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Biomedical subjects

D Schraufnagel

Publications and source records attributed to D Schraufnagel.

15 recordsLinked to original sources

Challenging Alexis Carrel: a study in alternate microvascular techniques.

INTRODUCTION: Alexis Carrel pioneered the full-thickness triangulated vascular repair technique, which led to a Nobel Prize in 1912. However, microvascular anastomotic techniques that do not violate the intima, such as the VCS microclip repair and partial-thickness suturing, limit trauma to the intima, thus minimizing the potential for thrombosis. Our study compares such techniques with the standard full thickness-anastomotic repair. METHODS: Thirty-two end-to-end anastomotic repairs were performed in rat femoral arteries 1 mm or less in diameter. Group I: thirteen full-thickness repairs were completed using 10-0 nylon on a BV75 microm needle. Nineteen extraluminal repairs were performed using either a partial thickness technique with an 11-0 nylon BV50 microm needle (Group II, n = 12) or VCS nonpenetrating clip (Group III, n=7). Casted samples, injected with methylmethacrylate, were harvested at 1 and 3 weeks for histopathological evaluation. The presence of thrombosis, inflammation, endothelialization, angiogenesis and intimal hyperplasia were described for each repair. RESULTS: Statistical analysis revealed no difference between the intraluminal and extraluminal techniques. Patency rates were similar between both groups: 92% (12/13) for Group I and 94% (17/18) for the extraluminal Groups II and III combined. One-hundred per cent of partial thickness suture repairs were patent. Histology revealed localized inflammation to the adventitia and media, as well as endothelialization at 1 week for anastomoses in Groups II and III. The intima of Group I demonstrated proliferative characteristics in contrast to the extraluminal groups, where secretory myofibroblasts were prevalent. The anastomotic microcirculation did not originate from the repaired artery in any of the groups. CONCLUSION: Patency rates with end-to-end anastomotic repairs using a partial thickness technique are comparable to the standard full-thickness technique. Repairs that do not include the intima revealed focal inflammatory responses to the outer layers and more rapid endothelialization, while neighboring vessels perfuse the healing anastomosis.

Anastomosis, Surgical↗

Alveolar fluid reabsorption is impaired by increased left atrial pressures in rats.

Cardiogenic pulmonary edema results from increased hydrostatic pressures across the pulmonary circulation. We studied active Na(+) transport and alveolar fluid reabsorption in isolated perfused rat lungs exposed to increasing levels of left atrial pressure (LAP; 0--20 cmH(2)O) for 60 min. Active Na(+) transport and fluid reabsorption did not change when LAP was increased to 5 and 10 cmH(2)O compared with that in the control group (0 cmH(2)O; 0.50 +/- 0.02 ml/h). However, alveolar fluid reabsorption decreased by approximately 50% in rat lungs in which the LAP was raised to 15 cmH(2)O (0.25 +/- 0.03 ml/h). The passive movement of small solutes ((22)Na(+) and [(3)H]mannitol) and large solutes (FITC-albumin) increased progressively in rats exposed to higher LAP. There was no significant edema in lungs with a LAP of 15 cmH(2)O when all active Na(+) transport was inhibited by hypothermia or amiloride (10(-4) M) and ouabain (5 x 10(-4) M). However, when LAP was increased to 20 cmH(2)O, there was a significant influx of fluid (-0.69 +/- 0.10 ml/h), precluding the ability to assess the rate of fluid reabsorption. In additional studies, LAP was decreased from 15 to 0 cmH(2)O in the second and third hours of the experimental protocol, which resulted in normalization of lung permeability to solutes and alveolar fluid reabsorption. These data suggest that in an increased LAP model, the changes in clearance and permeability are transient, reversible, and directly related to high pulmonary circulation pressures.

Absorption↗

Plasma membrane-bound and lysosomal peptidases in human alveolar macrophages.

Alveolar macrophages protect the lungs against noxious agents. Proteases and peptidases are essential for this defense and many metabolic activities. Human alveolar macrophages were evaluated for the presence of six important peptidases. Deamidase, a serine peptidase identical with the lysosomal protective protein and possibly with cathepsin A, had high specific activity in alveolar macrophages and is also present in cultured mouse J774A.1 and human U937 cells, used for the sake of comparison. In fractionated J774A cells, most of the deamidase activity was in the lysosomal fraction and in the final supernatant. Deamidase in human alveolar macrophages, obtained by bronchoalveolar lavage from 23 patients, cleaved dansyl-Phe-Leu-Arg at a rate of 2.26 mumol/h/mg protein and hydrolyzed the chemotactic peptide N-f-Met-Leu-Phe even faster, at a rate of 53.1 mumol/h/mg protein, the highest activity for this enzyme with any of the cells we tested. Rabbit antiserum, elicited with the recombinant partial sequence of the enzyme, immunoprecipitated 77-88% of the macrophage deamidase. In immunocytochemistry, this antiserum localized deamidase within the human macrophages. The enzyme was inhibited by diisopropylfluorophosphate (DFP; 1 mM) and by ebelactone B (10 microM), noncompetitively. The mRNA of deamidase was detected in mouse macrophages by Northern blot; the two protein chains of deamidase were shown in human macrophages by Western blot. In addition, two other serine peptidases were also highly active in macrophages: dipeptidyl peptidase IV (1.38 mumol/h/mg protein) and prolylcarboxypeptidase (0.72 mumol/h/mg protein). The activity of plasma membrane zinc metallopeptidases, neutral endopeptidase 24.11 and carboxypeptidase M, in contrast, was low or absent (angiotensin I converting enzyme; kininase II).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Tail signs.

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Adenocarcinoma, Bronchiolo-Alveolar↗

Pathogenesis of pulmonary infarction.

Pulmonary embolism discovered at autopsy is still as prevalent as previously reported in the last three to four decades. Only a certain percentage of pulmonary emboli result in pulmonary infarction. Recently published studies have suggested that importance of the size of the occluded pulmonary artery in the occurrence of infarction. Our study of 45 autopsy subjects in which there were pulmonary emboli shows a 31 percent incidence of pulmonary artery branches of 3 mm in diameter or less, but emboli in larger arteries may show frequent extensions into their smaller distal branches without producing infarct. Pulmonary infarction also occurs more commonly in patients dying of cardiovascular or malignant diseases than it does in those dying of other diseases, and the combination of shock and congestive left heart failure appears to be the most significant hemodynamic risk factor in the development of pulmonary infarction. However, the increased risk of pulmonary infarction in patients with malignancy may not be accounted for by the existence of these two hemodynamic risk factors alone.

Cardiomegaly↗

Differentiating bronchioloalveolar carcinoma from adenocarcinoma.

The recognition of bronchioloalveolar carcinoma (BAC) as distinct from adenocarcinoma of the lung, is controversial. Using strict pathologic criteria, 43 consecutive patients with BAC were matched by year of diagnosis and compared with a similar number of patients with adenocarcinoma, and for contrast, with those with squamous and oat cell carcinoma of the lung. We demonstrated that BAC is not sex related, and is not as smoking related as the other neoplasms. Unlike epidermoid carcinoma, BAC does not show a predilection for those occupations requiring manual labor. Also, BAC is frequently distinguishable radiologically from the other three by being smaller and peripheral. A pleural tag and an air bronchogram in a mass are rather specific, and BAC is less likely to have large airway involvement and adenopathy. The percentage of patients who were free of tumor after 2 yr was greater in the BAC group than in the others, but the overall survival rate between the BAC group and the adenocarcinoma group was not. Based on inter-observer variability, there is some overlap pathologically between these 2 groups. However, when the overlap between the adenocarcinoma and the BAC groups is compared with that between the adenocarcinoma and the squamous cell carcinoma groups, the difference is not significant. We conclude that BAC should be considered a distinct clinical entity.

Adenocarcinoma↗

A coded study of antitumor immunity to human lung cancer assayed by tube leukocyte adherence inhibition.

The present study was undertaken to evaluate the specificity of antitumor immunity to human lung cancer, measured by an in vitro assay--tube leukocyte adherence inhibition (LAI). We standardized and monitored the putative tumor antigen activity of the extracts by testing leukocytes from controls and patients with lung cancer in the Montreal General Hospital. A specific antitumor response to a lung cancer antigen was detected with coded leukocytes from 56% (20 out of 36) of patients with epidermoid lung cancer. By contrast, 4% (2 out of 53) of patients with inflammatory lung disease and none of 46 other patients with cancer metastatic to the lung or with other diagnoses had an LAI-positive result. The LAI response was inversely related to the extent of cancer: 80% (8 of 10) with Stage I, 66% (2 of 3) with Stage II, 54% (6 of 11) with localized Stage III, and 33% (4 of 12) with widespread Stage III were LAI positive. Leukocytes from patients with epidermoid, adenocarcinoma, or small cell lung cancer reacted to a common tumor antigen shared by extracts of epidermoid and small cell lung cancer. This study with coded samples from a remote hospital confirms the results of other investigators that the LAI measures an antitumor immune response to human organ-specific neoantigens.

Adenocarcinoma↗

The G syndrome: a case report.

A case of the G syndrome is reported in a baby boy who had an unusual facies (prominent forehead, telecanthus, posteriorly rotated ears, and anteverted nostrils), laryngeal cleft, hypospadias, cryptorchidism, and psychomotor development delay, possibly secondary to birth asphyxia and numerous medical and surgical complications. The mother had a similar facies.

Craniofacial Dysostosis↗