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Biomedical subjects

C Rupprecht

Publications and source records attributed to C Rupprecht.

At least 19 recordsLinked to original sources
PubMed2024

Oceanic islands act as drivers for the genetic diversity of marine species: Cardita calyculata (Linnaeus, 1758) in the NE Atlantic as a case-study.

Geographic distribution, as well as evolutionary and biogeographic processes and patterns of marine invertebrate benthic species are strongly shaped by dispersal ability during the life cycle. Remote oceanic islands lie at the brink of complex biotic and abiotic interactions which have significantly influenced the biodiversity patterns we see today. The interaction between geological environmental change and taxon-specific dispersal modes can influence species evolutionary patterns, eventually delimiting species-specific biogeographic regions. In this study, we compare the population genetic patterns of the marine bivalve Cardita calyculata in the northeast Atlantic, discussing the role of Macaronesian islands during past climatic cycles. The genetic structure and diversity patterns were outlined based on SSR-GBAS loci of 165 individuals and on the mitochondrial COI marker of 22 individuals from the Canary Islands, Madeira, Azores and the Mediterranean. The highly structured genetic pattern found among regions and within archipelagos suggests the central role of oceanic islands in promoting the divergence of the species in both the NE Atlantic and the Mediterranean. The high degree of divergence in the COI dataset (> 7%) suggests the existence of potential cryptic speciation that needs to be further explored with a more comprehensive sampling. Such patterns are only congruent with a scenario where C. calyculata populations were maintained during glacial/interglacial cycles, supporting the role of the studied archipelagos as drivers of diversity for marine biota. We stress the importance of developing studies for species with various life history and dispersal modes. In such a way, a more profound understanding of the biogeographic and evolutionary significance of oceanic islands can catalyse directed conservation efforts, especially in the context of the ongoing climate crisis.

Animals↗
PubMed2001

Prevalence of agglutinating antibodies to Sarcocystis neurona in raccoons, Procyon lotor, from the United States.

Equine protozoal myeloencephalitis (EPM) is the most important protozoal disease of horses in North America and it is caused by Sarcocystis neurona. Natural cases of encephalitis due to S. neurona have been reported in raccoons, Procyon lotor. We examined 99 raccoons for agglutinating antibodies to S. neurona using the S. neurona agglutination test (SAT) employing formalin-fixed merozoites as antigen. Raccoons originated in Florida (N=24, collected in 1996), New Jersey (N=25, collected in 1993), Pennsylvania (N=25, collected in 1999), and Massachusetts (N=25, collected in 1993 and 1994). We found that 58 (58.6%) of the 99 raccoons were positive for antibodies to S. neurona using the SAT; 44 of 99 raccoons (44%) had titers of > or =1:500. This prevalence is similar to the reported seroprevalence of 33-60% for S. neurona antibodies in horses from the United States using the Western blot test.

Agglutination Tests↗
PubMed2001

Prevalence of agglutinating antibodies to Neospora caninum in raccoons, Procyon lotor.

Neospora caninum is an apicomplexan parasite that causes neonatal neuromuscular disease in dogs and abortions in cattle. Dogs are the only proven definitive host. Little is known about the prevalence of antibodies to this parasite in wildlife. Sera from 99 raccoons (Procyon lotor) were examined for agglutinating antibodies to N. caninum using the modified agglutination test employing formalin-fixed tachyzoites as antigen. Raccoons originated in Florida (n = 24, collected in 1996), New Jersey (n = 25, collected in 1993), Pennsylvania (n = 25, collected in 1999), and Massachusetts (n = 25, collected in 1993 and 1994). Ten (10%) had antibodies to N. caninum; 9 had titers of 1:50, and 1 (1%) had a titer of 1:100. The present study indicates that raccoons have minimal exposure to N. caninum. The sera were also tested for agglutinating antibodies to Toxoplasma gondii and 46 (46%) were positive; 16 had titers of 1:50, 8 had titers of 1:100, and 22 had titers of > or = 1:500.

Agglutination Tests↗
PubMed1999

Different tachykinin receptors mediate chloride secretion in the distal colon through activation of submucosal neurones.

We investigated the role of tachykinin receptor subtypes on secretory responses in the guinea-pig distal colon using Ussing chamber experiments and intracellular recordings from submucosal neurones. Choline acetyltransferase (ChAT) and vasoactive intestinal polypeptide (VIP) were demonstrated in submucosal neurones by immunohistochemistry. In Ussing chamber experiments substance P (SP), the NK1-receptor agonist [SAR9,Met(O2)11]-SP and the NK-3-receptor agonist (MePhe7)-NKB increased dose-dependently short-circuit currents. The NK-2-receptor agonist (betaAla8)-NKA(4-10) had no effect. Responses to 1-100 nM SP, [(SAR9,Met(O2)11]-SP and (MePhe7)-NKB were tetrodotoxin-sensitive but hexamethonium-insensitive. While (MePhe7)-NKB-responses were atropine-sensitive at all concentrations, the atropine sensitivity of the secretory responses to SP and [SAR9,Met(O2)11]-SP dramatically decreased with increasing concentrations. [SAR9,Met(O2)11]-SP and (MePhe7)-NKB effects were blocked by the selective NK-I and NK-3 antagonists CP-99,994-1 (1 microM) and SR 142801 (1 microM), respectively. Combination of both antagonists blocked the SP-response. SR 142801 also suppressed the response to [SAR9,Met(O2)11]-SP. Desensitization with [SAR9,Met(O2)11]-SP significantly decreased (MePhe7)-NKB-responses but not vice versa. In intracellular recordings 90% of submucosal neurones were activated by both ISAR9,Met(O2)11]-SP and (MePhe7)-NKB as indicated by membrane depolarisation and enhanced spike discharge. These effects were tetrodotoxin-resistant and potentiated by atropine. NK-1-and NK-3-mediated responses occurred equally in ChAT-positive and in VIP-positive neurones. The results suggest the importance of NK-1- and NK-3-receptors on cholinergic and non-cholinergic submucosal neurones for secretory processes in the guinea-pig distal colon.

Action Potentials↗
PubMed1998

Polarized enteric submucosal circuits involved in secretory responses of the guinea-pig proximal colon.

1. Neuronal retrograde tracing with the dye DiI (1,1'-didodecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate), in combination with immunohistochemical detection of choline acetyltransferase (ChAT) and vasoactive intestinal peptide (VIP), were used to identify the innervation of the mucosa of the guinea-pig proximal colon by submucosal neurones. Ussing chamber experiments were performed to measure changes in short circuit current (delta Isc) evoked by electrical stimulation of the oral or anal end of the preparation. 2. The tracing studies revealed that the mucosa was primarily innervated by descending neurones (78%); the vast majority of these were VIP positive (85%). The numerically smaller ascending pathway (13%) was predominantly ChAT positive (69%). A small population (9%) of DiI-labelled neurones projected circumferentially. 3. Ussing chamber experiments revealed that oral electrical stimulation induced a significantly larger delta Isc than anal stimulation. The VIP antagonist VIP(6-28) significantly reduced only orally induced delta Isc. Anally induced delta Isc were significantly more atropine sensitive that orally induced delta Isc. Tissue incubation with carbachol or VIP significantly potentiated delta Isc induced by VIP and carbachol, respectively, indicating cross-potentiation. 4. This study provides the first functional demonstration of polarized innervation patterns from submucosal neurones to enteric mucosa. The ascending ChAT and descending VIP pathways suggest the existence of reflexes resulting in preferential release of VIP or acetylcholine. The distinct pathways might favour the observed cross-potentiation of cholinergic and VIPergic mediated secretion.

Action Potentials↗
PubMed1997

Knowledge and attitudes of residents in two areas of Massachusetts about rabies and an oral vaccination program in wildlife.

OBJECTIVE: To compare public knowledge and attitudes about rabies and an oral rabies vaccination program in raccoons. DESIGN: Random-digit dial telephone survey. SAMPLE POPULATION: Residents of 2 areas of Massachusetts. PROCEDURE: Residents of 2 areas of Massachusetts were called to participate in a telephone survey. One area (Cape Ann) included 8 towns, most of which have had rabies in raccoons since 1993. The second area (Cape Cod) included 7 towns, 5 of which have not had rabies in raccoons. Calls were made to 642 persons, and of these, 265 agreed to participate in the survey. Of the nonrespondents who were subsequently contacted again, half agreed to participate. Data were analyzed using a statistical program. Fisher's exact and chi 2 tests were used to determine associations. RESULTS: Residents from the area virtually free of rabies in raccoons were significantly less likely to consider rabies as a potential health threat for children in their household. The perception of rabies as a threat was higher for residents in the endemic area. Residents in both areas considered rabies control to be a high priority and supported use of state funding for an oral vaccination program. CLINICAL IMPLICATIONS: People recognize dangers associated with rabies and believe that oral vaccination programs will decrease the risk of exposure.

Administration, Oral↗
PubMed1997

Leukotriene-evoked cyclic chloride secretion is mediated by enteric neuronal modulation in guinea-pig colon.

Short term exposure to leukotrienes evoked a well known nerve mediated increase in short circuit current. It is unknown whether leukotrienes evoke in addition oscillations in chloride secretion, as has been reported for some of the other mediators released during inflammation. Therefore, the aim of this study was to characterize the effects of a long time exposure of leukotrienes on mucosal functions. Conventional Ussing chamber, and intracellular recording techniques were used to investigate the actions of leukotriene D4 and C4 on short-circuit current and excitability of submucosal neurons in guinea-pig distal colon. In Ussing chambers, long term exposure to leukotriene D4 or C4 evoked rhythmic oscillations in short-circuit current in 35% and 50% of tissues, respectively. These current bursts were blocked by tetrodotoxin, atropine, hexamethonium and piroxicam. Secretory response to short term exposure of leukotrienes was significantly higher in tissues exhibiting current bursts. Likewise, the potentiating effects of leukotrienes on the response to field stimulation was only observed in tissues exhibiting current bursts. In intracellular recording experiments, leukotriene C4 evoked activation of submucosal neurons that was partly sensitive to indomethacin; no oscillations in neuronal excitability could be demonstrated. Results suggested that long term exposure to leukotrienes evoked current bursts that were mediated by neural, cholinergic mechanisms as well as endogeneous prostaglandins.

Animals↗
PubMed1997

Differential effects of inflammatory mediators on ion secretion in the guinea-pig colon.

Bi-directional interactions between the enteric nervous system and the immune system play an important role in gut inflammation. We therefore investigated the effects of the inflammatory mediators, prostaglandin (PGD2, PGE2, PGI2, and PGF2 alpha) and leukotriene (LTC4), on guinea-pig colonic secretion and on electrophysiological behaviour of submucosal neurones. In Ussing chambers, all inflammatory mediators evoked a dose-dependent increase in short circuit current (Isc) that represented electrogenic chloride secretion. The secretory response was significantly reduced by tetrodotoxin (TTX) and atropine suggesting involvement of cholinergic submucosal neurones. Long-term application of prostaglandins and LTC4 induced TTX- and atropine-sensitive cyclical chloride secretions. Intracellular recordings revealed activation of submucosal neurones by all inflammatory mediators. This activation consisted of depolarisation of the membrane associated with increased spike discharge. Frequently, prostaglandins and LTC4 induced spontaneous occurrence of cholinergic fast excitatory postsynaptic potentials. Results suggest that the role of the enteric nervous system in neuroimmune interactions consists of a potentiation of the direct epithelial effect of inflammatory mediators by the activation of submucosal neurones. Ongoing nerve-mediated cyclical changes in chloride secretion may be interpreted as the induction of intrinsic alarm programs. The effects of inflammatory mediators may serve as a defense mechanism to dilute noxious substances in the lumen.

Animals↗
PubMed1996

The use of complementary therapies by cancer patients.

Since the beginning of time, persons with acute or chronic diseases have sought added control over their fates in the form of whatever therapies offered hope. Although conventional treatments for cancer have been proven to lower mortality rates significantly, patients continue to look for more ways to combat their illnesses. Little in the literature supports the actual frequency of use of such therapies, nor do we have published data to support the general assumption that their popularity is growing. This group of researchers reanalyzed data from the Cancer Survivorship Questionnaire of the 1992 National Health Interview Survey to compare the use of self-healing and psychosocial techniques before and after 1987. Using Martha Roger's conceptual framework of the Science of Unitary Human Beings, these therapies were viewed as unitary field practice modalities. Results of the secondary analysis of data from 2970 patients revealed that use of additional therapies increased by 63.9% after 1987.

Adult↗
PubMed1995

Effects of prostaglandin F2 alpha (PGF2 alpha) and prostaglandin I2 (PGI2) on nerve-mediated secretion in guinea-pig colon.

We have applied conventional flux-chamber and intracellular recording methods to investigate the effects of the prostaglandins PGF2 alpha and PGI2 upon epithelial ion transport and on the electrical behaviour of submucosal neurones in guinea-pig colon. In flux-chamber experiments on segments of colon, both prostaglandins evoked a dose-dependent increase in short-circuit current that was reduced in chloride-depleted Krebs solution and by serosal addition of tetrodotoxin or atropine, but was unaffected by hexamethonium. These results indicate activation of chloride secretion via submucosal neurones. The response to PGF2 alpha was decreased by piroxicam. Application of PGF2 alpha or PGI2 to submucosal neurones evoked depolarization of the membrane potential associated with an enhanced spike discharge. The depolarizing response was tetrodotoxin insensitive, indicating a direct effect of the prostaglandins on the impaled neurones. Membrane depolarization was frequently associated with the occurrence of fast excitatory postsynaptic potentials, suggesting in addition that part of the excitatory effect is mediated by the activation of neural circuits that drive the impaled neurone synaptically. The results of this study indicate that the secretory effects of prostaglandins are mediated in part by submucosal neurones and further suggest that the colonic submucosal plexus may function as an amplifier to enhance the epithelial response to inflammatory mediators.

Animals↗
PubMed1994

Effects of the inflammatory mediator prostaglandin D2 on submucosal neurons and secretion in guinea pig colon.

Conventional flux chamber and intracellular recording methods were used to investigate the mode of action of prostaglandin D2 (PGD2) on ion transport in muscle-stripped segments of guinea pig colon and on colonic submucosal ganglion cells. Application of PGD2 resulted in a dose-dependent increase in short-circuit current that was reduced by serosal addition of bumetanide, tetrodotoxin, atropine, or piroxicam, but not hexamethonium. Application of PGD2 to submucosal neurons evoked a depolarization of the membrane potential that was associated with an enhanced spike discharge. In AH/type 2 neurons, postspike afterhyperpolarizations were reduced in amplitude and duration. The depolarizing responses to PGD2 were not affected by tetrodotoxin, indicative of a direct effect of PGD2 on the impaled neurons. Whereas fast excitatory postsynaptic potentials (EPSPs) were not affected by PGD2, slow EPSPs were reduced by a presynaptic effect, indicating presynaptic suppression of noncholinergic neurotransmitter release. The study demonstrates that PGD2 acts as a neuromodulator to evoke nerve-mediated chloride secretion, predominantly through activation of cholinergic submucosal neurons. The results further indicate that PGD2 released from lamina propria immune cells during antigenic stimulation may influence mucosal function by altering electrical behavior of submucosal neurons.

Animals↗
PubMed1993

Rhein stimulates electrogenic chloride secretion by activation of submucosal neurons in guinea pig colon.

Conventional flux chamber methods were applied to investigate the mode of action of rhein, an active metabolite derived from colonic microbial fermentation of the naturally occurring sennoside laxatives, in muscle-stripped segments of guinea pig colon. Mucosal or serosal application of rhein (10 nmol/1 to 0.5 mmol/l) resulted in a dose-dependent increase in short-circuit current (Isc) that was superimposed by irregular fluctuations in Isc. The response to electrical field stimulation was increased. The rhein-evoked increase in Isc was reduced by serosal addition of 50 mumol/l bumetanide, 1 mumol/l tetrodotoxin, 1 mumol/l atropine and 10 mumol/l piroxicam but not 100 mumol/l hexamethonium, 1 mumol/l ICS 205 930 or 10 mumol/l cimetidine. The study suggests that rhein activates chloride secretion by excitation of submucosal neurons and release of acetylcholine and endogenous prostaglandins, but not by release of histamine or serotonin.

Acetylcholine↗
PubMed1992

MRI white matter hyperintensity in neuroleptic malignant syndrome (NMS)--a clue to pathogenesis?

The case of a young female patient with neuroleptic malignant syndrome (NMS) and extended MRI white matter hyperintensity in the left parietal and both occipital lobes is reported. MRI lesions resembled findings in hypertensive encephalopathy, they were not readily compatible with CNS vasculitis. Venous sinus thrombosis could be ruled out. Vascular encephalopathy with transient white matter edema and a small residual left parietal lesion is suggested. Neurochemical implications are discussed with particular reference to a possible involvement of excitatory amino acids in NMS pathogenesis.

Adult↗
PubMed1989

Triiodothyronine, thyroxine, and TSH response to dexamethasone in depressed patients and normal controls.

In view of recent investigations concerning alterations of thyroid function in depression, the pre- and postdexamethasone levels of T3, T4, and TSH of 14 patients during depression and after recovery were studied, in addition to those of 27 healthy controls. A reduction of T3 and TSH levels was shown to be dependent on the depressive state, with a tendency to lower T4 levels after recovery. Dexamethasone had a pronounced suppressive effect on TSH levels in healthy controls and in patients after recovery, but not during the depressive episode. These results point to an inadequate suppressibility of the hypothalamo-pituitary-thyroid (HPT) axis to dexamethasone during depression. There are close interrelations between the hypothalamo-pituitary-adrenal (HPA) and the HPT axes that are possibly affected during depressive illness.

Adult↗
PubMed1989

Effects of glucocorticoids on plasma catecholamines in depression.

To explore corticosteroid-catecholamine interactions in depression, plasma dopamine, norepinephrine, and epinephrine concentrations were studied both before and after dexamethasone in 16 patients during depression and after recovery, and in 28 healthy controls. Dexamethasone had a significant suppressive effect on plasma epinephrine levels in depressed patients and controls, while dopamine and norepinephrine levels were not significantly affected following dexamethasone administration. Levels of norepinephrine, epinephrine, and cortisol were positively correlated, while dopamine showed no correlation with cortisol values. These findings point to differentiated interrelations between certain catecholamines and glucocorticoids which possibly are affected during depressive illness.

Adult↗
PubMed1988

Gonadal steroid and gonadotropin response to dexamethasone: a study in sexual dysfunction and normal controls.

Numerous investigations have reported an alteration of hormonal response to dexamethasone in depressive disorder. No such data are available in psychogenic sexual dysfunction. Pre- and postdexamethasone levels of testosterone, estradiol, LH and FSH were studied in 20 male patients with sexual dysfunction and 20 male healthy controls. Dexamethasone had no influence on testosterone, estradiol, LH and FSH in normal controls. The patients showed an increase in testosterone and LH but not in FSH levels in the morning after dexamethasone administration. When compared with basal levels, the increase in postdexamethasone levels in sexual dysfunction was significant for testosterone (delta T) but not for LH (delta LH). The altered gonadal steroid and gonadotropin response to dexamethasone in sexual dysfunction might be due to disturbances of dexamethasone metabolism and glucocorticoid receptor density comparable to similar findings in depressive disorder.

Adult↗