Miracle-dz/UniFAR-FTUs huggingface dataset:
An empirical study of the correlations between function point elements [software metrics]

Researchers and practitioners have noted correlations between the five types of elements in function point analysis. Practitioners exploit them; researchers have raised concerns about them. Two previous studies of the correlations between the elements have agreed in some findings, but differed on others. A large data set is analyzed here to gain further insight into the correlations. Two elements (inputs and logical files) are found to be correlated always, and one element (external files) is found to be generally uncorrelated with the others. Correlations are strongest in new development projects that use 4GLs. These results confirm some findings of previous researchers, and suggest explanations for differences between previous findings.
Arsenic trioxide as effective therapy for relapsed acute promyelocytic leukemia.

The standard of treatment for newly diagnosed patients with acute promyelocytic leukemia (APL) is all-trans retinoic acid (ATRA) plus anthracycline-based cytotoxic chemotherapy, a combination that is highly effective for remission induction. However, 20%-30% of patients relapse and require salvage therapy. Reports from China on the striking efficacy and safety of arsenic trioxide in patients with APL led to clinical trials in the United States, which culminated in U.S. Food and Drug Administration approval in September 2000. Trisenox (Cell Therapeutics, Inc., Seattle, WA) is an injectable formulation of arsenic trioxide indicated in the treatment of refractory or relapsed APL. The common side effects of Trisenox therapy are mostly mild and self-limiting and do not require interruption of therapy. Serious adverse effects that can occur include hyperleukocytosis, electrocardiographic abnormalities, and APL differentiation syndrome. These effects can be prevented or managed successfully with careful patient monitoring during treatment. Trisenox has no known cross-resistance with ATRA or other anticancer agents. It does not cause hair loss and is not myelosuppressive in patients with APL. Oncology nurses can play a major role in educating patients about this new drug, explaining its clinical benefits and side effects and the precautions that are necessary for its use.
Essential Roles of Sphingosine‐1‐Phosphate and Platelet‐Derived Growth Factor in the Maintenance of Human Embryonic Stem Cells

Human embryonic stem cells (hESCs) have great potential for use in research and regenerative medicine, but very little is known about the factors that maintain these cells in the pluripotent state. We investigated the role of three major mitogenic agents present in serum—sphingosine‐1‐phosphate (S1P), lysophosphatidic acid (LPA), and platelet‐derived growth factor (PDGF)—in maintaining hESCs. We show here that although LPA does not affect hESC growth or differentiation, coincubation of S1P and PDGF in a serum‐free culture medium successfully maintains hESCs in an undifferentiated state. Our studies indicate that signaling pathways activated by tyrosine kinase receptors act synergistically with those downstream from lysophospholipid receptors to maintain hESCs in the undifferentiated state. This study is the first demonstration of a role for lysophospholipid receptor signaling in the maintenance of stem cell pluri‐potentiality.
Role of nitric oxide in hyperpnea-induced bronchoconstriction and airway microvascular permeability in guinea pigs

ABSTRACT The present study aimed to evaluate the role of nitric oxide (NO) on hyperpnea-induced bronchoconstriction (HIB) and airway microvascular hyperpermeability (AMP). Sixty-four guinea pigs were anesthetized, tracheotomized, cannulated, and connected to animal ventilator to obtain pulmonary baseline respiratory system resistance (Rrs). Animals were then submitted to 5 minutes hyperpnea and Rrs was evaluated during 15 minutes after hyperpnea. AMP was evaluated by Evans blue dye (25 mg/kg) extravasation in airway tissues. Constitutive and inductible NO was evaluated by pretreating animals with NG-nitro-l-arginine methyl ester (l-NAME) (50 mg/kg), aminoguadinine (AG) (50 mg/kg), and l-arginine (100 mg/kg) and exhaled NO (NOex) was evaluated before and after drug administration and hyperpnea. The results show that l-NAME potentiated (57%%) HIB and this effect was totally reversed by l-arginine pretreatment, whereas AG did not have effect on HIB. l-NAME decreased basal AMP (48%%), but neither l-NAME nor AG had any effect on hyperpnea-induced AMP. NOex levels were decreased by 50%% with l-NAME, effect that was reversed by l-arginine treatment. These results suggest that constitutive but not inducible NO could have a bronchoprotective effect on HIB in guinea pigs. The authors also observed that neither constitutive nor inducible NO seems to have any effect on hyperpnea-induced AMP.
A comparison of a 12-hour and eight-hour shift system in similar medical wards

Despite the increasing use of and discussion about 12-hour shifts, little work has been carried out in the United Kingdom to assess its impact. A study was carried out to compare two medical wards which had been operating a 12-hour shift for more than one year with two medical wards which had carried on with a conventional shift system over the same period of time. Staff questionnaires, interviews, patient interviews, documentation review, and analysis of a number of organizational issues were undertaken to evaluate the effect of the shift pattern worked. Viewing this shift pattern from a variety of perspectives indicates that there were no significant differences between the shift patterns with regard to staff perception, patient perception, documentation and organisational issues. However, some aspects of the 12-hour shift produced more favourable responses from the staff: less fatigue was reported by those working the 12-hour shift and documentation was more complete on these wards. However, the length of time available for the handover was identified as a problematic area. Staff surveyed had chosen to work these hours which may positively have influenced the impact of this shift pattern on both staff and patients. This work demonstrates the complexities in evaluating patterns of work in providing patient care over 24 hours.
Studies of cellular proliferation in human leukemia. I. Estimation of growth rates of leukemic and normal hematopoietic cells in two adults with acute leukemia given single injections of tritiated thymidine.

Two adults with rapidly progressive acute myeloblastic and myelomonoblastic leukemia were given single injections of tritiated thymidine, and measurements were made of the growth rates of their leukemic and normal hematopoietic cells by radioautographic methods. Although almost all leukemic blasts in both marrow and blood were metabolically active as shown by their ability to incorporate tritiated uridine and leucine in vitro, only 5.6% and 6.1% of the blasts in the marrow and even fewer in the blood incorporated tritiated thymidine. The mitotic indexes of the marrow blasts were 0.66% and 0.52%; no circulating blasts were dividing. The mean generation times of the actively proliferating blasts were estimated to be 49 and 83 hours. This cannot be equated with the doubling time of the total leukemic population as there is evidence that many blasts fail to continue dividing and die. The mean durations of the phases of the blasts' mitotic cycles were as follows: DNA synthesis (S) = 22 and 19 hours, premitosis (G(2)) = 3 hours, mitosis (M) = 0.47 and 0.62 hour (minimal estimates), and postmitosis (G(1)) = 24 and 61 hours. In both patients the maximal mean transit time of the blasts in the blood was 36 hours, and the minimal numbers of actively dividing blasts present were 1.6 and 2.6 x 10(9) per kg of body weight.Estimates were also made of the rates of proliferation and maturation of the residual normal erythrocytic and granulocytic cells in these two patients. Although total production was markedly diminished because of reduction in the number of normal elements, the relatively few remaining normal cells appeared to be dividing and maturing at rates that are about the same or only slightly slower than those found in normal subjects. We conclude that main reason leukemic blasts displace normal hematopoietic precursors in acute leukemia is that the blasts largely fail to differentiate. Many die but many others persist in the marrow and elsewhere as primitive cells and continue to proliferate. As the blasts accumulate, they gradually displace the normal hematopoietic cells, most of which continue their normal course of differentiation and leave the marrow as nondividing mature cells. It is not known why the over-all production of normal cells is not adequately increased to compensate for the anemia, granulocytopenia, and thrombocytopenia that develop, but apparently the leukemic cells somehow interfere with the proliferation or differentiation or both of normal stem cells.
Endurance exercise training and reproductive endocrine dysfunction in men: alterations in the hypothalamic-pituitary-testicular axis.

Research indicates that endurance exercise training has significant effects upon the reproductive endocrine system of humans. Until recently, this effect was thought to be limited primarily to women. However, a growing body of evidence demonstrates that the male reproductive endocrine system is also effected. Specifically, the circulating hormonal levels of testosterone are found to be at low concentrations; and, the hypothalamic-pituitary-testicular axis that regulates testosterone production is altered in endurance trained men. The physiological mechanism inducing the lower testosterone is currently unclear; but in many respects, these men display hypogonadotropic hypogonadism characteristics. Currently, the time course of the changes in the reproductive endocrine system is unresolved and in need of much furthers scientific investigation. The evidence available, however, suggests that a slowly developing process requiring years of exercise training results in these changes. Potentially, the lowered testosterone levels of the endurance-trained male could disrupt some of their anabolic or androgenic dependent processes. To date, there are only a limited number of findings suggesting that a consistent disruption of testosterone dependent processes occur due to endurance exercise training (e.g., oligo-spermatogenesis). Conversely, the alterations in testosterone concentration brought about by endurance training could have cardiovascular protective effects and thus be beneficial to the health of these men.
Predicting language impairment status: A risk factor model

Rudolph, Johanna M. Ph.D., Purdue University, December 2013. Predicting Language Impairment Status: A Risk Factor Model. Major Professor: Laurence B. Leonard. The etiology of specific language impairment (SLI) is multifactorial. Research has shown that genetic, environmental, and developmental factors may influence the course of its development. Because many of these factors are present even before a child is born, it is possible that a child’s risk of developing the disorder can be identified long before grammatical deficits are observed. The goal of this study was to develop and validate a screening tool to discriminate between children with SLI and typically developing (TD) children using only risk factor information including gender, family history of communication or reading disorders, socioeconomic status, maternal and paternal education level, birth order, premature birth, and birth weight. Participants included 211 children between the ages of 4;0 and 7;0. Two diagnostic classification schemes were used to examine the effects of clinical sample heterogeneity on risk factor model accuracy. In the first scheme, children were classified as SLI or TD based on their performance on a standardized expressive language test (SPELT classification). In the second scheme, children were classified based on their combined performance on both the standardized test and a measure of tense and agreement morpheme use (SPELT-FVM classification), thereby limiting the clinical sample to children with specific deficits in grammatical morphology. Step-wise logistic regression and five-fold cross-validation were used to derive risk factor models, probability equations, and cut-off scores for the two classification groups. Sensitivity, specificity, likelihood ratios, and diagnostic odds ratios were calculated for each cut-off value. Family history and maternal education arose as highly significant vari-
Efficacy of orally administered maropitant citrate in preventing vomiting associated with hydromorphone administration in dogs.

OBJECTIVE To evaluate the effectiveness of orally administered maropitant citrate in preventing vomiting after hydromorphone hydrochloride administration in dogs. DESIGN Randomized, blinded, prospective clinical study. ANIMALS 40 dogs with American Society of Anesthesiologists status of I or II, > 6 months of age, and weighing between 24 and 58.2 kg (52.8 and 128.04 lb). PROCEDURES Dogs were randomly selected to receive maropitant (2.0 to 4.0 mg/kg [0.9 to 1.8 mg/lb]) or placebo (lactose monohydrate) orally 2 hours prior to receiving hydromorphone (0.1 mg/kg [0.045 mg/lb], IM). A blinded observer recorded the occurrence of vomiting or signs of nausea (eg, salivation or lip-licking) during a 30-minute period after hydromorphone administration. Two-tailed Fisher exact tests were used to compare the incidences of vomiting and signs of nausea with or without vomiting between treatment groups. Results-Of the 20 dogs receiving maropitant, none vomited but 12 (60%) developed signs of nausea. Of the 20 dogs receiving placebo, 5 (25%) vomited and 11 (55%) developed signs of nausea; overall, 16 of 20 (80%) dogs in the placebo treatment group vomited or developed signs of nausea. Compared with the effects of placebo, maropitant significantly decreased the incidence of vomiting but not signs of nausea in dogs administered hydromorphone. CONCLUSIONS AND CLINICAL RELEVANCE Among the 40 study dogs, the incidence of vomiting associated with hydromorphone administration was 25%. Oral administration of maropitant prevented vomiting but not signs of nausea associated with hydromorphone administration in dogs.
Inflammation, Glutamate, and Glia in Depression: A Literature Review

ABSTRACT Multiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-α treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.
Impact of co-morbidities on self-rated health in self-reported COPD: An analysis of NHANES 2001–2008

Abstract Chronic Obstructive Pulmonary Disease (COPD) coexists with co-morbidities. While co-morbidity has been associated with poorer health status, it is unclear which conditions have the greatest impact on self-rated health. We sought to determine which, and how much, specific co-morbid conditions impact on self-rated health in current and former smokers with self-reported COPD. Using the 2001–2008 National Health and Nutrition Examination Survey we characterized the association between thirteen co-morbidities and health status among individuals self-reporting COPD. Adjusted odds ratios (ORs) were generated using ordinal logistic regression. Additionally we evaluated the impact of increasing number of co-morbidities with self-rated health. Eight illnesses had significant associations with worse self-rated health, however after mutually adjusting for these conditions, congestive heart failure (OR 3.07, 95% CI 1.69–5.58), arthritis (OR 1.69, 95% CI 1.13–2.52), diabetes (OR 1.63, 95% CI 1.01–2.64), and incontinence/prostate disease (OR 1.63, 95% CI 1.01–2.62) remained independent predictors of self-rated health. Each increase in co-morbidities was associated with a 43% higher chance of worse self-rated health (95% CI 1.27-1.62). Individuals with COPD have a substantial burden of co-morbidity, which is associated with worse self-rated health. CHF, arthritis, diabetes and incontinence/prostate disease have the most impact on self-rated health. Targeting these co-morbidities in COPD may result in improved self-rated health.
Manipulation of oxidative protein folding and PDI redox state in mammalian cells

In the endoplasmic reticulum (ER), disulfide bonds are simultaneously formed in nascent proteins and removed from incorrectly folded or assembled molecules. In this compartment, the redox state must be, therefore, precisely regulated. Here we show that both human Ero1‐Lα and Ero1‐Lβ (hEROs) facilitate disulfide bond formation in immunoglobulin subunits by selectively oxidizing PDI. Disulfide bond formation is controlled by hEROs, which stand at a crucial point of an electron‐flow starting from nascent secretory proteins and passing through PDI. The redox state of ERp57, another ER‐resident oxidoreductase, is not affected by over‐expression of Ero1‐Lα, suggesting that parallel and specific pathways control oxidative protein folding in the ER. Mutants in the Ero1‐Lα CXXCXXC motif act as dominant negatives by limiting immunoglobulin oxidation. PDI‐dependent oxidative folding in living cells can thus be manipulated by using hERO variants.
Expression of neutral endopeptidase (NEP/CD10) on pancreatic tumor cell lines, pancreatitis and pancreatic tumor tissues

Neutral endopeptidase (NEP/CD10) is a cell surface zinc metalloprotease cleaving peptide bounds on the amino terminus of hydrophobic amino acids and inactivating multiple physiologically active peptides. Loss or decrease in NEP/CD10 expression have been reported in many types of malignancies, but the role of NEP/CD10 in pancreatic carcinoma has not yet been identified. Using real‐time RT‐PCR, flow cytometry as well as immunohistochemistry, NEP/CD10 expression was quantified in both pancreatic carcinoma cell lines and in tumor specimens obtained from patients with primary pancreatic carcinomas. Three out of 8 pancreatic carcinoma cell lines exhibit heterogeneous NEP/CD10 expression levels: PATU‐8988T expressed the highest NEP/CD10 levels, whereas HUP‐T4 and HUP‐T3 cells showed a moderate to low NEP/CD10 expression. NEP/CD10 immunoreactivity was found in 6 of 24 pancreatic ductal adenocarcinomas, but also in 3 of 6 tissues of patients with chronic pancreatitis. NEP/CD10 expression in pancreatic tumor lesions and cell lines was not associated with tumor grading and staging. Treatment of PATU‐8988T cells with the histone deacetylase inhibitors sodium butyrate and valproic acid induced an increase of NEP/CD10 expression. This was accompanied by a reduced cell proliferation rate of PATU‐8988T cells, which was increased by the addition of the enzyme activity inhibitors phosphoramidon and thiorphan. Thus, NEP/CD10 is differentially expressed in pancreatic tumors and might be involved in the proliferative activity of pancreatic cancer cells. However, further studies are needed to provide more detailed information of the role of NEP/CD10 under physiological and pathophysiological conditions of the pancreas. © 2007 Wiley‐Liss, Inc.
Safety of sentinel node biopsy in breast cancer patients who receive a second radioisotope injection after visualization failure in lymphoscintigraphy

A failure to visualize axillary sentinel nodes in lymphoscintigraphy may lead to an unsuccessful sentinel node biopsy (SNB) and subsequent axillary lymph node dissection (ALND). To avoid unnecessary ALND, a second radioisotope injection may be given but has been considered hazardous. We investigated the axillary recurrence rate after tumor‐negative SNB in breast cancer patients who received a second tracer injection after axillary visualization failure in lymphoscintigraphy.
Anti‐homeostatic synaptic plasticity of glycine receptor function after chronic strychnine in developing cultured mouse spinal neurons

In this study, we describe a novel form of anti‐homeostatic plasticity produced after culturing spinal neurons with strychnine, but not bicuculline or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX). Strychnine caused a large increase in network excitability, detected as spontaneous synaptic currents and calcium transients. The calcium transients were associated with action potential firing and activation of γ‐aminobutyric acid (GABAA) and alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptors as they were blocked by tetrodotoxin (TTX), bicuculline, and CNQX. After chronic blockade of glycine receptors (GlyRs), the frequency of synaptic transmission showed a significant enhancement demonstrating the phenomenon of anti‐homeostatic plasticity. Spontaneous inhibitory glycinergic currents in treated cells showed a fourfold increase in frequency (from 0.55 to 2.4 Hz) and a 184% increase in average peak amplitude compared with control. Furthermore, the augmentation in excitability accelerated the decay time constant of miniature inhibitory post‐synaptic currents. Strychnine caused an increase in GlyR current density, without changes in the apparent affinity. These findings support the idea of a post‐synaptic action that partly explains the increase in synaptic transmission. This phenomenon of synaptic plasticity was blocked by TTX, an antibody against brain‐derived neurotrophic factor (BDNF) and K252a suggesting the involvement of the neuronal activity‐dependent BDNF‐TrkB signaling pathway. These results show that the properties of GlyRs are regulated by the degree of neuronal activity in the developing network.