Developmental effects of chronic maternal audiovisual stress on the rat fetus

Development ◽  
1966 ◽  
Vol 16 (1) ◽  
pp. 1-16
Author(s):  
William F. Geber
Keyword(s):  
Congenital Malformations ◽  
Wide Spectrum ◽  
Growth Patterns ◽  
Abnormal Behavior ◽  
Nutritional Deficiencies ◽  
Virus Infections ◽  
Intensive Study ◽  
Rat Fetus ◽  
Developmental Effects ◽  
Constant Source

A wide spectrum of agents and conditions has been imposed on the maternal organism in an effort to learn more about possible factors in the development of congenital malformations (Courrier & Marois, 1954; Ferm & Kilham, 1965; Fraser, Walker & Trasler, 1957; Gillman, Gilbert & Gillman, 1948; Grabowski, 1963; Ingalls, Curley & Prindle, 1952; Kalter & Warkany, 1959; Russell, 1950; Sikov & Noonan, 1958; Tuchmann-Duplessis & Mercier-Parot, 1960). The contribution of the genetic make-up of the organisms has received intensive study, as have the effects of nutritional deficiencies, drugs, irradiation, anoxia, trauma and virus infections. In the author's opinion, the most obvious and constant source of potential danger to the developing fetus, the maternal organism itself, has received relatively little experimental attention, although a number of investigators have indicated that various types of maternal stress may contribute to the production of abnormal behavior, metabolism and growth patterns of the progeny (Calhoun, 1962; Grollman & Grollman, 1962; Harris & Harris, 1946; Ibsen, 1928; Konstantinova, 1961; Malpas, 1937; Sontag, 1941; Spelt, 1948; Stott, 1961; Zondek & Tamari, 1960).

Otoconia formation in the chick embryo

1983 ◽  
Vol 41 ◽  
pp. 572-573
Author(s):  
C.D. Fermin ◽  
M. Igarashi
Keyword(s):  
Chick Embryo ◽  
Inner Ear ◽  
Gallus Domesticus ◽  
The Body ◽  
Abnormal Behavior ◽  
Intensive Study ◽  
Basic Fuchsin ◽  
Gestational Period ◽  
Sensory Epithelia ◽  
Transmission Electron

Otoconia are microscopic geometric structures that cover the sensory epithelia of the utricle and saccule (gravitational receptors) of mammals, and the lagena macula of birds. The importance of otoconia for maintanance of the body balance is evidenced by the abnormal behavior of species with genetic defects of otolith. Although a few reports have dealt with otoconia formation, some basic questions remain unanswered. The chick embryo is desirable for studying otoconial formation because its inner ear structures are easily accessible, and its gestational period is short (21 days of incubation).The results described here are part of an intensive study intended to examine the morphogenesis of the otoconia in the chick embryo (Gallus- domesticus) inner ear. We used chick embryos from the 4th day of incubation until hatching, and examined the specimens with light (LM) and transmission electron microscopy (TEM). The embryos were decapitated, and fixed by immersion with 3% cold glutaraldehyde. The ears and their parts were dissected out under the microscope; no decalcification was used. For LM, the ears were embedded in JB-4 plastic, cut serially at 5 micra and stained with 0.2% toluidine blue and 0.1% basic fuchsin in 25% alcohol.

A wide spectrum of rare clinical variants of Zinner syndrome

2021 ◽  
Vol 14 (1) ◽  
pp. e239254
Author(s):  
Harkirat Singh Talwar ◽  
Ankur Mittal ◽  
Tushar Aditya Narain ◽  
Vikas Kumar Panwar
Keyword(s):  
Congenital Malformations ◽  
Renal Agenesis ◽  
Wide Spectrum ◽  
Ejaculatory Duct ◽  
Seminal Vesicles ◽  
Duct Obstruction ◽  
Cyst Excision ◽  
Maintenance Haemodialysis ◽  
Clinical Variants ◽  
Ejaculatory Duct Obstruction

Congenital malformations of the seminal vesicles (SVs) are rare and are associated with abnormalities of the ipsilateral urinary tracts as embryologically both the ureteral buds and SVs arise from the mesonephric ducts. The triad of SV cysts, ipsilateral renal agenesis and ejaculatory duct obstruction is known as the Zinner syndrome. We, herein, present three very rare presentations of Zinner syndrome. Case 1 presented with haematuria, and was found to have a large SV cyst with stones and underwent a robotic cyst excision. Case 2 presented with primary infertility, and was found to have a variant of Zinner syndrome. Case 3 was a known case of chronic kidney disease on maintenance haemodialysis who presented with fever and oliguria. He was found to have Zinner syndrome and underwent aspiration of SV abscess. To the best of our knowledge, such varying presentations of Zinner syndrome have been rarely reported thus far.

scholarly journals Overview on Common Respiratory Virus

2018 ◽  
Vol 3 (03) ◽  
pp. 24-32
Author(s):  
P. Sagadevan ◽  
R. Ramya ◽  
S. Rathishkumar ◽  
S. Vijayakumar ◽  
L Surendran ◽  
...  
Keyword(s):  
Neonatal Intensive Care ◽  
Respiratory Virus ◽  
Wide Spectrum ◽  
Clinical Manifestations ◽  
Virus Infections ◽  
Respiratory Compromise ◽  
Hygiene Measures ◽  
Causative Agents ◽  
Virus Diagnostics ◽  
Common Respiratory Virus

Respiratory viruses have been recognised as causative agents for a wide spectrum of clinical manifestations and severe respiratory compromise in neonates during birth hospitalisation. Early-life respiratory virus infections have also been shown to be associated with adverse long-term consequences. Preventing virus infections by intensifying hygiene measures and cohorting infected infants should be a major goal for neonatal intensive care units, as well as more common use of virus diagnostics.

scholarly journals Shuni Virus Replicates at the Maternal-Fetal Interface of the Ovine and Human Placenta

Pathogens ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 17
Author(s):  
Judith Oymans ◽  
Lucien van Keulen ◽  
Guus M. Vermeulen ◽  
Paul J. Wichgers Schreur ◽  
Jeroen Kortekaas
Keyword(s):  
Congenital Malformations ◽  
Histopathological Examination ◽  
Placental Tissue ◽  
Virus Infections ◽  
Biting Midges ◽  
Wildlife Species ◽  
Human Sera ◽  
Ovine Placenta ◽  
The 1960S ◽  
Maternal Fetal Interface

Shuni virus (SHUV) is a neglected teratogenic and neurotropic orthobunyavirus that was discovered in the 1960s in Nigeria and was subsequently detected in South Africa, Zimbabwe, and Israel. The virus was isolated from field-collected biting midges and mosquitoes and shown to disseminate efficiently in laboratory-reared biting midges, suggesting that members of the families Culicidae and Ceratopogonidae may function as vectors. SHUV infections have been associated with severe neurological disease in horses, a variety of wildlife species, and domesticated ruminants. SHUV infection of ruminants is additionally associated with abortion, stillbirth, and congenital malformations. The detection of antibodies in human sera also suggests that the virus may have zoonotic potential. To understand how SHUV crosses the ruminant placenta, we here infected pregnant ewes and subsequently performed detailed clinical- and histopathological examination of placental tissue. We found that SHUV targets both maternal epithelial cells and fetal trophoblasts, that together form the maternal-fetal interface of the ovine placenta. Experiments with human placental explants, furthermore, revealed replication of SHUV in syncytiotrophoblasts, which are generally highly resistant to virus infections. Our findings provide novel insights into vertical transmission of SHUV in sheep and call for research on the potential risk of SHUV infection during human pregnancies.

scholarly journals Mice with mutations in Trpm1, a gene within the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.

2021 ◽  
Author(s):  
Tesshu Hori ◽  
Shohei Ikuta ◽  
Satoko Hattori ◽  
Keizo Takao ◽  
Tsuyoshi Miyakawa ◽  
...  
Keyword(s):  
Visual Impairment ◽  
Wide Spectrum ◽  
Genetic Disorder ◽  
Mutant Mice ◽  
Abnormal Behavior ◽  
Chromosome 15 ◽  
Microdeletion Syndrome ◽  
Visual Transduction ◽  
Null Mutant Mice ◽  
Relationship Of

Abstract 15q13.3 microdeletion syndrome is a genetic disorder caused by a deletion of a region containing seven genes on chromosome 15, MTMR10, FAN1, TRPM1, MIR211, KLF13, OTUD7A, and CHRNA7, and characterized by a wide spectrum of psychiatric disorders. The contribution of each gene in this syndrome has been studied using mutant mouse models, but no single mouse model recapitulates the whole spectrum of human 15q13.3 microdeletion syndrome. The behavior of Trpm1−/− mice with relation to 15q13.3 microdeletion syndrome has not been investigated due to the visual impairment in these mice, which may confound the results of behavioral tests that involve vision. We have now performed a comprehensive behavioral test battery in Trpm1 null mutant mice to demonstrate the role of Trpm1, which is thought to be solely expressed in the retina, in central nervous system and to examine the relationship of TRPM1 and 15q13.3 microdeletion syndrome. Our data indicate abnormal behavior of Trpm1−/− mice which may explain some phenotypes of 15q13.3 microdeletion syndrome, including reduction of anxiety-like behavior, abnormality of social interaction, attenuation in fear memory, and hyperactivity, which is the most prominent phenotype of Trpm1 mutant mice. While the ON visual transduction pathway is impaired in Trpm1−/− mice, we did not detect compensatory high sensitivities for other sensory modalities. Although Trpm1−/− mice share the same pathway for visual impairment with mGluR6-/- mice, hyperlocomotor activity has not been reported in mGluR6-/- mice. These data suggest that the phenotype of Trpm1−/− mice extends beyond that expected from visual impairment alone. This is the first evidence to associate TRPM1 with impairment of cognitive function similar to that found in the phenotypes of 15q13.3 microdeletion syndrome.

scholarly journals A 60-year experience in the treatment of pancreatic insulinoma in the Military Medical Academy, Belgrade

2014 ◽  
Vol 71 (3) ◽  
pp. 293-297 ◽  
Author(s):  
Ivan Tavcar ◽  
Sasa Kikovic ◽  
Mihailo Bezmarevic ◽  
Sinisa Rusovic ◽  
Nenad Perisic ◽  
...  
Keyword(s):  
Clinical Symptoms ◽  
Wide Spectrum ◽  
Operative Procedure ◽  
Clinical Manifestations ◽  
Diagnostic Procedures ◽  
Abnormal Behavior ◽  
Benign Tumors ◽  
Endocrine Tumors ◽  
Disturbance Of Consciousness

Background/Aim. Insulinomas are rare benign tumors in the most cases and the most frequent endocrine tumors of the pancreas. A wide spectrum of clinical manifestations in patients with insulinoma is the reason for difficult recognition of the disease with a long period of time between the onset of symptoms and the diagnosis. Diagnostic procedures include Whipple?s triad, 72-hour fast test and topographic assessment. The only currative therapy for patients with insulinoma is operative treatment. Methods. This retrospective study included 42 patients with diagnosis of insulinoma treated in our institution in a 60-year period. In all the patients a demographic and clinical data, types of biochemical methods for diagnosis, and diagnostic procedures for insulinoma localization were analyzed. Tumor size and localization, surgical procedures, postoperative complications and outcome were assessed. Results. A study included 42 patients, 29 women and 13 men. The median age at diagnosis was 43 years. Median time between the onset of symptoms and diagnosis was 3 years. The most common clinical symptoms and signs were disturbance of consciousness and abnormal behavior in 73%, confusion and convulsions in 61% of patients. The diagnosis of insulinoma was estimated by Whipple's triad and 72-hour fast test in 14 patients. Determination of insulinoma localization was assessed by angiography in 16 (36%) of the patients, by ultrasound (US) in 3 of 16 (18.8%) patients, by abdominal computed tomography (CT) in 8 of 18 (44.5%) patients, and magnetic resonance imaging (MRI) in 2 of 8 (25%) patients. Insulinoma was found in 13 of 13 (100%) patients by arterial stimulation with venous sampling (ASVS) and in 13 of 14 (93%) patients by endoscopic ultrasound (EUS). Of the 42 patients, 38 (90.5%) underwent operative procedure. Minimal resection was performed in 28 (73.6%) of the patients [tumor enucleation in 27 (71%) and central pancreatectomy in one (2.6%) of the patients], and the major resection was performed in 9 (23.6%) of the operated patients [distal splenopancreatectomy in 8 (21%) and pancreaticoduodenectomy in one (2.6%) patient]. The overall mortality rate in postoperative period was 2.6% (one patient). Conclusion. A combination of ASVS and EUS as diagnostic procedures ensures high accuracy for preoperative determination of insulinoma localization. Minimal resection such as enucleation shoud be performed whenever it is possible.

scholarly journals Chandipura Virus Utilizes the Prosurvival Function of RelA NF-κB for Its Propagation

2019 ◽  
Vol 93 (14) ◽  
Author(s):  
Sachendra S. Bais ◽  
Yashika Ratra ◽  
Naseem A. Khan ◽  
Rakesh Pandey ◽  
Pramod K. Kushawaha ◽  
...  
Keyword(s):  
Cell Death ◽  
Life Span ◽  
Rna Virus ◽  
Wide Spectrum ◽  
Virus Infections ◽  
Chandipura Virus ◽  
Infected Cells ◽  
Host Virus Interactions ◽  
Virus Interactions

ABSTRACT Chandipura virus (CHPV), a cytoplasmic RNA virus, has been implicated in several outbreaks of acute encephalitis in India. Despite the relevance of CHPV to human health, how the virus interacts with the host signaling machinery remains obscure. In response to viral infections, mammalian cells activate RelA/NF-κB heterodimers, which induce genes encoding interferon beta (IFN-β) and other immune mediators. Therefore, RelA is generally considered to be an antiviral transcription factor. However, RelA activates a wide spectrum of genes in physiological settings, and there is a paucity of direct genetic evidence substantiating antiviral RelA functions. Using mouse embryonic fibroblasts, we genetically dissected the role of RelA in CHPV pathogenesis. We found that CHPV indeed activated RelA and that RelA deficiency abrogated the expression of IFN-β in response to virus infections. Unexpectedly, infection of Rela−/− fibroblasts led to a decreased CHPV yield. Our investigation clarified that RelA-dependent synthesis of prosurvival factors restrained infection-inflicted cell death and that exacerbated cell death processes prevented multiplication of CHPV in RelA-deficient cells. Chikungunya virus, a cytopathic RNA virus associated also with epidemics, required RelA, and Japanese encephalitis virus, which produced relatively minor cytopathic effects in fibroblasts, circumvented the need of RelA for their propagation. In sum, we documented a proviral function of the pleiotropic factor RelA linked to its prosurvival properties. RelA promoted the growth of cytopathic RNA viruses by extending the life span of infected cells, which serve as the replicative niche of intracellular pathogens. We argue that our finding bears significance for understanding host-virus interactions and may have implications for antiviral therapeutic regimes. IMPORTANCE RelA/NF-κB participates in a wide spectrum of physiological processes, including shaping immune responses against invading pathogens. In virus-infected cells, RelA typically induces the expression of IFN-β, which restrains viral propagation in neighboring cells involving paracrine mechanisms. Our study suggested that RelA might also play a proviral role. A cell-autonomous RelA activity amplified the yield of Chandipura virus, a cytopathic RNA virus associated with human epidemics, by extending the life span of infected cells. Our finding necessitates a substantial revision of our understanding of host-virus interactions and indicates a dual role of NF-κB signaling during the course of RNA virus infections. Our study also bears significance for therapeutic regimes which alter NF-κB activities while alleviating the viral load.

scholarly journals Growth patterns and associated risk factors of congenital malformations in twins

2020 ◽  
Vol 46 (1) ◽  
Author(s):  
Ettore Piro ◽  
Ingrid Anne Mandy Schierz ◽  
Gregorio Serra ◽  
Giuseppe Puccio ◽  
Mario Giuffrè ◽  
...  
Keyword(s):  
Risk Factors ◽  
Congenital Malformations ◽  
Growth Patterns ◽  
Associated Risk Factors

scholarly journals Mice with Mutations in Trpm1, a Gene within the locus of 15q13.3 Microdeletion Syndrome, Display Pronounced Hyperactivity and Decreased Anxiety-Like Behavior.

2020 ◽  
Author(s):  
Tesshu Hori ◽  
Shohei Ikuta ◽  
Satoko Hattori ◽  
Keizo Takao ◽  
Tsuyoshi Miyakawa ◽  
...  
Keyword(s):  
Visual Impairment ◽  
Wide Spectrum ◽  
Genetic Disorder ◽  
Mutant Mice ◽  
Abnormal Behavior ◽  
Chromosome 15 ◽  
Microdeletion Syndrome ◽  
Visual Transduction ◽  
Null Mutant Mice ◽  
Relationship Of

Abstract 15q13.3 microdeletion syndrome is a genetic disorder caused by a deletion of a region containing seven genes on chromosome 15, MTMR10, FAN1, TRPM1, MIR211, KLF13, OTUD7A, and CHRNA7, and characterized by a wide spectrum of psychiatric disorders. The contribution of each gene in this syndrome has been studied using mutant mouse models, but the phenotypes of these mice do not account for human phenotypes and the results are still controversial. The behavior of Trpm1−/− mice with relation to 15q13.3 microdeletion syndrome has not been investigated due to the visual impairment in these mice, which may confound the results of behavior tests that involve vision. We have now applied a comprehensive behavioral test battery to examine the relationship of TRPM1 and 15q13.3 microdeletion syndrome by using Trpm1 null mutant mice. Our data indicate abnormal behavior of Trpm1−/− mice which may explain some phenotypes of 15q13.3 microdeletion syndrome, including reduction of anxiety behavior, abnormality of social interaction, attenuation in fear memory, and hyperactivity, which is the most prominent phenotype of Trpm1 mutant mice. While the ON visual transduction pathway is impared in Trpm1−/− mice, we did not detect compensatory high sensitivities for other sensory modalities. Although Trpm1−/− mice share the same pathway for visual impairment with mGluR6−/− mice, hyperlocomotion activity has not been reported in mGluR6−/− mice. These data suggest that the phenotype of Trpm1−/− mice extends beyond that expected from visual impairment alone. This is the first evidence to associate TRPM1 with impairment of cognitive function similar to that found in the phenotypes of 15q13.3 microdeletion syndrome.

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