;280:981-8. 9. Nicolson G, Nicolson N. Gulf War illnesses. Medicine, Conflict, and Survival 1998;14:156-65. 10. Magill AJ, Grogl M, Gasser RA, Wellington S, Oster CN. Viscerotropic leishmaniasis caused by Leishmania tropica in soldiers returning from Operation Desert Storm. N Engl J Med 1993;328:1383-7. 11. Magill AJ, Grogl M, Johnson SC, Gasser RA. Visceral infection due to Leishmania tropica in a veteran of Operation Desert Storm who presented two years after leaving Saudi Arabia. Clin Infect Dis 1994;19:805-6. 12. Ferrante MA, Dolan MJ. Q Fever meningoencephalitis in a soldier returning from the Persian Gulf War. Clin Infect Dis 1993;16:489-96. 13. Seaman J, Mercer AJ, Sondorp E. Epidemic of visceral Leishmaniasis in western upper Nile, southern Sudan: Course and impact from 1984 to 1994. Int J Epidemiol 1996;25:862-71. 14. Zilinskas RA. Iraqs biological weapons. JAMA 1997;278:418-24. Hospitalizations after the Gulf War—Reply to K.M. Leisure et al.
Capacity value of solar power: Report of the IEEE PES task force on capacity value of solar power

This paper reviews methods used for adequacy risk assessment considering solar power, and for assessment of the capacity value of solar power. The properties of solar power are described as seen from the perspective of the balancing authority, comparing differences in energy availability and capacity factors with those of wind. Methodology for risk calculations considering variable generation (VG) are then surveyed, including the probability background, statistical estimation approaches, and capacity value metrics. Issues in incorporating VG in capacity markets are described, followed by a review of applied studies considering solar power. Finally, recommendations for further research will be presented.
Hypoxia-inducible factor 1alpha and antiangiogenic activity of farnesyltransferase inhibitor SCH66336 in human aerodigestive tract cancer.

BACKGROUND The farnesyltransferase inhibitor SCH66336, in combination with other receptor tyrosine kinase inhibitors, inhibits the growth of non-small-cell lung cancer (NSCLC) cells. We examined whether SCH66336 inhibits angiogenesis of aerodigestive tract cancer cells. METHODS Antiangiogenic activities of SCH66336 against NSCLC, head and neck squamous cell carcinoma (HNSCC), and endothelial cells were examined with cell proliferation, capillary tube formation, and chick aorta (under hypoxic, normoxic, insulin-like growth factor I (IGF)-stimulated, and unstimulated conditions); reverse transcription-polymerase chain reaction; and western blot analyses. The specific roles of the ubiquitin-mediated proteasome machinery, mitogen-activated protein kinase (MAPK) and Akt pathways, and heat shock protein 90 (Hsp90) in the SCH66336-mediated degradation of hypoxia-inducible factor 1alpha (HIF-1alpha) were assessed with ubiquitin inhibitors and adenoviral vectors that express constitutively active MAP kinase kinase (MEK)1, constitutively active Akt, or Hsp90. RESULTS SCH66336 showed antiangiogenic activities and decreased the expression of vascular endothelial cell growth factor (VEGF) and HIF-1alpha in hypoxic, IGF-stimulated, and unstimulated aerodigestive tract cancer and endothelial cells. SCH66336 reduced the half-life of the HIF-1alpha protein, and ubiquitin inhibitors protected the hypoxia- or IGF-stimulated HIF-1alpha protein from SCH66336-mediated degradation. SCH66336 inhibited the interaction between HIF-1alpha and Hsp90. The overexpression of Hsp90, but not constitutive Akt or constitutive MEK, restored HIF-1alpha expression in IGF-stimulated or hypoxic cells but not in unstimulated cells. CONCLUSIONS SCH66336 appears to inhibit angiogenic activities of NSCLC and HNSCC cells by decreasing hypoxia- or IGF-stimulated HIF-1alpha expression and to inhibit VEGF production by inhibiting the interaction between HIF-1alpha and Hsp90, resulting in the proteasomal degradation of HIF-1alpha.
The Nature of Explanation in Qualitative Evaluation

In recent years evaluation has mushroomed dramatically as a discipline. A number of evaluation "models" or approaches have been conceived, and varieties of social science methods have been employed serving several evaluative purposes. Missing from the health profession's literature on evaluation is a discussion of the underlying explanatory purposes of evaluative inquiry. It can be argued that systematic accounts of a logical inquiry (evaluation)are inextricably bound to particular views or accounts of the logic of explanation. In this article those accounts of explanation that pertain to conventional and qualitative evaluation are reviewed and compared. The article describes what one has "bought off on" when applying the explanatory rationale underlying qualitative evaluation approaches. Problems and possibilities are described for the practice of qualitative evaluation in the health professions.
The effect of deprenyl and levodopa on the progression of Parkinson's disease

We have performed a 14‐month, prospective, randomized, double‐blind, placebo‐controlled study to evaluate the effect of deprenyl and levodopa/carbidopa (Sinemet) on the progression of signs and symptoms in patients with mild Parkinson's disease (PD). One hundred one untreated PD patients were randomly assigned to one of the following four treatment groups: Group I, deprenyl + Sinemet; Group II, placebo‐deprenyl + Sinemet; Group III, deprenyl + bromocriptine; and Group IV, placebo‐deprenyl + bromocriptine. The final visit was performed at 14 months, i.e., 2 months after withdrawal of deprenyl or its placebo and 7 days after withdrawal of Sinemet or bromocriptine. Deterioration in Unified Parkinson's Disease Rating Score (UPDRS) between untreated baseline and final visits was used as an index of disease progression. Placebo‐treated patients deteriorated by 5.8 ± 1.4 points, while deprenyl‐treated patients deteriorated by 0.4 ± 1.3 points (p < 0.001). This effect was sufficiently powerful that a significant deprenyl effect could be detected in the subgroup of 41 patients randomized to Sinemet (p < 0.01) as well as in the 23 patients who completed a 14‐day washout of Sinemet or bromocriptine (p < 0.05). No difference in the extent of deterioration was detected in patients randomized to Sinemet versus bromocriptine. This study demonstrates that deprenyl attenuates deterioration in UPDRS score in patients with early PD. These findings are not readily explained by the drug's symptomatic effects and are consistent with the hypothesis that deprenyl has a neuroprotective effect.
The molecular basis of severe hypertriglyceridemia: from genetic counseling to gene therapy.

C-II (Apo cII), lipase maturation factor 1 (LFM1), glycosylphosphatidylinositolanchored high density lipoprotein binding protein 1 (GPIHBP1) and apoprotein A5 (APO5) [7]. The accurate diagnosis of the genetic cause in a specific family is now feasible and enables detection of novel mutations in candidate genes, as shown by Behar et al. in their current report [6]. Another group is Israel used a similar approach to detect a mutation in the gene encoding glycerol 3 phosphate dehydrogenase 1 in two Arab Israeli families, which explains the phenotype of severe hypertriglyceridemia and fatty liver [8]. While accurate genetic counseling is very important, new modalities of therapy are now becoming feasible. At least one of the mutations in the LPL gene is a gain-offunction mutation (s447x). The presence of this variant enables better LPL enzyme activity and lowers triglyceride levels [9]. Several studies in humans have demonstrated that intramuscular injections of the LPL gene using an adenoviral-associated vector as the vehicle for the normal LPL gene prompts production of active LPL enzyme and corrects the LPL-deficient status of individuals born without LPL activity due to loss-of-function mutations in the LPL gene. This is believed to be a lasting gene implantation and these patients have a significant reduction in triglyceride levels [10]. In summary, recent advances in genetics have given us a powerful tool for the detection of large-effect monogenetic alleles responsible for extreme phenotypes s evere hypertriglyceridemia (fasting triglycerides above 1000 mg/dl) is a common condition that occurs in 1:600 individuals [1]. Clinical features include hepatomegaly, eruptive xantomatosis, lipemia retinalis and pancreatitis [2]. Hypertriglyceridemia also increases the risk of cardiovascular disease [3]. Genetic susceptibility to hypertriglyceridemia is now elucidated. extreme hypertriglyceridemia is less common and is caused by a simple monogenic disorder showing a typical Mendelian recessive inheritance presenting in early childhood and resulting from homozygosis for large-effect genetic mutations. Lipoprotein lipase is the enzyme responsible for lipolysis of triglyceride-rich lipoproteins [4]. More than 70 mutations are known in the LPL1 gene, causing about half the cases of extreme hypertriglyceridemia [5]. In this issue of IMAJ Behar and co-authors [6] report the detection of such a mutation in the LPL gene using the available tools of modern genetics and sequencing the LPL genes of the proband and his family. Other genes causing the same phenotype include Apo protein