Tracheal obstruction after placement of a metal wire expandable stent (Wallstent).

Metal wire expandable stents are increasingly being used to alleviate tracheal obstruction due to malignancies. Patients usually tolerate these stents well and experience good to excellent palliation of their symptoms [1]. We report a case in which severe tracheal obstruction occurred 5 days after placement of a Wallstent, caused by formation of fibrinoid plaques at the proximal end of the stent.

Sequences derived from the highly antigenic VP1 region 140 to 160 of foot-and-mouth disease virus do not prime for a bovine T-cell response against intact virus.

Although VP1 region 140 to 160 of foot-and-mouth disease virus (FMDV) is able to elicit neutralizing antibody in cattle, the protection against virus challenge that is conferred by peptide immunization is often poor. Here, we show that bovine T cells primed with peptides derived from this region generally show no reactivity to intact FMDV. In contrast, T-cell epitope VP4[20-34] is able to prime for a virus-specific response.

Adenosine deaminase activity, not diagnostic for tuberculous pleurisy.

We have measured adenosine deaminase (ADA) in pleural effusions of 95 patients, using a method optimalised for rapid determination on a Hitachi 705 analyzer. High ADA activity was found in four of the five patients with tuberculous pleurisy, in four of the seven with empyema and in three of the seven patients with mesothelioma. One patient with very high serum ADA activity due to liver disease also had a high activity in the pleural effusion. Low activity was found in all patients with other neoplastic pleural effusions, parapneumonic pleural effusions, transudates, and in pleural effusions due to some other diseases. We conclude that in a country with a low tuberculosis incidence a high ADA activity in pleural effusion in neither sensitive nor specific enough to rely on the diagnosis of tuberculous pleurisy. Routine determination of ADA is not recommended; in selected cases, however, it may be useful.

Transphrenic dissemination of actinomycosis.

Thoracic actinomycosis is an uncommon disease and often presents difficulty in diagnosis. Two cases are presented in which thoracic actinomycosis produced fistulae between the thoracic and abdominal cavities. Surgical drainage and high dose penicillin for at least 4-6 months was the treatment of choice.

Nasal application of a naturally processed and presented T cell epitope derived from TCR AV11 protects against adjuvant arthritis.

Reactivity towards TCR peptides plays an important role in the regulation of several experimental autoimmune diseases. In a previous paper, we showed the TCRAV11 usage by an arthritogenic T cell clone isolated from a rat with adjuvant arthritis (AA). Moreover, we identified three immunogenic peptides in AV11: AV11 24-40, 41-55 and 66-80. In the present study, we show that T cells directed towards all three epitopes are part of the immune repertoire. The strongest delayed-type hypersensitivity (DTH) reaction was observed against the peptide derived from the third framework region, peptide AV11 66-80. DTH reactions to this peptide were detectable in naive rats and increased significantly after AA induction. Interestingly, modulation of the AV11 66-80 T cell response by nasal AV11 66-80 administration resulted in reduced DTH responses and in a strong inhibition of AA. These findings suggest that during the natural course of AA, T cells directed towards the third framework region of AV11 do not have a disease regulatory function, but instead play a role in the deterioration of AA.

Twelve-minute walking test in a group of Dutch patients with chronic obstructive pulmonary diseases; relationship with functional capacity.

Limitations in exercise tolerance are characteristic for patients with chronic obstructive pulmonary disease. The twelve-minute walking test has been proposed as a simple, reproducible test to assess exercise tolerance in these patients. We investigated factors, that predicted the twelve-minute walking distance in a group of fifty patients with COPD, who had a maximal reversibility in the FEV1 of 20% after inhaled salbutamol. There was a strong correlation between walking distance and IVC (%pred) (p less than 0.001), RV% TLC (%pred) (p less than 0.001), FEV1 (ml) (p less than 0.001), FEV1 (%pred) (p less than 0.001) and PaO2 (mm Hg) (p less than 0.01). It is concluded that pathophysiological factors are the main determinants of the twelve-minute walking distance.

Adjuvant arthritis and immunity to the mycobacterial 65 kDa heat shock protein.

The mycobacterial 65 kDa heat shock protein (HSP65) is of critical significance in the model of adjuvant arthritis (AA). Arthritogenic and protective T cell clones obtained from arthritic rats recognized the 180-188 sequence of HSP65. Previous reports have shown that administration of HSP65 prior to disease induction led to resistance to arthritis in the AA model and in several other models of experimental arthritis. Here, we report the development of immunity to HSP65 and the critical 180-188 epitope during the course of AA. Following Mycobacterium tuberculosis (MT) immunization both antibodies and T cell responses to HSP65 were detected. Proliferative responses to the 180-188 epitope were seen exclusively in the local draining lymph node cells at day 14 after immunization. The anatomical distribution and course of T cell responses to HSP65 and its 180-188 epitope are compatible with T cell regulated control of the disease. Although lower HSP65 antibody levels were observed in the animals with severe arthritis, in individual animals no evidence was obtained for a relationship between development of HSP65 humoral immunity and arthritis severity. Nevertheless, during disease exacerbation, elicited by HSP65 immunization during disease development, elevated T cell responses against HSP65 and its 180-188 epitope were found. In contrast, we obtained evidence that successful transfer of arthritis resistance to naive recipients depends on the transfer of HSP65 specific T cells. On the basis of these results, it seems that HSP65 plays a crucial role in the T cell regulatory events involved in both the induction of, and protection against, AA.(ABSTRACT TRUNCATED AT 250 WORDS)

T cell-stimulatory fragments of foot-and-mouth disease virus released by mild treatment with cathepsin D.

Cathepsin D and cathepsin B are endosomal/lysosomal proteases that are thought to play a role during in vivo antigen processing, releasing fragments for binding to major histocompatibility complex class II products and subsequent presentation to T cells. Here we treated purified foot-and-mouth disease virus (FMDV) strain A10Holland with both enzymes. Cathepsin D, but not cathepsin B, was shown to release fragments from reduced or non-reduced FMDV under mild conditions in vitro. Twenty-eight predominant cathepsin D-released fragments were purified by HPLC and identified by amino acid composition analysis and sequencing. The unseparated set of fragments produced (the digest) was able to stimulate T cells from eight vaccinated cattle. With respect to the response to intact virus the extent of the response to the digest differed between animals: four animals could be classified as good responders, three as intermediate responders and one as a low responder. Subsequently, we investigated the proliferative T cell response to a large set of synthetic peptides in detail for two animals, one belonging to the group of good responders, the other being the low responder. The peptides covered all 28 cathepsin D-released fragments analysed and also several sequences not recovered from the digest. In this way seven T cell sites could be identified, five of which coincided with cathepsin D-released fragments. The other two T cell sites were VP2[54-72], being a homologue of a T cell site identified for FMDV strain O1K and the N terminus of VP4. Whether the most dominantly recognized T cell site was recovered from the digest or not was shown to be related to the good or low response to the digest. These findings suggest a role for cathepsin D in the release of some but not all T cell-stimulatory fragments from FMDV.