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Biomedical subjects

M Grüb

Publications and source records attributed to M Grüb.

17 recordsLinked to original sources
PubMed2006

[On the socio-economic relevance of glaucoma].

About 800,000 people in Germany suffer from glaucoma. As the population ages, the prevalence of glaucoma will rise and the socio-economic impact of the disease increase. The costs of glaucoma include those of diagnosis, medical, laser and surgical treatment, and costs of blindness as a result of glaucoma. So far the costs of diagnosis and screening programs are not well known but there is substantial knowledge of the therapeutic costs. Daily therapy costs are about 0.50 to 1.00 euro per patient. Every year the German statutory health insurance system pays about 1,000 euro per glaucoma patient. In addition, blindness due to glaucoma costs the German government over euro 150 million annually in Social Security benefits, lost income tax revenues, and health care expenditures. Demographic changes and scientific progress will even aggravate the socio-economic burden of this disease.

Cost of Illness↗
PubMed2006

[About the frequency of excessive epithelial basement membrane thickening in keratoconus].

BACKGROUND: In spite of a huge amount of morphological and biochemical findings the aetiology of keratoconus (KC) is still unclear. While the primary changes are seen and found mainly within the anterior corneal stroma, some authors believe that the corneal epithelium plays the major role in KC formation. Consequently, the epithelial basement membrane (BM) has become a matter of interest in KC research. MATERIAL AND METHODS: The study included 55 consecutive patients who had a perforating keratoplasty performed because of KC. The corneal explants were processed for light microscopy in the usual manner. Slides were stained with PAS. The whole explant was investigated although the focus of interest was put on the epithelial BM. 10 normal corneas of eyes which had to be enucleated because of a choroidal melanoma served as a control. RESULTS: In 3 patients (5.5 %) there was a significant linear thickening of the BM (thickness of the BM more than 5 % but less than 30 % of the thickness of Bowman's layer). Only in one patient (1.8 %) there was an excessive BM thickening (thickness of the BM more than 30 % of that of Bowman's layer) with focal (central) BM warts directed against the epithelium ("inverse cornea guttata"). In general, thickening of the BM was most pronounced paracentrally. None of the control corneas had a significantly thickened BM. CONCLUSIONS: A massively thickened epithelial BM can be occasionally observed in KC but is rare on the whole. It is most likely an unspecific secondary phenomenon and not a prerequisite for KC development. The "inverse cornea guttata" was a unique finding.

Adult↗
PubMed2006

[Effect of timolol on central corneal thickness and endothelial cell density].

BACKGROUND: The measurement of corneal thickness plays an increasing role in glaucoma screening and diagnosis. The influence of a variety of drugs on corneal thickness is well established. Especially for antiglaucomateous drugs this effect seems to be important. However, little is known about the influence of beta receptor antagonists on corneal thickness. The aim of this study was to provide evidence of the effect of timolol on central corneal thickness and endothelial cell density. MATERIALS AND METHODS: Ten healthy volunteers (five women and five men) with a mean age of 29 years (range 25 to 56 years) were examined in a double-blind, prospective and randomised pilot study. Intraocular pressure, corneal thickness and endothelial cell density was estimated before as well as fifteen minutes, 24, 48, 72 and 96 hours after application of timolol 0.5 % eye drops twice daily. The partner eye received sodium hyaluronate eye drops twice daily and served as a control. RESULTS: The application of timolol showed a decrease of intraocular pressure from initially 12 mmHg to 9 mmHg after four days (p = 0,0188) as well as an increase of corneal thickness from 537 microm to 557 microm after four days (p = 0,0659). There was no change of intraocular pressure (p = 0,9935) or corneal thickness (p = 0,9998) in the control eyes. There was also no effect of timolol (p = 0,2782) or sodium hyaluronate (p = 0,1940) on endothelial cell density. CONCLUSIONS: The study provides evidence of the influence of beta receptor antagonists on corneal thickness. This effect may be caused by receptor mediated influences on corneal ion and fluid transport. Further studies are needed to show if the increase of corneal thickness after application of topical timolol has clinical importance.

Adult↗
PubMed2006

[Protein kinase C isoforms in corneal epithelium and endothelium].

BACKGROUND: Protein kinase C (PKC) plays a key role in cell metabolism. Three subgroups and 12 isoforms have been isolated so far, catalysing specific functions in cell metabolism. The demonstration of PKC subtypes in corneal tissue has been inconsistent. The aim of this study was to verify the expression of several PKC subgroups and isoforms in human and bovine corneal epithelial and endothelial cells. MATERIALS AND METHODS: PKC subgroups and isoforms were studied using polyclonal antibodies. RESULTS: Antibodies to PKC-alpha, -delta, -epsilon and -zeta, representing all three PKC subgroups, bound in human and bovine corneal epithelium and endothelium. No binding was found for antibodies to PKC-beta2. CONCLUSIONS: For the first time the presence of all three PKC subgroups was demonstrated in human and bovine corneal epithelial and endothelial cells. Further studies are needed to show the role of these subgroups in cellular functions such as cell proliferation and differentiation.

Adult↗
PubMed2005

[Epidemic keratoconjunctivitis. Detecting adenoviruses].

OBJECTIVE: The validity of the 15-min adenovirus assay SAS Adenotest was evaluated compared with virus detection by polymerase chain reaction (PCR) from conjunctival swabs. METHODS: In 75 patients with assumed epidemic keratoconjunctivitis, adenovirus detection from conjunctival swabs was performed by the immunochromatographic assay SAS Adenotest and PCR. RESULTS: In 25 patients adenovirus was detected by PCR, 18 of whom were detected by the SAS Adenotest and 7 of whom were not. No false positive results occurred. Sensitivity was 72% and specificity was 100%. CONCLUSIONS: The results indicate that rapid adenovirus detection with the SAS Adenotest is a useful tool in early epidemic keratoconjunctivitis. An additional PCR should be performed when clinical symptoms persist for 5 days or more.

Adenoviridae↗
PubMed2005

[Inflammatory glaucomas].

The prevalence of glaucoma in patients with intra- or extraocular inflammation is five to twenty percent. The etiopathogenesis is manifold, including classical secondary open and closed angle mechanisms as well as specific inflammatory elements. Diagnosis and follow-up studies of inflammatory glaucomas are often difficult. The therapeutic options are limited or are poorly evaluated. The development of a secondary glaucoma is a severe complication of intra- or extraocular inflammation and may even lead to blindness. Further investigations, especially with regard to the treatment of inflammatory glaucomas, are necessary to improve the prognosis.

Glaucoma↗
PubMed2005

[Neoplastic secondary glaucomas].

With few exceptions all intraocular tumours can principally induce elevation of intraocular pressure (IOP). The frequency of IOP-elevation is mainly dependent on the biologic behaviour of the neoplasm (benign / malignant), its dimensions, localization, and its ability to provoke secondary changes like retinal detachment, hemorrhages, inflammation, and necroses. There are many and diverse pathomechanisms which may cause a "neoplastic glaucoma". The leading mechanisms are direct invasion of the chamber angle by tumour cells, rubeosis iridis, and forward displacement of the iris-lens-diaphragm with (lens induced) pupillary block. As intraocular tumours may have pressure-lowering effects too, eyes bearing a tumour may also be hypotonic or normotonic inspite of a "glaucomatous chamber angle morphology". The therapy of the tumour-induced glaucomas is hardly validated and generally follows the treatment of the other secondary glaucomas. However, filtration procedures are contraindicated when a malignant tumour is diagnosed or suspected. Because of the progress of tumour therapy with salvation of eyes which had to be enucleated in former times and prolongation of survival in some tumour entities (like Non Hodgkin's lymphoma and metastases) the significance of tumour-induced glaucomas will probably further increase in the future.

Eye Neoplasms↗
PubMed2004

[Aqueous humor dynamics].

Intraocular pressure is mainly controlled by the rate of aqueous humor production and the resistance to its outflow. Aqueous humor formation is the result of fast unidirectional secretion and slow contradirectional reabsorption. The most striking evidence of endogenous regulation of the ciliary epithelial secretion is provided by the observation of the circadian rhythm. Aqueous humor formation is mainly controlled by the interaction of inhibiting alpha(2)-adrenoreceptors and stimulating beta-adrenoceptors. The role of the central nervous system in the regulation of this process remains unclear and the precise mechanism of outflow regulation is not fully understood. The aqueous humor passes into the anterior chamber and leaves the eye by two routes: the direct outflow pathway through the trabecular meshwork or the indirect outflow pathway through the ciliary muscle. Further biochemical, biological and pharmacological investigations are necessary to determine the fundamental process of aqueous humor formation, outflow and regulation.

Absorption↗
PubMed2004

[Optical coherence tomography in the diagnosis and follow-up of patients with uveitic macular edema].

BACKGROUND: Optical coherence tomography (OCT) is a relatively new, noninvasive method and has been well established as an effective diagnostic procedure for the investigation of several macular diseases. Knowledge about the efficacy of OCT in the diagnosis and follow-up of macular edema in uveitis patients is still limited. PATIENTS AND METHODS: In the first part of the study, OCT was performed in 22 eyes of 18 patients with anterior or intermediate uveitis who showed angiographic and fundoscopic evidence of macular edema. The OCT results were compared with the visual acuity and fundoscopic and angiographic appearance of macular edema. In the second part of the study, the same patients were followed over a period of approximately 5 months (+/-2 months) and OCT was repeated at different time points during treatment of uveitic macula edema. RESULTS: OCT investigation also showed clear evidence of macular edema in all eyes and was not compromised by a low or medium degree of optical haze. Furthermore, OCT investigation revealed marked differences in the individual degree of macular edema (foveal heights 168-810 microm). Diffuse macular edema ( n = 4 ) and different types of cystoid macular edema (several distinguished cysts n = 6, partially or completely confluent cysts n = 11, one marked cyst n = 1) were observed. During the follow-up of the patients, OCT results, visual acuity, and fundoscopic appearance of the macula showed a comparable behavior. In some eyes, a stable visual acuity was accompanied by changes of foveal edema demonstrated by OCT. CONCLUSION: Optical coherence tomography is a safe and highly effective method in the diagnosis of macular edema in uveitis associated with low or medium haze of the optical media. Furthermore, OCT investigation seems to be useful in the follow-up of uveitic macular edema under treatment.

Fluorescein Angiography↗
PubMed2003

Inhibition of MMP-9 expression by PPARgamma activators in human bronchial epithelial cells.

BACKGROUND: The release of matrix degrading enzymes such as matrix metalloproteinase 9 (MMP-9) from bronchial epithelial cells is critically involved in airway wall remodelling in chronic inflammatory processes of the respiratory system. MMP-9 expression is induced by inflammatory mediators such as tumour necrosis factor (TNF)-alpha, but to date nothing is known about the mechanisms of inhibition of MMP-9 expression in these cells. METHODS: A study was undertaken to examine whether activators of the nuclear transcription factor peroxisome proliferator activated receptor gamma (PPARgamma) might modulate MMP-9 expression in two different bronchial epithelial cell lines. RESULTS: PPARgamma was expressed and was functionally active in NL20 and BEAS cells. Activation of PPARgamma by rosiglitazone or pioglitazone significantly reduced TNF-alpha and PMA induced MMP-9 gelatinolytic activity in a concentration dependent manner in both cell lines, but did not alter the expression of tissue inhibitor of MMPs type 1 (TIMP-1), the local inhibitor of MMP-9. Northern blot analysis revealed a decrease in MMP-9 mRNA expression following treatment with PPARgamma which resulted from the inhibition of NF-kappaB activation in these cells, as determined by transient transfection assays and electromobility shift assays. CONCLUSION: Activation of PPARgamma in human bronchial epithelial cells limits the expression of matrix degrading MMP-9. This might have therapeutic applications in chronic inflammatory processes of the respiratory system.

Blotting, Northern↗
PubMed2001

[Bee sting of the cornea - a case report].

BACKGROUND: Bee stings of the cornea are very rare, though its response can range from minimal inflammation to severe damage like lens dislocation, cataract formation, iris atrophy, ophthalmoplegia and optic neuropathy. We report on a patient with typical, severe findings. PATIENT: A 42-year-old patient presented with an acute, corneal bee sting of the left eye, after he was stung only a few hours ago. The patient suffered from pain, blurred vision and epiphora. The left eye showed edema of the upper and lower eyelid, conjunctival hyperemia, chemosis, striate keratitis, a purulent infiltration of the cornea above the limbus at the 7 o'clock meridian and a massive hypopyon. Further examinations showed regular ophthalmological findings. Vision acuity was 1,0/0,4. Under therapy inflammation decreased quickly. One week after we could lokalize the stinger in the depth of the corneal infiltration and it was removed surgically. After one month the eye only showed a minimal infiltration of the cornea with fine neovascularisations. Visual acuity was 0,8. CONCLUSION: Clinical reactions to bee stings of the cornea are caused by toxical and immunological effects of different components of the bee venom. These toxical and/or inflammatory reactions can lead to severe intraocular damage. Treatment of choice is the systemic and local application of steroids and antibiotics as well as local therapy with antihistamins.

Adult↗
PubMed1998

Effect of hypoglycemia on beta-adrenergic sensitivity in normal and type 1 diabetic subjects.

OBJECTIVE: The purpose of this study was to assess the potential role of reduced tissue sensitivity to catecholamines in the pathogenesis of hypoglycemia unawareness in patients with type 1 diabetes. RESEARCH DESIGN AND METHODS: The effect of a single episode of hypoglycemia on beta-adrenergic sensitivity was studied in 10 type 1 diabetic patients with apparently normal awareness of hypoglycemia (age 29 +/- 5 years, diabetes duration 13 +/- 8 years, HbA1c 7.3 +/- 0.9%) and 10 age-matched healthy control subjects. Beta-adrenergic sensitivity was measured with the isoproterenol test after a hyperinsulinemic euglycemic clamp and after a hyperinsulinemic hypoglycemic clamp. Beta-adrenergic sensitivity was expressed as the dose of intravenous isoproterenol that increased the heart rate by 25 beats/min (IC25). RESULTS: During hypoglycemia, diabetic subjects had an impaired plasma epinephrine response compared with that of the control subjects (16.7 +/- 5.0 vs. 40.1 +/- 6.8 ng/ml, P = 0.02). In control subjects, the IC25 was lower after hypoglycemia than after euglycemia (0.83 +/- 0.22 vs. 1.13 +/- 0.21 microg, P = 0.02) indicating an increase in beta-adrenergic sensitivity. In diabetic subjects, on the other hand, the IC25 was greater after hypoglycemia than after euglycemia (1.00 +/- 0.26 vs. 0.65 +/- 0.14 microg, P = 0.04), indicating a decrease in beta-adrenergic sensitivity. CONCLUSIONS: In normal subjects, a single episode of hypoglycemia increases beta-adrenergic sensitivity. In diabetic subjects, in contrast, hypoglycemia reduces beta-adrenergic sensitivity. These results provide evidence that in type 1 diabetic patients, some maladaptation of tissue sensitivity to catecholamines contributes to the development of hypoglycemia unawareness. A unifying hypothesis is presented for the pathogenesis of hypoglycemia unawareness in type 1 diabetic patients incorporating the concepts of both a reduced catecholamine response and reduced adrenergic sensitivity

Adrenergic beta-Agonists↗