Maturation of Social-Vocal Communication in Prairie Vole (Microtus ochrogaster) Pups

Impairments in social communication are common among neurodevelopmental disorders. While traditional animal models have advanced our understanding of the physiological and pathological development of social behavior, they do not recapitulate some aspects where social communication is essential, such as biparental care and the ability to form long-lasting social bonds. Prairie voles (Microtus ochrogaster) have emerged as a valuable rodent model in social neuroscience because they naturally display these behaviors. Nonetheless, the role of vocalizations in prairie vole social communication remains unclear. Here, we studied the ontogeny [from postnatal days (P) 8–16] of prairie vole pup ultrasonic vocalizations (USVs), both when isolated and when the mother was present but physically unattainable. In contrast to other similarly sized rodents such as mice, prairie vole pups of all ages produced isolation USVs with a relatively low fundamental frequency between 22 and 50 kHz, often with strong harmonic structure. Males consistently emitted vocalizations with a lower frequency than females. With age, pups vocalized less, and the acoustic features of vocalizations (e.g., duration and bandwidth) became more stereotyped. Manipulating an isolated pup's social environment by introducing its mother significantly increased vocal production at older (P12–16) but not younger ages, when pups were likely unable to hear or see her. Our data provide the first indication of a maturation in social context-dependent vocal emission, which may facilitate more active acoustic communication. These results help lay a foundation for the use of prairie voles as a model organism to probe the role of early life experience in the development of social-vocal communication.

The clinical and (dermato) pathological signifcance of neural crest cells. Blaschko lines and dermatoses. Neurocristopathies

In the course of their migration the neural crest cells reach all parts of the developing embryo. The frst wave of the derivatives of these cells the melanoblasts and melanocytes harbour in the epidermis and hair follicles during the dorsolateral migration. A number of signal molecules and proteases play an important role in the course of melanocyte migration through the extracellular matrix. The Mongolian spots appear as a consequence of the transient inhibition of melanocyte migration and in the case of fnal obstruction the Ota-, or. Ito nevuses. The Blaschko lines based on cutaneous mosaicism are of great diagnostic importance and on the ground of these lines the blaschkitises can appear under the exogenous factors. The blaschkolinear acquired infammatory skin eruption (BLAISE) is an acquired infammatory process. One of its variants is the lichen striatus and the other is the blaschkitis. The blaschkolinear dermatoses can appear usually as a nevoid disease. The pathological development of the neural crest cells can induce pathological processes in other tissues of the body as well, which may appear in the form of the so-called neurocristopathies including approximately ffty manifestations. The knowledge of the diferent pigmentation forms as well as the pathological symptoms of neurocristopathies is of great importance for the clinican from a diagnostic point of view.

New insights into the pathological development of dyslipidemia in patients with hypothyroidism

According to the previous reports, hypothyroidism has been shown to be strongly correlated with increased circulating concentrations of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG). Notably, thyroid hormones are confirmed to modulate the production, clearance, and transformation process of cholesterol within circulation of mammals. Moreover, emerging evidence suggests that the thyroid-stimulating hormone could also participate in modulating serum lipid metabolism independently of thyroid hormones, which further induces the pathological development of dyslipidemia. However, the underlying mechanism is still not fully elucidated. Recently, several research studies have demonstrated that the pathogenic progression of hypothyroidism-related dyslipidemia might be correlated with the decreased serum concentrations of thyroid hormones and the increased serum concentrations of thyroid-stimulating hormones. Thus, this indicates that hypothyroidism could induce dyslipidemia and its related cardio-metabolic disorder diseases. In addition, several newly identified modulatory biomarkers, such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTLs), and fibroblast growth factors (FGFs), might play an important role in the regulation of dyslipidemia induced by hypothyroidism. Furthermore, under the status of hypothyroidism, significantly dysfunctional HDL particles could also be observed. In the current review, we summarized the recent knowledge of the relationship between the development of hypothyroidism with dyslipidemia. We also discussed the updated understanding of the mechanisms whereby hypothyroidism induces the risk and the development of dyslipidemia and cardio-metabolic diseases.

Neural Circuits for Social Interactions: From Microcircuits to Input-Output Circuits

Social behaviors entail responses to social information and requires the perception and integration of social cues through a complex cognition process that involves attention, memory, motivation, and emotion. Neurobiological and molecular mechanisms underlying social behavior are highly conserved across species, and inter- and intra-specific variability observed in social behavior can be explained to large extent by differential activity of a conserved neural network. However, neural microcircuits and precise networks involved in social behavior remain mysterious. In this review, we summarize the microcircuits and input-output circuits on the molecular, cellular, and network levels of different social interactions, such as social exploration, social hierarchy, social memory, and social preference. This review provides a broad view of how multiple microcircuits and input-output circuits converge on the medial prefrontal cortex, hippocampus, and amygdala to regulate complex social behaviors, as well as a potential novel view for better control over pathological development.

Karl Mannheim on Fascism: Sociological Lessons About Populism and Democracy Today?

The parallels and differences between current forms of populism and early 20th-century fascism have been the focus for much discussion. This article examines the relevance today of Karl Mannheim’s analysis of fascism and of its relationship to democracy in the 1930s. He argued that the threat of fascism arose from the very nature of liberal democratic society, rather than being a product of external forces. He claimed that liberal democracy is transitional, rather than stable in character, and that the new emerging form of governance that was required to replace it shared a key component with fascism: a high level of social and economic planning. At the same time, he insisted that, as a pathological development, fascism served to illustrate the disastrous consequences that a failure to engage realistically with the process of societal development can have for upholding Western civilisational ideals. This article explores Mannheim’s arguments against the background of current thinking about populism and ‘post-democracy’.

Ileal mucosa-associated microbiota overgrowth associated with pathogenesis of primary biliary cholangitis

The small intestinal mucosa-associated microbiota (MAM) can potentially impact the etiology of primary biliary cholangitis (PBC). Herein, we investigate the MAM profile to determine its association with liver pathology in patients with PBC. Thirty-four patients with PBC and 21 healthy controls who underwent colonoscopy at our hospital were enrolled in our study. We performed 16S ribosomal RNA gene sequencing of MAM samples obtained from the mucosa of the terminal ileum and examined the relationship between the abundance of ileal MAM and chronic nonsuppurative destructive cholangitis using liver specimens from patients with PBC. There was a significant reduction in microbial diversity within individuals with PBC (P = 0.039). Dysbiosis of ileal MAM was observed in patients with PBC, with a characteristic overgrowth of Sphingomonadaceae and Pseudomonas. Multivariate analysis showed that the overgrowth of Sphingomonadaceae and Pseudomonas is an independent association factor for PBC (P = 0.0429, P = 0.026). Moreover, the abundance of Sphingomonadaceae was associated with chronic nonsuppurative destructive cholangitis in PBC (P = 0.00981). The overgrowth of Sphingomonadaceae and Pseudomonas in ileal MAM was found in patients with PBC. Sphingomonadaceae may be associated with the pathological development of PBC.

C1q/TNF-Related Protein 3 Prevents Diabetic Retinopathy via AMPK Dependent Stabilization of Blood-Retinal Barrier Tight Junctions

Background The impairment of the inner blood-retinal barrier (iBRB) increases the pathological development of diabetic retinopathy (DR), a severe complication in diabetic patients. Identifying approaches to preserving iBRB integrity and function is a major challenge in DR. C1q/tumor necrosis factor-related proteins-3 (CTRP3) is a newly discovered adipokine and an important biomarker predicting DR severity. We sought to determine whether and how CTRP3 affects the pathological development of non-proliferative diabetic retinopathy (NPDR). Methods To clarify the pathophysiologic progress of the blood-retinal barrier in NPDR and explore its potential mechanism, a mouse type 2 diabetic model of diabetic retinopathy was used. The capillary leakage was assessed by confocal microscope with fluorescent-labeled protein in vivo. Furthermore, the effect of CTRP3 on the inner blood-retinal barrier (iBRB) and its molecular mechanism was clarified. Results The results demonstrated that CTRP3 protects iBRB integrity and resists the vascular permeability induced by DR. Mechanistically, the administration of CTRP3 activates AMPK signaling pathway and enhances the expression of Occludin and Claudin-5 (tight junction protein) in vivo and in vitro. Meanwhile, CTRP3 improves the injury of human retinal endothelial cells (HRMECs) induced by high glucose/high lipids (HG/HL) and its protective effects are AMPK dependent. Conclusions In summary, we report for the first time that CTRP3 prevents diabetes-induced retinal vascular permeability via stabilizing the tight junctions of the iBRB and AMPK-dependent Occludin/Claudin-5 signaling pathway, thus critically affecting the development of NPDR.

A Focus on Male Homosexuality in Psychoanalytic Literature

Homosexuality has long been classified by many authors as a form of psychic immaturity. Today, it is widely accepted that homosexuality is not by definition a pathological development. In this article, I will focus on male homosexuality because I have been working with homosexual men for quite some time. In the first part, we will see that the Freudian and post-Freudian authors examined have largely emphasized the narcissistic failings of male homosexuals. In the Jungian corpus, which also serves as a reference, the homosexual is frequently considered as an individual whose relationship to his inner feminine is the result of a fusional identification with his mother. The abstract concepts of anima/animus have done little to remove homosexuality from the category of identity disorders. In the second part, I assume the possible existence of a homosexual instinct which everyone is confronted with and which would manifest itself in specific conditions. Certainly, no distinction between men and women should be made regarding my hypothesis of a homosexual instinct. However, from a scientific point of view, it has been impossible for me to prove that such an instinct really exists.

The Many Faces of Astrocytes in Alzheimer's Disease

Alzheimer's disease (AD) is a progressive neurodegenerative disease and is the most common cause of dementia in an aging population. The majority of research effort has focused on the role of neurons in neurodegeneration and current therapies have limited ability to slow disease progression. Recently more attention has been given to the role of astrocytes in the process of neurodegeneration. Specifically, reactive astrocytes have both advantageous and adverse effects during neurodegeneration. The ability to isolate and depict astrocyte phenotype has been challenging. However, with the recent development of single-cell sequencing technologies researchers are provided with the resource to delineate specific biomarkers associated with reactive astrocytes in AD. In this review, we will focus on the role of astrocytes in normal conditions and the pathological development of AD. We will further review recent developments in the understanding of astrocyte heterogeneity and associated biomarkers. A better understanding of astrocyte contributions and phenotypic changes in AD can ultimately lead to more effective therapeutic targets.

Critical functions of lncRNA DGCR5 in cancers of the digestive system

Background: Long non-coding RNAs (lncRNAs) has no protein-coding potential due to the lack of an apparent open reading frame. There is growing evidence that lncRNA DGCR5 has a vital regulatory role in human illnesses' pathological development, particularly in the digestive system's carcinogenesis and progression. Abnormal DGCR5 expression affects different cellular functions such as proliferation, aggression, and metastasis. This paper aims to probe into the pathophysiological functions and molecular mechanisms of DGCR5 in cancers of the digestive system. Methods: This review summarizes and analyzes the biological functions and mechanisms of lncRNA DGCR5 in digestive system cancers occurrence. Relevant studies were conducted and reviewed by searching PubMed for articles with lncRNA DGCR5 and digestive system cancer as keywords in recent years. Results: DCGR5, as a novel tumor-related lncRNA, is recently identified to be abnormally expressed in digestive system cancers, such as pancreatic ductal adenocarcinoma, pancreatic cancer, gastric cancer, gallbladder cancer, colorectal cancer, and hepatocellular carcinoma. The role played by DCGR5 is vital and varies in different digestive cancers. Taken together, aberrant expression of DCGR5 regulates the progression of digestive cancers by affecting cancer cell proliferation, aggression, metastasis, and drug resistance. Conclusion: LncRNA DGCR5 might be a viable marker or a promising therapeutic target in digestive system cancers.