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"Russell, Bruce"
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Is it still cheating if I don't get caught?
Presents five ethical principles that can provide the basis for discussion and solutions for handling school, sports, Internet, or family situations that involve cheating. Includes an index of dilemmas.
Book
A Dilemma for Sterba
James Sterba argues that a good God is not logically possible. He argues that what he calls the Pauline Principle, which says that we should never do evil that good may come of it, implies that a good God would prevent horrendous evil consequences of immoral actions. However, there are plenty of examples of such actions in our world. So, a good God does not exist. I offer an example from Derek Parfit, and one of my own, that calls the Pauline Principle into question. Sterba believes that what he calls Moral Evil Prevention Requirements (MEPRs) follow from the Pauline Principle, and that they are necessary truths which imply that a good God would prevent horrendous evil consequences of immoral actions. Whether these (MEPRs) follow from the Pauline Principle or do not, they may be necessary truths that could form the basis of Sterba’s argument. However, I argue that they are not necessary truths. If modified to become such, Sterba faces a challenge from the Skeptical Theists that can only be met by turning his argument into an evidential version of the problem of evil. I compare Sterba’s argument with my version of the evidential argument from evil that says that if God exists, there is not excessive, unnecessary suffering and whose second premise says there is. I argue that it is easier to establish that there is excessive, unnecessary suffering than to establish Sterba’s second premise (once his principles are modified). That second premise will say that there are no goods that logically require God to allow immoral actions that have horrendous evil consequences. Sterba faces a dilemma: either he has an unsound logical argument or a weak evidential argument for the non-existence of God. In either case, he does not have a good logical argument for atheism.
Journal Article
Ethics and Theism
In this essay I argue that there are necessarily true synthetic a priori moral propositions whose truth does not depend on the existence of God. To make my case, I appeal to an analogy with arithmetic truths such as 2 + 2 = 4 whose truth does not depend on the existence of God. I criticize views like Peter Railton’s that hold that moral truths are like truths about natural kinds such as water and heat, and non-cognitivists who hold that there are no robust moral truths. The point of my criticisms is to answer challenges to my view that there are necessarily true synthetic a priori moral propositions and, in the case of Railton, to block an argument by Robert Adams for a Divine Command Theory of ethics. Second, I argue by example that there can be conflicts between what is best for me and those for whom I care and what is morally required that cannot be reconciled by a theistic ethics. It can be rational to violate moral requirements that have the same contents as the commands of a loving God even if there would be most reason to adhere to those requirements IF God exists, just as it can be rational to leave your umbrella at home even if there would be most reason to take it IF it rained. This will be true regardless of whether the reason to adhere to God’s commands, IF God exists, is because our greatest good is the love of God (and that requires adhering to his commands) or because God will punish you if you do not and reward you if you do. The problem of evil is the primary reason to believe that God does not exist, and so to believe that there are no divine commands that there would be most reason to follow if God did exist.
Journal Article
Evaluating employee performance through Christian virtues
In this book the authors create a statistically validated scale measuring the display of each of the nine fruit of the spirit in employees. The authors will discuss how biblical values are applicable to contemporary organizational leadership and management. These nine virtues span a wide breadth of important personal and organizational attributes including benevolence, affection, gladness, relational harmony, tranquility, perseverance, helpfulness, caring for the welfare of others, adherence to the beliefs and value of others, power used soberly, and mastering one's desires. While diverse in nature, the list also suggests a holistic development of personal and organizational character. Understanding the manner in which these traits can be measured will be a significant benefit to HRM and HRD scholars conducting research in Christian servant leadership.
Book
Variability and magnitude of brain glutamate levels in schizophrenia: a meta and mega-analysis
Glutamatergic dysfunction is implicated in schizophrenia pathoaetiology, but this may vary in extent between patients. It is unclear whether inter-individual variability in glutamate is greater in schizophrenia than the general population. We conducted meta-analyses to assess (1) variability of glutamate measures in patients relative to controls (log coefficient of variation ratio: CVR); (2) standardised mean differences (SMD) using Hedges g; (3) modal distribution of individual-level glutamate data (Hartigan’s unimodality dip test). MEDLINE and EMBASE databases were searched from inception to September 2022 for proton magnetic resonance spectroscopy (1H-MRS) studies reporting glutamate, glutamine or Glx in schizophrenia. 123 studies reporting on 8256 patients and 7532 controls were included. Compared with controls, patients demonstrated greater variability in glutamatergic metabolites in the medial frontal cortex (MFC, glutamate: CVR = 0.15,
p
< 0.001; glutamine: CVR = 0.15,
p
= 0.003; Glx: CVR = 0.11,
p
= 0.002), dorsolateral prefrontal cortex (glutamine: CVR = 0.14,
p
= 0.05; Glx: CVR = 0.25,
p
< 0.001) and thalamus (glutamate: CVR = 0.16,
p
= 0.008; Glx: CVR = 0.19,
p
= 0.008). Studies in younger, more symptomatic patients were associated with greater variability in the basal ganglia (BG glutamate with age:
z
= −0.03,
p
= 0.003, symptoms:
z
= 0.007,
p
= 0.02) and temporal lobe (glutamate with age:
z
= −0.03,
p
= 0.02), while studies with older, more symptomatic patients associated with greater variability in MFC (glutamate with age:
z
= 0.01,
p
= 0.02, glutamine with symptoms:
z
= 0.01,
p
= 0.02). For individual patient data, most studies showed a unimodal distribution of glutamatergic metabolites. Meta-analysis of mean differences found lower MFC glutamate (
g
= −0.15,
p
= 0.03), higher thalamic glutamine (
g
= 0.53,
p
< 0.001) and higher BG Glx in patients relative to controls (
g
= 0.28,
p
< 0.001). Proportion of males was negatively associated with MFC glutamate (
z
= −0.02,
p
< 0.001) and frontal white matter Glx (
z
= −0.03,
p
= 0.02) in patients relative to controls. Patient PANSS total score was positively associated with glutamate SMD in BG (
z
= 0.01,
p
= 0.01) and temporal lobe (
z
= 0.05,
p
= 0.008). Further research into the mechanisms underlying greater glutamatergic metabolite variability in schizophrenia and their clinical consequences may inform the identification of patient subgroups for future treatment strategies.
Journal Article
Sticking for a Cause: The Falciparum Malaria Parasites Cytoadherence Paradigm
After a successful invasion, malaria parasite
extensively remodels the infected erythrocyte cellular architecture, conferring cytoadhesive properties to the infected erythrocytes. Cytoadherence plays a central role in the parasite's immune-escape mechanism, at the same time contributing to the pathogenesis of severe falciparum malaria. In this review, we discuss the cytoadhesive interactions between
infected erythrocytes and various host cell types, and how these events are linked to malaria pathogenesis. We also highlight the limitations faced by studies attempting to correlate diversity in parasite ligands and host receptors with the development of severe malaria.
Journal Article
Glutamatergic Neurometabolites in Clozapine-Responsive and -Resistant Schizophrenia
Background:According to the current schizophrenia treatment guidelines, 3 levels of responsiveness to antipsychotic medication exist: those who respond to first-line antipsychotics, those with treatment-resistant schizophrenia who respond to clozapine, and those with clozapine-resistant or ultra-treatment resistant schizophrenia. Proton magnetic resonance spectroscopy studies indicate that antipsychotic medication decreases glutamate or total glutamate + glutamine in the brains of patients with schizophrenia and may represent a biomarker of treatment response; however, the 3 levels of treatment responsiveness have not been evaluated.Methods:Proton magnetic resonance spectroscopy spectra were acquired at 3 Tesla from patients taking a second generation non-clozapine antipsychotic (first-line responders), patients with treatment-resistant schizophrenia taking clozapine, patients with ultra-treatment resistant schizophrenia taking a combination of antipsychotics, and healthy comparison subjects.Results:Group differences in cerebrospinal fluid-corrected total glutamate + glutamine levels scaled to creatine were detected in the dorsolateral prefrontal cortex [df(3,48); F = 3.07, P = .04, partial η2 = 0.16] and the putamen [df(3,32); F = 2.93, P = .05, partial η2 = 0.22]. The first-line responder group had higher dorsolateral prefrontal cortex total glutamate + glutamine levels scaled to creatine than those with ultra-treatment resistant schizophrenia [mean difference = 0.25, standard error = 0.09, P = .04, family-wise error-corrected]. Those with treatment-resistant schizophrenia had higher total glutamate + glutamine levels scaled to creatine in the putamen than the first-line responders (mean difference = 0.31, standard error = 0.12, P = .05, family-wise error-corrected) and those with ultra-treatment-resistant schizophrenia (mean difference = 0.39, standard error = 0.12, P = .02, family-wise error-corrected).Conclusions:Total glutamate + glutamine levels scaled to creatine in the putamen may represent a marker of response to clozapine. Future studies should investigate glutamatergic anomalies prior to clozapine initiation and following successful treatment.
Journal Article
Right frontal anxiolytic-sensitive EEG ‘theta’ rhythm in the stop-signal task is a theory-based anxiety disorder biomarker
Psychiatric diagnoses currently rely on a patient’s presenting symptoms or signs, lacking much-needed theory-based biomarkers. Our neuropsychological theory of anxiety, recently supported by human imaging, is founded on a longstanding, reliable, rodent ‘theta’ brain rhythm model of human clinical anxiolytic drug action. We have now developed a human scalp EEG homolog—goal-conflict-specific rhythmicity (GCSR), i.e., EEG rhythmicity specific to a balanced conflict between goals (e.g., approach-avoidance). Critically, GCSR is consistently reduced by different classes of anxiolytic drug and correlates with clinically-relevant trait anxiety scores (STAI-T). Here we show elevated GCSR in student volunteers divided, after testing, on their STAI-T scores into low, medium, and high (typical of clinical anxiety) groups. We then tested anxiety disorder patients (meeting diagnostic criteria) and similar controls recruited separately from the community. The patient group had higher average GCSR than their controls—with a mixture of high and low GCSR that varied with, but cut across, conventional disorder diagnosis. Consequently, GCSR scores should provide the first theoretically-based biomarker that could help diagnose, and so redefine, a psychiatric disorder.
Journal Article
Evaluation of splenic accumulation and colocalization of immature reticulocytes and Plasmodium vivax in asymptomatic malaria: A prospective human splenectomy study
A very large biomass of intact asexual-stage malaria parasites accumulates in the spleen of asymptomatic human individuals infected with Plasmodium vivax. The mechanisms underlying this intense tropism are not clear. We hypothesised that immature reticulocytes, in which P. vivax develops, may display high densities in the spleen, thereby providing a niche for parasite survival.
We examined spleen tissue in 22 mostly untreated individuals naturally exposed to P. vivax and Plasmodium falciparum undergoing splenectomy for any clinical indication in malaria-endemic Papua, Indonesia (2015 to 2017). Infection, parasite and immature reticulocyte density, and splenic distribution were analysed by optical microscopy, flow cytometry, and molecular assays. Nine non-endemic control spleens from individuals undergoing spleno-pancreatectomy in France (2017 to 2020) were also examined for reticulocyte densities. There were no exclusion criteria or sample size considerations in both patient cohorts for this demanding approach. In Indonesia, 95.5% (21/22) of splenectomy patients had asymptomatic splenic Plasmodium infection (7 P. vivax, 13 P. falciparum, and 1 mixed infection). Significant splenic accumulation of immature CD71 intermediate- and high-expressing reticulocytes was seen, with concentrations 11 times greater than in peripheral blood. Accordingly, in France, reticulocyte concentrations in the splenic effluent were higher than in peripheral blood. Greater rigidity of reticulocytes in splenic than in peripheral blood, and their higher densities in splenic cords both suggest a mechanical retention process. Asexual-stage P. vivax-infected erythrocytes of all developmental stages accumulated in the spleen, with non-phagocytosed parasite densities 3,590 times (IQR: 2,600 to 4,130) higher than in circulating blood, and median total splenic parasite loads 81 (IQR: 14 to 205) times greater, accounting for 98.7% (IQR: 95.1% to 98.9%) of the estimated total-body P. vivax biomass. More reticulocytes were in contact with sinus lumen endothelial cells in P. vivax- than in P. falciparum-infected spleens. Histological analyses revealed 96% of P. vivax rings/trophozoites and 46% of schizonts colocalised with 92% of immature reticulocytes in the cords and sinus lumens of the red pulp. Larger splenic cohort studies and similar investigations in untreated symptomatic malaria are warranted.
Immature CD71+ reticulocytes and splenic P. vivax-infected erythrocytes of all asexual stages accumulate in the same splenic compartments, suggesting the existence of a cryptic endosplenic lifecycle in chronic P. vivax infection. Findings provide insight into P. vivax-specific adaptions that have evolved to maximise survival and replication in the spleen.
Journal Article