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Most studies concerning parasitic infections in European bison have been performed on free-ranging animals: comparatively little is known about the abomasal nematodes of captive wisents, which are widely used in reintroduction programmes. The aim of the study was to determine the infection level and species composition of abomasal nematodes in captive European bison in enclosures (including zoos) and breeding centres compared to free-ranging individuals. It also includes a morphological analysis of the parasites based on figures and measurement data. Altogether, 11 species of nematodes were detected, with both captive and free-ranging animals demonstrating similar species compositions. Among those, 2 species of blood-sucking nematodes were detected, including Ashworthius sidemi and Haemonchus contortus. Interestingly, A. sidemi was found in almost all free-roaming animals, but only in 1 captive European bison. In addition, H. contortus was predominant in captive animals. The morphological identification was confirmed molecularly for 5 nematode species: A. sidemi, H. contortus, Ostertagia kolchida, O. ostertagi and Spiculopteragia boehmi. The identification was performed using small subunit ribosomal rDNA. The study provides the first available set of specular lengths of the gastric nematodes of European bison, and the first molecular data of O. kolchida and S. boehmi derived from the same host species. Our findings may simplify the morphometrical and molecular identification of Trichostrongylidae species infecting European bison, and can be useful in developing new management strategies for populations of this near-threatened species in Europe.
We conducted a retrospective, analytical cross-sectional and single-centre study that included 190 hospitalised COVID-19 patients in the Fujian Provincial Hospital South Branch between December 2022 and January 2023 to analyse the correlation of viral loads of throat swabs with clinical progression and outcomes. To normalise the Ct value as quantification of viral loads, we used RNase P gene as internal control gene and subtracted the Ct value of SARS-CoV-2 N gene from the Ct value of RNase P gene, termed △Ct. Most patients were discharged (84.2%), and only 10 (5.6%) individuals who had a lower △Ct value died. The initial △Ct value of participants was also significantly correlated with some abnormal laboratory characteristics, and the duration time of SARS-CoV-2 was longer in patients with severe symptoms and a lower △Ct value at admission. Our study suggested that the △Ct value may be used as a predictor of disease progression and outcomes in hospitalised COVID-19 patients.
How does a person curious about or wanting to do science learn it? The thesis of this book is learning science requires not only digging deeply into the subject but learning how to learn. It is not enough to learn facts about the history of science or to study chemistry, biology, or physics per se. One must also have a sense of the roles of psychological and social factors in science. We can read about the development of Newtonian mechanics or quantum physics, but that does not tell us why Newton, or Planck, Bohr, Born, or Heisenberg studied these subjects in the first place or what thought processes they used in their work. It does not tell us how their personalities and intuition drove their work. It also does not tell us why the work of these scientists was or was not accepted by the scientific community, rightly or wrongly. Most importantly, it does not tell us why we think we know what we do or even if what we study is real. Epistemology and metaphysics are required here. This chapter explains why such knowledge is obligatory if one is to do science well.
Melatonin supplementation to obese mothers during gestation and lactation might benefit the pancreatic islet cellular composition and beta-cell function in male offspring adulthood. C57BL/6 females (mothers) were assigned to two groups (n = 20/each) based on their consumption in control (C 17% kJ as fat) or high-fat diet (HF 49% kJ as fat). Mothers were supplemented with melatonin (Mel) (10 mg/kg daily) during gestation and lactation, or vehicle, forming the groups (n = 10/each): C, CMel, HF, and HFMel. The male offspring were studied, considering they only received the C diet after weaning until three months old. The HF mothers and their offspring showed higher body weight, glucose intolerance, insulin resistance, and low insulin sensitivity than the C ones. However, HFMel mothers and their offspring showed improved glucose metabolism and weight loss than the HF ones. Also, the offspring’s higher expressions of pro-inflammatory markers and endoplasmic reticulum (ER) stress were observed in HF but reduced in HFMel. Contrarily, antioxidant enzymes were less expressed in HF but improved in HFMel. In addition, HF showed increased beta-cell mass and hyperinsulinemia but diminished in HFMel. Besides, the beta-cell maturity and identity gene expressions diminished in HF but enhanced in HFMel. In conclusion, obese mothers supplemented with melatonin benefit their offspring’s islet cell remodeling and function. In addition, improving pro-inflammatory markers, oxidative stress, and ER stress resulted in better glucose and insulin levels control. Consequently, pancreatic islets and functioning beta cells were preserved in the offspring of obese mothers supplemented with melatonin.
Toxigenic diphtheria is rare in Australia with generally fewer than 10 cases reported annually; however, since 2020, there has been an increase in toxin gene-bearing isolates of Corynebacterium diphtheriae cases in North Queensland, with an approximately 300% escalation in cases in 2022. Genomic analysis on both toxin gene-bearing and non-toxin gene-bearing C. diphtheriae isolated from this region between 2017 and 2022 demonstrated that the surge in cases was largely due to one sequence type (ST), ST381, all of which carried the toxin gene. ST381 isolates collected between 2020 and 2022 were highly genetically related to each other, and less closely related to ST381 isolates collected prior to 2020. The most common ST in non-toxin gene-bearing isolates from North Queensland was ST39, an ST that has also been increasing in numbers since 2018. Phylogenetic analysis demonstrated that ST381 isolates were not closely related to any of the non-toxin gene-bearing isolates collected from this region, suggesting that the increase in toxigenic C. diphtheriae is likely due to the expansion of a toxin gene-bearing clone that has moved into the region rather than an already endemic non-toxigenic strain acquiring the toxin gene.
Lobbying, scientific elasticity, and serendipity can all lead to divergent research paths. But there is also an alternative method of changing the trajectory of discovery, which is the focus of Chapter 19: convergence. Conceptually, convergence can loosely be defined as the trajectories of different fields meeting at a common point or area. While very similar to the concept of interdisciplinarity, convergence is more structural and fundamental than the simple exchange of ideas denoted by interdisciplinarity. It doesn’t merely imply people from different backgrounds working together, but rather the effect of entire fields fusing - such as computing and biology combining to create computational biology - opening new avenues of thought and discovery. Chapter 19 is about how convergence can increase the rate of medical discovery, as well as how we can more systematically cultivate convergence in medical science.
Owing to the lack of effective POST herbicide options, producers typically rely on nicosulfuron as the main POST grass herbicide in sweet corn production systems. In 2019, a Wisconsin sweet corn producer reported fall panicum control escapes after spraying nicosulfuron. Seeds from mature plants were collected to (1) measure fall panicum response to acetolactate synthase (ALS)-inhibiting herbicides, (2) elucidate the resistance mechanism, and (3) evaluate its response to alternative POST herbicides. Greenhouse and laboratory investigations were conducted to assess fall panicum response to ALS-inhibiting herbicides and elucidate the resistance mechanism. Dose–response results showed that fall panicum was highly resistant to nicosulfuron with a resistance ratio of >12.9-fold (survived rates >254 g ai ha−1, or 8× the field label rate). Molecular and genetic studies indicated that there are multiple ALS gene copies in fall panicum and that resistance was due to a mutation in one copy, resulting in an Asp-376-Glu amino acid substitution. Additional greenhouse experiments indicate that clethodim (105 g ai ha−1), quizalofop-p-ethyl (70 g ae ha−1), glyphosate (864 g ae ha−1), and glufosinate (650 g ai ha−1) are effective POST options to manage the ALS-resistant fall panicum (>90.0% control and 96.8% biomass reduction) in rotational years. The 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicides isoxaflutole (105 g ai ha−1), mesotrione (105 g ai ha−1), tembotrione (92 g ai ha−1), and tolpyralate (39 g ai ha−1) did not provide effective POST fall panicum control. Because these herbicides are commonly used for POST weed control in sweet corn, more investigations are required to evaluate combinations of HPPD-inhibiting herbicides with herbicides from other sites of action for POST fall panicum control. Herein we confirm the first case of herbicide resistance in fall panicum in the United States.
Humans are the end point of almost four billion years of evolution. The generally accepted explanatory theory is Charles Darwin’s theory of evolution through natural selection, brought on by a struggle for existence. Darwin bolstered his case through a “consilience of inductions,” showing how evolution through selection explained in many areas right across the life sciences – behavior, fossil record, geographical distributions, morphology, taxonomy, and embryology. The missing element was an adequate theory of heredity, supplied by the Moravian monk Gregor Mendel. A major problem was why random change in the units of heredity, mutations of the genes, should provide enough suitable material for selection to work on. Theodosius Dobzhansky solved this problem by hypothesizing that all populations contain much variation, quite enough for selection to work on. His student, Richard Lewontin, using molecular techniques – gel electrophoresis – showed that Dobzhansky’s hypothesis was right.
The work reported in this research communication investigated the occurrence of Mycoplasma bovis (M. bovis) in milk samples from cows with clinical mastitis on dairy farms from seven Brazilian states. We hypothesized that M. bovis was present in bovine clinical mastitis milk in Brazil. A total of 561 milk samples were cultured on Hayflick agar and incubated in a microaerophilic atmosphere at 5% CO2. Polymerase chain reaction (PCR) was performed for the detection of Mycoplasma spp. and Mycoplasma bovis in milk samples. Mycoplasma spp. were isolated in 2% of the milk samples, and Mycoplasma bovis was verified in 3% of the milk samples by PCR. The results showed that Mycoplasma bovis is involved in clinical mastitis in Brazilian dairy herds. We emphasize the need for further studies to investigate the infection by this agent in clinical mastitis cases, particularly in Brazil, due to the lack of knowledge about its prevalence.
The family Ctenophthalmidae (Order Siphonaptera) has been considered as a ‘catchall’ for a wide range of divergent taxa showing a paraphyletic origin. In turn, Ctenophthalmus sp. (Ctenophthalmidae) includes 300 valid described taxa. Within this genus, males are easily distinguishable basing on the size, shape, and chaetotaxy of their genitalia; however, females show slight morphological differences with each other. The main objective of this work was to carry out a comparative morphometric, phylogenetic, and molecular study of two different subspecies: Ctenophthalmus baeticus boisseauorum and Ctenophthalmus apertus allani in order to clarify and discuss its taxonomic status. From a morphological and biometrical point of view, we found clear differences between modified abdominal segments of males of both subspecies and slight differences in the margin of sternum VII of all female specimens which did not correspond with molecular and phylogenetic results based on four different molecular markers (Internal Transcribed Spacer 1 and 2 of ribosomal DNA, and the partial cytochrome c oxidase subunit 1 and cytochrome b of mitochondrial DNA). Thus, we observed a phenotypic plasticity between both subspecies, which did not correspond with a real genotypic variability nor different environmental or ecological conditions. Basing on these results, we could consider that there are no solid arguments to consider these two ‘morphosubspecies’ as two different taxa. We propose that C. b. boisseauorum should be considered as a junior synonym of C. a. allani.
Dystrobrevin binding protein 1 (DTNBP1), or dysbindin, is thought to be critical in regulating the glutamatergic system. While the dopamine pathway is known to be important in the aetiology of schizophrenia, it seems likely that glutamatergic dysfunction can lead to the development of schizophrenia. DTNBP1 is widely expressed in brain, levels are reduced in brains of schizophrenia patients and a DTNBP1 polymorphism has been associated with reduced brain expression. Despite numerous genetic studies no DTNBP1 polymorphism has been strongly implicated in schizophrenia aetiology. Using a haplotype block-based gene-tagging approach we genotyped 13 SNPs in DTNBP1 to investigate possible associations with DTNBP1 and schizophrenia. Four polymorphisms were found to be significantly associated with schizophrenia. The strongest association was found with an A/C SNP in intron 7 (rs9370822). Homozygotes for the C allele of rs9370822 were more than two and a half times as likely to have schizophrenia compared to controls. The other polymorphisms showed much weaker association and are less likely to be biologically significant. These results suggest that DTNBP1 is a good candidate for schizophrenia risk and rs9370822 is either functionally important or in disequilibrium with a functional SNP, although our observations should be viewed with caution until they are independently replicated.
The monoamine hypothesis of depression and its direct derivation, the receptor theory, have constituted for several years a frame of reference for researchers working in the field of biological psychiatry. Although most of the data are derived from animal findings and must be considered inconclusive in view of various controversies, some guidelines may be identified: these would suggest that changes in postsynaptic beta-adrenoreceptors, presynaptic alpha 2-adrenoreceptors, as well as in type 2 serotonin receptors and dopaminergic autoreceptors may be involved in the mode of action of antidepressant drugs and, consequently, in the pathophysiology of depression. Nowadays, any attempt to correlate depression with the dysfunction of a single neurotransmitter or receptor is no longer tenable, since it is clear that depression is a heterogeneous disorder which involves abnormalities in the interactive relationships between neurotransmitters and receptors. If, on the one hand, this new model has opened up new fields of research and has led to the investigation of new systems, eg the GABAergic and GABA B receptors, on the other hand, it has been strongly limited by the lack of research tools and reliable peripheral CNS models for in vivo studies. A possible approach to this unresolved dilemma may be provided by molecular biology techniques, which have permitted the identification of the genes and sequencing of the primary structure of several membrane receptors. It is now established that receptors may be grouped into four superfamilies; in depression, there exists compelling evidence of alterations mainly in receptors belonging to the G-protein-coupled family: it is plausible that depression may be related to a disorder of the G-protein-coupled receptor superfamily. Such an hypothesis would represent an attempt to unify the different receptor abnormalities found in depression or following antidepressant treatments, and to shift from the monoamine paradigm to a new heuristic model. In addition, it would accommodate the various dysfunctions likely to be encountered and would open up new theoretical perspectives in the treatment of depression.
Psychosis-proneness or schizotypy is a personality organisation mirroring individual risk for schizophrenia-development. Believed to be a fully dimensional construct sharing considerable geno- and phenotypal variance with clinical schizophrenia, it has become an increasingly promising tool for basic psychosis-research. Although many studies show genetic commonalities between schizotypy and schizophrenia, changes in regulation of gene expression have never been examined in schizotypy before. We therefore extracted RNA from the blood, a valid surrogate for brain tissue, of a large sample of 67 healthy male volunteers and correlated the activities of all genes relevant for dopaminergic neurotransmission with the positive schizotypy-scale of the O-LIFE. We found significant negative correlations regarding the expression of the genes COMT, MAOB, DRD4, DRD5 and FOS, indicating that increased schizotypy coincides with higher levels of dopaminergic dysregulation on the mRNA-level. Considering the advantages of this method, we suggest that it be applied more often in fundamental psychosis-research.
The neurotrophic factors (NTF) hypothesis of depression was postulated nearly a decade ago and is nowadays widely acknowledged. Previous reports suggest that cerebral concentrations of NTF may be reduced in suicide victims who received minimal or no antidepressant pharmacotherapy. Recent evidence suggests that antidepressant treatment may improve or normalise cerebral concentrations of neurotrophic factors. Therefore, we examined the concentration of brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) in different brain regions (cortex, cingulate gyrus, thalamus, hippocampus, putamen and nucleus caudatus) of 21 individuals – 7 patients of which 4 patients with major depressive disorder (MDD) and overall age 86.8 ± 5 years who received antidepressant pharmacotherapy (selective serotonin re-uptake inhibitors [SSRI]; tricyclic antidepressants [TCA]), 3 patients with MDD without antidepressant treatment and overall age 84.3 ± 5 years versus 14 unaffected subjects at age 70.3 ± 13.8. We detected significant elevation of BDNF (parietal cortex) and NT3 (parietal, temporal and occipital cortex, cingulate gyrus, thalamus, putamen and nucleus caudatus regions) in MDD patients who received antidepressant medication compared to MDD untreated patients and controls. Moreover, we detected a significant decrease of NT3 levels in the parietal cortex of patients suffering from MDD non-treated patients without treatment compared to healthy individuals. Although the limited statistical power due to the small sample size in this proof of concept study corroborates data from previous studies, which show that treatment with antidepressants mediates alterations in neuroplasticity via the action of NTF. However, more research using post-mortem brain tissue with larger samples needs to be carried out as well as longitudinal studies to further verify these results.
Technological advances in the field of molecular genetics have improved the ability to classify brain tumors into subgroups with distinct clinical features and important therapeutic implications. The World Health Organization’s newest update on classification of gliomas (2016) incorporated isocitrate dehydrogenase 1 and 2 mutations, ATRX loss, 1p/19q codeletion status, and TP53 mutations to allow for improved classification of glioblastomas, low-grade and anaplastic gliomas. This paper reviews current advances in the understanding of diffuse glioma classification and the impact of molecular markers and DNA methylation studies on survival of patients with these tumors. We also discuss whether the classification and grading of diffuse gliomas should be based on histological findings, molecular markers, or DNA methylation subgroups in future iterations of the classification system.
Metabolic syndrome and impaired insulin sensitivity may occur as side effects of atypical antipsychotic drugs. However, studies of peripheral insulin resistance using the homeostatic model assessment of insulin resistance (HOMA-IR) or oral glucose tolerance tests (OGTT) suggest that abnormal glucose metabolism is already present in drug-naive first-episode schizophrenia (DNFES). We hypothesized impairments of neuronal insulin signaling in DNFES.
Methods:
To gain insight into neuronal insulin-signaling in vivo, we analyzed peripheral blood extracellular vesicles enriched for neuronal origin (nEVs). Phosphorylated insulin signal transduction serine-threonine kinases pS312-IRS-1, pY-IRS-1, pS473-AKT, pS9-GSK3β, pS2448-mTOR, pT389-p70S6K and respective total protein levels were determined in plasma nEVs from 48 DNFES patients and healthy matched controls after overnight fasting.
Results:
Upstream pS312-IRS-1 was reduced at trend level (p = 0.071; this condition may amplify IRS-1 signaling). Exploratory omnibus analysis of downstream serine-threonine kinases (AKT, GSK3β, mTOR, p70S6K) revealed lower phosphorylated/total protein ratios in DNFES vs. controls (p = 0.013), confirming decreased pathway activation. Post-hoc-tests indicated in particular a reduced phosphorylation ratio of mTOR (p = 0.027). Phosphorylation ratios of p70S6K (p = 0.029), GSK3β (p = 0.039), and at trend level AKT (p = 0.061), showed diagnosis-dependent statistical interactions with insulin blood levels. The phosphorylation ratio of AKT correlated inversely with PANSS-G and PANSS-total scores, and other ratios showed similar trends.
Conclusion:
These findings support the hypothesis of neuronal insulin resistance in DNFES, small sample sizes notwithstanding. The counterintuitive trend towards reduced pS312-IRS-1 in DNFES may result from adaptive feedback mechanisms. The observed changes in insulin signaling could be clinically meaningful as suggested by their association with higher PANSS scores.
The disease caused by the influenza virus is a global public health problem due to its high rates of morbidity and mortality. Thus, analysis of the information generated by epidemiological surveillance systems has vital importance for health decision making. A retrospective analysis was performed using data generated by the four molecular diagnostic laboratories of the Mexican Social Security Institute between 2010 and 2016. Demographics, influenza positivity, seasonality, treatment choices and vaccination status analyses were performed for the vaccine according to its composition for each season. In all cases, both the different influenza subtypes and different age groups were considered separately. The circulation of A/H1N1pdm09 (48.7%), influenza A/H3N2 (21.1%), influenza B (12.6%), influenza A not subtyped (11%) and influenza A/H1N1 (6.6%) exhibited well-defined annual seasonality between November and March, and there were significant increases in the number of cases every 2 years. An inadequate use of oseltamivir was determined in 38% of cases, and the vaccination status in general varied between 12.1 and 18.5% depending on the season. Our results provide current information about influenza in Mexico and demonstrate the need to update both operational case definitions and medical practice guidelines to reduce the inappropriate use of antibiotics and antivirals.
Strongyloidiosis by Strongyloides stercoralis is a disease of increasing interest in human and animal medicine. The scientific knowledge on canine strongyloidiosis is hindered by the poor diagnostics available. To assess the most sensitive and specific diagnostic method, feces and blood from 100 shelter dogs were screened for S. stercoralis by coprological, molecular and serological tests. Thirty-six dogs (36%) scored positive to S. stercoralis by coprology (22.3% to Baermann) and/or 30% to real time-polymerase chain reaction (rt-PCR). According to two composite reference standards (CRS) based on all coprological methods and rt-PCR (first CRS) or in combination with serology (second CRS), the most sensitive test was IFAT (93.8%; CI 82.8–98.7), followed by rt-PCR (80.6%; 95% CI 64–91.8) and Baermann (60.6%; 95% CI 42.1–77.1). The inconsistent shedding of L1 during the 4-week follow-up in infected dogs suggests the importance of multiple faecal collections for a reliable diagnosis. A combination of serological and coprological tests is recommended for the surveillance and diagnosis of S. stercoralis infection in dogs.