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Biomedical subjects

J Richter

Publications and source records attributed to J Richter.

At least 199 records · Page 11Linked to original sources
PubMed1996

Lansoprazole prevents recurrence of erosive reflux esophagitis previously resistant to H2-RA therapy. The Lansoprazole Maintenance Study Group.

OBJECTIVE: This randomized, double-blind study was designed to determine whether the proton pump inhibitor lansoprazole could prevent relapse among patients with healed erosive reflux esophagitis that had been resistant to healing with at least 3 months of H2-receptor antagonist therapy. RESULTS: By the end of the year, 13% of placebo patients remained healed compared with 67% of lansoprazole 15 mg and 55% of lansoprazole 30 mg patients (p < 0.001 for time to first relapse). All placebo patients were symptomatic by the end of the study whereas only one-third of the lansoprazole patients was symptomatic at the end of the 12-month study period. The two lansoprazole doses were comparably effective in maintaining healing and in symptom control and were well tolerated. Fasting serum gastrin values increased significantly to about 1.5-2 times the baseline values over the first 2 months of lansoprazole treatment; no further increase was noted. CONCLUSION: Erosive relapse can be prevented in most patients for up to 1 yr with lansoprazole 15 mg or 30 mg once daily.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

[Diagnosis of acute rupture of the anterior cruciate ligament. Value of ultrasonic in addition to clinical examination].

Post-traumatic knee injuries often deteriorate if reuptures of anterior cruciate ligaments (ACL) are not treated adequately. Further diagnostic procedures are required if pain-induced muscle contraction impairs clinical examination. The clinical relevance of sonography, however, for the diagnosis of ACL ruptures is controversial. Within 25 months, 74 patients were preoperatively evaluated clinically and by ultrasound. 58 ruptures of the ACL and 21 lesions of the collateral ligaments were confirmed by arthroscopy or arthrotomy. In 16 cases a menisceal tear was found, four patients had a luxation of the patella, and two had PCL ruptures. The sensitivity of the Lachman test was 93%, of the anterior drawer test 68% and of the pivot shift test 48%. Ultrasound diagnosis revealed 88% of all ACL ruptures (91% if patients with bony ruptures of the ACL were excluded). In 75% of ACL ruptures, a popping sensation was reported by the patients. In the case of uncertain diagnosis, examination with ultrasound could be easily performed before further operative diagnostic procedures are scheduled.

Acute Disease↗
PubMed1995

TNF-induced superoxide anion production in adherent human neutrophils involves both the p55 and p75 TNF receptor.

TNF, a potent activator of neutrophil granulocytes, acts via two cell-surface receptors: the p55-TNF receptor (TNF-R55) and the p75-TNF receptor (TNF-R75), which can be cleaved from the cell surface and thus form soluble TNF-binding proteins (TNF-BP). The role of the two receptors in activation of the neutrophil respiratory burst was investigated. Two mAbs reacting with TNF-R55 (H398 and TBP2) induced O2 release in a similar manner but to a lesser extent than TNF. TBP2, however, required preincubation at 4 degrees C to exert its effect. Preincubation of neutrophils (both at 4 and 37 degrees C) with mAb to TNF-R75 decreased TNF-induced superoxide anion production by 67 and 64%, respectively, indicating the essential role also for TNF-R75 in neutrophil activation. This inhibitory effect could not be explained by cross-down-regulation of TNF-R55 because the TNF-R75 mAb had no effect on TNF binding to TNF-R55 as determined by binding of 125I-labeled TNF or release of TNF-R55-BP as measured by ELISA. Furthermore, the TNF-R75 mAb did not decrease superoxide anion generation induced by the TNF-R55 mAb H398, thus ruling out that the inhibitory effect of the TNF-R75 mAb is due to inhibition of the signaling pathway downstream of TNF-R55. In contrast to the TNF-R75 mAb, TNF-R55 mAbs induced down-regulation of TNF-R75 and shedding of both TNF-R55-BP and TNF-R75-BP. We conclude that both TNF-R55 and TNF-R75 are involved in TNF-induced activation of the neutrophil respiratory burst.

Antibodies, Monoclonal↗
PubMed1995

Morphometric evaluation of volume shifts between intra- and extra-cellular space before and during global ischemia.

BACKGROUND: It is well known that all forms of cardiac arrest lead to global ischemia combined with alterations in cellular and interstitial volume. The aim of this study was to investigate the nature of these alterations with respect to different methods of cardiac arrest and establish the extent of their mutual influence at the onset as well as during the course of global ischemia. METHODS: Three tested clinical methods were employed to induce cardiac arrest by a) aortic cross clamping, b) coronary perfusion with the cardioplegic solution St. Thomas, and c) coronary perfusion with the cardioplegic solution histidine-tryptophane-ketoglutarate (HTK). The arrested hearts were subjected to global ischemia at 25 degrees C. The size of the myocytes, as well as the interstitial space of myocytes, was determined morphometrically. The contraction state of myocytes was evaluated according to a score. RESULTS: We found that the degree of contraction, as well as nature of alterations in the cellular and interstitial volumes, depended both on the form of cardiac arrest and on the duration of ischemia. The following relationships were established. High contraction at the onset of ischemia leads to expulsion of fluid from the interstitium between bundles of myocytes into the tissue clefts increasing their size. The decrease in contraction during ischemia leads to narrower tissue clefts. Cellular swelling at the onset of and during ischemia is caused by volume shifts between intracellular and interstitial space. An increase in cellular volume during global ischemia and/or additional contraction reduce the interstitium within bundles of myocytes. Sufficient relaxation and/or interstitial edema enlarge the interstitium. CONCLUSIONS: Cellular and interstitial alterations seen at the onset and during the course of ischemia are dependent upon the method of cardiac arrest. Furthermore, a considerable mutual influence is exerted by the alterations in cellular and interstitial spaces.

Animals↗
PubMed1995

Morphometric characterisation of the fine structure of human type II pneumocytes.

BACKGROUND: Pulmonary type II pneumocytes have been examined by scanning electron microscopy (SEM), transmission electron microscopy (TEM), and morphometry in numerous mammals. Until now, the fine structure of the human type II pneumocyte has not been studied by means of morphometry. METHODS: Eleven human donor lungs, which could not be made available for a suitable recipient, were preserved with Euro Collins solution (ECS) according to clinical organ preservation techniques. The lungs were fixed via the airways. Systematic random samples were analyzed by SEM, TEM, and classical stereological methods. RESULTS: Type II pneumocytes showed normal fine structural characteristics. Morphometry revealed that although inter-individual variation due to some oedematous swelling was present, the cells were in a normal size range as indicated by an estimated mean volume of 763 +/- 64 microns 3. The volume densities were: nucleus 21.9 +/- 2.2%, mitochondria 5.8 +/- 0.9%, lamellar bodies 9.8 +/- 3.6%, and remaining cytoplasmic components 62.4 +/- 2.9% of the cell volume. Since the inter-individual variations in the volume densities referred to the cell may, to variable degrees, reflect the variation in the reference space, the volume densities referred to the constant test point system and the respective volume-to-surface ratios were used for inter-individual comparisons. These parameters indicate that lamellar bodies were independent of cellular swelling, while mitochondria < nucleus < remaining cytoplasmic components increased in size with increasing cell size. CONCLUSIONS: Two to 7.5 hours of cold ischemia following ECS preservation do not deteriorate the fine structure of type II pneumocytes of human donor lungs. For reliable assessment of fine structural variations, morphometric parameters are required that are independent of variations in cell size.

Cell Nucleus↗
PubMed1995

Cellular distribution patterns of lanthanum and morphometry of rat hearts exposed to different degrees of ischemic stress.

BACKGROUND: The element lanthanum (La) can be used as a tracer for verification of membrane permeability. The aim of this study was to establish whether 1) distribution of La in the myocardium of rat hearts depends on the degree of ischemic stress and 2) morphometrically determined cell and mitochondrial swelling correlates with the La distribution. MATERIALS AND METHODS: Isolated beating rat hearts were arrested by coronary perfusion with the cardioplegic solution Custodiol (controls) or by aortic cross clamping followed by exposure to different degrees of ischemic stress. The solutions for perfusion-and postfixation as well as for rinsing contained 1.1% La(NO3)3. Cellular and mitochondrial swelling were determined morphometrically and myocytes exhibiting intracellular La were quantified and stated as percentage of test fields. RESULTS: Immediately after cardiac arrest La was present as precipitates only in a few myocytes adjacent to the outer mitochondrial membrane as seen by cTEM and ESI. In such cells La was also detected by EELS in mitochondrial matrix and myofibrils. Advanced ischemic stress led to an increase of the percentage of myocytes containing detectable intracellular La. After 45 min ischemia at 30 degrees C, myocytes and mitochondria showed a remarkable edema and different intracellular distribution patterns of La. After 90 min of ischemia at 20 degrees C interruptions of sarcolemma could only be detected in a few of the swollen myocytes. Roundish La granules were seen in the myofibrils. The percentage of myocytes containing intracellular La and the extent of cellular and mitochondrial swelling showed a significant correlation. CONCLUSIONS: Patterns of intracellular La distribution depend on the degree of ischemic stress and correspond to the degree of cellular as well as mitochondrial edema. These results point at a direct relation between alterations of membrane permeability and development of edema.

Animals↗
PubMed1995

Aggressive course of primary plasma cell leukemia with unusual morphological and cytogenetic features.

A case of aggressive plasma cell leukemia with unusual morphological and cytogenetic features is reported. A 65-year-old man was admitted to hospital due to anemia, thrombocytopenia, and renal insufficiency. Bone marrow examination and peripheral blood smear revealed a large number of pleomorphic cells with convoluted and multilobulated nuclei. Immunohistochemistry of the bone marrow biopsy was negative for anti-keratin antibodies CAM.5.2 and AE1/AE3, but positive for EMA. The immunophenotypic features of these cells were suggestive of plasma cell origin with positivity for CD38, CD56, CD9, and CD44 and a weak positivity for CD71 and CD45 (40% of the cells), while all other markers of hematopoietic origin were negative. Furthermore, a serum protein electrophoresis showed a monoclonal component type IgG-kappa of 70 g/l. The cytogenetic analysis demonstrated a hypotetraploid clone with multiple numerical and structural abnormalities. Although some of the aberrations found are associated with plasma cell malignancies--e.g., structural rearrangement of chromosome 1, del(6q), and monosomy 13--the karyotypic complexity in the present case is unusual. The course of the disease was very aggressive, and the patient died 3 days after admission.

Aged↗
PubMed1995

Modeling reductive dehalogenation with quantum chemically derived descriptors.

Existing models for the reductive dehalogenation reaction under environmentally relevant conditions use Hammett and Taft coefficients as descriptors. Drawbacks of these descriptors are the limited possibilities for interpretation in terms of reaction mechanisms, and the limited availability of these descriptors for more "exotic' substituents. Therefore, in this study new descriptors are tested, using semi-empirical molecular orbital calculations. These descriptors are based on the energetic and electronic properties of the reaction sites and should be able to account for the systematics of the rate constants in a better way than substituent coefficient models. This approach is expected to give reliable estimates of the rate constants even for compounds containing less common structural features. Several relationships for a series of halogenated aromatics are presented here, relating the experimental rate constants to, among others, the calculated activation energy of the rate limiting step in the reductive dehalogenation process. Results show that semi-empirical molecular orbital descriptors are capable of describing the reaction kinetics within a homologous series of compounds. All descriptors can be explained for in terms of reaction mechanisms, thus corroborating the hypothesis about mechanisms taking place in the environment.

Chemical Phenomena↗
PubMed1995

Functional and fine structural changes in isolated rat lungs challenged with endotoxin ex vivo and in vitro.

The aim of this study was to relate changes in rat lung functions caused by the endotoxin lipopolysaccharide (LPS) to alterations in structure. The following four experimental groups were used: 1), control in vitro, perfusion for 150 minutes; 2), LPS in vitro, perfusion for 150 minutes and infusion of 5 mg of LPS after 40 minutes; 3), control ex vivo, perfusion for 10 minutes; and 4), LPS ex vivo, lungs perfused for 10 minutes from rats treated for 110 minutes with 20 mg/kg LPS intraperitoneally. Histologically, blood-derived leukocytes were detectable only in lungs from group 4, where neutrophils were found in capillaries, interstitium, and endothelial pouches. LPS treatment increased pulmonary resistance and decreased pulmonary compliance in group 4 (ex vivo), and, to a greater extent, in group 2 (in vitro). In these two groups, formation of giant lamellar bodies in the type II pneumocytes was observed. By histological examination, the bronchoconstriction induced by LPS in vitro was localized to the terminal bronchioles. At 2 hours after LPS treatment, no edema and no change in precapillary and postcapillary resistance, capillary pressure, vascular compliance, capillary permeability, and the wet/dry ratio was observed. Thus, our major findings are that LPS induced constriction of the terminal bronchioles in vitro, formation of giant lamellar bodies in type II pneumocytes ex vivo and in vitro, and trapping of neutrophils in endothelial pouches in vivo.

Animals↗
PubMed1995

[Medial femoral neck fracture--femur head preserving therapeutic concepts].

Intracapsular femoral neck fractures of patients younger than 65 should be treated by open or closed reduction and internal fixation with two to four lag screws. Garden I fractures should also be treated by percutaneous screw fixation to prevent a delayed dislocation. If the fracture is dislocated (Garden II-IV) immediate reduction and internal fixation is mandatory to improve the blood flow by "unkinking" of the supporting vessels. The rate of femoral head necrosis is about ten to fifty percent, according to the grade of posttraumatic dislocation. Early stages of total or partial femoral head necrosis can be successfully treated by vascularized cortical bone grafts. In our institute a graft vascularized by the quadratus femoris muscle is preferred. Valgisation osteotomy, alloarthroplasties and arthrodeses in very young people are performed in cases of irreversible total femoral head necrosis.

Adolescent↗
PubMed1995

[Diagnosis and therapy of local infections after surgical management of proximal femoral fractures].

Postoperative infections after trochanteric and intracapsular hip fractures are rare. Critical clinical observation of the wound during the early postoperative period and the evaluation by sonography as well as the determination of the C-reactive protein are important factors in the diagnosis of early haematoma and wound infections. If revision surgery of suspected infections is immediately performed, good long-term results are to be expected. Infected hemialloarthroplasties and loosened total hip arthroplasties (THR) should be retrieved. If a mild infection is present, one stage revision arthroplasty is indicated. In case of gram-negative infections, however, alloarthroplasties should be removed and the total hip replacement should be delayed for 3 to 6 months.

Diagnostic Imaging↗
PubMed1994

Adherence of neutrophils induces release of soluble tumor necrosis factor receptor forms.

TNF is a potent activator of neutrophil granulocytes which acts via two cell surface receptors: the p55-TNF receptor (TNF-R55) and the p75-TNF receptor (TNF-R75). The extracellular region of the receptors can be released by proteolytic cleavage and form soluble TNF-binding proteins, TNF-R55-BP and TNF-R75-BP, respectively. The phorbol ester PMA, the chemotactic peptide FMLP, and TNF were all found to induce release of TNF-R55-BP and TNF-R75-BP from neutrophils in suspension in a time- and dose-dependent manner as measured by ELISA. Exposure of neutrophils to 10 ng/ml of PMA for 60 min resulted in release of 900 pg of TNF-R55-BP and 350 pg of TNF-R75-BP per 5 million cells, corresponding to approximately 4800 receptors per cell. In addition, adherence by itself of neutrophils to fibrinogen-coated culture plates and other surfaces resulted in a release of TNF-R55-BP of the same magnitude as seen in response of neutrophils in suspension to 1 nM TNF, whereas the release of TNF-R75-BP was less pronounced. The protein kinase C inhibitors staurosporin and calphostin C inhibited both the TNF-, PMA-, and adherence-induced release of soluble forms of TNFRs. Ab to the common beta-chain of the leukocyte integrins (CD18) did not affect adherence-induced TNF-R55-BP release, indicating that non-integrin-dependent mechanisms are involved in receptor cleavage. However, cross-linking of anti-CD18 Ab (IB4) with a Fab2 fragment resulted in a decrease of specific binding of 125I-TNF to neutrophils indicating that the leukocyte integrins can modulate TNFR expression on neutrophils. Thus, adherence to a biological surface, without additional stimuli, induces release of soluble TNFR form from neutrophils. TNFR expression can be modulated by protein kinase C as well as both leukocyte integrins and non-integrin-dependent adherence mechanisms.

Antigens, CD↗
PubMed1994

L-selectin mediates downregulation of neutrophil TNF receptors.

Tumor necrosis factor (TNF) is a potent activator of neutrophil granulocytes, which acts via two cell-surface receptors: the p55-TNF receptor (TNF-R55) and the p75-TNF receptor (TNF-R75). Proteolytic cleavage of the extracellular region of the receptors results in formation of soluble TNF-binding proteins, TNF-R55-BP and TNF-R75-BP. We recently reported that adherence alone, without any further stimuli, causes release of both TNF-R55-BP and TNF-R75-BP and that both leukocyte-integrin-dependent and non-integrin-dependent adherence mechanisms can modulate TNF receptor expression. In the present work we show that crosslinking of a mAb to the adhesion protein L-selectin (TQ1) on the surface of neutrophils results in downregulation of TNF-receptor binding capacity. Furthermore, when the fluctuations of cytosolic free calcium found in adherent neutrophils were blocked with the cell-permeable calcium chelator BAPTA, adherence-induced release of TNF-R55-BP was inhibited. We have shown that adherence, via mechanisms involving two adhesion proteins, L-selectin and the CD11/CD18 leukocyte integrins, and fluctuations of cytosolic free calcium, can result in downregulation of neutrophil TNF-receptors.

Antigens, CD↗
PubMed1994

Regional deep hypothermia of the spinal cord protects against ischemic injury during thoracic aortic cross-clamping.

We tested in pigs the hypothesis that regional deep hypothermia of the spinal cord achieved by cerebrospinal fluid cooling will protect against ischemic injury during thoracic aortic cross-clamping. Eight control animals underwent aortic cross-clamping at the distal aortic arch and just above the diaphragm for 30 minutes. Eight experimental animals had placement of two subarachnoid perfusion catheters through laminectomies at T4 and the lower lumbar region. The subarachnoid space was perfused with normal saline solution at 6 degrees C delivered by gravity infusion, with infusion rates adjusted to maintain cord temperatures at less than 20 degrees C. After 30 minutes of aortic cross-clamping, the infusion was stopped and the cord allowed to warm to body temperature. Hind limb neurologic function was graded by Tarlov's scale. All of the animals in the control group had complete hind limb paraplegia (Tarlov grade 0) postoperatively. Seven of the 8 animals in the experimental group had preservation of hind limb motor function (Tarlov grade 2), and 1 animal had complete hind limb paraplegia (Tarlov grade 0) (p = 0.002, Fisher's exact test). We conclude that regional deep hypothermia of the spinal cord in pigs does provide some protection from ischemic injury during thoracic aortic cross-clamping. Clinically this may be a useful adjunct for prevention of paraplegia during thoracic aortic operations.

Animals↗