Negotiation of software requirements in an asynchronous collaborative environment

The effect of task structure and negotiation sequence on collaborative software requirements negotiation is investigated. This work began with an extensive literature review that focused on current research in collaborative software engineering and, in particular, on the negotiation of software requirements and the requisite collaboration for the development of such requirements. A formal detailed experiment was then conducted to evaluate the effects of negotiation sequence and task structure in an asynchronous group meeting environment. The experiment tested the impact of these structures on groups negotiating the requirements for an emergency response information system. The results reported here show that these structures can have a positive impact on solution quality but a negative impact on process satisfaction, although following a negotiation sequence and task structure can help asynchronous groups come to agreement faster. Details of the experimental procedures, statistical analysis, and discussion of the results of the experiment are also presented, as are suggestions for improving this work and a plan for future research

Handcrafting Attachment: A User-Centered Approach

Management, above all, is the controlling element responsible for coordinating the three basic business functions; production, marketing, and finance. Mechanisms exist to facilitate the finance function with influence coming from outside regulatory bodies such as the AICPA, IIA, SEC, and other regulators. Integrating the finance function into organizations, then, becomes somewhat generic (although some would argue this point). Coordinating the functions of marketing and production is a much more difficult endeavor because it lacks the standardization seen in finance. This paper suggests employing a more user-focused approach as a means to improving the overall quality of products, and eventually, the success of the organization. Specifically, this paper explores the role of the human brain in the calculus of choice, discusses the role of consumer involvement as it leads to product attachment, and offers suggestions for employing contextual research to improve product design and quality

The Usage of Skeletal Muscle Oxygenation and Heart Rate Variability as Predictors of Aerobic Fitness.

Heart rate variability (HRV) is used to assess the autonomic nervous system’s (ANS) activity on the heart, while skeletal muscle oxygenation (SmO2) measures how well muscles uptake oxygen from the blood. Both measurements have demonstrated strong associations with cardiorespiratory fitness and are altered with increased exercise workloads. Both have been used to assess athletic performance. While the gold standard for assessing cardiorespiratory fitness is VO2 max testing, several situations preclude the usage of a true VO2 max. Purpose: To determine if HRV and SmO2 possess predictive qualities to accurately assess cardiorespiratory fitness levels. Methods: Thirty-six healthy fit individuals (n = 22 men; n = 14 women; age 37.6 + 12.4 yr; BF% 19.2 + 7.1%; VO2max 41.8 + 7.4 ml/kg/min) completed a single VO2 max ramp protocol treadmill test while wearing an infrared oxyhemoglobin (MOXY) Sensor to assess SmO2 while HRV was assessed via Polar (Bluetooth monitor (Polar H7)) heart rate (HR) monitor. The MOXY Sensor was placed on the lateral-posterior belly of the gastrocnemius while the Polar HR monitor was placed on the distal third of the sternum using an elastic belt. The data was analyzed using a Pearson Correlation to compare SmO2, HRV indices, and VO2max associations. In addition, a multiple linear regression analysis was performed to examine the relationship between HRV indices and SmO2 to VO2 max. All analyses were performed using SPSS (v. 28.0.1.1). Results: There was a significant correlation between VO2 max, mean of RR intervals (mRR) (r = 0.440, p = 0.007), and THb Max (r = 0.509, p = 0.002). mRR and THb Max were able to significantly predictive (r2 = 0.365, p = 0.001) VO2 max outcomes. Conclusion: The combination of SmO2 measurements and HRV can assist in predicting VO2 max levels, but further research is needed to determine the accuracy at which it will predict. This can be a useful and simple method for predicting cardiorespiratory fitness when a VO2 max test is unavailable, or an individual is unfit to perform one. This can aid in better exercise prescription for chronic diseased individuals

The Influence of Age and Cardiorespiratory Fitness on Cardiac Autonomic Modulation. A Pilot Study.

Maximal rate of oxygen consumption (VO2max) is traditionally viewed as the gold standard of determining cardiorespiratory fitness (CF) in healthy and diseased populations. CF has a significant influence on the improvement of cardiac autonomic modulation (CAM) and the risk of morbidity and mortality rates. Heart rate variability (HRV) is a non-invasive way to assess CAM. Age is another factor that influences CAM and CF in healthy and diseased populations. However, what is not fully elucidated, is if CF is maintained at a high level throughout adulthood, will CAM remain relatively unchanged. PURPOSE: To determine if age and CF are significantly correlated to variables of HRV to determine CAM in healthy fit individuals. METHODS: Twenty-two healthy individuals (n = 14 male; n = 8 female, Age 33.2 ± 11.8 years, %BF 18.3 ± 6.0, VO2max 42.0 ± 6.2 ml/ /kg/min) completed a single health assessment to quantify CF and HRV. HRV was measured for 5 mins in the supine position and during a standard VO2max test using an elastic belt and Bluetooth monitor (Polar H7). CardioMood software was used to process HRV variables high frequency (HF), low frequency (LF), total power (TP) were assessed for frequency domain, and standard deviation of all NN intervals (SDNN) and the square root of the mean of the squares of successive R-R interval differences (RMSSD) for the time domain. Pearson correlation was used to check associations between age and CF, and CAM. Multiple regression was implemented to determine if there were any differences in HRV variables in relation to age and VO2max. A paired sample t-test was used to determine changes in HRV variables from rest to VO2max. All analyses were performed using SAS (v.9.3). RESULTS: HRV variables were significantly altered from rest to VO2max (p \u3c 0.05). HRV time and frequency domain variables were not significantly correlated to age and CF level (p \u3e 0.05). The multiple regression analysis indicated that the only significance was max heart rate is 0.642 bpm lower during exercise for each 1-year increase in age (p = 0.035). CONCLUSION: The analysis of pilot data focused on determining the impact of CF and age on CAM appears not to be significantly correlated when utilizing HRV. However, due to the project\u27s continuation and further data collection, significant outcomes may still be observed

All the Brain\u27s a Stage for Serotonin: The Forgotten Story of Serotonin Diffusion across Cell Membranes

In the conventional model of serotonin neurotransmission, serotonin released by neurons in the midbrain raphe nuclei exerts its actions on forebrain neurons by interacting with a large family of post-synaptic receptors. The actions of serotonin are terminated by active transport of serotonin back into the releasing neuron, which is mediated by the serotonin reuptake transporter (SERT). Because SERT is expressed pre-synaptically and is widely thought to be the only serotonin transporter in the forebrain, the conventional model does not include serotonin transport into post-synaptic neurons. However, a large body of evidence accumulating since the 1970s has shown that serotonin, despite having a positive charge, can cross cell membranes through a diffusion-like process. Multiple low-affinity, high-capacity, sodium-independent transporters, widely expressed in the brain, allow the carrier-mediated diffusion of serotonin into forebrain neurons. The amount of serotonin crossing cell membranes through this mechanism under physiological conditions is considerable. Most prominent textbooks fail to include this alternative method of serotonin uptake in the brain, and even most neuroscientists are unaware of it. This failure has limited our understanding of a key regulator of serotonergic neurotransmission, impeded research on the potential intracellular actions of serotonin in post-synaptic neurons and glial cells, and may have impeded our understanding of the mechanism by which antidepressant medications reduce depressive symptoms

Parent-mediated social communication therapy for young children with autism (PACT):long-term follow-up of a randomised controlled trial

SummaryBackgroundIt is not known whether early intervention can improve long-term autism symptom outcomes. We aimed to follow-up the Preschool Autism Communication Trial (PACT), to investigate whether the PACT intervention had a long-term effect on autism symptoms and continued effects on parent and child social interaction.MethodsPACT was a randomised controlled trial of a parent-mediated social communication intervention for children aged 2–4 years with core autism. Follow-up ascertainment was done at three specialised clinical services centres in the UK (London, Manchester, and Newcastle) at a median of 5·75 years (IQR 5·42–5·92) from the original trial endpoint. The main blinded outcomes were the comparative severity score (CSS) from the Autism Diagnostic Observation Schedule (ADOS), the Dyadic Communication Assessment Measure (DCMA) of the proportion of child initiatiations when interacting with the parent, and an expressive-receptive language composite. All analyses followed the intention-to-treat principle. PACT is registered with the ISRCTN registry, number ISRCTN58133827.Findings121 (80%) of the 152 trial participants (59 [77%] of 77 assigned to PACT intervention vs 62 [83%] of 75 assigned to treatment as usual) were traced and consented to be assessed between July, 2013, and September, 2014. Mean age at follow-up was 10·5 years (SD 0·8). Group difference in favour of the PACT intervention based on ADOS CSS of log-odds effect size (ES) was 0·64 (95% CI 0·07 to 1·20) at treatment endpoint and ES 0·70 (95% CI −0·05 to 1·47) at follow-up, giving an overall reduction in symptom severity over the course of the whole trial and follow-up period (ES 0·55, 95% CI 0·14 to 0·91, p=0·004). Group difference in DCMA child initiations at follow-up showed a Cohen's d ES of 0·29 (95% CI −0.02 to 0.57) and was significant over the course of the study (ES 0·33, 95% CI 0·11 to 0·57, p=0·004). There were no group differences in the language composite at follow-up (ES 0·15, 95% CI −0·23 to 0·53).InterpretationThe results are the first to show long-term symptom reduction after a randomised controlled trial of early intervention in autism spectrum disorder. They support the clinical value of the PACT intervention and have implications for developmental theory.FundingMedical Research Council

Mycobacterium abscessus and Children with Cystic Fibrosis

We prospectively studied 298 patients with cystic fibrosis (mean age 11.3 years; range 2 months to 32 years; sex ratio, 0.47) for nontuberculous mycobacteria in respiratory samples from January 1, 1996, to December 31, 1999. Mycobacterium abscessus was by far the most prevalent nontuberculous mycobacterium: 15 patients (6 male, 9 female; mean age 11.9 years; range 2.5–22 years) had at least one positive sample for this microorganism (versus 6 patients positive for M. avium complex), including 10 with >3 positive samples (versus 3 patients for M. avium complex). The M. abscessus isolates from 14 patients were typed by pulsed-field gel electrophoresis: each of the 14 patients harbored a unique strain, ruling out a common environmental reservoir or person-to-person transmission. Water samples collected in the cystic fibrosis center were negative for M. abscessus. This major mycobacterial pathogen in children and teenagers with cystic fibrosis does not appear to be acquired nosocomially

A monoclonal antibody raised against a thermo-stabilised β1-adrenoceptor interacts with extracellular loop 2 and acts as a negative allosteric modulator of a sub-set of 1- adrenoceptors expressed in stable cell lines

Recent interest has focused on antibodies that can discriminate between different receptor conformations. Here we have characterised the effect of a monoclonal antibody (mAb3), raised against a purified thermo-stabilised turkey β1-adrenoceptor (β1AR-m23 StaR), on β1-ARs expressed in CHO-K1 or HEK 293 cells. Immunohistochemical and radioligand-binding studies demonstrated that mAb3 was able to bind to ECL2 of the tβ1-AR, but not its human homologue. Specific binding of mAb3 to tβ1-AR was inhibited by a peptide based on the turkey, but not the human, ECL2 sequence. Studies with [3H]-CGP 12177 demonstrated that mAb3 prevented the binding of orthosteric ligands to a subset (circa 40%) of turkey 1-receptors expressed in both CHO K1 and HEK 293 cells. MAb3 significantly reduced the maximum specific binding capacity of [3H]-CGP-12177 without influencing its binding affinity. Substitution of ECL2 of tβ1-AR with its human equivalent, or mutation of residues D186S, P187D, Q188E prevented the inhibition of [3H]-CGP 12177 binding by mAb3. MAb3 also elicited a negative allosteric effect on agonist-stimulated cAMP responses. The identity of the subset of turkey β1-adrenoceptors influenced by mAb3 remains to be established but mAb3 should become an important tool to investigate the nature of β1-AR conformational states and oligomeric complexes

Primary Coenzyme Q Deficiency in Pdss2 Mutant Mice Causes Isolated Renal Disease

Coenzyme Q (CoQ) is an essential electron carrier in the respiratory chain whose deficiency has been implicated in a wide variety of human mitochondrial disease manifestations. Its multi-step biosynthesis involves production of polyisoprenoid diphosphate in a reaction that requires the enzymes be encoded by PDSS1 and PDSS2. Homozygous mutations in either of these genes, in humans, lead to severe neuromuscular disease, with nephrotic syndrome seen in PDSS2 deficiency. We now show that a presumed autoimmune kidney disease in mice with the missense Pdss2kd/kd genotype can be attributed to a mitochondrial CoQ biosynthetic defect. Levels of CoQ9 and CoQ10 in kidney homogenates from B6.Pdss2kd/kd mutants were significantly lower than those in B6 control mice. Disease manifestations originate specifically in glomerular podocytes, as renal disease is seen in Podocin/cre,Pdss2loxP/loxP knockout mice but not in conditional knockouts targeted to renal tubular epithelium, monocytes, or hepatocytes. Liver-conditional B6.Alb/cre,Pdss2loxP/loxP knockout mice have no overt disease despite demonstration that their livers have undetectable CoQ9 levels, impaired respiratory capacity, and significantly altered intermediary metabolism as evidenced by transcriptional profiling and amino acid quantitation. These data suggest that disease manifestations of CoQ deficiency relate to tissue-specific respiratory capacity thresholds, with glomerular podocytes displaying the greatest sensitivity to Pdss2 impairment