[Evisceration of intestines following abdominal stab wounds: epidemiology and clinical aspects of emergency room management]. / Eviszeration von Darm nach Stichverletzung des Abdomens: Häufigkeit und klinische Aspekte des klinischen Schockraummanagements.

STUDY AIM: The aim of the study was an estimation of the incidence and clinical aspects of emergency room (ER) parameters of penetrating abdominal injury patients with bowel evisceration. STUDY DESIGN AND METHODS: The study involved a retrospective cohort analysis of ER data from the Chris Hani Baragwanath Academic Hospitals, Soweto, Johannesburg, South Africa between September 2000 to May 2005. RESULTS: Out of 9,010 ER patients, 4,390 suffered penetrating injuries with 8 out of 71 eviscerations due to a single gunshot wound, 60 out of 71 eviscerations due to single stab wounds and 3 further patients suffered multiple injuries. The ER mortality was 1 out of 71(1.6 %) with an average ER mortality of 4.2 %. The only death seen was a single abdominal gunshot wound with vascular injury. The causative mortality due to abdominal stab wounds with evisceration of the bowels was therefore zero. The heart rate in patients with abdominal stab wounds with and without bowel evisceration showed no significant difference, thus mesentery tearing or vagal overstimulation could not be seen, neither with bradycardia nor hypotension. CONCLUSION: Evisceration itself is not a cause for increased mortality or cardiovascular instability seen in the ER. There is ample time for diagnostic procedures before laparotomy is performed.

Local tumor inflammation, lymph node metastasis, and survival of operated bronchus carcinoma patients.

Three hundred and fifty-three resection specimens with primary lung carcinomas were cut into serial sections, and the tumor volume was computed. Resected lymph nodes were cut into 0.3-mm serial sections and analyzed for metastasis. The inflammatory reaction of lung tissue was analyzed by grading the amount of inflammatory infiltrations of a complete tumor cross section. Survival of patients was evaluated by consulting the house physician every 3 months after surgical treatment. Percentage of specimens with severe inflammatory reaction of host tissue increased remarkably in tumors with a volume of 35-60 cm3. Percentage of patients with detectable lymph node metastasis increased with tumor volume but decreased at the tumor volume of 35-45 cm3. Mean tumor volume in patients with no detectable lymph node metastasis was increased if severe inflammatory response of host tissue existed. Survival of patients with severe inflammatory infiltrations was superior to survival of patients with no inflammatory infiltrations if grouped for tumor volume. Data indicated that inflammatory infiltrations in primary lung carcinoma may partly be related to the immunologic response of host tissue to tumor growth. Inflammatory infiltrations may delay tumor cell propagation into lymph nodes or may be even able to destroy small tumor cell agglutinations.

MDR1 gene expression in lung cancer.

The MDR1 gene (also known as PGY1) is frequently overexpressed in multidrug-resistant cell lines. We investigated the role of MDR1 gene expression in lung cancer by performing RNA slot blot analysis in samples from a panel of 24 lung cancers, 10 corresponding nontumorous lung tissues, and 67 tumor cell lines of several histologic types. Almost all of the tumors, nontumorous lung tissues, and cell lines expressed low levels of MDR1 RNA. Relatively higher levels were found in only one type of lung cancer, a subgroup of non-small cell lung cancers expressing neuroendocrine markers. No evidence of MDR1 gene amplification or rearrangements was detected. We found no correlation between MDR1 gene expression in cell lines and (a) in vitro chemosensitivity of the cells, (b) prior therapy status of the patients, or (c) clinical response to therapy. We conclude that the clinical multidrug resistance of many lung cancers cannot be explained solely on the basis of expression of the MDR1 gene.

Digitized pathology: theory and experiences in automated tissue-based virtual diagnosis.

AIMS: To describe the theory and develop an automated virtual slide screening system. Theoretical considerations. Tissue-based diagnosis separates into (a) sampling procedure to allocate the slide area containing diagnostic information, and (b) evaluation of diagnosis from the selected area. Nyquist's theorem broadly applied in acoustics, serves to presetting the sampling accuracy. Tissue-based diagnosis relies on two different information systems: (a) texture, and (b) object information. Texture information can be derived by recursive formulas without image segmentation. Object information requires image segmentation and feature extraction. Both algorithms complete another to a "self-learning" classification system. METHODS: Non-overlapping compartments of the original virtual slide (image) are chosen at random with predefined error-rate (Nyquist's theorem). The standardized image compartments are subject for texture and object analysis. The recursive formula of texture analysis computes median gray values and local noise distribution. Object analysis includes automated measurements of immunohistochemically stained slides. The computations performed at different magnifications (x 2, x 4.5, x 10, x 20, x 40) are subject to multivariate statistically analysis and diagnosis classification. RESULTS: A total of 808 lung cancer cases of diagnoses groups: cohort (1) normal lung (318 cases) - cancer (490 cases); cancer subdivided: cohort (2) small cell lung cancer (10 cases) - non-small cell lung cancer (480 cases); non-small cell lung cancer subdivided: cohort (3) squamous cell carcinoma (318 cases) - adenocarcinoma (194 cases) - large cell carcinoma (70 cases) was analyzed. Cohorts (1) and (2) were classified correctly in 100%, cohort (3) in more than 95%. The selected area can be limited to 10% of the original image without increased error rate. A second approach included 233 breast tissue cases (105 normal, 128 breast carcinomas) and 88 lung tissue cases (58 normal, 38 cancer). Texture analysis revealed a correct classification with only 10 training set cases in >92% for both, breast and lung tissue. CONCLUSIONS: The developed system is a fast and reliable procedure to fulfill all requirements for an automated "pre-screening" of virtual slides in tissue-based diagnosis.

HMGI-C rearrangements as the molecular basis for the majority of pulmonary chondroid hamartomas: a survey of 30 tumors.

Pulmonary chondroid hamartomas (PCH) are benign tumors of the lung characterized by a more or less high degree of mesenchymal metaplasia. In our series we investigated 30 PCH by a combination of cytogenetic and molecular methods. 18 tumors (60%) had cytogenetically detectable aberrations involving either 12q14-15 or 6p21 with a clear predominance of chromosomal abnormalities involving 12q14-15 (15 tumors). As in subgroups of pleomorphic adenomas of the salivary glands, leiomyomas of the uterus, and lipomas with 12q14-15 abnormalities the HMGI-C gene is frequently rearranged we tested PCH with either 12q14-15 abnormalities or normal karyotype by FISH and 3' RACE experiments for rearrangements of HMGI-C. Rearrangements were found in all cases with chromosomal 12q14-15 abnormalities and further six cases with an apparently normal karyotype. By the combination of cytogenetics with molecular techniques the percentage of cases with intragenic rearrangements of HMGI-C or rearrangements of its immediate surrounding was thus increased to 70% (21/30 cases). Considering all types of aberrations within this series 80% (24/30) of all PCH were aberrant. This is the first report on a combined molecular and cytogenetic analysis of a large series of pulmonary chondroid hamartomas indicating that rearrangements of HMGI-C, a member of the high mobility group protein gene family, are the leading molecular events in the genesis of PCH.

Expression of CD44 splice variants in normal respiratory epithelium and bronchial carcinomas: no evidence for altered CD44 splicing in metastasis.

Expression of alternatively spliced CD44 adhesion molecules has been implicated in metastatic spread of various rodent and human tumors. To determine whether specific CD44 splice variants contribute to metastatic spread of bronchial cancers, we compared the expression of CD44 splice variants in normal bronchial epithelium and bronchial cancers, including tumors which already spread to regional lymph nodes or distant organs. Variant CD44 expression was analysed by immunohistochemistry using variant exon-specific monoclonal antibodies. The precise composition of CD44 transcripts was delineated by exon-specific RT-PCR. The concurring data obtained by both methods revealed that high levels of standard CD44 and variants v5 and v6 as well as low levels of variants v7 and v10 are expressed both in normal bronchial epithelium and squamous cell lung cancers. No CD44 expression was observed in the highly metastatic small cell lung cancers and adenocarcinomas with the exception of bronchioalveolar cancers showing weak expression of standard CD44. These data suggest that expression of alternatively spliced CD44 molecules in the bronchial tract is related to the distinct differentiation of the respiratory epithelium. No correlation between expression of specific CD44 splice variants and metastasis of bronchial cancers was observed.

Triple vessel coronary artery endarterectomy and reconstruction: results in 144 patients.

Coronary artery endarterectomy and reconstruction are valuable adjuncts to conventional bypass surgery when attempting to revascularize "diffusely" diseased coronary arteries. One hundred forty-four consecutive patients were operated on through February 1986, all of whom required endarterectomy and reconstruction of the left anterior descending, left circumflex and right coronary arteries. There were 130 men (90%), ranging in age from 29 to 83 years (average 55.8), whose left ventricular ejection fraction ranged from 0.20 to 0.75 (average 0.54). One hundred thirty-one patients (91%) had angina preoperatively, which was Canadian Cardiovascular Society class III or IV in 85 (59%). Fifteen operations (10%) were repeat procedures. All operations were performed using intermittent ischemic arrest. There was an average of 5.0 grafts per patient (range 3 to 8), with an average of 3.8 endarterectomized vessels per patient (range 3 to 7). There were 14 surgical deaths (10%), all cardiac in origin. Statistically significant (p less than 0.01) risk factors for increased operative mortality included repeat surgery, ejection fraction less than or equal to 0.30 and age greater than or equal to 70 years. The operative mortality rate in 106 low risk patients (male gender, age less than 70 years, ejection fraction greater than 0.30, first operation) was 3.8% (4 patients). Nonfatal complications included 13 perioperative myocardial infarctions (10%). Long-term follow-up data are available for all 102 surviving patients for an average of 30 months (range 7 to 92). There were 12 late deaths 1 to 52 months postoperatively. The 5 year actuarial survival rate is 71% for the entire group and 87% for the 106 low risk patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchioloalveolar carcinoma: a new cancer in Peutz-Jeghers syndrome.

Besides gastrointestinal hamartomatous polyposis and melanin spots in the skin and mucosa, patients with the Peutz-Jeghers syndrome (PJS) have repeatedly been observed with a variety of tumours, including lung cancer. Available data indicate an increased cancer risk among PJS patients, which suggests that the gene involved in PJS, STK11 on chromosome 19p13.3, may be a tumour suppressor gene. Herein, bronchioloalveolar carcinoma (BAC) of mucinous type is reported in a 22-year old male PJS patient with a novel germline frameshift insertion in exon 2 at codon 118 of the STK11 gene. Molecular studies of his BAC indicated loss of heterozygosity (LOH) in the region of STK11 on chromosome 19p13.3. This observation supports the hypothesis that STK11 is a tumour suppressor gene which is involved in the development of lung adenocarcinoma.

Processes in vertical-flow reed beds: nitrification, oxygen transfer and soil clogging.

Vertical-flow reed beds (VF) with intermittent feeding are extremely reliable regarding aerobic processes. For a save operation with high nitrification rates and without soil clogging it is essential to preserve aerobic conditions in the filter. The challenge is to keep aerobic conditions in the filter without oversizing the system (economical aspects). It is very difficult to determine the current oxygen content in the filters because it ultimately results from complex interactions of a large number of different influencing parameters such as loading rate, degree of clogging, temperature, and hydraulic behaviour of the reed bed. To gain better knowledge of this complex system, different tests and examinations were carried out over several years. Focusing on the questions of identification and the description of conversion and transport processes (water/gas), a full-scale treatment plant under clogged and non-clogged conditions was investigated in detail. Additionally soil column test were carried out. The results make it possible to describe some of the processes and their interactions in the filter body. Recommendations for a safe and controlled operation can be derived.

Phenotype and genotype associations of lung carcinoma with atypical adenomatoid hyperplasia, squamous cell dysplasia, and chromosome alterations in non-neoplastic bronchial mucosa.

The frequency of preneoplastic lesions of the lung and bronchial mucosa as well as potential genotype alterations in spatial relationship to pulmonary malignancies still need intensive investigations in order to understand the occurrence and manifestation of lung cancer in detail. To investigate the contemporary manifestation of lung cancer precursor lesions, peripheral (non-neoplastic) lung parenchyma and bronchial mucosa of operated lung carcinomas were analyzed at distinct distances (1, 2, 3, and 4 cm) from the tumor boundary for pre-neoplastic lesions--atypical adenomatoid hyperplasia (AAH) and squamous cell dysplasia (SCD), in 150 surgical specimens. Short-term tissue cultures of additional 55 primary and secondary lung tumors and their surrounding non-neoplastic bronchial mucosa were performed at the same distances in order to search for chromosome alterations, i.e. genotype aberrations. In phenotype observations, atypical adenomatoid hyperplasia was noted in 19/150 (13%) cases, and squamous cell dysplasia in 46/150 (31%) cases. The degree of cellular atypia decreased with increasing distance from the tumor boundary in both AAH and SCM. AAH was observed more frequently in adenocarcinomas, SCQ more frequently in squamous cell carcinomas. In genotype observations, the average number of abnormal metaphases measured 4.5/10 high power fields (HPF) in primary lung carcinomas, and only 2/10 in metastases. Data indicate that the so-called preneoplastic lesions in the lung are not completely tumor-precursor lesions, but, in addition, induced by the tumor itself.

Glutathione-S-transferase M1, M3, T1 and P1 polymorphisms and susceptibility to non-small-cell lung cancer subtypes and hamartomas.

Polymorphic glutathione-S-transferase (GST) genes causing variations in enzyme activity may influence individual susceptibility to lung cancer. In this case-control study (consisting of 389 Caucasian lung cancer patients, including 151 adenocarcinomas (ACs) and 172 squamous cell carcinomas (SCCs), and 353 hospital control subjects without malignant disease, genotype frequencies for GSTM1, GSTM3, GSTP1 and GSTT1 were determined by polymerase chain reaction (PCR)/ restriction fragment length polymorphism (RFLP)-based methods. While adjusted odds ratios (ORs) indicated no significantly increased risk for lung cancer overall due to any single GST genotype, the risk alleles for GSTM1, GSTM3 and GSTP1 conferring reduced enzyme activity were present at higher frequency in SCC than in AC patients. This is consistent with a reduced detoxification of carcinogenic polycyclic aromatic hydrocarbons (PAHs) from cigarette smoke that are more important for the development of SCC than for AC. An explorative data analysis also identified statistically significantly increased ORs for the combinations GSTT1 non-null and GSTP1 GG or AG for lung cancer overall (OR 2.23, CI 1.11-4.45), and for SCC (OR 2.69, CI 1.03-6.99). For lung cancer overall, and especially among SCC patients, the GSTT1 null genotype was underrepresented (SCC 11.2% v. control subjects 19%, P = 0.026, OR 0.57, CI 0.30-1.06). Additionally, in 28 patients with hamartomas, the GSTT1 null genotype was also protective (P = 0.013), while GSTP1 variant allele carriers were overrepresented (OR 2.48, CI 1.06-6.51). In conclusion, GST genotypes may act differently, either by detoxifying harmful tobacco carcinogens and/or by eliminating lung cancer chemopreventive agents. The latter role for GSTT1 would explain the observed lower risk of SCC and hamartoma associated with GSTT1 null. Further confirmatory studies are required.

Relevance of N-acetyltransferase 1 and 2 (NAT1, NAT2) genetic polymorphisms in non-small cell lung cancer susceptibility.

The highly polymorphic N-acetyltransferases (NAT1 and NAT2) are involved in both activation and inactivation reactions of numerous carcinogens, such as tobacco derived aromatic amines. The potential effect of the NAT genotypes in individual susceptibility to lung cancer was examined in a hospital based case-control study consisting of 392 Caucasian lung cancer patients [152 adenocarcinomas, 173 squamous cell carcinomas (SCC) and 67 other primary lung tumours] and 351 controls. In addition to the wild-type allele NAT1*4, seven variant NAT1 alleles (NAT1*3, *10, *11, *14, *15, *17 and *22) were analysed. A new method based on the LightCycler (Roche Diagnostics Inc.) technology was applied for the detection of the polymorphic NAT1 sites at nt 1088 and nt 1095. The NAT2 polymorphic sites at nt 481, 590, 803 and 857 were detected by polymerase chain reaction-restriction fragment length polymorphism or LightCycler. Multivariate logistic regression analyses were performed taking into account levels of smoking, age, gender and occupational exposure. An increased risk for adenocarcinoma among the NAT1 putative fast acetylators [odds ratio (OR) 1.92 (1.16-3.16)] was found but could not be detected for SCC or the total case group. NAT2 genotypes alone appeared not to modify individual lung cancer risk, however, individuals with combined NAT1 fast and NAT2 slow genotype had significantly elevated adenocarcinoma risk [OR 2.22 (1.03-4.81)] compared to persons with other genotype combinations. These data clearly show the importance of separating different histological lung tumour subtypes in studies on genetic susceptibility factors and implicate the NAT1*10 allele as a risk factor for adenocarcinoma.

Correlation of expression of binding sites for synthetic blood group A-, B- and H-trisaccharides and for sarcolectin with survival of patients with bronchial carcinoma.

Carrier-immobilised carbohydrates were used to monitor the presence of specific carbohydrate-binding sites in tissue sections. Sarcolectin, an interferon-alpha/beta antagonist and growth regulator, had been shown to bind the lymphokine macrophage migration inhibitory factor (MIF). The lectin is thus a MIF-specific probe. Biotinylated sarcolectin, neoglycoproteins with lactose or N-acetylglucosamine residues, and polyacrylamide-attached trisaccharides, that represent the ABH histo-blood group antigens, were applied to sections of 187 primary lung carcinomas. The panel of cases consisted of 57 epidermoid carcinomas, 55 adenocarcinomas, 43 large cell anaplastic carcinomas and 32 small cell anaplastic carcinomas. 47 cases with intrapulmonary metastatic tumours were also included. Expression of binding sites of both sarcolectin and trisaccharides of histo-blood group antigens A and H correlated with patient survival in lung cancer. In view of the widely performed analysis of the presence of histo-blood group antigens, concomitant profiling of binding sites for these sugar components is suggested to be of potential benefit.

Subjective and objective confirmation of the ability to self-awaken at a self-predetermined time without using external means.

The ability to awaken oneself from sleep at a preselected time without external means (such as alarm clocks) was studied using, first, subjective and, second, objective methods. First, in a telephone survey of 269 unselected adults, over one-half said that they never use an alarm clock (or other external means) or always awaken before it. Another 24% said that they sometimes awaken before the alarm. Furthermore, this ability positively correlated with age and was related to consistency in the amount of nightly sleep but not consistency in wake-up time. Second, 15 people who said they regularly self-awaken were objectively tested for this ability in their own beds using actigraphy for three consecutive nights while choosing their own wake-up times. Five awoke within 10 minutes of their target time (mostly before) on each night, five did so on two of the three nights, and of the remaining five, four did so on one night. Choice of target times varied considerably within subjects but more so for those who were more successful. Taken together these results show that many people have the ability to regularly awaken themselves from sleep at a desired time and that such an ability is of practicable utility.

The galactoside-specific lectin from mistletoe as biological response modifier.

Experience with herbal extracts can guide the isolation of substances that effectively amend aspects of the host's defence system against tumor growth and spread. This capacity appears to be conferred to mistletoe (Viscum album) extract by a rather small dose range of the galactoside-specific lectin (VAA). It is a biochemically characterized dimer, consisting of a toxic subunit that acts as a RNA N-glycosidase (depurination of A-4324 in 28S rRNA) and a carbohydrate-binding B-chain. The binding of this subunit to galactose-exposing glycoligands on mononuclear cells elicits cytokine secretion in vitro and antitumoral/antimetastatic capacity in vivo in lymphosarcoma/sarcoma model systems. Increases in NK cell number, the activity of peritoneal macrophages and NK cells as well as the response of splenic T cells to mitogens are detectable. Immunophenotyping of blood samples from lectin-treated patients reveals increases in the number of helper/inducer T cells, NK cells and CD25-positive cells. Since the response to the treatment is assumed to be dependent on the presence of lectin-specific ligands on inflammatory host cells, histopathological monitoring of tumor specimens with labelled lectin is conceivable to be one factor of relevance to predict a response to the treatment in animal models or within clinical trials.

Disease type-associated increases of the plasma levels and ligand expression for natural alpha- or beta-galactoside-binding immunoglobulin G subfractions in patients with lung cancer.

The presence of natural carbohydrate-binding antibodies may play a role in host defence against malignant cells in addition to elicitation of an immune response by artificial carbohydrate antigens. Human serum contains immunoglobulin G(2) (IgG) fractions with selectivity to alpha- and to beta-galactosides, respectively, irrespective of the type of blood group of the donor. To determine whether these naturally occurring subfractions may have any relevance for tumor disease control, their binding to malignant cells was ascertained by cytofluorimetric assays in vitro with a number of human tumor cell lines of different histogenetic origin. The affinity of cell binding was comparable to that of binding to lactosylated or melibiosylated neoglycoconjugates as model ligands in solid-phase assays and K-D values were found to be in the range of 5-300 nM. Cross-reactivity of the anomer-selective subfractions to the other type of ligand was observed to be rather low. When the IgG contents of plasma samples of patients with diverse types of lung cancer were assessed, the concentrations of both galactoside-binding immunoglobulin G subfractions were significantly increased in association with presence of small cell lung carcinoma and of metastatic lesions to the lung without any marked change in the overall IgG plasma level. Such an apparently general enhancement was seen for patients with adenocarcinoma and included both subfractions with no impact on their percentage in the total IEC content. When detergent extracts of tumor and tumor-free specimens of the same patient were analyzed with the affinity purified antibody subfractions to comparatively determine ligand presentation, increases in sugar-inhibitable binding were especially noted for the tumor tissue of small cell lung carcinomas and apparently tumor-free samples of cases with lung metastasis. Material from other types of lung cancer revealed no significant indication for disease-related alterations with the exception of carcinoids. These data demonstrate that plasma levels and ligand expression for two types of natural galactoside-binding immunoglobulin G fractions can show nonuniform responses in patients within the class of lung cancer. They encourage to deliberately monitor these parameters of the natural carbohydrate-directed antibody fractions in cancer patients with various types of disease to clarify the clinical significance of respective malignancy-associated changes.

Prognostic relevance of detection of ligands for vertebrate galectins and a Lewis(Y)-specific monoclonal antibody.

Tissue sections taken from 157 potentially curatively operated lung carcinoma patients (70 epidermoid carcinomas, 68 adenocarcinomas, 15 large cell anaplastic, and 4 small cell anaplastic carcinomas) were examined by a standardized histochemical protocol in a prospective study evaluating the extent of various types of probes to serve as prognostic indicators in lung cancer. Detailed clinical records and survival data (minimum 56 weeks, maximum 96 weeks) were correlated to the results of the histochemical reactions. The study centres on monitoring the expression of galactoside-containing epitopes in tumor cells by human, animal and plant lectins: and with a monoclonal antibody. In addition, affinity-purified subfractions of natural antibodies from human serum with preferential affinity to alpha- and beta-galactosides, respectively, were employed. Significant contributions to the estimation of the survival of patients are given by clinical parameters (pT, pN stage), number of resected and positive lymph nodes and presence of tumor metastases into specific lymph nodes (No. 5 and No. 6 right and left). With respect to the relevance of subsets of beta-galactosides, the galectin from chicken liver (CL-16) and the Le(y)-specific monoclonal antibody unveiled a negative correlation at a statistically significant level. The predictive value of binding of the animal lectin CL-16 was especially pronounced for patients with advanced tumor stages, pointing to a potential role of such lectin-reactive beta-galactosides in late tumor stages or progression.

Glycohistochemical properties of malignancies of lung and pleura.

Based upon the reasoning that protein-carbohydrate recognition is involved in diverse intercellular activities including growth control and cell motility 14 probes have been employed to characterize epitope presence in sections of 80 cases with operated lung carcinomas, 20 patients with mesothelioma, and 20 cases with non-malignant lung diseases. As parts of the innate immune system with supposed relevance for host defense the mannan-binding lectin (MBL) and serum amyloid P component (SAP) were employed. The naturally occurring immunoglobulin G fractions with selectivity for alphaa-galactosides (alpha+) and beta-galactosides (beta+) and their subfractions with enhanced target selectivity (alpha+beta-,alpha-beta+) allowed the monitoring of expression of reactive sites for these autoantibodies as a step to elucidate potential anti-tumor activity. Due to the diversity of cellular galactoside-containing glycoconjugates two galectins and a plant lectin were included. As a measure of receptor activities for carbohydrates, neoglycoconjugates with alpha-galactose, the B-disaccharide, the Forssman-disaccharide, and alpha-glucose as histochemically crucial ligand part were tested in addition to an antibody against heparin-binding lectin. Quantitative image analysis revealed significant differences between cases with small cell and non-small cell lung cancer for the plant lectin and one galectin, cases with non-tumorous lung disease and lung carcinoma for serum amyloid P component and the beta-galactoside-selective autoantibody fraction. Prognostic relevance was observed for the presence of glucose-specific sites in small cell lung cancer and meso-thelioma cases, and of galectin- and alpha-galactoside-selective immunoglobulin G fraction-binding sites in non-small cell lung cancer patients.

Histopathologic evaluation of application of labeled neoglycoproteins in primary bronchus carcinoma.

Neoglycoproteins are readily available conjugates of a histochemically inert carrier protein and histochemically crucial carbohydrate moieties which are covalently attached to the carrier protein by chemical synthesis. Biotinylation renders these conjugates detectable in formalin-fixed, paraffin-embedded tissue sections of human lung cancer by standard staining protocols, thereby localizing endogenous receptors for carbohydrate moieties. Examination of 30 cases of main types of human lung cancer revealed the presence of alpha-fucosyl-, alpha-mannosyl-, and alpha-glucosyl-specific receptors in adenocarcinomas or epidermoid carcinomas with high positivity rates. The extent of the expression of receptors for alpha- and beta-galactosides appeared to be comparatively lower. Within the standard protocol, using a concentration of the biotinylated probes of 10 micrograms/mL, this panel of probes consistently failed to detect endogenous sugar receptors in ten cases of small cell anaplastic carcinoma of the lung. Whereas none of the sections from the tumor cases bound the sulfated fucan fucoidan, the accompanying inflammatory cells, especially the granulocytes, expressed receptors for the sulfated fucan. Pronounced labeling for macrophages was observed for the alpha-galactoside-specific probe, whereas no binding to inflammatory cells and pneumocytes was detectable for the beta-galactoside-specific probe. The results indicate that expression of endogenous receptors for neoglycoproteins may be useful in discriminating between small cell and non-small cell lung carcinoma and carcinomatous cells from accompanying inflammatory cells.

Telepathology overview: from concept to implementation.

Telepathology is the practice of pathology at a distance by using video imaging and telecommunications. Significant progress has been made in telepathology. To date, 12 classes of telepathology systems have been engineered. Rapid and ultrarapid virtual slide processors may further expand the range of telepathology applications. Next-generation digital imaging light microscopes, such as miniaturized microscope arrays (MMA), may make virtual slide processing a routine laboratory tool. Diagnostic accuracy of telepathology is comparable with that of conventional light microscopy for most diagnoses. Current telepathology applications include intraoperative frozen sections services, routine surgical pathology services, second opinions, and subspecialty consultations. Three telepathology practice models are discussed: the subspecialty practice (SSP) model; the case triage practice (CTP) model; and the virtual group practice (VGP) model. Human factors influence performance with telepathology. Experience with 500 telepathology cases from multiple organs significantly reduces the video viewing time per case (P < .01). Many technology innovations can be represented as S-curves. After long incubation periods, technology use and/or efficiency may accelerate. Telepathology appears to be following an S-curve for a technical innovation.