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Biomedical subjects

E Lundberg

Publications and source records attributed to E Lundberg.

At least 19 recordsLinked to original sources

Autocrine growth factors in human periodontal ligament cells cultured on enamel matrix derivative.

OBJECTIVE: Enamel extracellular matrix proteins in the form of the enamel matrix derivative EMDOGAIN (EMD) have been successfully employed to mimic natural cementogenesis to restore fully functional periodontal ligament, cementum and alveolar bone in patients with severe periodontitis. When applied to denuded root surfaces EMD forms a matrix that locally facilitates regenerative responses in the adjacent periodontal tissues. The cellular mechanism(s), e.g. autocrine growth factors, extracellular matrix synthesis and cell growth, underlying PDL regeneration with EMD is however poorly investigated. MATERIAL AND METHODS: Human periodontal ligament (PDL) cells were cultured on EMD and monitored for cellular attachment rate, proliferation, DNA replication and metabolism. Furthermore, intracellular cyclic-AMP levels and autocrine production of selected growth factors were monitored by immunological assays. Controls included PDL and epithelial cells in parallel cultures. RESULTS: PDL cell attachment rate, growth and metabolism were all significantly increased when EMD was present in cultures. Also, cells exposed to EMD showed increased intracellular cAMP signalling and autocrine production of TGF-beta1, IL-6 and PDGF AB when compared to controls. Epithelial cells increased cAMP and PDGF AB secretion when EMD was present, but proliferation and growth were inhibited. CONCLUSION: Cultured PDL cells exposed to EMD increase attachment rate, growth rate and metabolism, and subsequently release several growth factors into the medium. The cellular interaction with EMD generates an intracellular cAMP signal, after which cells secrete TGF-beta1, IL-6 and PDGF AB. Epithelial cell growth however, is inhibited by the same signal. This suggest that EMD favours mesenchymal cell growth over epithelium, and that autocrine growth factors released by PDL cells exposed to EMD contribute to periodontal healing and regeneration in a process mimicking natural root development.

Cell Adhesion↗

Enamel matrix derivative promotes reparative processes in the dental pulp.

During odontogenesis, amelogenins from the preameloblasts are translocated to differentiating odontoblasts in the dental papilla, suggesting that amelogenins may be associated with odontoblast changes during development. In the present study, we have explored the effects of enamel matrix derivative (EMD) on the healing of a pulpal wound. Coronal pulp tissue of permanent maxillary premolars of miniature swine were exposed through buccal class V cavities. The exposed pulp was capped with EMD. The contralateral teeth served as controls and were capped with a calcium hydroxide paste (Dycal). The cavities were sealed with glass-ionomer cement. After 2 and 4 weeks, the histology of the teeth was analyzed. In the EMD-treated teeth, large amounts of newly formed dentin-like hard tissue with associated formative cells outlined the pulpal wound separating the cavity area from the remaining pulp tissue. Inflammatory cells were present in the wound area but not subjacent to the newly formed hard tissue. Morphometric analysis showed that the amount of hard tissue formed in EMD-treated teeth was more than twice that of the calcium-hydroxide-treated control teeth (p < 0.001), suggesting that EMD is capable of promoting reparative processes in the wounded pulp more strongly than is calcium hydroxide.

Animals↗

Reversal of meconium inhibition of pulmonary surfactant by ferric chloride, copper chloride, and acetic acid.

Meconium inhibits pulmonary surfactant function. We investigated the in vitro effect of meconium on three different commercial surfactants. The dynamic surface properties of these surfactants were evaluated at the concentration of 5 mg/ml with a pulsating bubble system. The inhibitory effect of 2.75 mg/ml meconium was significantly less on Alveofact than on Curosurf and Survanta. Ferric chloride and copper chloride completely reversed the inhibitory effect of meconium. Meconium also prevented effective spreading of surfactant in a Wilhelmy balance system, and this inhibitory effect was counteracted by addition of ferric chloride. Image analysis of Curosurf demonstrated that meconium reduced the total number of microbubbles in 15 light-microscopic fields (4.35 mm(2)) from 1,748 +/- 481 to 180 +/- 166. Ferric chloride restored the number of microbubbles. Addition of ferric chloride or copper chloride to surfactant/meconium lowers pH, and pH adjustment by acetic acid also reversed the inhibitory effect of meconium. Together with the fact that the iron-chelator deferoxamine did not attenuate the effect of ferric chloride this suggests that the observed contrainhibition is caused by lowering of pH, and that meconium inhibition of surfactant is pH-dependent. Lowering pH from 6.2 to 5-5.5 abolished the inhibitory effects of meconium on surfactant. Inhibition of 2.5 mg/ml of Curosurf with plasma could also be reversed by increasing amounts of ferric chloride. We conclude that the inhibitory effect of meconium on surfactant in vitro can be abolished by addition of ferric chloride, copper chloride, or acetic acid.

Acetic Acid↗

The effect of immediate-hypersensitivity reactions on the level of SLPI, granulocyte elastase, alpha1-antitrypsin, and albumin in nasal secretions, by the method of unilateral antigen challenge.

BACKGROUND: The aim of this paper was to investigate the role of SLPI in patients with allergic rhinitis. From this point of view, we also examined leukocyte elastase, alpha1-antitrypsin, and albumin. SLPI is an inhibitor of serine proteases such as leukocyte elastase, cathepsin G, and mast-cell chymase. Since chymase is considered to participate in mast-cell degranulation and histamine release, SLPI might act as a regulator of allergic reactions. Recent interest has been focused on leukocytes and allergy. Since SLPI is a strong inhibitor of leukocyte elastase, we also focused on the function of elastase in allergic rhinitis. METHODS: We used the method of nasal lavage after unilateral nasal antigen challenge in atopic and healthy subjects. The ELISA quantified SLPI and elastase. Albumin and alpha1-antitrypsin were quantified by electroimmunoassay. Gel filtration was used to separate native SLPI from its complex with elastase. RESULTS: There was a higher level of SLPI in lavage fluid from healthy subjects than from atopic patients. SLPI was increased on the contralateral side in atopic subjects after allergen challenge. The absence of increase in SLPI on the challenged side may be attributed to the increase in elastase and its binding to SLPI, which might have an effect on the immunoreactivity and interfere with the ELISA. It may then be assumed that there is an augmentation of SLPI on the challenged side as well. No increase was seen in healthy subjects. There was a higher concentration of elastase, alpha1-antitrypsin, and albumin before antigen challenge in atopic patients outside the pollen season than in healthy subjects. As expected, an increase was also seen in the challenged side exclusively in atopic subjects. CONCLUSIONS: The lower concentration of SLPI in nasal lavage fluid among the atopic patients than the healthy subjects indicates damaged mucosa. Neural reflexes are involved in SLPI release since there was an increase even in the contralateral nostril. A higher level of elastase and albumin before allergen challenge suggests chronic inflammation in nasal mucosa outside the pollen season. Leukocyte recruitment takes place in response to IgE-mediated reactions, which are reflected in an increase in elastase in response to allergen challenge.

Adult↗

The subacromial impingement syndrome. A study of results of treatment with special emphasis on predictive factors and pain-generating mechanisms.

Forty-two patients with subacromial impingement syndrome entered a randomized prospective study comparing open anterior acromioplasty with a physiotherapy regime. The criterion for a successful outcome of treatment was a reduction of the initial pain score of more than 50% using the visual analogue scale (VAS) technique. The evaluation was performed by an independent observer. At the 6-month follow-up, treatment in the surgical group had been successful in 12/21 (57%) patients versus 6/18 (33%) in the physiotherapy group. A one-year evaluation revealed 16/21 (76%) "successes" in the surgical group. A direct and unbiased comparison with the physiotherapy group was not possible at one year, since 13 patients chose surgery after initial physiotherapy. However, in "an intention to treat" analysis outcome at one year was significantly better in those randomized to surgery. We found two standardized, composite, active movements--the "Pour out of a Pot" manoeuvre requiring the emptying of a pot of water, and the "Hand in Neck" manoeuvre--to be of predictive value for the outcome of surgery. When combining three pain-related variables into a criterion for prediction of success, a sensitivity of 78% (p < 0.02) and a specificity of 90% (p < 0.03) were attained. We advance the hypothesis that pain in the impingement syndrome is mainly elicited by comparison of the subacromial bursa. In some patients a traction-responsive pain generator in the supraspinatus tendon may be present as well.

Adult↗

IgE-mediated histamine release from nasal mucosa is inhibited by SLPI (secretory leukocyte protease inhibitor) to the level of spontaneous release.

The secretory leukocyte protease inhibitor (SLPI) is a low-molecular-weight inhibitor of proteases, such as elastase and cathepsin G which are released from leukocytes during phagocytosis. The purpose of this study was to determine whether or not SLPI is able to inhibit IgE-mediated histamine release. Nasal mucosa from 11 test subjects without atopic disposition was used for this in vitro study. We found that SLPI inhibited histamine release in a dose-dependent way but was without influence on the spontaneous release.

Histamine Release↗

Production and secretion of pancreatic secretory trypsin inhibitor in normal human small intestine.

The aim of this study was to prove the production and secretion of pancreatic secretory trypsin inhibitor (PSTI) in human small intestine. To achieve this we analyzed the content of immunoreactive PSTI (irPSTI) in rinsing fluid from isolated small intestine, using the urea method to estimate the volume of epithelial lining fluid recovered. IrPSTI, measured by an enzyme-linked, immunosorbent assay (ELISA), was present in both free and complexed form. The free PSTI showed intact biologic activity, binding trypsin in stable complexes. The complexed PSTI was dissociated on acidification. With the reverse transcriptase polymerase chain reaction (RT-PCR) and Southern blot hybridization, PSTI mRNA was demonstrated in the mucosa of the ileum. These findings indicate that PSTI is produced and secreted in the small intestinal epithelium and may be part of defence system in intestinal mucosa.

Adult↗

Leukocyte activation detected by increased plasma levels of inflammatory mediators in patients with ischemic cerebrovascular diseases.

BACKGROUND AND PURPOSE: Leukocytes have been implicated in the development of ischemic atherosclerotic vascular diseases. In a prospective study we investigated whether the plasma concentrations of inflammatory mediators, ie, proteases and cytokines, as markers for systemic leukocyte activation, are increased in patients with acute ischemic cerebrovascular diseases. METHODS: Using enzyme-linked immunosorbent assays, we measured the plasma levels of neutrophil gelatinase-associated lipocalin (NGAL), neutrophil proteinase 4 (NP4), tumor necrosis factor-alpha (TNF), and soluble TNF receptor protein-1 p55 (sTNFR-1) in 120 patients with acute ischemic cerebrovascular insult (72 with stroke and 48 with transient ischemic attack [TIA]) and in 35 age- and sex-matched healthy subjects. RESULTS: Compared with the control group, plasma NGAL levels were higher in the stroke group (P < .0001) and the TIA group (P < .01); plasma NP4 levels were higher in the stroke group (P < .0001) and the TIA group (P < .01); and plasma sTNFR-1 levels were higher in the stroke group (P < .04). There was significant correlation between the plasma levels of fibrinogen and those of both sTNFR-1 (r = .32; P = .005) and NGAL (r = .40; P = .0001) and between the erythrocyte sedimentation rate and the plasma levels of both sTNFR-1 (r = .35; P = .001) and NGAL (r = .34; P = .002). CONCLUSIONS: Our study demonstrated that markers for systemic leukocyte activation, ie, plasma levels of cytokines and proteases, were higher in patients with acute ischemic cerebrovascular disease than in healthy control subjects. Activated leukocytes and leukocytic mediators may have an important role in acute cerebrovascular ischemia and its consequences.

Aged↗

Release of cytokines and proteases from human peripheral blood mononuclear and polymorphonuclear cells following phagocytosis and LPS stimulation.

Release and cellular contents of pro- and anti-inflammatory cytokines, neutrophilic elastase and secretory leukocyte proteinase inhibitor (SLPI) were measured with enzyme-linked immunosorbent assay in peripheral blood mono- and polymorphonuclear cells stimulated with preopsonized yeast cells or lipopolysaccharide. Tumour necrosis factor alpha (TNF alpha) was also measured with a bioassay. TNF alpha production and soluble TNF alpha receptor I (sTNF RI) were demonstrated in the environment of both cell populations. The bioassay indicated levels of TNF alpha far below those detected by ELISA. The overall secretion of cytokines and their inhibitors was found to favour an anti-inflammatory balance in the environment of the stimulated cells. The interleukin-1 receptor antagonist (IL1-ra), compared with interleukin-1 beta (IL-1 beta), dominated the secretions from both cell types with a 100- to 1000-fold excess respectively. Most of the translated IL-1 beta was not secreted but found associated with the cellular compartments. In contrast to lipopolysaccharide (LPS) stimulation, preopsonized yeast cells stimulated a massive release of elastase from neutrophil cells.

Cell Line↗

Release of bacterial DNA by marine nanoflagellates, an intermediate step in phosphorus regeneration.

The concentrations of dissolved DNA and nanoflagellates were found to covary during a study of diel dynamics of the microbial food web in the Adriatic Sea. This observation was further investigated in a continuous seawater culture when nanoflagellates were fed bacteria grown in filtered seawater. Analysis of dissolved organic phosphorus and dissolved DNA showed a sixfold increase of dissolved DNA in the presence of the nanoflagellates (Ochromonas sp.). The amount of DNA released suggested that the majority of the consumed bacterial DNA was ejected. Phagotrophic nanoflagellates thus represent an important source of origin for dissolved DNA. The rate of breakdown of dissolved DNA and release of inorganic phosphorus in the pelagic ecosystem is suggested to be dependent on the ambient phosphate pool. In the P-limited northern Adriatic Sea, rapid degradation of the labelled DNA could be demonstrated, whereas the N-limited southern California bight water showed a much lower rate. Phosphorus originating from dissolved DNA was shown to be transferred mainly to organisms in the <3-mum-size fractions. On the basis of the C/P ratios, we suggest that a significant fraction of the phosphorus demand by the autotrophs may be sustained by the released DNA during stratified conditions. Thus, the nucleic acid-rich bacterial biomass grazed by protozoa plays an important role in the biogeochemical cycling of phosphorus in the marine environment.

Journal Article↗

Release of immunoreactive human neutrophil proteinase 4, normally and in peritonitis.

A specific enzyme-linked immunoassay (ELISA) has been developed for the determination of neutrophil proteinase 4 (NP4) in human plasma/serum and tissue fluids. Comparison of the sequence for the first 20 N-terminal amino acids of NP4, neutrophil elastase and cathepsin G shows that NP4 is distinct from the other two proteases. However, all three show considerable homology. Neither elastase nor cathepsin G show any immunoreactivity when tested in the present ELISA. Normal human plasma contains about 38 micrograms/l of NP4, identified as alpha 1-proteinase inhibitor complexes. This represents about 50% of the total amount of NP4 released in plasma. The remaining 50% is bound by alpha 2-macroglobulin. Blood coagulation leads to a rapid release of NP4 from the leukocytes. Peritonitis is accompanied by a pronounced release of NP4, as shown by a three-to 10-fold increase of NP4 plasma levels and by the NP4 level in peritoneal exudates, which reaches about 40 mg/l in severe cases.

Amino Acid Sequence↗

[Intensive dynamic back exercises for patients with chronic low back pain. A controlled study].

The effect of intensive dynamic back extensor exercises for patients with chronic low back was investigated in a controlled clinical trial where the patients underwent a three months intensive training program a total 30 sessions. The 105 patients were divided into three groups: a treatment group, an alternative group which underwent 1/5 of the treatment group's exercise program per session, and an alternative group in which the treatment consisted of thermotherapy, massage and mild exercise. Regardless of whether the outcome of treatment is assessed qualitatively or quantitatively, a statistically significant, favourable difference was found between the results for the treatment group and those for the alternative groups. The therapy was found to be without risk, but patients with clinical signs of current lumbar nerve root compression or radiological signs of spondylolysis or halisteresis of the column were excluded from the study. The authors recommend the introduction of this form of treatment as a general offer in the primary and secondary health sector. Back exercises can advantageously be conducted in a group; thus, the resources required for this treatment do not differ significantly from those required for many of the other forms of treatment generally employed, which often require individual attention.

Adult↗

The course of renal amyloidosis with uraemia.

The course of uraemia in 47 patients with renal amyloidosis has been studied. The median survival with a S-creatinine of 150 mumol/l was approximately 18 months, but 15% survived for more than 3 years. Deterioration arose often suddenly and was of unclear cause. Approximately 25% of the patients improved for a while and the reason for this temporary improvement is also unclear. The unsteady course during the uraemia period for amyloidosis patients makes prognosis calculations very much less accurate than for patients with cystic kidneys.

Amyloidosis↗