Daniel Carlson

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Organic chemistry lab experiments to identify organic functional groups in a sample

DanCo writings , 2023

• To equip students with the use of litmus paper to determine the acidity/basicity of solutions. ... more • To equip students with the use of litmus paper to determine the acidity/basicity of solutions. • To determine the solubility of samples in different solutions. • To know the processes involved in identifying organic functional groups in compounds. • To be able to study the chemical properties of commonly encountered functional groups.

Impairment of blood volume restitution after large hemorrhage: a mathematical model

American Journal of Physiology-regulatory Integrative and Comparative Physiology, May 1, 1996

A mathematical model tests possible mechanisms for the progressive failure of blood volume restit... more A mathematical model tests possible mechanisms for the progressive failure of blood volume restitution seen after larger hemorrhages ( &gt; 26%) with increasing changes in plasma osmolality. After 10% hemorrhage, the model requires a decrease in net hydrostatic capillary pressure, the release of solute into the extracellular space, and the release of Na+ and K+ from a bound pool in equilibrium with the interstitium to match the experimental data. The solute and released cations expand the interstitium to drive the restitution of volume and protein from 3 to 24 h. After 30% hemorrhage, the best prediction of the average experimental responses occurs when the Na(+)-K(+)-adenosinetriphosphatase (ATPase) in the cell membrane is inhibited by 38.7% from 0.8 to 3 h, and the proportionality between capillary pressure and blood volume is reduced by 68% from its value for 10% hemorrhage. When the change in plasma osmolality is doubled after 30% hemorrhage, an increase in the inhibition of the ATPase to 85% and extension of its duration to 24 h are necessary to match experimental findings. The associated defect in sodium transport may occur after large hemorrhage so that sodium and water move into cells. This response may oppose osmotically driven expansion of the interstitium and thus account for the failure of restitution.

Locus coeruleus monoaminergic activity and plasma corticotropin after hemorrhage in cats

American Journal of Physiology-regulatory Integrative and Comparative Physiology, Feb 1, 1988

Temporal changes in monoaminergic activity in the locus coeruleus (LC) in response to hemorrhage ... more Temporal changes in monoaminergic activity in the locus coeruleus (LC) in response to hemorrhage of 10 or 20% of blood volume were assessed using normal pulse voltammetry in alpha-chloralose-urethan-anesthetized cats. Oxidation current was measured with a carbon microelectrode, and changes at 230 and 450 mV were used as estimates of catecholaminergic and indolaminergic activity, respectively. Plasma adrenocorticotropin (ACTH) was measured by radioimmunoassay. Hemorrhage of 20% blood volume caused a transient increase in the catecholaminergic activity in a compact area in the ventral LC (vLC) that preceded increases in the plasma ACTH. The increase in oxidation current at 450 mV was similar to that at 230 mV, suggesting no significant contribution from indolamines. Dorsal rostral pontine sites outside this area exhibited either sustained decreases in oxidation current or no change in response to hemorrhage. The proportion of sites that exhibited transient increases in oxidation current in the vLC after the 10% blood loss was less than that after the 20% blood loss, suggesting that this response was dependent on the magnitude of hemorrhage. Since the LC was implicated previously in the control of ACTH release, we suggest that hemodynamic signals traversing the LC activate catecholaminergic mechanisms that, in turn, participate in the regulation of ACTH release after hemorrhage.

Noradrenergic turnover increases in locus coeruleus after hemorrhage in cats

American Journal of Physiology-regulatory Integrative and Comparative Physiology, Feb 1, 1988

Push-pull perfusion was used to determine monoaminergic activity in the locus coeruleus (LC) of a... more Push-pull perfusion was used to determine monoaminergic activity in the locus coeruleus (LC) of alpha-chloralose-urethan-anesthetized cats after 20% hemorrhage. Blood was withdrawn from 0 to 3 min and reinfused from 10 to 13 min. Continuous 5-min interval samples of perfusate were collected from -5 to 15 min. Concentrations of the monoamines were determined using high-performance liquid chromatography with electrochemical detection. The perfusion sites (n = 21) were identified histologically. In a group of eight contiguous sites in the ventral LC (vLC), 4-hydroxy-3-methoxy-phenyl(ethylene)glycol (MHPG) increased significantly from 0.50 +/- 0.22 (control) to 1.19 +/- 0.42 pmol/5 min during the first 5 min after hemorrhage (P less than 0.05). This response differed significantly from that obtained at the remaining 13 sites. Other metabolites were not often detectable for many sites either within or outside vLC, and their responses to hemorrhage were not significant. The response of MHPG in the vLC indicates that norepinephrine (NE) turnover increases in this area selectively and implicates NE in the increase in the catecholamine oxidation current reported previously using in vivo voltammetry. Since the vLC was shown previously to facilitate adrenocorticotropin (ACTH) release, the increase in NE turnover after hemorrhage could induce ACTH release. This increase may also act locally to modulate the ascending hemodynamic signal.

The Acceleration of Mitochondrial Respiration by Atp May Provide Protection Against Oxidant Lung Injury

Shock, 2004

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Hypotensive Hemorrhage Increases Calcium Uptake Capacity and BCL-XL Content of Liver Mitochondria

Shock, 2007

This study examines the hypothesis that HTS preserves renal blood flow following II/R injury. Ane... more This study examines the hypothesis that HTS preserves renal blood flow following II/R injury. Anesthetized male Sprague Dawley rats (300 gms) had microdialysis probes placed in the cortex (Cor,2 mm) and medullar (Med,4 mm) and perfused at 3 2l/min to measure basal and post II/R NO, PGE 2 , and thromboxane B 2 (TxB 2 ) synthesis. Laser Doppler fibers were placed similarly to continuously measure cortical and medullary blood flow (BF). The animals underwent superior mesenteric artery clipping (or sham, SH) for 30 minute followed by 60 minutes of reperfusion (30/60 II/R) with resuscitation with increasing concentrations of NS (10 cc/kg). Creatinine Clearance (mls/min, CrCL) was also measured. Data are reported as percent of baseline following 30/60 II/R (Mean T SEM, N 9 7, *P G 0.05 by ANOVA compared to Sham). These data show that II/R caused a decrease in cortical and medullary blood flow with an attempt of the cortex to compensate by increasing endogenous synthesis of NO and PGE 2 , both potent renal vasodilators. Treatment with 7.5% saline restored both cortical blood flow and endogenous NO and PGE 2 synthesis following II/R but not renal function. These data suggest that 7.5% saline can preserve cortical blood flow following distant II/R injury. Sham 30/60 .9%S 3%S 7.5%S Med-BF 18 T 6 3T 3* j7 T 4* j1 T 4* .6 T 4* Cor-BF 16 T 8 j1 T 4* j4 T 5* j6 T 6* 5 T 8

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Control of Release of Adrenocorticotropin and Vasopressin by the Supraoptic and Paraventricular Nuclei*

Endocrinology, 1981

To determine the relative roles of the hypothalamic supraoptic (SON) and paraventricular (PVN) nu... more To determine the relative roles of the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei in the control of the release of vasopressin and of ACTH, we have examined the hormonal responses to electrical stimulation (200 microA, 0.2 msec, 100 Hz, 20 sec) of these regions. Cats were anesthetized with chloralose-urethane. Blood samples were taken 30 sec before stimulation and 1.5 min poststimulation. ACTH and vasopressin were measured by RIA. Electrical stimulation of the caudal pole of the SON increased vasopressin in plasma (1.82 +/- 0.41 microU/ml, n = 17, P less than 0.01) and decreased ACTH (-26 +/- 4 pg/ml, n = 13, P less than 0.01). In contrast, stimulation of the PVN increased vasopressin (2.01 +/- 0.60 microU/ml, n = 7, P less than 0.001) and increased ACTH (107 +/- 20 pg/ml, n = 32, P less than 0.01). Previous work has shown that vasopressinergic neurons of PVN, but not of SON, project to the zona externa of the median eminence. Other have suggested that the retrograde flow of blood from the neural lobe to the median eminence and thence to the anterior lobe would allow vasopressin to influence the release of ACTH. The present results indicate that both SON and PVN facilitate the release of vasopressin. However, PVN facilitates, but SON inhibits the release of ACTH. These findings suggest that the projection from PVN to the zona externa of the median eminence mediates the release of ACTH and that retrograde flow from the neural lobe is not important in the control of ACTH release during modest and transient increases in the release of vasopressin.

Vasopressin-Dependent and -Independent Control of the Release of ADRENOCORTICOTROPIN1

Endocrinology, 1982

We tested the possibility that vasopressin mediates the responses of adrenocorticotropin (ACTH) t... more We tested the possibility that vasopressin mediates the responses of adrenocorticotropin (ACTH) to electrical stimulation of various areas of the hypothalamus. Thirty-three cats were anesthetized with chloralose-urethane, immobilized with gallamine, and respired artificially. Plasma ACTH was measured by RIA. Intraventricular administration of antiserum to vasopressin blocked the release of ACTH induced by electrical stimulation of the paraventricular nucleus (PVN), suggesting a role for the vasopressinergic projection from PVN to the external zone of the median eminence. In contrast, the release of ACTH induced by stimulation of areas ventral to PVN was unaffected by the antiserum. Thus, there is at least one corticotropin releasing factor released from nuclei other than PVN that is distinct from vasopressin.

Organization of the Lateral Hypothalamus for Control of Adrenocorticotropin Release in the Cat*

Endocrinology, 1980

Regions in the ventral midbrain that project to the lateral hypothalamus have been implicated in ... more Regions in the ventral midbrain that project to the lateral hypothalamus have been implicated in the control of ACTH release. To define further those areas in the lateral hypothalamus through which afferent signals might pass, we electrically stimulated 188 sites in the lateral hypothalamus of 20 cats anesthetized with chloralose-urethane. Stimulations were monophasic pulses of DC (200 microA; 0.2 msec; 100 Hz; 20 sec). Venous samples were drawn over 30 sec 0.5 min before and 1.5 min after stimulation. Equal volumes of warmed isoncotic dextran were infused during sampling to prevent hypovolemia. ACTH was assayed by RIA. Areas were defined in which stimulation led to increased, decreased,, or unchanged ACTH. Mean changes in ACTH were tested by analysis of variance. The present data indicate that the ACTH-active areas defined previously in the midbrain may join the medial forebrain bundle in the subthalamic area and nucleus to traverse the lateral hypothalamus. At the level of the mammillary bodies, a facilitatory area occupied the ventral portion of the medial forebrain bundle. This area extended rostrally and medially to join the medial aspect of the medial forebrain bundle. Continuity with the mediobasal hypothalamus was seen only anteriorly in the area of the supraoptic decussations. An inhibitory area occupied the dorsal extent of the medial forebrain bundle at the level of the mammillary bodies. It extended rostrally and laterally around the caudal pole of the supraoptic nucleus and then medially at the level of the optic chiasm. There appear to be no other medial projections of the lateral lying ACTH-active areas to the mediobasal hypothalamus. The lateral hypothalamus may serve as a site of passage and/or of processing of information that ascends from the midbrain and descends from the limbic system.

Response of Plasma Adrenocorticotropin to Injections of L-Glutamate or Norepinephrine in the Dorsal Rostral Pons of Cats*

Endocrinology, 1991

Previously, electrical stimulation of several nuclei in the dorsal rostral pons of the cat was sh... more Previously, electrical stimulation of several nuclei in the dorsal rostral pons of the cat was shown to modulate the release of ACTH. However, the stimulation may have activated fibers of passage. To determine if there are specific groups of neurons within the pons that modulate plasma ACTH when stimulated with glutamate, 30 cats were prepared acutely under chloralose anesthesia. Microinjections of several agents were made at each of 2 sites in the pons of each cat. ACTH was measured by RIA. Injections of 150 mM L-glutamate (100 nl/min.2 min) elicited increases in arterial pressure that were related to the loci of injection. The responses did not decrease significantly when the rate and volume of the injection were reduced by half. Eight sites in a lateral area that extended rostrally from the parabracheal nucleus elicited a significant pressor response that was greater in duration and magnitude than a second significant pressor response that was obtained from 18 sites in a medial area that included the rostral locus coeruleus. Pressor responses did not occur when 0.1 mM norepinephrine or vehicle was substituted for L-glutamate in any area. The larger, but not the smaller, dose of L-glutamate elicited changes in plasma ACTH that were related to the loci of injection. Eight sites in a caudal area that included the ventral locus coeruleus and was within the medial pressor area elicited a significant increase in ACTH. Seven sites in an area rostral to the ventral locus coeruleus that included the rostromedial locus subcoeruleus elicited a significant decrease in plasma ACTH. ACTH responses were not observed when 0.1 mM norepinephrine or vehicle was substituted for L-glutamate in any area. In conclusion, the ventral locus coeruleus and the rostrally adjacent locus subcoeruleus contain neurons with receptors for L-glutamate that can modulate plasma ACTH and arterial pressure independently of a second pathway that includes the parabracheal region and influences arterial pressure. Because the neurons in the coeruleus are known to respond to hemodynamic input, they may participate in the hemodynamic control of ACTH release.

Alpha-adrenergic input in the locus coeruleus modulates plasma adrenocorticotropin in cats

Endocrinology, 1992

Previous evidence suggested that noradrenergic activity in the vicinity of the ventrorostral locu... more Previous evidence suggested that noradrenergic activity in the vicinity of the ventrorostral locus coeruleus (LC) increased in response to hemorrhage. To investigate the possible role of this response in the control of ACTH release, microinjections (100 nl/min for 2 min) of several agents were made at 59 sites in 35 cats anesthetized with chloralose. Injections were as follows: vehicle (all sites); 150 mM L-glutamate (GLU; 51 sites); an alpha 2-agonist, 1 mM clonidine (19 sites); an alpha 2-antagonist, 1 mM yohimbine (32 sites); an alpha 1-agonist, 1 mM phenylephrine (PE; 42 sites); and an alpha 1-antagonist, 0.05 mM prazosin (20 sites). Plasma ACTH was measured by RIA. Responses were tested statistically by repeated measures analysis of variance. GLU at 12 sites in the region of the ventrorostral LC facilitated plasma ACTH (P less than 0.01), whereas GLU at 6 sites in the caudal LC inhibited ACTH (P less than 0.05). Clonidine at 9 sites in an area that included the ventrorostral LC inhibited ACTH (P less than 0.05), and yohimbine at 7 sites within this latter area facilitated ACTH (P less than 0.01). PE within the ventrorostral LC had no effect on ACTH. However, PE at 10 sites within the caudal LC and along the ventromedial border of the ventrorostral LC facilitated ACTH. The responses for all of these areas to the respective agents differed from those to vehicle, whereas responses from other areas to the former agents or from all areas to prazosin did not. An increase in noradrenergic turnover in the LC may provide inhibitory alpha 2 modulation to the neurons in the LC that are activated by hemorrhage. This modulation and possible alpha 1 input in areas adjacent to the ventrorostral LC may influence the hemodynamic control of ACTH release.

Acid- and Base-Catalyzed Hydrolysis of Chloroacetamide Herbicides

Journal of Agricultural and Food Chemistry, Jun 1, 2006

Supporting Information describes methods used to synthesize two chloroacetamide degradates, along... more Supporting Information describes methods used to synthesize two chloroacetamide degradates, along with data pertaining to their mass spectra and 1 NMR spectra. Also included are mass spectra of hydrolysis products observed in this study, as well as a scheme outlining proposed pathways in acid hydrolysis of N-alkoxyethyl substituted chloroacetamides.

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Improved Liquid Mixture Viscosity Predictions with the Tlvmie Force Field

SSRN Electronic Journal

Improved liquid viscosity prediction with the novel TLVMie force field for branched hydrocarbons

Fluid Phase Equilibria

Liquid viscosity oriented parameterization of the Mie potential for reliable predictions of normal alkanes and alkylbenzenes

Fluid Phase Equilibria

Influence of oocyte selection, activation with a zinc chelator and inhibition of histone deacetylases on cloned porcine embryo and chemically activated oocytes development

Zygote, 2020

SummaryThe aim of this study was to evaluate the effects of alternative protocols to improve oocy... more SummaryThe aim of this study was to evaluate the effects of alternative protocols to improve oocyte selection, embryo activation and genomic reprogramming on in vitro development of porcine embryos cloned by somatic cell nuclear transfer (SCNT). In Experiment 1, in vitro-matured oocytes were selected by exposure to a hyperosmotic sucrose solution prior to micromanipulation. In Experiment 2, an alternative chemical activation protocol using a zinc chelator as an adjuvant (ionomycin + N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) + N-6-dimethylaminopurine (6-DMAP)) was compared with a standard protocol (ionomycin + 6-DMAP) for the activation of porcine oocytes or SCNT embryos. In Experiment 3, presumptive cloned zygotes were incubated after chemical activation in a histone deacetylase inhibitor (Scriptaid) for 15 h, with the evaluation of embryo yield and total cell number in day 7 blastocysts. In Experiment 1, cleavage rates tended to be higher in sucrose-treated oocytes ...

Dysregulated ribonucleoprotein granules promote cardiomyopathy in RBM20 gene-edited pigs

Nature Medicine, 2020

Ribonucleoprotein (RNP) granules are biomolecular condensates-liquid-liquid phase-separated dropl... more Ribonucleoprotein (RNP) granules are biomolecular condensates-liquid-liquid phase-separated droplets that organize and manage messenger RNA metabolism, cell signaling, biopolymer assembly, biochemical reactions and stress granule responses to cellular adversity. Dysregulated RNP granules drive neuromuscular degenerative disease but have not previously been linked to heart failure. By exploring the molecular basis of congenital dilated cardiomyopathy (DCM) in genome-edited pigs homozygous for an RBM20 allele encoding the pathogenic R636S variant of human RNA-binding motif protein-20 (RBM20), we discovered that RNP granules accumulated abnormally in the sarcoplasm, and we confirmed this finding in myocardium and reprogrammed cardiomyocytes from patients with DCM carrying the R636S allele. Dysregulated sarcoplasmic RBM20 RNP granules displayed liquid-like material properties, docked at precisely spaced intervals along cytoskeletal elements, promoted phase partitioning of cardiac biomolecules and fused with stress granules. Our results link dysregulated RNP granules to myocardial cellular pathobiology and heart failure in gene-edited pigs and patients with DCM caused by RBM20 mutation.

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Editing Myosin VB Gene to Create Porcine Model of Microvillus Inclusion Disease, With Microvillus-Lined Inclusions and Alterations in Sodium Transporters

Gastroenterology, 2020

BACKGROUND & AIMS: Microvillus inclusion disease (MVID) is caused by inactivating mutations in th... more BACKGROUND & AIMS: Microvillus inclusion disease (MVID) is caused by inactivating mutations in the myosin VB gene (MYO5B). MVID is a complex disorder characterized by chronic, watery, lifethreatening diarrhea that usually begins in the first hours to days of life. We developed a large animal model of MVID to better understand its pathophysiology. METHODS: Pigs were cloned by transfer of chromatin from swine primary fetal fibroblasts, which were edited with TALENs and single-strand oligonucleotide to introduce a P663-L663 substitution in the endogenous swine MYO5B (corresponding to the P660L mutation in human MYO5B, associated with MVID) to fertilized oocytes. We analyzed duodenal tissues from patients with MVID (with the MYO5B P660L mutation) and without (controls), and from pigs using immunohistochemistry. Enteroids were generated from pigs with MYO5B(P663L) and without the substitution (control pigs). RESULTS: Duodenal tissues from patients with MVID lacked MYO5B at the base of the apical membrane of intestinal cells; instead MYO5B was intracellular. Intestinal tissues and derived enteroids from MYO5B(P663L) piglets had reduced apical levels and diffuse subapical levels of sodium hydrogen exchanger 3 and SGLT1, which regulate transport of sodium, glucose, and water, compared with tissues from control piglets. However, intestinal tissues and derived enteroids from MYO5B(P663L) piglets maintained CFTR on apical membranes, like tissues from control pigs. Liver tissues from MYO5B(P663L) piglets had alterations in bile salt export pump, a transporter that facilitates bile flow, which is normally expressed in the bile canaliculi in the liver. CONCLUSIONS: We developed a large animal model of MVID that has many features of the human disease. Studies of this model could provide information about the functions of MYO5B and MVID pathogenesis, and might lead to new treatments.

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