First measurement of the 14N/15N ratio in the analogue of the Sun progenitor OMC-2 FIR4

We present a complete census of the 14N/15N isotopic ratio in the most abundant N-bearing molecules towards the cold envelope of the protocluster OMC-2 FIR4, the best known Sun progenitor. To this scope, we analysed the unbiased spectral survey obtained with the IRAM-30m telescope at 3mm, 2mm and 1mm. We detected several lines of CN, HCN, HNC, HC3N, N2H+, and their respective 13C and 15N isotopologues. The lines relative fluxes are compatible with LTE conditions and moderate line opacities have been corrected via a Population Diagram method or theoretical relative intensity ratios of the hyperfine structures. The five species lead to very similar 14N/15N isotopic ratios, without any systematic difference between amine and nitrile bearing species as previously found in other protostellar sources. The weighted average of the 14N/15N isotopic ratio is 270 +/- 30. This 14N/15N value is remarkably consistent with the [250-350] range measured for the local galactic ratio but significantly differs from the ratio measured in comets (around 140). High-angular resolution observations are needed to examine whether this discrepancy is maintained at smaller scales. In addition, using the CN, HCN and HC3N lines, we derived a 12C/13C isotopic ratio of 50 +/- 5.Comment: Accepted for publication in ApJ ; 19 pages, 5 tables, 12 figure

Deedle Deedle Dum

https://digitalcommons.library.umaine.edu/mmb-vp/1294/thumbnail.jp

Virology under the microscope-A call for rational discourse

Viruses have brought humanity many challenges: respiratory infection, cancer, neurological impairment and immunosuppression to name a few. Virology research over the last 60+ years has responded to reduce this disease burden with vaccines and antivirals. Despite this long history, the COVID-19 pandemic has brought unprecedented attention to the field of virology. Some of this attention is focused on concern about the safe conduct of research with human pathogens. A small but vocal group of individuals has seized upon these concerns - conflating legitimate questions about safely conducting virus-related research with uncertainties over the origins of SARS-CoV-2. The result has fueled public confusion and, in many instances, ill-informed condemnation of virology. With this article, we seek to promote a return to rational discourse. We explain the use of gain-of-function approaches in science, discuss the possible origins of SARS-CoV-2 and outline current regulatory structures that provide oversight for virological research in the United States. By offering our expertise, we - a broad group of working virologists - seek to aid policy makers in navigating these controversial issues. Balanced, evidence-based discourse is essential to addressing public concern while maintaining and expanding much-needed research in virology

Essential evidence for guiding health system priorities and policies: anticipating epidemiological transition in Africa

KIMBACKGROUND: Despite indications that infection-related mortality in sub-Saharan Africa may be decreasing and the burden of non-communicable diseases increasing, the overwhelming reality is that health information systems across most of sub-Saharan Africa remain too weak to track epidemiological transition in a meaningful and effective way. PROPOSALS: We propose a minimum dataset as the basis of a functional health information system in countries where health information is lacking. This would involve continuous monitoring of cause-specific mortality through routine civil registration, regular documentation of exposure to leading risk factors, and monitoring effective coverage of key preventive and curative interventions in the health sector. Consideration must be given as to how these minimum data requirements can be effectively integrated within national health information systems, what methods and tools are needed, and ensuring that ethical and political issues are addressed. A more strategic approach to health information systems in sub-Saharan African countries, along these lines, is essential if epidemiological changes are to be tracked effectively for the benefit of local health planners and policy makers. CONCLUSION: African countries have a unique opportunity to capitalize on modern information and communications technology in order to achieve this. Methodological standards need to be established and political momentum fostered so that the African continent's health status can be reliably tracked. This will greatly strengthen the evidence base for health policies and facilitate the effective delivery of services

Impact of stress, fear and anxiety on the nociceptive responses of larval zebrafish

Both adult and larval zebrafish have been demonstrated to show behavioural responses to noxious stimulation but also to potentially stress- and fear or anxiety- eliciting situations. The pain or nociceptive response can be altered and modulated by these situations in adult fish through a mechanism called stress-induced analgesia. However, this phenomenon has not been described in larval fish yet. Therefore, this study explores the behavioural changes in larval zebrafish after noxious stimulation and exposure to challenges that can trigger a stress, fear or anxiety reaction. Five-day post fertilization zebrafish were exposed to either a stressor (air emersion), a predatory fear cue (alarm substance) or an anxiogenic (caffeine) alone or prior to immersion in acetic acid 0.1%. Pre- and post-stimulation behaviour (swimming velocity and time spent active) was recorded using a novel tracking software in 25 fish at once. Results show that larvae reduced both velocity and activity after exposure to the air emersion and alarm substance challenges and that these changes were attenuated using etomidate and diazepam, respectively. Exposure to acetic acid decreased velocity and activity as well, whereas air emersion and alarm substance inhibited these responses, showing no differences between pre- and post-stimulation. Therefore, we hypothesize that an antinociceptive mechanism, activated by stress and/or fear, occur in 5dpf zebrafish, which could have prevented the larvae to display the characteristic responses to pain

The Impact of Ventilation on the Development of Brain Injury in Asphyxiated Newborns Treated with Hypothermia

Birth asphyxia and the resulting neonatal encephalopathy are a significant cause of mortality and long-term morbidity in children. Hypothermia is currently the only neuroprotective treatment to have been clinically tested in large trials to prevent the development of brain injury in some term asphyxiated newborns. Most of the asphyxiated newborns treated with hypothermia are intubated at birth as per resuscitation measures and remain on mechanical ventilation during some part of the hypothermia treatment or during the whole length of the treatment. They also may present with oxygenation problems. Very often, they present with hypocapnia that can be worsened with the use of mechanical ventilation during the first days of life. When taking care of these newborns, a few important points should be remembered about the impact of asphyxia and therapeutic hypothermia on oxygenation and ventilation. In this article, we review some of the physiopathology behind neonatal encephalopathy and the implications of brain cooling from a respiratory point of view. Strategies to optimize oxygenation and ventilation for these newborns, as well as to prevent further brain injury, are also discussed based on a current literature review

The Role of Oral Microbiota in Periodontitis and Alzheimer\u27s Disease

Background: Periodontal disease (PD), affecting 20-50% of the global population is marked by biofilm-induced inflammation in oral tissues. Chronic PD results in systemic complications such as heart disease, stroke, and Alzheimer\u27s. The red complex microbes, Porphyromonas gingivalis and Treponema denticola, play a pivotal role, penetrating the blood-brain barrier and contributing to neurodegeneration. Alzheimer\u27s disease (AD), an irreversible neurodegenerative disorder, is linked to abnormal protein cleavage and potentially involves microbiologic components, including gram-positive cocci. Research suggests the presence of bacteria such as Porphyromonas, Actinomyces, and Treponema in autopsied AD brains. Investigating the microbiologic connection between PD and AD is crucial, considering the potential neuroanatomic pathways and enhanced neurotropism exhibited by specific microbes. This exploration is vital for identifying interventions that could mitigate the severity of these prevalent global conditions, addressing the substantial burden they impose on the population. Methods: A comprehensive systematic review from 2010 to 2023 was conducted across electronic databases like PubMed, PLOS ONE, Nature, Springer, and Sage. The search strategy used keywords related to Porphyromonas gingivalis, Treponema denticola, periodontal disease, and “oral pathogens in neurocognitive disorders.” Inclusion criteria considered peer-reviewed English studies investigating the pathogens or the P. gingivalis and T. denticola relationship in Alzheimer\u27s disease (AD), encompassing both in vitro and in vivo research. Excluded were non-peer-reviewed, case reports, reviews, commentaries, and non-English studies. Two independent reviewers screened titles and abstracts, followed by a full-text review of relevant articles. Data extraction included authors, publication year, sample size, methods, findings, tables, figures, and conclusions. The review adhered to PRISMA guidelines, ensuring transparency and comprehensiveness in reporting the research process and findings. Ethical considerations were unnecessary, given the reliance on publicly available data from previously published studies. Results: Multiple clinical studies establish a link between periodontitis and Alzheimer\u27s disease (AD). Red complex pathogens, P. gingivalis and T. denticola, can move from the oral cavity to the brain through inflammation. T. denticola is associated with increased neuronal apoptosis by down-regulating key proteins combating Aβ accumulation in the hippocampi. Additionally, it may induce Aβ accumulation and cause neuronal apoptosis through mitochondrial pathways. However, further research is needed to confirm this. P. gingivalis can enter the brain, causing inflammation and subsequent neuron degeneration. Both pathogens increase Aβ accumulation in the hippocampi, but P. gingivalis also induces increased production of NFTs and neuron loss. Conclusions: In conclusion, the collective evidence from multiple clinical studies solidly establishes a compelling link between periodontitis and Alzheimer\u27s disease (AD). The red complex pathogens, namely P. gingivalis and T. denticola, demonstrate a capacity to traverse from the oral cavity to the brain, propelled by inflammation. T. denticola\u27s association with heightened neuronal apoptosis, particularly through the down-regulation of crucial proteins combatting Aβ accumulation in the hippocampi, suggests a potential mechanistic role. Although further research is imperative to corroborate these findings, the observed cognitive impairment in severe periodontitis patients being three times greater than those with mild or no periodontitis suggests that both pathogens, through their synergistic action, exacerbate AD development by enhancing inflammation

Singular Character of Critical Points in Nuclei

The concept of critical points in nuclear phase transitional regions is discussed from the standpoints of Q-invariants, simple observables and wave function entropy. It is shown that these critical points very closely coincide with the turning points of the discussed quantities, establishing the singular character of these points in nuclear phase transition regions between vibrational and rotational nuclei, with a finite number of particles.Comment: 12 pages, 7 figures, elsart, revised version, considerable changes and addition

Astrocytes Infected with Chlamydia Pneumoniae Demonstrate Altered Expression and Activity of Secretases Involved in the Generation of Β-amyloid Found in Alzheimer Disease

BACKGROUND: Epidemiologic studies strongly suggest that the pathophysiology of late-onset Alzheimer disease (AD) versus early-onset AD has environmental rather than genetic causes, thus revealing potentially novel therapeutic targets to limit disease progression. Several studies supporting the pathogen hypothesis of AD demonstrate a strong association between pathogens and the production of β-amyloid, the pathologic hallmark of AD. Although the mechanism of pathogen-induced neurodegeneration of AD remains unclear, astrocytes, a key player of the CNS innate immune response and producer/metabolizer of β-amyloid, have been implicated. We hypothesized that Chlamydia pneumoniae infection of human astrocytes alters the expression of the amyloid precursor protein (APP)-processing secretases, ADAM10, BACE1, and PSEN1, to promote β-amyloid formation. Utilizing immunofluorescent microscopy, molecular, and biochemical approaches, these studies explore the role of an intracellular respiratory pathogen, Chlamydia pneumoniae, as an environmental trigger for AD pathology. Human astrocytoma cells in vitro were infected with Chlamydia pneumoniae over the course of 6-72 h. The gene and protein expression, as well as the enzymatic activity of non-amyloidogenic (ADAM10), and pro-amyloidogenic (BACE1 and PSEN1) secretases were qualitatively and quantitatively assessed. In addition, the formation of toxic amyloid products as an outcome of pro-amyloidogenic APP processing was evaluated through various modalities. RESULTS: Chlamydia pneumoniae infection of human astrocytoma cells promoted the transcriptional upregulation of numerous genes implicated in host neuroinflammation, lipid homeostasis, microtubule function, and APP processing. Relative to that of uninfected astrocytes, BACE1 and PSEN1 protein levels were enhanced by nearly twofold at 48-72 h post-Chlamydia pneumoniae infection. The processing of APP in Chlamydia pneumoniae-infected astrocytes favors the pro-amyloidogenic pathway, as demonstrated by an increase in enzymatic activity of BACE1, while that of ADAM10 was decreased. Fluorescence intensity of β-amyloid and ELISA-quantified levels of soluble-APP by products revealed temporally similar increases, confirming a BACE1/PSEN1-mediated processing of APP. CONCLUSIONS: Our findings suggest that Chlamydia pneumoniae infection of human astrocytes promotes the pro-amyloidogenic pathway of APP processing through the upregulation of expression and activity of β-secretase, upregulated expression of γ-secretase, and decreased activity of α-secretase. These effects of astrocyte infection provide evidence for a direct link between Chlamydia pneumoniae and AD pathology

Report on OTHER proposals for SSPEX

The only unifying factor among the experiments discussed is that they are all unique Opportunities and/or Techniques for High-caliber Experimental Research (OTHER). Thirteen of the experiments are briefly described