Perinatal hyperoxia for 14 days increases nerve conduction time and the acute unitary response to hypoxia of rat carotid body chemoreceptors

2005 ◽  
Vol 99 (1) ◽  
pp. 114-119 ◽  
Author(s):  
David F. Donnelly ◽  
Insook Kim ◽  
Claire Carle ◽  
John L. Carroll
Keyword(s):  
Functional Impairment ◽  
Nerve Conduction ◽  
Single Unit ◽  
Acute Hypoxia ◽  
Adult Life ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Conduction Time ◽  
Activity Levels

Hyperoxia in the immediate perinatal period, but not in adult life, is associated with a life-long impairment of the ventilatory response to acute hypoxia. This effect is attributed to a functional impairment of peripheral chemoreceptors, including a reduction in the number of chemoreceptor afferent fibers and a reduction in “whole nerve” afferent activity. The purpose of the present study was to assess the activity levels of single chemoreceptor units in the immediate posthyperoxic period to determine whether functional impairment extended to single chemoreceptor units and whether the impairment was only induced by hyperoxia exposure in the immediate postnatal period. Two groups of rat pups were exposed to 60% inspired O2 fraction for 2 wk at ages 0–14 days and 14–28 days, at which time single-unit activities were isolated and recorded in vitro. Compared with control pups, hyperoxia-treated pups had a 10-fold reduction in baseline (normoxia) spiking activity. Peak unit responses to 12, 5, and 0% O2 were reduced and nerve conduction time was significantly slower in both hyperoxia-treated groups compared with control groups. We conclude that 1) hyperoxia greatly reduces single-unit chemoreceptor activities during normoxia and acute hypoxia, 2) the treatment effect is not limited to the immediate newborn period, and 3) at least part of the impairment may be due to changes in the afferent axonal excitability.

An important functional role of persistent Na+ current in carotid body hypoxia transduction

2006 ◽  
Vol 101 (4) ◽  
pp. 1076-1084 ◽  
Author(s):  
Edward Vincent S. Faustino ◽  
David F. Donnelly
Keyword(s):  
Carotid Body ◽  
Acute Hypoxia ◽  
Whole Body ◽  
Conduction Time ◽  
Afferent Neurons ◽  
Patch Clamp Recording ◽  
Peripheral Chemoreceptor ◽  
Whole Cell Patch Clamp ◽  
Old Rats

Systemic hypoxia in mammals is sensed and transduced by the carotid body into increased action potential (AP) frequency on the sinus nerve, resulting in increased ventilation. The mechanism of hypoxia transduction is not resolved, but previous work suggested that fast Na+ channels play an important role in determining the rate and timing of APs (Donnelly, DF, Panisello JM, and Boggs D. J Physiol. 511: 301–311, 1998). We speculated that Na+ channel activity between APs, termed persistent Na+ current ( INaP), is responsible for AP generation that and riluzole and phenytoin, which inhibit this current, would impair organ function. Using whole cell patch clamp recording of intact petrosal neurons with projections to the carotid body, we demonstrated that INaP is present in chemoreceptor afferent neurons and is inhibited by riluzole. Furthermore, discharge frequencies of single-unit, chemoreceptor activity, in vitro, during normoxia (Po2 150 Torr) and during acute hypoxia (Po2 90 Torr) were significantly reduced by riluzole concentrations at or above 5 μM, and by phenytoin at 100 μM, without significant affect on nerve conduction time, AP magnitude (inferred from extracellular field), and AP duration. The effect of both drugs appeared solely postsynaptic because hypoxia-induced catecholamine release in the carotid body was not altered by either drug. The respiratory response of unanesthetized, unrestrained 2-wk-old rats to acute hypoxia (12% inspired O2 fraction), which was measured with whole body plethysmography, was significantly reduced after treatment with riluzole (2 mg/kg ip) and phenytoin (20 mg/kg ip). We conclude that INaP is present in chemoreceptor afferent neurons and serves an important role in peripheral chemoreceptor function and, hence, in the ventilatory response to hypoxia.

scholarly journals Lactate as an oxidizable substrate for rat brain in vitro during the perinatal period

1983 ◽  
Vol 214 (2) ◽  
pp. 633-635 ◽  
Author(s):  
C Arizmendi ◽  
J M Medina
Keyword(s):  
Neonatal Period ◽  
Brain Slices ◽  
High Capacity ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Late Gestation ◽  
Lactate Oxidation ◽  
Energy Substrate ◽  
The Brain

Foetal brain slices showed a high capacity for lactate oxidation in vitro during late gestation. This capacity remained high during the very early postnatal period, suggesting that lactate may play an important role as an energy substrate in the brain during the early neonatal period. The capacity for lactate oxidation decreased markedly during the first 2 days of extra-uterine life and thereafter remained low.

scholarly journals Nellore cloned calf viability during the postnatal period

2021 ◽  
Vol 51 (7) ◽  
Author(s):  
Guilherme Gonçalves Fabretti Santos ◽  
Bruno Fornitano Cholfe ◽  
Igor Augusto Andreta Paiola ◽  
João Morelli Júnior ◽  
Eduardo Harry Birgel Junior ◽  
...  
Keyword(s):  
Somatic Cell Nuclear Transfer ◽  
Nuclear Transfer ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Total Calcium ◽  
Vitro Fertilization ◽  
Group I ◽  
High Incidence ◽  
Mucous Membranes

ABSTRACT: This study evaluated the viability of Nellore cloned calves derived from somatic cell nuclear transfer (SCNT) and compare their viability with animals of the same breed derived from in vitro fertilization (IVF). Thus, two groups were formed. Group I (GI) consisted of 10 calves derived from SCNT and group II (GII) consisted of 10 calves derived from IVF. The differences detected between the groups were in the physical examination of the respiratory tract in GI, which represented the most common clinical-pathological disturbances. The Apgar index score indicated that 80% of GI animals were depressed and all had pale mucous membranes. Thus, anemia was reported in GI. In GII, this started at 12 h of life and was probably caused by an iron deficiency. Moreover, total calcium and ionized calcium levels were higher in GI immediately after birth. These alterations probably resulted in a high incidence of mortality in GI, reaching 90% of the calves, whereas mortality was only 20% for the calves in GII. In conclusion, cloned calves, which were derived from SCNT, had physiological and metabolic alterations after delivery, leading to a higher mortality rate during the perinatal period.

scholarly journals Time Efficiency of Digitally and Conventionally Produced Single-Unit Restorations

2021 ◽  
Vol 9 (6) ◽  
pp. 62
Author(s):  
Sofia Stromeyer ◽  
Daniel Wiedemeier ◽  
Albert Mehl ◽  
Andreas Ender
Keyword(s):  
Single Unit ◽  
Operating Time ◽  
In Vitro Study ◽  
Working Time ◽  
Control Group ◽  
Similar Amount ◽  
Scan Design ◽  
Time Efficiency ◽  
Dental Professional

The purpose of this in vitro study was to compare the time efficiency of digital chairside and labside workflows with a conventional workflow for single-unit restorations. The time efficiency in this specific sense was defined as the time, which has to be spent in a dental office by a dental professional performing the relevant steps. A model with interchangeable teeth on position 36 was created. These teeth were differently prepared, responding to several clinical situations to perform single-unit restorations. Different manufacturing techniques were used: For the digital workflows, CEREC Omnicam (CER) and Trios 3 (TN/TI) were used. The conventional workflow, using a dual-arch tray impression technique, served as the control group. For the labside workflow (_L) and the conventional impression procedure (CO), the time necessary for the impressions and temporary restorations was recorded and served as operating time. The chairside workflow time was divided by the time for the entire workflow (_C) including scan, design, milling and finishing the milled restoration, and in the actual working time (_CW) leaving out the chairside milling of the restoration. Labside workflow time ranged from 9 min 27 s (CER_L) to 12 min 41 s (TI_L). Entire chairside time ranged from 43 min 35 s (CER_C) to 58 min 43 s (TI_C). Pure chairside working time ranged from 15 min 21 s (CER_CW) to 23 min 17 s (TI_CW). Conventional workflow time was 10 min 39 s (CO) on average. The digital labside workflow and the conventional workflow require a similar amount of time. The digital chairside workflow is more time consuming.

scholarly journals Bone marrow mesenchymal stem cells promote prostate cancer cell stemness via cell–cell contact to activate the Jagged1/Notch1 pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ji-wen Cheng ◽  
Li-xia Duan ◽  
Yang Yu ◽  
Pu Wang ◽  
Jia-le Feng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Western Blot ◽  
Cell Contact ◽  
Activity Levels ◽  
Tumor Resistance ◽  
Cell Cell

Abstract Background Mesenchymal stem cells (MSCs) play a crucial role in cancer development and tumor resistance to therapy in prostate cancer, but the influence of MSCs on the stemness potential of PCa cells by cell–cell contact remains unclear. In this study, we investigated the effect of direct contact of PCa cells with MSCs on the stemness of PCa and its mechanisms. Methods First, the flow cytometry, colony formation, and sphere formation were performed to determine the stemness of PCaMSCs, and the expression of stemness-related molecules (Sox2, Oct4, and Nanog) was investigated by western blot analysis. Then, we used western blot and qPCR to determine the activity levels of two candidate pathways and their downstream stemness-associated pathway. Finally, we verified the role of the significantly changed pathway by assessing the key factors in this pathway via in vitro and in vivo experiments. Results We established that MSCs promoted the stemness of PCa cells by cell–cell contact. We here established that the enhanced stemness of PCaMSCs was independent of the CCL5/CCR5 pathway. We also found that PCaMSCs up-regulated the expression of Notch signaling-related genes, and inhibition of Jagged1-Notch1 signaling in PCaMSCs cells significantly inhibited MSCs-induced stemness and tumorigenesis in vitro and in vivo. Conclusions Our results reveal a novel interaction between MSCs and PCa cells in promoting tumorigenesis through activation of the Jagged1/Notch1 pathway, providing a new therapeutic target for the treatment of PCa.

Homozygous Expression of a Dominant Gene Causing Peroneal Muscular Atrophy (Charcot-Marie-Tooth Disease)

1974 ◽  
Vol 23 (S1) ◽  
pp. 217-220 ◽  
Author(s):  
H. Warner Kloepfer ◽  
James M. Killian
Keyword(s):  
Clinical Features ◽  
Nerve Conduction ◽  
Peripheral Nerves ◽  
Muscular Atrophy ◽  
Dominant Gene ◽  
Conduction Time ◽  
Charcot Marie Tooth ◽  
Charcot Marie Tooth Disease ◽  
Peroneal Muscular Atrophy ◽  
Tooth Disease

This study involves the presentation of a kindred from Southwestern Louisiana showing 66 individuals who were heterozygous for a rare dominant gene for a type of Charcot-Marie-Tooth disease with hypertrophy of peripheral nerves. Two marriages between heterozygotes resulted in the occurrence of five homozygous offsprings. Clinical features of these previously undescribed homozygotes are compared to the clinical features of the classic type of heterozygote. The value of using nerve-conduction time to detect the asymptomatic heterozygote for Charcot-Marie-Tooth disease is discussed.

scholarly journals Telomerase RNA Template Mutations Reveal Sequence-Specific Requirements for the Activation and Repression of Telomerase Action at Telomeres

2000 ◽  
Vol 20 (8) ◽  
pp. 2941-2948 ◽  
Author(s):  
John C. Prescott ◽  
Elizabeth H. Blackburn
Keyword(s):  
Enzymatic Activity ◽  
Activity Levels ◽  
Telomeric Dna ◽  
Telomere Shortening ◽  
Telomere Elongation ◽  
Telomere Binding Protein ◽  
Telomere Function ◽  
Double Base ◽  
Telomere Lengthening

ABSTRACT Telomeric DNA is maintained within a length range characteristic of an organism or cell type. Significant deviations outside this range are associated with altered telomere function. The yeast telomere-binding protein Rap1p negatively regulates telomere length. Telomere elongation is responsive to both the number of Rap1p molecules bound to a telomere and the Rap1p-centered DNA-protein complex at the extreme telomeric end. Previously, we showed that a specific trinucleotide substitution in the Saccharomyces cerevisiae telomerase gene (TLC1) RNA template abolished the enzymatic activity of telomerase, causing the same cell senescence and telomere shortening phenotypes as a complete tlc1 deletion. Here we analyze effects of six single- and double-base changes within these same three positions. All six mutant telomerases had in vitro enzymatic activity levels similar to the wild-type levels. The base changes predicted from the mutations all disrupted Rap1p binding in vitro to the corresponding duplex DNAs. However, they caused two classes of effects on telomere homeostasis: (i) rapid, RAD52-independent telomere lengthening and poor length regulation, whose severity correlated with the decrease in in vitro Rap1p binding affinity (this is consistent with loss of negative regulation of telomerase action at these telomeres; and (ii) telomere shortening that, depending on the template mutation, either established a new short telomere set length with normal cell growth or was progressive and led to cellular senescence. Hence, disrupting Rap1p binding at the telomeric terminus is not sufficient to deregulate telomere elongation. This provides further evidence that both positive and negativecis-acting regulators of telomerase act at telomeres.

In vitro evidence that LHRH stimulates the recruitment of prolactin mRNA-expressing cells during the postnatal period in the rat

1994 ◽  
Vol 12 (1) ◽  
pp. 107-118 ◽  
Author(s):  
A Van Bael ◽  
R Huygen ◽  
B Himpens ◽  
C Denef
Keyword(s):  
Cell Cycle ◽  
Cell Population ◽  
Blot Hybridization ◽  
Postnatal Period ◽  
S Phase ◽  
Female Rats ◽  
Mrna Levels ◽  
Dot Blot ◽  
Total Cell Population

ABSTRACT We have studied the effect of LHRH and neuropeptide Y (NPY) on prolactin (PRL) mRNA levels in pituitary reaggregate cell cultures from 14-day-old female rats, by means of in situ hybridization and Northern blot analysis. As estimated by computer-image analysis, addition of LHRH on day 5 in culture for 40 h resulted in a 37% increase in the total cytoplasmic areas of cells containing PRL mRNA, visualized using a digoxigenin-labelled PRL cRNA. The size of individual PRL-expressing cells was not influenced, nor was the content of PRL mRNA per cell. A similar effect of LHRH was found by dot blot hybridization of extracted RNA. PRL mRNA levels were not affected by NPY. LHRH induced a 29% increase in the number of PRL mRNA-expressing cells processing through the S phase of the cell cycle, visualized by the incorporation of [3H]thymidine ([3H]T) into DNA over 16 h. The fraction of [3H]T-labelled cells was 10–12% of the total cell population. NPY did not influence the number of [3H]T-positive cells expressing PRL mRNA, but completely blocked the effect of LHRH on the latter population. The present data suggest that LHRH, probably via a paracrine action of gonadotrophs, stimulates the recruitment of new lactotrophs, an action which is negatively modulated by NPY. Since the magnitude of this effect was the same in the total pituitary cell population as in cells processing through the S phase of the cell cycle and presumably mitosis, recruitment of lactotrophs seems to be based on differentiation of progenitor or immature cells into PRL-expressing cells, rather than on a mitogenic action on pre-existing lactotrophs alone.

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