PubMed Health⌕ Search

Biomedical subjects

J de Koning

Publications and source records attributed to J de Koning.

At least 37 records · Page 2Linked to original sources
PubMed1995

Respiratory failure in leptospirosis (Weil's disease).

Two patients with leptospirosis (Weil's disease), with acute respiratory failure necessitating mechanical ventilation, are described. Adult respiratory distress syndrome (ARDS) in one patient and profuse pulmonary bleeding in the other were the respective causes of respiratory failure. One patient died after developing the multiple organ dysfunction syndrome (MODS), the other patient recovered completely. Respiratory failure is an uncommon complication of leptospirosis and is due to severe pulmonary bleeding and/or ARDS.

Adult↗
PubMed1995

Improved outcome for patients with a cardiac arrest by supervision of the emergency medical services system.

BACKGROUND: The outcome for patients with an out-of-hospital cardiac arrest can only be improved through optimal pre-hospital therapy by the emergency medical services (EMS) system. So far it is not clear if physician supervision of the EMS system is necessary for an optimal result. METHODS: In a retrospective and prospective case series we describe the changes in outcome for patients with an out-of-hospital cardiac arrest after the implementation of limited physician supervision of the EMS system. We also analysed the factors that were responsible for these changes. RESULTS: We studied 479 consecutive patients with an out-of-hospital cardiac arrest. In the pre-intervention period, the survival rate for patients with an out-of-hospital cardiac arrest was 13%. This increased to 21.6% when physician supervision was implemented (p = 0.013). This increase in survival coincided with an improvement in pre-hospital advanced cardiac life support with an increase in the number of patients who arrived with a stable cardiac rhythm in the emergency department (p < 0.001). CONCLUSIONS: Limited physician supervision of an EMS system in a non-metropolitan area may improve the outcome for patients with an out-of-hospital cardiac arrest.

Adult↗
PubMed1995

Gonadotrophin surge-inhibiting/attenuating factor governs luteinizing hormone secretion during the ovarian cycle: physiology and pathology.

The stabilization of low luteinizing hormone (LH) concentrations during the period of the ovarian cycle preceding the mid-cycle LH surge seems to be of importance for embryo viability and survival. Several studies have stressed the importance of the timely excess of threshold levels of LH for optimal oocyte quality: LH already initiates the resumption of meiosis when a relatively low threshold level is reached, whereas a further outburst of LH release is necessary to reach the threshold level to induce ovulation. Hence, the mechanism of LH release should have the ability, on the one hand, to limit the LH secretion rate, and on the other, to allow an increased secretion rate, as during the LH surge. The functional antagonistic coupling of gonadotrophin-releasing hormone (GnRH) and the ovarian protein gonadotrophin surge-inhibiting factor or -attenuating factor (GnSIF/AF) provides such a mode of action for the control of LH concentration during the ovarian cycle. One of the important regulatory steps in this process is the de-novo synthesis of the so far unidentified pituitary proteins induced by GnRH. The induction of these proteins is a prerequisite for the increase in the rate of LH release. Because their synthesis is a time-consuming process, the effect becomes visible in the typical biphasic pituitary LH responses to the pulsatile or continuous administration of GnRH: initially low, with an increase after some time. This phenomenon is also known as the GnRH self-priming action. It is assumed that the synthesis of these self-priming-associated proteins is necessary to eliminate the inhibitory effect of GnSIF/AF. GnSIF/AF eliminates the effect of self-priming by neutralizing the biological activity of the pituitary proteins, which are responsible for the increased rate of LH release. Thus, the pituitary gland is kept in a GnRH-hyporesponsive state. The major advantage of such a slow protein synthesis-dependent regulatory mechanism is that it prevents sudden increases in the LH secretion rate in response to GnRH. Thus it stabilizes low LH concentrations to prevent the premature reinitiation of meiosis. However, the enhanced secretion of GnRH and/or the suppressed release or action of GnSIF/AF may finally lead to the restoration of the intrinsic LH responsiveness of the gonadotrophs at the start of the mid-cycle LH surge. The antagonistic interaction between GnRH and GnSIF/AF, and its implication in the control of LH release under physiological and pathological conditions, are discussed.

Animals↗
PubMed1995

From basal luteinizing hormone (LH) concentrations to the pre-ovulatory LH surge: titration of the physiological effect of gonadotrophin surge-inhibiting/attenuating factor.

Pulsatile luteinizing hormone (LH) release is thought to be controlled by the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the putative ovarian factor gonadotrophin surge-inhibiting/attenuating factor (GnSIF/AF). Our experiments were designed to titrate the input of endogenous basal and follicle stimulating hormone (FSH)-stimulated GnSIF/AF in this system. The effects were studied of five consecutive pulses of GnRH administration (10-250 pmol/pulse/kg rat), 1 h apart, on the self-priming effect in pro-oestrus phenobarbital-blocked rats injected with FSH or saline. In response to the two high pulses of GnRH, a clear GnRH self-priming was demonstrated. However, pulses of 25 pmol GnRH induced only a minor self-priming effect and the LH blood concentrations were within the physiological range. Pulses of 10 pmol GnRH had no effect. FSH suppressed the unprimed LH response and delayed GnRH self-priming by approximately 1 h. Increasing the GnRH pulse frequency of the 25 pmol GnRH pulses from one to three per hour induced pre-ovulatory-like LH surges. The effect was facilitated by ovariectomy to eliminate GnSIF/AF. Thus, the results are consistent with relative inputs of GnRH and GnSIF/AF being responsible for the changes in LH concentration during the ovarian cycle, including the generation of the mid-cycle LH surge.

Animals↗
PubMed1995

Acrodermatitis chronica atrophicans: a light and electron microscopic study.

Degeneration of the elastica and collagen fibres in skin biopsies from patients with acrodermatitis chronica atrophicans was studied with light and electron microscopy. Elastic fibres were involved in the infiltrative stage while the elastin plexus was still present. In the atrophic phase, only fragments of elastic and oxytalan fibres were seen and the elaunin plexus was absent. Some collagen fibres were surrounded by osmiophilic material. In all biopsies, myelin sheaths were collapsed without axon structures. Spirochetes could be demonstrated in 69% of the biopsies and were most numerous in infiltrative and nodular lesions. The loss of elasticity of the skin in the atrophic phase may be caused by the destruction of both elastic and elastin fibres.

Acrodermatitis↗
PubMed1995

The influence of ovarian steroids on hypothalamic-pituitary-adrenal regulation in the female rat.

The present study examined the association between hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-ovarian axes. HPA activity determined by plasma levels of adrenocorticotropin (ACTH) and corticosterone (B) was assessed in intact female rats as a function of oestrous cycle stage under resting conditions and after exposure to a 20 min restraint stress. To delineate the roles of oestradiol and progesterone in HPA axis modulation, plasma concentrations of ACTH and B were determined in ovariectomised (OVX) animals treated with oestradiol and/or progesterone under resting conditions and during exposure to the stress of a novel environment. The effects of these steroid treatments on the transcription and/or binding properties of the two corticosteroid receptors, the mineralocorticoid (MR) and glucocorticoid (GR) receptors, were also examined in hippocampal tissue, (i) Fluctuations in basal and stress-induced plasma ACTH and B concentrations were found during the oestrous cycle with highest levels at late pro-oestrus. (ii) In OVX steroid-replaced animals, basal and stress-induced activity was enhanced in oestradiol and oestradiol plus progesterone-treated animals compared with OVX controls. (iii) Cytosol binding assays revealed an oestradiol-induced decrease in hippocampal MR capacity. This decrease appears to be due to an effect of the steroid on MR transcription as in situ hybridisation analysis of MR mRNA showed an oestradiol-induced decrease in MR transcript in all hippocampal subfields. (iv) Treatment of oestradiol-primed animals with progesterone reversed the oestradiol-induced decrease in hippocampal MR capacity. Data from MR mRNA hybridisation in situ experiments indicate that this reversal may be due to an antagonism of the oestradiol effect on MR transcription. (v) Progesterone treatment with or without prior oestradiol-priming induced a significant decrease in the apparent binding affinity of hippocampal MR. We show that progesterone and its 11 beta-hydroxylated derivative have a high affinity for the hippocampal MR. (vi) Neither oestradiol nor progesterone affected GR binding parameters in the hippocampus. In conclusion, we find that sex steroids modulate HPA activity and suggest that the observed effects of these steroids on hippocampal MR may underlie their concerted mechanism of action in inducing an enhanced activity at the period of late pro-oestrus.

Adrenocorticotropic Hormone↗
PubMed1994

On the dynamics between gonadotrophin surge-inhibiting factor and gonadotrophin releasing hormone (GnRH): role of self-priming and desensitization in the luteinizing hormone response to GnRH after follicle stimulating hormone treatment.

The effects were studied of follicle stimulating hormone (FSH)-induced production of gonadotrophin surge-inhibiting factor (GnSIF) on three phases of the pituitary responsiveness to gonadotrophin releasing hormone (GnRH): the unprimed, primed and desensitized phases. Rats were injected with FSH on two occasions during the oestrous cycle. Spontaneous luteinizing hormone (LH) surges were measured as well as GnRH-induced LH surges on the day of pro-oestrus during infusions with 100-4000 pmol GnRH/rat/10 h, in phenobarbital blocked rats. The spontaneous LH surges were attenuated or completely inhibited by the FSH treatment. FSH suppresses and prolongs the unprimed LH response and delays GnRH self-priming, especially during infusions with low concentrations of GnRH. This treatment does not affect the total LH response (area under curve) to the highest concentrations of GnRH and after ovariectomy. On the other hand, this response is suppressed during infusions with the lower concentrations of GnRH. Hence, FSH, via GnSIF, delays maximal priming of the LH response to GnRH, whereas the suppression of LH release is a consequence of the GnRH-induced progressed state of desensitization. The inconsistent effects of FSH on the mid-cycle LH surges are explained as a result of the interaction between the relative strengths of GnRH and GnSIF.

Animals↗
PubMed1994

Treponemal infections in hares in The Netherlands.

Treponemal infections in wild European brown hares (Lepus europaeus) from The Netherlands were diagnosed by means of serological tests for human syphilis and histological demonstration of spirochetes by the Bosma-Steiner silver impregnation method in histological sections of skin lesions. The treponeme should probably be classified as "Treponema paraluisleporis."

Animals↗
PubMed1994

Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates.

Anterior pituitary cells cultured as three-dimensional cell aggregates and incubated with gonadotropin-releasing hormone (GnRH) show a biphasic pattern of luteinizing hormone (LH) release when steroid-free bovine follicle fluid is added to the culture medium. Initially, the GnRH-induced LH release is low (lag-phase response), but LH release increases during further incubations with GnRH (primed-state response). Also, in aggregates of dispersed cells from long-term ovariectomized rats cultured for 2 days in the presence of 1% bovine follicle fluid, a low initial LH responsiveness to GnRH could be restored. Cycloheximide was found to block the induction of the primed state, indicating the protein synthesis dependency of GnRH self-priming. In aggregates from gonadotroph-enriched cell populations obtained by velocity sedimentation in a bovine serum albumin gradient, addition of 1% bovine follicle fluid to the culture medium also restored a biphasic pattern of GnRH-induced LH release. However, co-culturing the gonadotroph-enriched cell aggregates with a folliculo-stellate (FS) cell-enriched population resulted in the attenuation of the differences in LH secretion rate between early and late responses to GnRH. The present example of the attenuation by folliculo-stellate cells of pituitary hormone secretion responses demonstrates that the cells regulate the cellular processes leading to a priming of the LH response to GnRH, rather than interfering with the access of GnRH to its receptor in gonadotrophs. Finally, it was found that stimulation of the adenylate cyclase enzyme with maximal effective doses of forskolin counteracted the inhibitory effect of bovine follicle fluid on the initial LH response to GnRH, but did not completely abolish the biphasic pattern of LH release. It is concluded that coupling to the adenylate cyclase enzyme is presumably involved in the LH surge inhibiting feedback action on the pituitary cells, but also other messenger pathways and intercellular interactions between pituitary cells may play a role in establishing a biphasic LH release at the pituitary level following GnRH administration.

Animals↗
PubMed1994

Erythromycin-induced torsades de pointes and ventricular fibrillation in a patient with Legionella pneumonia.

Several case reports of erythromycin-induced torsades de pointes (TDP) arrhythmia have been reported in the literature. However, this potentially lethal side-effect of a frequently prescribed drug is not generally known. We report a patient who developed TDP followed by ventricular fibrillation during rapid infusion of erythromycin lactobionate. Although the patient used diuretics, probably predisposing her to arrhythmias due to hypokalaemia, several ECG abnormalities predisposing to TDP, all related to erythromycin infusion, occurred during observation in the ICU, establishing the precipitating role of erythromycin. The diagnosis was made only after QT prolongation, TDP and ventricular fibrillation were observed during rapid intravenous infusion of erythromycin lactobionate, one of the reasons no doubt being the assumed lack of serious side-effects of this frequently prescribed drug.

Aged↗
PubMed1993

Borrelia burgdorferi myositis: report of eight patients.

Myositis is a rare manifestation of Lyme disease of unknown pathogenesis. This study describes the course of disease in eight patients with Lyme disease, aged 37-70 years, all of whom were suffering from histologically proven myositis. The clinical, electrophysiological, and myopathological findings are reported. One patient showed signs and symptoms of myositis of all limbs. In six patients myositis was localized in the vicinity of skin lesions, arthritis or neuropathy caused by Borrelia burgdorferi. In another patient suffering from pronounced muscle weakness of the legs and cardiac arrest, inflammation of the myocardium, the conducting system and skeletal muscles was revealed at autopsy. Muscle biopsy revealed lymphoplasmocellular infiltrates combined with few fibre degenerations in three patients. The lymphoplasmocellular infiltrates were found predominantly in the vicinity of small vessels. Several spirochetes were stained in six of seven muscle biopsy samples by means of the immunogold-silver technique. Culturing of B. Burgdorferi from the muscle biopsy samples was, however, unsuccessful. Antibiotic treatment succeeded in curing the myositis in four of six patients. In one patients signs and symptoms improved. One patient died from cardiac arrest caused by myocarditis and Guillain-Barré syndrome. The outcome is unknown in one patient. Clinical and myopathological findings indicate that Lyme myositis can be caused either by local spreading of B. burgdorferi or an unknown antigen or toxin from adjacent tissues or haematogenously.

Adult↗
PubMed1993

Myositis in Lyme borreliosis: an immunohistochemical study of seven patients.

Myositis is a rare complication of Lyme disease. In order to get information about the pathogenesis of this disorder, muscle specimens of 7 patients suffering from myositis as a manifestation of Lyme borreliosis were examined by immunohistology. Lyme spirochetes could be found in muscle biopsies of 6 patients. Infiltrates consisted mainly of macrophages and T helper/inducer cells. The T4/T8 ratio was 1.7 in the endomysium and 2.1 in the perimysium. Increased expression of MHC-I molecules by several muscle fibers was observed in 2 subjects only. No MHC-II molecules were expressed by muscle fibers. Lymphocytes expressing the interleukin-2 receptor were detected in 2 patients. Leu-15+ and Leu-11+ cells were found only to a slight extent in 2 patients. In conclusion the immunohistochemical findings in myositis due to Lyme borreliosis are different from other manifestations of this disease, and also from other forms of myositis.

Adult↗
PubMed1993

Lesions in the hypothalamus after active immunisation against GnRH in the pig.

The terminals of the hypothalamic gonadotrophin hormone-releasing hormone (GnRH) neurons are located within the median eminence and thereby extend beyond the protection of the blood-brain barrier. Thus, these terminals may be subjected to direct autoimmune action in animals that are actively immunised against GnRH. Boars (male pigs) (n = 108) were actively immunised against GnRH by two successive injections with synthetic GnRH, covalently coupled to KLH and dissolved in CFA or IFA. They were killed at 26 weeks of age. Immunised boars were selected on the basis of the resultant testes size, which indicates the effectiveness of the immunisation. The hypothalami of 25 selected animals were studied by histological and immunocytochemical techniques and compared with the hypothalami of three sham- and nine control animals. In the immunised animals, changes in the GnRH system had taken place. These comprised dystrophy of the perikarya and a sharp decrease of the GnRH immunocytochemical reactivity in the terminals within the median eminence. In addition, various degrees of inflammatory reactions were present, particularly within the median eminence. These consisted of tissue disruption by edema, collapse of the capillaries, fibrosis and infiltration with fibroblasts. In addition, accumulations of neurosecretum within the median eminence in combination with hypertrophy of magnocellular neurons within the hypothalamus were present. The reactions were restricted to the median eminence and did not involve other neurohemal organs or other parts of the hypothalamus. A correlation could be established between the incidence of the lesions and the effectiveness of the GnRH autoimmunity (as indicated by the size and endocrine function of the gonads and the anti-GnRH titres). Changes in extra- and intracellular IgG immunocytochemical reactivity within the median eminence indicated the involvement of IgG. The effects were absent from control and sham vaccinated animals and after vaccinations with other compositions of the vaccine. Thus, hypothalamic lesions have been observed in this selected group of animals, vaccinated against GnRH with this particular vaccine.

Amino Acid Sequence↗
PubMed1993

Induction of the gonadotrophin surge-inhibiting factor by FSH and its elimination: a sex difference in the efficacy of the priming effect of gonadotrophin-releasing hormone on the rat pituitary gland.

This study was designed to explore the efficacy of gonadotrophin-releasing hormone (GnRH) to antagonize the effect of gonadotrophin surge-inhibiting factor (GnSIF) on the timing of the induction by GnRH of the maximal self-priming effect on pituitary LH responsiveness. The GnSIF levels were increased by FSH treatment and reduced after gonadectomy. Female rats were injected s.c. with 10 IU FSH or saline (control) on three occasions during the 4-day cycle. Serial i.v. injections of GnRH (500 pmol/kg body weight) were administered to intact rats on the afternoon of pro-oestrus or 15-30 min after ovariectomy. Intact male rats were given 10 IU FSH and 500 or 2000 pmol GnRH/kg body weight on an equivalent time-schedule. Endogenous GnRH release was suppressed with phenobarbital. In intact female control rats, the timing of the maximally primed LH response was delayed as the GnRH pulse-interval increased. FSH treatment of female rats induced a suppression of the initial unprimed LH response and delayed the maximally primed LH response, which showed further delay as the GnRH pulse-interval was increased. When the pulsatile administration of GnRH was started 15-30 min after ovariectomy, the priming effect of GnRH did not change as the GnRH pulse-interval was increased in the saline-treated rats. However, FSH treatment caused a suppression of the unprimed LH response, a delay in the primed LH response and decreased the delay of the maximally primed LH response to GnRH when the GnRH pulse-interval was decreased. Increasing the interval between ovariectomy and the first GnRH pulse to 4 h diminished the efficacy of the FSH treatment: GnRH-induced priming was delayed by only one pulse instead of the two pulses in control rats. In intact males but not in orchidectomized rats, a self-priming effect was demonstrated during GnRH pulses which were 1 h apart. The effect of 2 nmol GnRH/kg body weight was the most pronounced. Compared with intact female rats, the timing of the maximally primed LH response was delayed by 1 h. FSH treatment did not affect the pituitary LH response to both dose levels of GnRH. It is concluded that FSH treatment increased the release of GnSIF by the ovary, then induced a state of low responsiveness of the pituitary gland to GnRH and subsequently delayed GnRH-induced maximal self-priming. The efficacy of GnRH to prime the pituitary gland was higher when GnSIF levels were decreasing after removal of the ovaries.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Effects of the opioid antagonist naltrexone-estrone azine on the luteinizing hormone-releasing hormone induced release of luteinizing hormone from the pituitary glands of ovariectomized rats.

The effects were studied of in vivo administration of the new opioid antagonist-estrogen hybrid, naltrexone-estrone azine (EH-NX), on subsequent luteinizing hormone-releasing hormone (LHRH)-stimulated luteinizing hormone (LH) release by the pituitary gland in vitro. It is well known that administration of estrogen exerts negative and positive effects on the pituitary LH response to LHRH, respectively after short-term and long-term treatment. Rats were injected subcutaneously with either 17 beta-estradiol-3-benzoate (EB), EH-NX or oil on days 18 and 19 (long-term treatment), and on day 21 (short-term treatment) following ovariectomy. Twenty minutes later the animals were killed and the pituitary glands were incubated in the presence of LHRH (1000 ng/ml) for 4 h. Whereas short-term treatment with EB on day 21 did not affect LH release in vitro, EH-NX significantly decreased the pituitary LH response to LHRH in oil pretreated rats. This inhibitory effect was partially blocked by the opioid antagonist naltrexone. After long-term EB or EH-NX, followed by short-term oil treatment, the pituitary LH response to LHRH was increased considerably, compared to the long-term oil controls. These observations demonstrate that the opioid antagonist estrogen hybrid EH-NX has estrogenic activity at the level of the pituitary gland. This hybridized drug is more effective in time than EB and an equimolar amount of EH (estrone hydrazone) to induce the negative estrogenic effect.

Animals↗
PubMed1992

Estrogenic effects of the new opioid antagonist naltrexone-estrone azine on pituitary luteinizing hormone secretion in ovariectomized rats.

The effect of the new opioid antagonist naltrexone-estrone azine (EH-NX) on pituitary luteinizing hormone (LH) secretion in the ovariectomized rat was studied. EH-NX is a hybrid between the steroid component estrone and the opioid antagonist naltrexone (NX). It is a potent and long-acting opioid antagonist in vitro and in vivo, but its effect upon in vivo LH secretion has not been tested before. The aims of the study were to investigate whether, unlike naltrexone, EH-NX can stimulate LH secretion without the need of additional estrogen pretreatment and whether EH-NX has peripheral estrogenic effects upon the uterine weight, when administered chronically to long-term ovariectomized rats. Female rats were injected subcutaneously with EH-NX 21 days after ovariectomy. The effects of EH-NX injections on LH secretion were compared to the effects of NX and estrone hydrazone (EH) alone, or in combination, with or without estradiol-benzoate (EB) pretreatment. Inhibition of LH secretion and uterine proliferation were observed in rats treated chronically with EH-NX in dosages of 0.250 mg/kg bw and higher. These effects were similar to those caused by EH and EB. In short-term OVX rats EH-NX appeared to act faster than EH. In contrast to NX, no stimulatory effect on LH secretion was seen with EH-NX in EB primed OVX rats. These results surprisingly demonstrate that EH-NX behaves like an estrogen and not like an opioid antagonist. The unexpected pharmacological profile of this new drug may open up doors for several medical applications.

Animals↗
PubMed1992

Unusual manifestations of Yersinia enterocolitica infections diagnosed using novel methods.

We report the cases of two patients who had infections due to Yersinia enterocolitica. The first patient exhibited chronic recurrent fever, hepatic and splenic granulomas, and bone marrow abnormalities, and the second patient presented with enterocolitis with leukocytoclastic vasculitis of the skin. Cultures and agglutination titers were negative. Indirect immunofluorescence techniques with use of serotype-specific antisera and antisera to Yersinia outer-membrane proteins (Yops) were applied to biopsy specimens, and immunoblotting techniques for determining class-specific circulating antibodies to Yops were used for demonstrating these unusual manifestations of Y. enterocolitica infections.

Adult↗