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T Kossmann

Publications and source records attributed to T Kossmann.

69 records · Page 4Linked to original sources
PubMed1993

[Arthroscopy of the shoulder joint. Technique, indications, surgery and complications].

Diagnostic and operative arthroscopy of the shoulder joint has gained considerable importance in traumatology and orthopedic surgery over the last years. Injuries of the limbus glenoidalis, in particular traumatic shoulder luxation, injuries of the rotator cuff, infection of the glenohumeral joint and unclear posttraumatic pain are indications for diagnostic and operative arthroscopy. Arthroscopy of the shoulder is a procedure, which offers exact diagnosis and the possibility of immediate surgery at the same time. The technique of the shoulder joint arthroscopy has to be carried out carefully and according to a standard protocol. The complication rate of around 5% of shoulder arthroscopy has not to be neglected.

Arthroscopy↗
PubMed1993

Rat model for limb lengthening by callus distraction.

Limb lengthening and treatment of bone defects by using the method of callus distraction has become very important in traumatology and orthopedics. Despite increasing clinical use and ongoing research, many questions still remain unanswered. The biochemical processes that occur during matrix-induced bone formation have been elucidated, while the mechanisms of bone formation induced by callus distraction are still unclear. This study details the development of a new animal model in which rats undergo limb lengthening by callus distraction, offering the possibility of using modern immunological, and molecular biological techniques, which have already been developed for this animal species. The application of limb lengthening by callus distraction in this animal model has proven to be a practicable, reproducible, and economical procedure, which can increase our understanding of the callus distraction process.

Animals↗
PubMed1993

[Osteosynthesis of subcapital humerus fracture with unconventionally applied implants].

The osteosynthesis of proximal humerus fractures with the commonly used plates is often critical because of the small space subacromial, the irritation of the blood supply by the broad plates and the poor proximal anchorage without angle stability. The osteosynthesis with a children hip plate or a angle plate like modified DC-plate is thought to be a reliable alternative.

Adult↗
PubMed1993

[Opportunistic infections in patients with disordered immune status].

Dysfunction of the immune system can result in opportunistic infections, which are frequently responsible for high morbidity and mortality. With regard to surgery, opportunistic infections are found in specific risk groups, including individuals with tumors, AIDS, thermic or mechanical trauma and organ transplantation. These infections can be caused by bacteria, fungi, viruses and protozoa. If there are indications of a possible opportunistic infection, a rapid diagnosis is required, followed by immediate therapeutic intervention.

AIDS-Related Opportunistic Infections↗
PubMed1993

[Necrotizing soft tissue infections].

Necrotizing soft tissue infections are a group of life- and limb-threatening infections. They are caused by aerobic and anaerobic bacteria occasionally in a synergistic polymicrobial combination. The literature describing necrotizing soft tissue infections is controversial and often contradictory. Depending on their clinical appearance, tissue level and microbiological findings, necrotizing soft tissue infections are classified into two major groups, infections within the subcutaneous/fascia niveau and within the muscle level. Necrotizing infections of the subcutaneous level are further differentiated in hemolytic streptococcal gangrene, necrotizing fasciitis, clostridium fasciitis, and anaerobic nonclostridium fasciitis. In particular, necrotizing fasciitis is a rapidly progressing process, which is characterized by suppurative fasciitis, following by vascular thrombosis and cutaneous gangrene and is often accompanied by severe systemic toxicity, seen as septic-toxic shock and progressive (multi-) organ failure. Nineteen cases of necrotizing soft tissue infections were treated at the Department of Surgery, University Hospital of Zurich, between 1989 and 1992. These infections originated from "neglected trauma" in 9 (9/19), drug injections in 4 (4/19), acute infections in 3 (3/19), operative wounds in 2 (2/19) and perforation of the intestine in 1 case (1/19). Most of the patients (13/19) suffered from chronic debilitating diseases and were compromised by a suppressed immune system. We treated two groups of patients, one with septic-toxic clinical course and the other without. Eleven patients (11/19) belonged to group one and four of them, showing necrotizing fasciitis of the trunk, died as a result of multiorgan failure (MOF). Furthermore, three patients in this group had a limb amputated. In the other group without septic-toxic signs, no one died or lost a limb. The two groups differed also in length of hospital stay, an average of 60 days in group one (23 days intensive care) and 25 days in group two. Our results suggest that prompt recognition and treatment of necrotizing soft tissue infections are essential for the patient's survival. Often the full extent of the infections is underestimated initially, resulting in delayed surgical therapy. To control the rapidly spreading necrosis, early diagnosis and radical debridement of the affected tissue are essential and should be done without compromise, even if the affected limb must be amputated.

Adult↗
PubMed1992

Autocrine and paracrine regulation of astrocyte function by transforming growth factor-beta.

Recent evidence indicates that astrocytes have a wide range of functions, usually attributed to cells of the immune system, which are critical for maintaining a balanced homeostatic environment in the central nervous system (CNS). Moreover, these cells are known to participate in inflammatory events within the CNS by secreting cytokines such as transforming growth factor-beta (TGF-beta). In this study we have investigated the ability of TGF-beta to influence astrocyte functions. TGF-beta 1 mRNA is constitutively expressed by astrocytes in vitro, and when cultures are stimulated with exogenous TGF-beta 1 an increase in the expression of this mRNA can be shown, suggesting both autocrine and paracrine regulation. In in vitro assays, TGF-beta 1 is chemotactic for astrocytes in a dose-dependent fashion and inhibits astrocyte proliferation. These results indicating signal transduction by TGF-beta 1-prompted studies to explore receptor-ligand interactions on isolated astrocyte populations. In a receptor binding assay, we demonstrate that astrocytes appear to express three distinct TGF-beta receptor subtypes with nearly 10,000 receptors per cell. Thus, TGF-beta may play an important role in regulating astrocyte functions pivotal to the evolution of intracerebral immune responses including recruitment and activation of glial cells at local inflammatory sites within the CNS.

Animals↗
PubMed1992

Cytokines and neuropathology.

Inflammatory processes in the brain require the cooperation of immunocompetent cells and glial cells, which communicate by secreting bidirectional mediators. Resident cells within the nervous system can synthesize and secrete inflammatory cytokines, as well as neuropeptides, contributing to the response within the CNS to injury or immunological challenge. Although the mechanisms of cell activation and immune interaction are poorly understood, accumulating evidence implicates these pathways in neuropathogenesis, as described here by Sharon Wahl and colleagues. For example, in the acquired immune deficiency syndrome (AIDS), HIV-1-induced nervous system dysfunction and dementia are associated with the presence of infiltrating leukocytes and the release of inflammatory cytokines. Defining the pathways of cytokine dysregulation and neurotoxicity invoked by the infiltrating leukocytes, as well as the contribution of the neural cells themselves, may help to identify mechanisms of intervention in this and other debilitating CNS diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Kupffer cells express type I TGF-beta receptors, migrate to TGF-beta and participate in streptococcal cell wall induced hepatic granuloma formation.

Intraperitoneal injection of Group A streptococcal cell wall (SCW) fragments into female Lewis rats results in the induction of an acute hepatic inflammation that progresses to granulomatous lesions. Kupffer cells have been shown to rapidly clear circulating SCW which triggers production of TGF-beta. In this study, we examined Kupffer cells for the expression of TGF-beta receptors to determine if these cells might be modulated in an autocrine/paracrine fashion by TGF-beta during SCW-hepatic inflammation. By receptor crosslinking and subsequent SDS-PAGE analysis we demonstrate that Kupffer cells express Type I TGF-beta receptors, but not Types II and III. Scatchard analysis indicated a receptor density of approximately 1100 receptors per cell. Functionally, TGF-beta was found to be chemotactic for Kupffer cells in vitro and this chemotactic response was higher in cells isolated from rats 1-21 days post SCW-injection. Although TGF-beta 1 mRNA is constitutively expressed by Kupffer cells, in vitro stimulation of the cultures with purified TGF-beta augments the expression of TGF-beta 1 mRNA and protein synthesis suggesting autocrine/paracrine regulation. These results indicate that TGF beta secreted by Kupffer cells during SCW-induced hepatic inflammation may amplify its own expression and regulate Kupffer cell functions relevant to the formation of granulomatous lesions within the liver.

Animals↗
PubMed1992

Role of Kupffer cells in developing streptococcal cell wall granulomas. Streptococcal cell wall induction of inflammatory cytokines and mediators.

Hepatic granulomas are induced by intraperitoneal injection of streptococcal cell walls (SCW) into Lewis rats. Kupffer cells rapidly clear SCW from the blood, and the authors examined Kupffer cells further for a role in SCW-hepatic inflammation. Isolated Kupffer cells cultured with SCW secreted high levels of tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), transforming growth factor beta (TGF beta), and prostaglandin E2 (PGE2). SCW transiently induced increased steady-state levels of IL-1 beta and TNF alpha mRNA; in contrast, constitutive expression of TGF beta 1 mRNA in Kupffer cells was not affected by SCW. Low concentrations of SCW induced the accumulation of intracellular IL-1 and TGF beta bioactivity, with intracellular IL-1 bioactivity remaining high through at least 72 hours of culture. Kupffer cells isolated 1, 7, and 21 days after SCW injection did not express IL-1 beta or TNF alpha mRNA greater than control levels and exhibited marked hyporesponsiveness to secondary in vitro stimulation with SCW or LPS. SCW transiently induces Kupffer cells to secrete a variety of soluble mediators that contribute to hepatic inflammation by inducing leukocyte recruitment and activation and fibroproliferation. The transient nature of the Kupffer cell response and the hyporesponsiveness to secondary stimulation may be a mechanism by which the hepatic inflammation is negatively regulated.

Animals↗
PubMed1991

Macrophage- and astrocyte-derived transforming growth factor beta as a mediator of central nervous system dysfunction in acquired immune deficiency syndrome.

The multifunctional cytokine, transforming growth factor beta (TGF-beta), was identified by immunocytochemistry in the brain tissues of four patients with acquired immune deficiency syndrome (AIDS), but not in control brain tissue. The TGF-beta staining was localized to cells of monocytic lineage as well as astrocytes, especially in areas of brain pathology. In addition, the brain tissues from the AIDS patients contained transcripts for human immunodeficiency virus 1 (HIV-1) by in situ hybridization, suggesting a correlation between the presence of HIV-1 in the brain and the expression of TGF-beta. However, the expression of TGF-beta was not limited to HIV-1-positive cells, raising the possibility of alternative mechanisms for the induction of TGF-beta in these AIDS patients' brains. To investigate these mechanisms, purified human monocytes were infected in vitro with HIV-1 and were shown to secrete increased levels of TGF-beta. In addition, HIV-1-infected monocytes released a factor(s) capable of triggering cultured astrocytes that are not infected with HIV-1 to secrete TGF-beta. The release of TGF-beta, which is an extremely potent chemotactic factor, may contribute to the recruitment of HIV-1-infected monocytic cells, enabling viral spread to and within the central nervous system (CNS). Moreover, TGF-beta augments cytokine production, including cytokines known to be neurotoxic. The identification of TGF-beta within the CNS implicates this cytokine in the immunopathologic processes responsible for AIDS-related CNS dysfunction.

AIDS Dementia Complex↗
PubMed1991

Transferred triage to a level I trauma center in a mass catastrophe of patients; many of them with burns.

Three airplanes were involved in an airshow accident at the Ramstein military airbase on 28th of August 1988 causing immediate 45 dead and approximate 400 injured people. As a Level I Trauma facility we received 47 patients in different state of distress direct from airfield within an hour. The disaster plan was activated and sufficient personal and infrastructure could be mobilized.

Accidents, Aviation↗
PubMed1987

Structural and biochemical analysis of skinned smooth muscle preparations.

This paper describes a biochemical and immunocytochemical analysis of smooth muscle strips that were chemically skinned and subjected to contraction and relaxation cycles according to procedures commonly employed in current skinned smooth muscle work. The fate of four major proteins, myosin, filamin, caldesmon and actin, was followed with respect to the proportionate loss of these proteins to the bathing medium as well as to their structural redistribution within the cells in the muscle strips. Large losses (of the order of 50%) of both myosin and filamin occurred at the skinning step, using either Triton X-100 or Saponin as the detergent; losses of actin were up to 30% with Triton X-100 and around 15% with Saponin. Losses of caldesmon were difficult to assess due to the rapid degradation of this protein in the bathing medium. Subsequent cycles of contraction and relaxation resulted in accumulated loss, notably of myosin and filamin, so that after the third contraction as little as 20% and 40% respectively of the original complement of these proteins remained in the muscle strips. These changes in protein composition were accompanied by a drastic redistribution of the proteins in the muscle cells. Most marked were the changes seen with myosin, significant amounts of this protein being already found in the connective tissue space after the first relaxation. These findings point to the need for a careful reappraisal of the conditions currently used in skinned smooth muscle research.

Animals↗
PubMedDate not supplied

Effect of peritoneal fluid pH on outcome of aminoglycoside treatment of intraabdominal infections.

Netilmicin and clindamycin were administered to 47 patients with an intraabdominal infection who underwent emergency laparotomy. Thirty-one patients were cured, seven were improved, and therapy failed in nine patients despite the fact that all aerobic bacteria isolated from these patients were sensitive to netilmicin as determined by standard in vitro susceptibility tests. The pH of peritoneal and drainage fluid collected intraoperatively and during follow-up correlated with clinical outcome. Acidic pH was found in 21 of 33 (64%) specimens sampled from patients with therapeutic failure compared to 17 of 80 (21%) obtained from the categories "cured" and "improved" (p < 0.001). Netilmicin concentrations in serum or peritoneal/drainage fluid did not correlate with clinical outcome. Netilmicin levels were above the minimal inhibitory concentration of the pathogens in 59 of 64 (92%) drainage fluid specimens in which aerobic bacteria were isolated. Aerobic bacteria were isolated in 91% of drainage fluid specimens if the pH was less than 7.0, compared to 37% if pH was more than 7.0 (p < 0.001). Reduction of pH antagonized aminoglycoside activity in vitro against clinical isolates of Escherichia coli. Surgical reexploration should be considered in cases of deterioration following a laparotomy associated with detection of acidic drainage fluid.

Abdomen↗