Surgical therapy of dens fracture

The use of Anderson/D'Alonso or Aebi/Nazarian classification of dens fractures is the basis for exact selection of therapy. The ventral screw-fixation of Anderson type-II-Fracture is today the common standard of treatment, especially in the elderly. The stabilisation of the fracture with maintenance of atlanto-axial rotation-function, the minimal rate of pseudarthrosis compared with conservative therapy, the minimal operation trauma and the immediate mobilisation with high patient comfort are decisive benefits of this method. Reposition of the fracture, visualisation in two planes and the use of adequate instruments are important conditions to get optimal operation results. In-vitro-experiments have shown that there is no difference of stability in one- or two-screw-technique. Flexion injuries with oblique fracture plane, insufficient stability after anterior screw fixation and typ-III-fractures are indications for dorsal, atlanto-axial screw fixation. The conservative treatment(HALO-vest) is recommended only in otherwise inoperable patients.     

Monocyte procoagulant activity induced by adherence to an artificial surface is reduced by end-point immobilized heparin-coating of the surface

Heparin-coating improves the biocompatibility of blood contacting artificial surfaces. This led us to investigate the impact of heparin-coating (Carmeda AB, Stockholm) of polymetylmetacrylate on the expression of monocyte tissue factor procoagulant activity (TF-PCA) by surface adhesion. Also, the anticoagulant effect of heparin-coating in the presence or absence of adherent procoagulant monocytes was assessed. This is of particular interest, since activation of extrinsic coagulation by adherent monocyte TF-PCA may play a significant role in thrombin generation during extracorporeal circulation. Monocytes exposed to heparin-coated or non-coated polymetylmetacrylate expressed TF-PCA. The heparin coat did not affect the rate of monocyte adhesion. However, heparin-coating reduced the induction of TF-PCA of non-adherent and adherent monocytes by 17 and 33% (p <0.001 and p <0.0003), respectively. Heparin-coating in the absence of monocytes, totally inhibited the clotting of recalcified plasma (p <0.003). In contrast, in the presence of adherent monocytes expressing TF-PCA, surface-bound heparin did not inhibit clotting. However, inclusion of heparin in a plasma concentration of 8.9 IU/ml totally inhibited the activation of coagulation. It is apparent that heparin-coating of an artificial surface is an efficient means to inhibit coagulation of recalcified plasma, but much less so when procoagulant monocytes are adherent to the coated surface. The present findings are of clinical relevance, since monocytes will adhere to blood contacting surfaces of extracorporeal circuits or to implanted vascular prostheses and subsequently express TF-PCA, and this may promote thromboembolism.     

Basophilic blast crisis in chronic myeloid leukemia

Acute nonoliguric renal failure developed in a 13-year-old girl, 1 month after the institution of isoniazid therapy because of a positive tuberculin test at school screening. A renal biopsy demonstrated severe crescentic glomerulonephritis with focal interstitial changes. Discontinuation of isoniazid and a short course of steroids and cyclophosphamide therapy were followed by complete recovery. Whereas isoniazid has been shown to induce a lupus-like syndrome and antihistone antinuclear antibodies, our patient displayed none of the clinical or immunological features that are characteristic of drug-induced lupus. Furthermore, none of the identifiable causes for crescentic glomerulonephritis was evident in this girl. To the best of our knowledge this is the first report suggesting a possible association of crescentic glomerulonephritis to isoniazid treatment.     

Three cases of tuberculosis after heart transplantation in Spain

The fibrinolytic capacity of patients with acute myocardial infarction (AMI) is known to be impaired. The primary regulatory element of the fibrinolytic system is plasminogen activator inhibitor (PAI). It has been previously observed that there are 2 peaks in the plasma PAI level of AMI patients at 4h and 16h after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA). Lanoteplase/SUN9216 is a mutant tPA with a biological half-life longer than that of rtPA. Thrombolytic therapy with mutant tPA or rtPA was carried out consecutively in 21 patients with AMI (8 patients as the mutant tPA group, and 13 patients as the rtPA group). The recanalization time of the mutant tPA group was significantly faster than that of the rtPA group (16.1 +/- 3.9 min vs 39.6 +/- 4.8 min, p<0.01). The PAI activity at 4h after the initiation of thrombolysis was significantly lower in the mutant tPA group than in the rtPA group (8.74 +/- 5.46IU/L vs 26.74 +/- 3.35 IU/L, p<0.01). There was a one mild peak in serial plasma PAI activity levels 24h after the initiation of thrombolysis. The results suggest that thrombolytic therapy with mutant tPA reduced the impairment of fibrinolytic capacity. The mutant tPA gives faster recanalization and lower PAI activity after successful thrombolysis, compared with rtPA.     

Liquid chromatographic determination of five benzoylurea insecticides in fruit and vegetables

A liquid chromatographic (LC) method was developed to determine 5 benzoylureas--diflubenzuron, hexaflumuron, teflubenzuron, flufenozuron, and lufenuron--in peppers, tomatoes, eggplants, cucumbers, and oranges. Preparation of samples involve extraction with acetone and partitioning into dichloromethane-petroleum ether. A portion of this extract is cleaned up with a solid-phase extraction aminopropyl disposable column. With LC analysis using an RP-8-DB microbore column, acetonitrile-water (70 + 30, v/v) as mobile phase, and photodiode array detection at 254 nm, recovery and repeatability data were collected for the 5 benzoylureas on 4 vegetables and citrus in the range 0.04-2.0 mg/kg. Validated limits of detection and quantitation were 0.01 and 0.04 mg/kg, respectively. The method is reliable for routine analysis of vegetables and fruits.     

The simian T-lymphotropic virus STLV-PP1664 from Pan paniscus is distinctly related to HTLV-2 but differs in genomic organization

We have isolated a highly divergent simian T-lymphotropic virus, STLV-PP1664, from a wild-caught bonobo (Pan paniscus). Previous phylogenetic analysis suggested that this virus represents an additional type of STLV but this has now become a matter of discussion. We have now obtained and analyzed the entire genome of STLV-PP1664. All major genes and their corresponding viral messengers were identified. Sequence comparison and phylogenetic analysis indicated that this virus, together with the closely related panp isolate, belongs to an early lineage within the PTLV-2 clade, differing from HTLV-2 by about 25%. In contrast to the HTLV-1 and HTLV-2 LTR, only two 21-bp repeats instead of three were found in the STLV-PP1664 LTR. Additional messengers, resulting from alternative splicing, potentially encode five different accessory proteins from open reading frames in the pX region: prorfI, porfII, ptorfV', and two isoforms of Rex. The amino acid sequences of these proteins are only distinctly related to the accessory proteins from HTLV-2. These data suggest a different genomic organization of the STLV-PP1664 pX region than that of HTLV-2. We conclude that STLV-PP1664, although related to HTLV-2, has some distinct features in the LTR and the pX regions, the impact of which needs further investigation. Although arguments pro and contra a distinct classification are nearly equally balanced, we propose to classify this virus as an STLV-2, designated STLV-2PP1664.     

Differential chromosome sensitivity to 5-azacytidine in Alzheimer''s disease

The chemiluminescence (CL) technique with scavengers for superoxide anion (superoxide dismutase) and hydrogen peroxide (catalase) was used to characterize the generation of reactive oxygen species (ROS) inside and outside the human neutrophil after stimulation with both soluble (formyl-methionyl-leucyl-phenylalanine, FMLP) and particulate (urate crystals, zymosan, oxidized LDL) stimuli. Depending on the stimulus used, ROS generation differed in composition and absolute amounts. The ratio between extracellularly and intracellularly produced ROS ranged from 0.3 (zymosan) to 4.2 (FMLP). While enhancing substantially FMLP-stimulated CL, horseradish peroxidase inhibited CL induced by particulate stimuli by 40-80%. Furthermore, an azide-insensitive and therefore peroxidase-independent part of CL was found in FMLP-, LDL- and zymosan-stimulated cells. The results indicate that different agonists may lead through distinct chemical pathways to neutrophil luminol-amplified light generation.     

Therapeutic approach in blast injuries of the ear

Otic blast injury is caused by arrhythmic air blast wave. The perforation of the tympanic membrane is the commonet finding associated with lacerations of mucosa in the middle ear. Makki [6] published 34 cases of myringoplasty after war blast injuries. However, healing of such perforations is common; Kerr [7] noted a healing rate of 83% after the blast injury. The aim of the study was to evaluate different therapic procedures of otic blast injuries. There were 74 patients with bilateral otic blast injuries, who underwent otomycroscopic examination. The following parameters were noted: Integrity of tympanic membrane and size of perforation, presence of haemorrhagic exudate in the middle ear and median value of conductive deafness (Table 2). Main symptoms, presented in Table 1 were: pain, deafness and otohaematorrhoea. The first group of 19 patients received antibiotics by parenteral way during 7 days according to the bacterial finding in ear exudate. Healing rate was dependent on the size of tympanic membrane perforation, and rated from 71% in perforation of one third of tympanic membrane to 25% in total perforation of tympanic membrane. Data are presented in Table 3. The second group of 24 patients received the same therapy as the first treatment, plus otomycroscopic removal of haemorrhagic exudate, lacerated middle ear mucosa, and repair of tympanic membrane lacerations. Healing rate was significantly better than the one obtained in the first group (Table 4). Persistent tympanic perforation, as indicator of failed therapy, was present in 5 (35%) of all examined ears with two thirds of tympanic membrane perforation in the first group, while in the second group the rate was 3 (12%). The third group received the same therapy as the second treatment, including administration of amicacyn into the external auditory canal. The results were statistically compared by chi 2 test, and we found that the second therapy protocol was significantly better. There was no significant difference between the second and the third therapy protocols. We found blast ruptures of tympanic membrane and auditory ossicles chain discontinuity in 88% of examined ears. In our material the high incidence of total tympanic membrane ruptures and subtotal ruptures (48%) is quite different in comparison to other authors [5-7]. We consider it as the effect of high power blast wave. Loss of conductive hearing was present in 91% of blast injured patients, while 7.4% of patients had mixed, predominantly senzoneural deafness. Consequently, in addition to mechanic blast injuries acoustic trauma could profoundly damage the inner ear. Spontaneous healing of tympanic membrane occurred in 71% of injured persons and this was a better result than the results obtained by other authors [3, 4, 6]. The spontaneous healing of tympanic membrane failed if infection of the middle ear occurred or blast caused the total tympanic membrane perforation. In the second and third therapy protocols significantly higher healing of tympanic membrane ruptures was evident; it rated from 88% to 91%. Better results could be explained by the effect of optimal healing conditions, based on removal of exudate from the middle ear and necrotic parts of tympanic membrane, completed by fitting of lacerated parts of tympanic membrane and antibiotic prophylaxis. Healing of tympanic membrane without scars and adhesions was more frequent than in patients treated only with antibiotics. Incidence of undesired outcome of persistent perforation of tympanic membrane was reduced. To prevent posttraumatic complications in the middle ear, we recommend early cleaning of margins, reposition of lacerated fragments of tympanic membrane, and removal of haemorrhagic exudate. Myringoplasty should be performed if spontaneous healing of tympanic membrane did not occur after 6 months. CONCLUSION: Otic blast injury was frequently found in war induced trauma. (ABSTRACT TRUNCATED)