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S Dijkstra

Publications and source records attributed to S Dijkstra.

At least 19 recordsLinked to original sources
PubMed2006

Intraspinal administration of an antibody against CD81 enhances functional recovery and tissue sparing after experimental spinal cord injury.

We previously demonstrated that the tetraspanin protein CD81 is up-regulated by astrocytes and microglia after traumatic spinal cord injury in rats and that CD81 is involved in adhesion and proliferation of cultured astrocytes and microglia. Since these reactive glial cells contribute to secondary damage and glial scar formation, we studied the effect of local administration of an anti-CD81 antibody in experimental spinal cord injury. Adult rats were subjected to a moderate spinal cord contusion injury and treated for 2 weeks with different doses of the anti-CD81 antibody AMP1 (0.5-5 microg/h) or non-immune IgG (5.0 microg/h). A technique was developed to infuse the antibodies directly into the lesion site via an intraspinal cannula connected to a pump. Functional recovery was monitored during 8 postoperative weeks by means of the Basso, Beattie and Bresnahan (BBB) locomotor rating scale, the BBB subscore and Grid-walk test. At the end of the study, quantitative histology was performed to assess tissue sparing. Our data showed that by itself cannulation of the lesion site resulted in minimal functional and histological impairments. Application of 0.5 microg/h AMP1 resulted in a marked functional recovery (BBB 2 points; Grid-walk 30% less errors compared to control). This recovery was accompanied by an 18% increase in tissue sparing at the lesion epicentre. No gross histological changes in glial scarring were apparent. Our data demonstrate beneficial effects of an anti-CD81 antibody on functional recovery in spinal cord injured rats and suggest that this effect is mediated through a reduction in secondary tissue loss.

Animals↗
PubMed2006

Mathematical modeling of gravitational effects on the circulation: importance of the time course of venous pooling and blood volume changes in the lungs.

A dip in blood pressure (BP) in response to head-up tilt (HUT) or active standing might be due to rapid pooling in the veins below the heart (preload) or muscle activation-induced drop in systemic vascular resistance (afterload). We hypothesized that, in the cardiovascular response to passive HUT, where, in contrast to active standing, little BP dip is observed, features affecting the preload play a key role. We developed a baroreflex model combined with a lumped-parameter model of the circulation, including viscoelastic stress-relaxation of the systemic veins. Cardiac contraction is modeled using the varying-elastance concept. Gravity affects not only the systemic, but also the pulmonary, circulation. In accordance with the experimental results, model simulations do not show a BP dip on HUT; the tilt-back response is also realistic. If it is assumed that venous capacities are steady-state values, the introduction of stress-relaxation initially reduces venous pooling. The resulting time course of venous pooling is comparable to measured impedance changes. When venous pressure-volume dynamics are neglected, rapid (completed within 30 s) venous pooling leads to a drop in BP. The direct effect of gravity on the pulmonary circulation influences the BP response in the first approximately 5 s after HUT and tilt back. In conclusion, the initial BP response to HUT is mainly determined by the response of the venous system. The time course of lower body pooling is essential in understanding the response to passive HUT.

Adult↗
PubMed2002

Ischaemic heart disease in Turkish migrants with type 2 diabetes mellitus in The Netherlands: wait for the next generation?

OBJECTIVE: To study the prevalence of ischaemic heart disease in Turkish and Surinam-Asian migrants with type 2 diabetes mellitus in the Netherlands as compared with Europeans. METHODS: In a consecutive case-control study, 59 Turkish and 62 Surinam-Asian patients were compared with 185 Europeans referred to a diabetes clinic for treatment of type 2 diabetes in the period 1992 to 1998. Main outcome measures were ischaemic heart disease and its associated risk factors. RESULTS: The prevalence of ischaemic heart disease was lower (9%) in the Turks (p < 0.02), but higher (29%) in the Surinam-Asians compared with the Europeans (23%). The Turks (52 +/- 10 years) and Surinam-Asians (46 +/- 12 years) were younger than the Europeans (64 +/- 11 years, p < 0.001). Body mass index was 32 +/- 5 (p < 0.001) in the Turks, 27 +/- 5 in the Surinam-Asians (p < 0.05) and 29 +/- 5 in the Europeans. Turkish patients smoked less (23%, p < 0.05) and used less alcohol (4%, p < 0.05) than the Europeans. Proteinuria was found in 24% of the Turks (p < 0.05), 37% of the Surinam-Asians (NS) and 46% of the Europeans. In univariate analysis ischaemic heart disease was related to Turkish origin, OR 0.34 (0.14-0.83) p < 0.02, to Surinam-Asian origin, OR 1.84 (1.00-3.38) p = 0.05, and smoking, OR 1.78 (1.18-2.68) p < 0.01. Other variables were not related to ischaemic heart disease. Multivariate analysis in a model with ethnicity and smoking showed significant relations between ischaemic heart disease and Turkish ethnicity, OR 0.19 (0.06-0.65) p = 0.007, Surinam-Asian origin, OR 2.77 (1.45-5.28) p = 0.002, and smoking, OR 1.79 (1.20-2.66) p = 0.004. CONCLUSION: Type 2 diabetes mellitus in different ethnic groups results in a significant difference in incidence of ischaemic heart disease. The most remarkable finding is a low incidence of ischaemic heart disease in the Turkish patients with type 2 diabetes, independent of smoking. The high prevalence of ischaemic heart disease in young migrant Asians with diabetes is confirmed.

Case-Control Studies↗
PubMed2001

CD81 and microglial activation in vitro: proliferation, phagocytosis and nitric oxide production.

CD81 (TAPA), a member of the tetraspanin family of proteins, is upregulated by astrocytes and microglia after traumatic injury to the rat central nervous system (CNS). To further understand the role of CD81 in the microglial response to injury, we analysed the functional effects of a CD81 antibody, AMP1, on cultured rat microglia. We found that AMP1 suppressed microglial proliferation in a dose-dependent manner. Furthermore, AMP1 stimulated myelin phagocytosis, probably by opsonizing the myelin. The phagocytosis of latex beads, as well as the production of nitric oxide, were not significantly influenced by AMP1. These data indicate that CD81 is involved in an important subset of microglial effector functions after CNS injury.

Animals↗
PubMed2000

Up-regulation of CD81 (target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat.

We examined the expression of CD81 (also known as TAPA, or target of the antiproliferative antibody) after traumatic spinal cord injury in the rat. CD81, a member of the tetraspanin family of proteins, is thought to be involved in reactive gliosis. This is based on the antiproliferative and antiadhesive effects of antibodies against CD81 on cultured astrocytes, as well as its up-regulation after penetrating brain injury. CD81 expression following dorsal hemisection of the spinal cord was determined immunohistochemically at time points ranging from 1 day to 2 months postlesion (p.l.). In the unlesioned cord a low background level of CD81 was observed, with the exception of the ependyma of the central canal and the pia mater, which were strongly CD81-positive. One day p.l., CD81 was diffusely up-regulated in the spinal cord parenchyma surrounding the lesion site. From 3 days onward, intensely CD81-positive round cells entered the lesion site, completely filling it by 7 days p.l. Staining with the microglial markers OX-42 and Iba1 revealed that these cells were reactive microglia/macrophages. At this time, no significant CD81 expression by GFAP-positive reactive astrocytes was noted. From the second week onward, CD81 was gradually down-regulated; i.e., its spatial distribution became more restricted. The CD81-positive microglia/macrophages disappeared from the lesion site, leaving behind large cavities. After 2 months, astrocytes that formed the wall of these cavities were strongly CD81-positive. In addition, CD81 was present on reactive astrocytes in the dorsal funiculus distal from the lesion in degenerated white matter tracts. In conclusion, the spatiotemporal expression pattern of CD81 by reactive microglia and astrocytes indicates that CD81 is involved in the glial response to spinal cord injury.

Animals↗
PubMed2000

Collagen IV deposits do not prevent regrowing axons from penetrating the lesion site in spinal cord injury.

Scarring is suggested to impede axon regrowth across the lesion site in the injured adult mammalian central nervous system. Collagen Type IV, as a major component of the scar formed after injury, is an impediment for successful axonal regeneration and a decrease in its amount is a prerequisite for regrowing axons to cross the lesion in the postcommissural fornix in the injured adult rat (Stichel et al. [1999] Neurosci. 93:321-333). The aim of the present study was to analyze the relationship between collagen IV deposits and regrowing axons at various times after dorsal hemi-section of the adult rat spinal cord. Immunohistochemical double staining revealed that penetrating neurofilament-positive axons and collagen IV deposits were co-localized in the lesion site in the initial stages of axonal sprouting (between 7 and 14 days post-operatively) and were still present 1 and 2 months post-operatively. Interestingly, collagen IV-immunoreactive areas located around cystic cavities formed at the site of injury 1 month post-operatively, were devoid of axons. In conclusion, our observations indicate that collagen IV deposits after spinal cord injury do not prevent neurofilament-positive regrowing axons from penetrating the lesion site.

Animals↗
PubMed1999

Selective stimulation of dendrite outgrowth from identified corticospinal neurons by homotopic astrocytes.

Corticospinal neurons were identified in primary cultures of cortical neurons established from rats that had been injected with a fluorescent tracer to retrogradely label the corticospinal tract. We measured neurite outgrowth from corticospinal neurons after they had been co-cultured with astrocytes derived from either the cerebral cortex (homotopic region) or spinal cord (target region) of postnatal rats. The axon length of corticospinal neurons was increased when they were cultured on astroglial monolayers compared to a control monolayer (fibroblasts). However, no difference in axon length was noted on cortical versus spinal cord-derived astrocytes. On the other hand, total dendritic length was increased on cortical compared to spinal cord astrocytes. This increase in total dendrite length was not the result of differences in the length of primary dendrites, but primarily of a higher number of dendrites and increased branching on the cortical astroglia. If the corticospinal neurons were co-cultured without physical contact with the astrocytes, axonal and dendritic outgrowth were not stimulated when compared to the fibroblast control. The data indicate that dendritic growth from corticospinal neurons is preferentially promoted by astrocytes from the cerebral cortex, whereas axonal growth is not influenced by the anatomical origin of the astrocytes. The impact of these findings on our understanding of the role of astrocytes in the development and regeneration of the corticospinal tract is discussed.

Animals↗
PubMed1999

The prognosis and outcome of patients referred to an outpatient clinic for rheumatic diseases characterized by the presence of antinuclear antibodies (ANA).

To evaluate if patients with symptoms related to the musculoskeletal system, characterized by the presence of ANA, are prone to develop SLE or other specific rheumatic diseases, a follow-up study was started to investigate all patients who for the first time visited the outpatient clinic of the Department of Rheumatology in the period from 1983 to 1986 and who had detectable ANA. Patients with anti-dsDNA antibodies were excluded from evaluation. In total 65 patients could be included in the study, with a mean duration of follow-up of 9.3 years (range 2-16 years). During follow-up a specific rheumatic diagnosis could be established in 38 patients, on 75% of the patients within 2 years of follow-up, and in 90% within 5 years. Five patients developed a non-rheumatic disease. For the remaining 22 patients, diagnosis was not conclusive. These patients without a conclusive diagnosis had a mild clinical picture, which remained stable during follow-up. In conclusion 58% of patients presented with rheumatic symptoms and detectable ANA developed an overt rheumatic disease, usually within the first 5 years of follow-up.

Antibodies, Antinuclear↗
PubMed1997

Diabetic patients with foot burns.

We describe six patients with non-insulin dependent (Type 2) diabetes mellitus (NIDDM) and thermal foot injury admitted to the Burn Centre in Rotterdam. They were all male with a mean age of 56.8 (range 47-63) years. The median patients' delay before admission was 27 (range 1-56) days. Five patients needed amputation. Healing of the wounds took a mean period of 9.5 (range 2-27) months. In two patients healing of the wounds took more than 1 year; these two patients also had recurrent foot burns. Neurological evaluation in four patients confirmed severe polyneuropathy and severe loss of heat pain, warmth, and cold sensation.

Burns↗
PubMed1996

Treatment of pathological fractures of the humeral shaft due to bone metastases: a comparison of intramedullary locking nail and plate osteosynthesis with adjunctive bone cement.

In a retrospective study 37 patients were surgically treated for 38 fractures (27 actual and 11 impending) caused by metastatic lesions of the humerus shaft. A comparison between plate osteosynthesis with bone cement (20 cases) and intramedullary nailing (18 cases) was made. There was no mortality related to the surgical procedure. The patients' survival rate was 61% after 3 months and 44% after 6 months; six were alive after 1 year. Overall, a subjective and objective relief of pain was achieved in 92% and 79%, respectively. Restoration of arm function was improved in 95%. The operative course was complicated in six patients after plate osteosynthesis (three local and three systemic complications) and in four patients after intramedullary nailing (one local and three systemic complications). Fixation failed in four patients, instability developed twice after intramedullary fixation without bipolar static locking. No significant difference in survival rate, pain relief, restoration of function and complications were associated with methods of treatment, or with operation of actual or impending pathological fractures. Despite the poor life expectancy our results indicate that intramedullary nailing with bipolar static locking and post-operative irradiation or plate osteosynthesis with bone cement for treatment of pathological (impending) fractures of the humerus shaft are safe ways to restore arm function and improve quality of life.

Adult↗
PubMed1994

Effects of dinitrophenol on active-transport processes and cell membranes in the Malpighian tubule of Formica.

In Formica Malpighian tubules KCl secretion is driven by a V-type H+ ATPase in the luminal membrane in parallel with a H+/K+ antiporter. The effect of the protonophore dinitrophenol (DNP) was investigated on the isolated, symmetrically perfused tubule. DNP was applied in two different concentrations: 0.2 mmol/l and 1 mmol/l. The effects were fast and rapidly reversible. The equivalent short-circuit current (Isc) was reduced significantly to respectively 25 +/- 3% Cn = 4) and -3 +/- 7% (n = 11) of the control value when 0.2 mmol/l or 1 mmol/l was added to the bath. When 1 mmol/l DNP was applied the transepithelial resistance (Rte) decreased significantly to 74 +/- 11% of the control value (n = 11), and the luminal over basolateral voltage divider ratio (VDR), providing an estimate of luminal over basolateral membrane resistance, decreased to 37 +/- 12% of the control (n = 6). A concentration of 1 mmol/l DNP was also applied from the lumen. The decrease in Isc was significant, but much less pronounced (74 +/- 5% of control; n = 6) and no significant changes in Rte and VDR were observed. It is argued that, when the concentration in the bath is high enough, DNP may cross the cell and have a protonophoric effect not only on the mitochondria but also across the luminal cell membrane explaining the drop in transepithelial and in relative luminal membrane resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1994

Mechanisms of K+ uptake across the basal membrane of malpighian tubules of Formica polyctena: the effect of ions and inhibitors.

In the presence of 6 mmol l-1 Ba2+, known to block the K+ channels in the basal membrane, a rise in bath [K+] ([K+]bl) induced an increase in intracellular K+ concentration ([K+]i) similar in amount and in time course to that obtained in the absence of Ba2+. The presence of active and passive (other than through K+ channels) K+ uptake mechanisms across the basal membrane was investigated in different bath K+ concentrations. Dihydro-ouabain (10(-3) mol l-1), a blocker of the Na+/K(+)-ATPase, tested in low bath [K+], and Sch28080 (10(-4) mol l-1), a K+/H(+)-ATPase inhibitor, were without effect on fluid secretion. Dihydro-ouabain was also without effect on electrical potential differences either in the absence or in the presence of Ba2+. Vanadate (10(-3) mol l-1), in contrast, strongly reduced fluid secretion not only in control solution but also in high-K+, Na(+)-free medium and reduced the transepithelial and the apical membrane potential differences but not the basal membrane potential difference of [K+]i. Omitting Na+ from the bathing medium, replacing Cl- by Br- or applying bumetanide (10(-5) mol l-1) inhibited fluid secretion only in a low-K+ (10 mmol l-1) medium. In 51 mmol l-1 [K+]bl, omitting Na+ was without effect and 10(-4) mol l-1 bumetanide was needed to inhibit secretion. Replacing Cl- by Br- stimulated fluid secretion at this K+ concentration. Bumetanide (10(-4) mol l-1) had no effect in 113 mmol l-1 [K+]bl. Bumetanide (10(-4) mol l-1) in 51 mmol l-1 [K+]bl did not affect membrane potentials, did not lower [K+]i and did not affect the rise in [K+]i observed on an increase in [K+]bl. The results were summarized in a model proposing that K+ channels play a dominant role in high-K+ (113 mmol l-1) bathing medium. A K+/Cl- cotransporter may become more important in 51 mmol l-1 [K+]bl and a K+/Na+/2Cl- cotransporter may gain in importance in 10 mmol l-1 [K+]bl. Active mechanisms for K+ uptake across the basal membrane seem to play no detectable role in sustaining fluid secretion. The response to vanadate might be due to an effect on the apical electrogenic H+ pump.

Animals↗