Objective: To evaluate the prediction performance of 1st trimester fasting plasma glucose (FPG) levels, as compared to gestational diabetes (GDM), for type 2 diabetes mellitus (T2DM), in a 5-year follow-up after pregnancy. Design: A retrospective analysis of prospectively collected data Setting: Mehuedet HMO, Israel Population or sample: 69,001 parturients with FPG levels measured at 1st-trimester and T2DM data up to 5 years after delivery. Methods: T2DM diagnosis was stratified by FPG levels divided into categories with 10 mg/dl increments. GDM was diagnosed using the two-step strategy. Prediction performance for T2DM was determined using ROC-AUC statistics with the utilization of the Youden index(YI) for the calculation of the best FPG cut-off for T2DM prediction. Survival analysis was applied to calculate hazard ratios(HRs) for T2DM prediction with further stratification to maternal obesity status. Main outcome measures: T2DM, as determined by the Israeli National Diabetes Registry.. Results: The determined FPG cut-off for predicting the risk of T2DM was 86.5mg/dl (sensitivity 53.3%, specificity 72.4%). This cutoff demonstrated superior predictive performance when compared to GDM diagnosis (0.615 vs. 0.586). Furthermore, all FPG level categories exceeding 80 mg/dL were associated with an increased risk of developing T2DM. FPG levels equal to or greater than 110 mg/dL exhibited even stronger predictive performance for T2DM compared to GDM diagnosis (HR 4.92 and 3.92, respectively). When stratified by maternal obesity, FPG levels displayed enhanced predictive capabilities for T2DM, particularly among women without obesity. Conclusions: 1st trimester FPG levels are associated with increased risk for T2DM, at least as GDM.

We examined the proteomic profiles of three registered opium poppy cultivars having different alkaloid content. The study was conducted on both stem and capsule organs. A high number of DEPs were identified between the cultivars and the organs. We analyzed DEPs for their contribution in GO terms and KEGG pathways. The up-regulated DEGs were significantly enriched in photosynthesis and translation for morphine-rich and noscapine-rich cultivars, respectively. The data depicted that photosynthesis is crucial for BIA biosynthesis, but different processes are also effective on morphine and noscapine biosynthesis which occur at different branches in the biosynthetic pathway. The protomic profiles revealed that energy demand is more effective in morphine biosynthesis, while translational control has leading role in noscapine biosynthesis. This is the first report demonstrating the organ-based and cultivar-based protein expression differences in mature poppy plant.

Should we stay or should we go – the ever-growing role of Twitter (X) in Neuroscience dissemination and a quandary of conscience for a field.Kenneth A. Foxe and John J. Foxe

The Janzen-Connell hypothesis is one of the most important hypotheses in ecology, but is mostly tested indirectly without accounting for the underlying plant-associated organisms, or only for highly host-specific organisms. Advances in massive sequencing allow to sample, for example, the fungi communities associated with different plant species, and spatial analysis can reveal spatial patterns in the number of organisms (species) shared by plant species and their neighbours. We show how combining these tools provides new perspectives for testing the Janzen Connell hypothesis. We illustrate our approach using a natural experiment in two fully-mapped Mediterranean forest plots, where the dominant dry- and fleshy-fruited species have distinctly different seed deposition patterns, leading to contrasting expectation about the emerging spatial structures. Our analysis confirmed these expectations and provided deep insights into how the neighbourhood load of plant-associated fungi and herbivorous insects changes during plant ontogeny and how seed dispersal mechanisms modulates Janzen-Connell effects.

A document by Hyun Chae Lee. Click on the document to view its contents.

Acute kidney injury (AKI) is a common disease characterized by a sharp decline of kidney function within a short time and is associated with high morbidity and mortality in recent years. Although the development of clinical therapy for AKI has taken a certain degree of effect, these treatments do little to improve the prognosis of patients suffering from AKI. Mounting researches have demonstrated that AKI is an independent and important risk factor for chronic kidney disease (CKD), and the transition from AKI to CKD involves various mechanisms. Recently, in addition to the pathophysiology of tubular epithelial cells (TECs) and macrophages aberrant polarization, the crosstalk between them has garnered significant attention after kidney injury. The crosstalk between TECs and macrophages polarization is closely related to inflammation, repair and fibrosis after kidney injury, which are all key points in the transition from AKI to CKD. Exploring the progression of AKI to CKD is of great significance for clinical treatment. Therefore, this review aims to summarize the current researches on tubular epithelial cells, macrophages and the crosstalk them to provide effective reference for subsequent research and help to find potential therapeutic targets to prevent the progression of AKI to CKD.

Background and Purpose: Traumatic brain injury (TBI) imposes life-long physical, psychological, and financial burdens on affected individuals. The current study investigated the effects of chronic nicotine exposure via E-cigarette (E-cig) on TBI-associated behavioral and biochemical changes. Experimental Approach: Adult C57/BL6J male mice were subjected to controlled cortical impact (CCI) followed by daily exposure to E-cigarette (E-Cig) vapor for six weeks. The effects of chronic nicotine exposure on sensorimotor functions, locomotion, and sociability were evaluated by nesting, open field, and social approach, respectively. Immunoblots were performed to assess changes of mature brain-derived neurotrophic factor (mBDNF) and associated downstream signaling proteins (p-Akt and p-Erk). Histological analyses of the cortex were performed to evaluate the effects of chronic nicotine exposure on Microglia-mediated neuroinflammation. Key Results: Post-injury chronic nicotine exposure significantly improved nesting performance in CCI mice. Histology analysis revealed that chronic nicotine exposure increased the survival of cortical neurons in the perilesion cortex. Immunoblots of cortical tissue revealed that chronic nicotine exposure significantly upregulated mBDNF expression, P-Erk, and p-Akt in the perilesion cortical tissue of CCI mice. Additional IF microscopy revealed elevated mBDNF and p-Akt expression was predominantly localized in cortical neurons of CCI mice. Furthermore, immunolabeling of Iba1 showed that chronic nicotine exposure attenuates microglia-mediated chronic neuroinflammation in the perilesional cortex of CCI mice. Conclusions and Implications: Post-injury chronic nicotine exposure via vaping facilitates sensorimotor function recovery by upregulating neuroprotective mBDNF/TrkB/Akt/Erk signaling. Results from this study support the neuroprotective properties of nicotine, further investigation is needed due to its highly addictive nature.

Introduction Oral propranolol is a first-line treatment for infantile hemangiomas (IH). This study aims to describe the results of treating IH with propranolol only or initial propranolol therapy followed by laser therapy, surgical excision, corticosteroid therapy, or a second cycle of propranolol. Methods Our patient population included pediatric patients (<18 years of age) diagnosed with IH at Monroe Carell Junior Children’s Hospital at Vanderbilt University Medical Center between August 2009 to July 2017. Patient demographics, IH clinical features, and treatment data were extracted from the electronic medical record. Results Three hundred forty patients with IH were included in this study, with a prevalence of focal lesions (71%) and a total of 279 (82%) IH located on the head/neck. Lesions of the head had a statistically significant association with PHACE syndrome (p<0.001). Most patients initiated propanolol treatment before the age of 6 months (71%), with continuation for ≥6 months (69%). Upon discontinuation of propranolol, 14 (4%) patients required a second cycle of propranolol for regrowth. After controlling for IH location, patients with a family history of hemangiomas or cardiac abnormalities were 3.6 times more likely to need a second round of propranolol treatment (OR, 3.6; 95% Confidence Interval 1.14-11.19) (P=0.03). Conclusion The study confirms propranolol’s effectiveness and safety, reinforcing the need for early intervention and close monitoring following treatment termination to prevent regrowth. Ultimately, this research contributes to advancing the understanding and treatment of IH, aiming to optimize patient outcomes and reduce morbidity.

Nutrient deficiency, excitotoxic injury, and oxidative stress caused by cerebral ischemia/reperfusion injury are important inducing factors of mitophagy and ferroptosis in neurons. Ferroptosis is an iron-dependent mode of cell death usually accompanied by a large accumulation of iron ions and lipid peroxides. Mitophagy is one of the forms of selective autophagy, which can maintain mitochondrial and cellular homeostasis by eliminating dysfunctional mitochondria. Mitophagy and ferroptosis are closely related to the pathological mechanism of ischemia/reperfusion injury. However, the function and mechanism of mitophagy in regulating ferroptosis are only beginning to be understood, and the relationship between mitophagy and ferroptosis after cerebral ischemia/reperfusion has not been elucidated. This article reviews the mechanism pathways of mitophagy and ferroptosis after cerebral ischemia/reperfusion, especially discusses the common regulatory factors of mitophagy and ferroptosis in cerebral reperfusion injury, and focuses on the therapeutic potential of mitophagy in regulating ferroptosis, in order to provide ideas for targeted treatment of cerebral ischemia/reperfusion injury.

Early-life stress has been shown to have long-lasting consequences on adult neuropsychology and is a known risk factor for various neuropsychiatric disorders, namely schizophrenia and major depressive disorder. The amygdala, prefrontal cortex, and hippocampus are key brain regions affected by this stress, with the amygdala playing a crucial role in stress activation and memory formation. Animal models provide valuable insights into the neurobiological alterations caused by stress in these regions and are essential to our understanding of stress-related disorders in humans. This paper will analyze the impact of stress on the activation of the amygdala and its effects on the prefrontal cortex and hippocampus, focusing on the utility and necessity of animal studies in research of stress-related pathologies.

Cartilage is frequently used as scaffolds for repairing and reconstructing body surface organs. However, after successful plastic surgery, transplanted cartilage scaffolds often exhibit deformation and absorption over time. To enhance the shapping stability of cartilage scaffolds and improve patients’ satisfaction after reconstructions, we employed the ear folding models in New Zealand rabbit to confirm whether the 1064nm Nd:YAG laser could promote cartilage reshapping. There was an increase in collagen and aromatase (Cyp19) expression within the ear cartilage after laser treatment. Moreover, we have discovered that the Cyp19 inhibitor can suppress the shaping effect of the laser on cartilage, as well as the expression of collagen and Cyp19. The overall findings suggest that treatment with 1064nm Nd:YAG laser irradiation can enhance estrogen levels in local cartilage tissues by upregulating Cyp19 expression in chondrocytes through photobiomodulation, thereby promoting the proliferation and collagen secretion of chondrocytes to improve cartilage reshaping and stability.

This paper explores the sensitivity of the human visual system to the quantum entangled photons. We examine the possibility of human subjects perceiving higher dimensional quantum entangled photons through psychophysical experiments. Our focus begins with a two-photon entangled state to make a comparative study with the literature by taking into account additive noise for false positive on two-photon entanglement perception by humans. After that, we limit our similar investigation to a three-photon entangled state for simplicity in higher dimensions. To model the photodetection by humans, we employ the probability of seeing determined for coherently amplified photons in Fock number states, including an additive noise. Our results indicate that detecting two-photon and three-photon entanglement with the human eye is possible for a certain range of additive noise levels and visual thresholds.

Incorporating the Internet of Things (IoT) with cloud computing has significantly changed various industries and improved the quality of life. Despite these advantages, cloud computing is not enough for real-time applications due to the dynamic nature of IoT Devices (IoTDs) and their unpredictable locations, heterogeneity constraints, fault sensitivity, and power supply limitations. Accordingly, Cisco has introduced fog computing as a solution that relocates computation to the network’s edge. This article presents a Systematic Literature Review (SLR) of 109 research articles published between 2016 and 2023 on modern fog resource management approaches. Based on a comprehensive taxonomy, these approaches are classified and compared considering several technological benchmarks, including Quality of Service (QoS) parameters, algorithms, techniques, evaluation methods, case studies, and their strengths, limitations, and novel findings. Additionally, a separate section extensively discusses future trends and open issues in fog computing resource management. In this study, security issues are not addressed, which is suggested for future studies.

Background: Starting from May 31 st, 2023, the local transmission of monkeypox (Mpox) in mainland China began in Beijing. Till now, the transmission characteristics have not been explored. Method: Based on the daily Mpox incidence data in the first three weeks of Beijing (from May 31 st to June 21 st, 2023) , we employed the instant-individual heterogeneity transmission model to simultaneously calculate the effective reproduction number ( R e) and the degree of heterogeneity ( k) of the Beijing epidemic. We additionally simulated the monthly infection size in Beijing from July to September and compared with the reported data to project subsequent transmission dynamics. Results: We estimated R e to be 1.68 [95% HPD:1.12, 2.41], and k to be 2.57 [95% HPD: 0.54, 83.88], suggesting the transmission of Mpox in Beijing was supercritical and didn’t have considerable transmission heterogeneity. We projected that R e fell in the range of 0.95 to 1.0 from July to September, highlighting more efforts needed to further reduce the Mpox transmissibility. Conclusion: Our findings revealed supercritical and homogeneous transmission of the Mpox epidemic in Beijing. Our results may provide reference for understanding and predicting of the on-going Mpox transmission in other regions of China and assess the effect of control measures.

Background and purpose: Bardoxolone methyl (2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid methyl ester, CDDO-Me) is a potent activator of nuclear factor erythroid 2-related factor (Nrf)2, which induces anti-oxidative-associated genes. CDDO-Me is known to exert protective effects against chronic inflammatory diseases in the kidney and lungs. However, its pharmacological effects on non-alcoholic steatohepatitis (NASH) caused by fat accumulation remain unknown. In this study, we examined the hepatoprotective effects of CDDO-Me in a diet-induced NASH mouse model, and elucidated its pharmacological mechanisms using RNA-seq analysis. Experimental approach: CDDO-Me was orally administered to mice fed a choline-deficient, L-amino acid-defined, high-fat diet, and histological, biochemical, and transcriptome analyses were performed on the livers of mice that developed NASH. Key results: CDDO-Me administration induced the expression of antioxidant genes and cholesterol transporters downstream of Nrf2 and significantly improved the symptoms of NASH. Whole-transcriptome analysis revealed that CDDO-Me inhibited the inflammatory pathway that leads to phagocyte recruitment, in addition to activating the Nrf2-dependent pathway. Among inflammatory pathways, CC chemokine ligand (CCL)3 and CCL4 in the downstream of NF-B, which are associated with the recruitment of macrophages expressing CC chemokine receptor (CCR)1 and CCR5, were released into blood in NASH mice. In contrast, CDDO-Me directly inhibited the expression of CCL3-CCR1 and CCL4-CCR5 in macrophages. Conclusions and Implications: Overall, this study revealed the potent hepatoprotective effect of CDDO-Me in a NASH mouse model, and demonstrated that its pharmacological effects were closely associated with the reduction of macrophage infiltration through CCL3-CCR1 and CCL4-CCR5 inhibition, in addition to Nrf2-mediated hepatoprotective effects.

Background and Purpose: Oligomeric Aβ1-42 (oAβ42) exhibits agonist-like action at human α7- and α7β2-nicotinic receptors (collectively, α7*-nAChR). Aβ1-42 and an N-terminal Aβ peptide fragment (N-Aβ fragment: Aβ1-15/16) have been shown to modulate presynaptic Ca2+ and enhance hippocampus-based synaptic plasticity via α7* nAChR. Both the N-Aβ fragment and its essential core sequence, the N-Aβcore hexapeptide (Aβ10-15), protect against Aβ-associated synapto- and neurotoxicity, also involving nAChR. Here, we investigated how oAβ42, the N-Aβ fragment and N-Aβcore regulate the functional activity of α7*-nAChRs. Experimental approach: Single-channel patch clamp recordings measured the impact of ACh, oAβ42, the N-Aβ fragment, and the N-Aβcore on the function of concatenated, human α7- and α7β2-containing nAChR expressed in nAChR-null SH-EP1 cells. Molecular dynamics simulations identified potential sites of interaction between the N-Aβ fragment and the orthosteric α7*-nAChR binding interfaces. Key Results: Relative to the effects of ACh alone, oAβ42 preferentially enhanced α7β2-nAChR open probability and open-dwell times. Co-application with the N-Aβcore neutralized these effects. Further, we demonstrate that the N-Aβ fragment alone, or in combination with ACh or oAβ42, resulted in selective enhancement of α7-nAChR single-channel open probability and open-dwell times (compared to ACh or oAβ42). Conclusions and Implications: Our findings show the functional diversity of Aβ peptides in regulating α7*-nAChR function, with implications for a wide range of nAChR-mediated functions in AD. Single-channel recordings of the differential effects of oAβ42, N-Aβ fragment and/or N-Aβcore on α7*-nAChR isoform function revealed the complexities of their interactions with α7*-nAChR, with new insights into the neuroprotective actions of these N-Aβ-derived peptides.

A document by James Higham. Click on the document to view its contents.

Epilepsy, characterized by recurrent seizures, encompasses various complex syndromes with varied origins. To unravel the intricate biology of epilepsy and explore novel Antiseizure treatments, researchers have developed over 100 in vitro and in vivo epilepsy models, each simulating different seizure types. These experimental models serve as indispensable tools for investigating the neurochemical, neurophysiological, cellular, and molecular mechanisms governing epileptic seizures, offering a comprehensive understanding of this condition. This article provides a comprehensive overview of diverse experimental models crucial for studying Antiseizure Medication and seizures, including Generalized Tonic-Clonic Seizure (GTCS), Temporal Lobe Epilepsy (TLE), Absence Seizure, Myoclonus, and Status Epilepticus (SE) Models. Researchers leverage these models to gain critical insights into epilepsy’s underlying causes, available therapies, and potential therapeutic targets. The study digs into a thorough analysis of the benefits and drawbacks related to various chemical models used in epilepsy treatment. This dual approach adds to the continuing discussion in epilepsy research by clarifying the complicated issues surrounding therapeutic strategies and improving our understanding of the complexity of epilepsy. This article includes discusses GTCS, SE, and TLE subtypes such as WAG/Rij rats, coriaria lactone-induced TLE, pilocarpine-induced TLE, Tottering 6j mouse, GHB-induced seizure model, PTZ-induced model, NMDA-induced seizure models, and flurothyl-induced seizure model. Penicillin-induced TLE, Theiler’s virus-induced TLE, and many more.

In this paper, we consider the Ricker model with delay and constant or periodic stocking. The impact of delay and stocking on stability is known to reflect opposing effect, which motivates investigating the interaction between these factors and their influence on overall stability. We found that the high stocking density tends to neutralize the delay effect. Conditions are established on the parameters in order to guarantee the global stability of the equilibrium solution in the case of constant stocking, as well as the global stability of the 2-periodic solution in the case of 2-periodic stocking. Our approach extensively relies on the utilization of the embedding technique. Whether constant stocking or periodic stocking, the mode has the potential to undergo a Neimark-Sacker bifurcation in both cases. However, the Neimark-Sacker bifurcation in the 2-periodic case results in the emergence of two invariant curves that collectively function as a single attractor. Finally, we pose open questions in the form of conjectures about global stability for certain choices of the parameters.

A document by Carlos Zetina Rosales. Click on the document to view its contents.

A document by Jitendra Maharana. Click on the document to view its contents.

Early Diagnosis of Thoracic Spinal Dural Arteriovenous Fistula Using Lumbar Magnetic Resonance Imaging: A Case Report

Empyema necessitans as a rare manifestation ofStaphylococcus aureusNazanin Zeinali Nezhad1,Aazam Gholami Shahrebabak2*, Amirhossein Shahpar31 Faculty of Medicine, Kerman University of Medical Sciences, Haft Bagh Alavi Blvd, Kerman, Iran Postal Code: 76169135552 Department of Medical Education, Medical Education Research Center, Kerman University of Medical Sciences, Haft Bagh Alavi Blvd, Kerman, Iran Postal Code: 76169135553 Faculty of Medicine, Kerman University of Medical Sciences, Haft Bagh Alavi Blvd, Kerman, Iran Postal Code: 7616913555*Corresponding author : Aazam Gholami Shahrebabak, Assistant Professor of Pediatrics, Department of Medical Education, Medical Education Research Center, Kerman University of Medical Sciences, Haft Bagh Alavi Blvd, Kerman, IranEmail: a.gholami@kmu.ac.ir

Marfan syndrome (MFS) is an autosomal dominant connective tissue disease that is often accompanied by heart valve abnormalities and aortic aneurysms. It is usually associated with a mutation in the FBN-1 gene. Pregnancy is generally contraindicated in patients with MFS. In this report, we present the case of a pregnant woman