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In an attempt to establish the etiologic role of Helicobacter pylori (H. pylori) in gastric and/or duodenal pathology, 169 patients were tested and compared with a control group of 25 healthy subjects, for a total of 194 subjects. Data on sex, age, familiarity, smoking, coffee and alcohol habits were collected and each patient underwent histological, microbiological and immunological tests. 80 (41.2%) subjects were found positive to H. pylori. This bacterium was detected in 53.3% of patients with gastric ulcer while IgG were found in 86.7%; in 50% of patients with chronic atrophic gastritis while IgG were detected in 80%; in 48.5% of patients with duodenal ulcer while IgG were found in 87.9%; in 41.8% of patients with superficial chronic gastritis while IgG were detected in 80.2%. In the control group of healthy patients H. pylori was found in 28% of patients while IgG were detected in 62.5%. The results do not confirm a direct clear-cut correlation between this microorganism and the pathologies studied.

We describe here a modified nonenzymatic method for the isolation of rat aortic endothelial cells with vasoformative properties. Aortic rings placed on plastic or gelatin-coated surfaces generated outgrowths primarily composed of endothelial cells. Prompt removal of aortic explants after endothelial migration minimized fibroblast contamination. However, fibroblasts, because of their high proliferative rate tended to overgrow the endothelial cells even when present in small numbers. This potential pitfall was avoided by weeding out fibroblasts with the rounded tip of a bent glass pipette. Primary endothelial colonies free of fibroblasts were segregated in cloning rings, trypsin-treated, and transferred to gelatin-coated dishes. Endothelial cells were cultured in MCDB 131 growth medium containing 10% fetal bovine serum, endothelial cell growth supplement, and heparin. Using this technique, pure endothelial cell strains were obtained from single aortic rings. Confluent endothelial cells formed a contact-inhibited monolayer with typical cobblestone pattern. The endothelial cells were positive for Factor VIII-related antigen, took up DiI-Ac-LDL, and bound the Griffonia Simplicifolia-isolectin-B4. Endothelial cells cultured on collagen gel formed a polarized monolayer, produced basement membrane, displayed Weibel-Palade bodies and caveolae, and were connected by tight junctions. In addition, they reorganized into a network of microvascular cords and tubes when overlaid with a second layer of collagen and formed microvascular sprouts in response to fibroblast-conditioned medium. This isolation procedure yields stable strains of vasoformative endothelial cells, which can be used to study aortic endothelium-related angiogenesis and its mechanisms.

Background: Thrombospondin (TSP), a cell-matrix adhesion protein, and cysteine-serine-valine-threonine-cysteine-glycine (CSVTCG), a major TSP cell adhesive domain, have recently been shown to play a role in tumor cell metastasis. In this study we immunohistochemically localized TSP and its newly discovered CSVTCG-specific receptor in normal, benign, and neoplastic breast tissues., Experimental Design: Paraffin sections of normal, benign, and neoplastic breast tissue were examined immunohistochemically for the presence of TSP and its CSVTCG-specific receptor using the avidin-biotin complex immunoperoxidase staining procedure., Results: Positive staining using polyclonal antibodies for TSP and its tumor cell adhesion receptor, isolated from a human adenocarcinoma of the lung, was observed in all primary breast ductal carcinomas examined (N = 11). In contrast, all benign lesions and normal breast tissue stained negative for TSP and its receptor with the exception of two fibrocystic breast samples with hyperplasia. One of the samples showed strong TSP staining of ductal apocrine cells, whereas the other showed apical receptor staining of hyperplastic ductal cells. The negatively staining normal and benign tissues consisted of 1 normal breast, 1 gynecomastia, 5 fibroadenomas, and 6 fibrocystic samples. Positive staining for TSP in ductal carcinoma was only localized in the dense stromal collagen adjacent to tumor, whereas the TSP receptor localized to the tumor cells. Consistent with these immunohistochemical staining results was the observation that protein extracts of breast carcinoma cells contained receptor with no detectable TSP as revealed by Western blotting. Capillary endothelium was focally positive for receptor in regions proximal to ductal epithelium in 8 of 11 neoplastic tissues and in 6 of 14 benign samples., Conclusions: Our results indicate that increasing expression of stromal TSP and the CSVTCG-specific TSP receptor in ductal epithelium correlates with neoplastic transformation. In addition, our results indicate that both malignant and benign breast tissue can stimulate surrounding capillaries to express the TSP receptor, whereas only carcinoma has the capacity to stimulate surrounding nonendothelial stromal cells, such as myofibroblasts, to secrete a TSP-rich matrix that may contribute to the desmoplastic stromal reaction characteristic of ductal carcinoma tumor. The TSP-rich matrix may then promote tumor cell attachment, migration, and angiogenesis, factors important in tumor growth. The receptor-rich capillary endothelium may promote the cell adhesive interactions important in tumor intravasation. Taken together the results of this study provide a rational basis for a role of TSP in tumor angiogenesis and metastasis.

Thrombospondin (TSP) is a multidomain adhesive protein postulated to play an important role in the biological activity of the extracellular matrix. To test this hypothesis, TSP-containing fibrin and collagen matrices were evaluated for their capacity to support angiogenesis and cell growth from explants of rat aorta. This serum-free model allowed us to study the angiogenic effect of TSP without the interference of attachment and growth factors present in serum. TSP promoted dose-dependent growth of microvessels and fibroblast-like cells. The number of microvessels in TSP-containing collagen and fibrin gels increased by 136 and 94%, respectively. The TSP effect was due in part to cell proliferation since a 97% increase in [3H]thymidine incorporation by the aortic culture was observed. The effect was TSP-specific because TSP preparations adsorbed with anti-TSP antibody showed no activity. TSP did not promote angiogenesis directly since no TSP-dependent growth of isolated endothelial cells could be demonstrated. Rather TSP directly stimulated the growth of aortic culture-derived myofibroblasts which in turn promoted microvessel formation when cocultured with the aortic explants. Angiogenesis was also stimulated by myofibroblast-conditioned medium. Partial characterization of the conditioned medium suggests that the angiogenic activity is due to heparin-binding protein(s) with molecular weight > 30 kD. These results indicate that matrix-bound TSP can indirectly promote microvessel formation through growth-promoting effects on myofibroblasts and that TSP may be an important stimulator of angiogenesis and wound healing in vivo.

A 68-yr-old woman was hospitalized because of abdominal pain, an enlarged pancreatic head by CT, and a questionable 4-cm mass in the liver. Fine-needle aspiration (FNA) of the pancreatic head disclosed a highly cellular specimen consisting of clusters of cytologically bland, monotonous, small nuclei and variable but generally sparse cytoplasm. Because of the differentiated monomorphic character of the cell clusters, the postaspiration differential cytopathologic diagnosis included islet cell tumor, acinic cell tumor, carcinoid, lymphoma, and well differentiated ductal adenocarcinoma. Pancreaticoduodenectomy and hepatic biopsy yielded a grossly normal pancreas and a cirrhotic liver. Histologic examination of the pancreas revealed a spotty but extensive spectrum of islet changes ranging from normal to bland hyperplasia, nesidioblastosis, microadenosis, and neuroendocrine microadenomas, all appearing in a light and electron microscopic context of an otherwise normal pancreas. This case highlights the differential diagnostic ambiguities presented by a continuum of pancreatic islet cell proliferations, especially among patients in whom there are no known predisposing factors for such diffuse preneoplastic or neoplastic changes.

The autocrine role of basic fibroblast growth factor (bFGF) in angiogenesis was studied in the rat aortic ring-collagen gel model using serum-free culture conditions. Immunohistochemical staining of the rat aorta showed bFGF in the cytoplasm of endothelial and smooth muscle cells. Aortic rings mechanically injured during the dissection procedure released bFGF, which was demonstrated in the conditioned medium by slot and Western blot analysis. bFGF-containing aorta-conditioned medium and purified bFGF increased both the number and length of microvessels sprouting from the explants. This effect was particularly evident during the second week of culture, when the release of endogenous bFGF was minimal. Neutralizing anti-bFGF antibodies induced a 40% reduction of angiogenesis. Regression of microvessels, which regularly occurred toward the end of the second week, was prevented by purified bFGF. These data support the idea that bFGF released by vascular cells plays an important role in the autoregulation of angiogenesis after injury.

Fibronectin is a component of the extracellular matrix of developing microvessels whose role in angiogenesis is poorly understood. This study evaluated the effect of plasma fibronectin on angiogenesis in serum-free collagen gel culture of rat aorta. Aortic explants embedded in collagen gels generated microvascular outgrowths. Fibronectin incorporated in the collagen gel promoted a selective dose-dependent elongation of the newly formed microvessels without stimulating vascular proliferation. The fibronectin-treated microvessels were longer due to a proportional increase in the number of microvascular cells. However, fibronectin had no effect on microvascular DNA synthesis and mitotic activity. Fibronectin stimulated microvascular length also in cultures in which mitotic activity was suppressed and angiogenesis was markedly reduced by pretreating the aortic explants with mitomycin C. The synthetic peptide Gly-Arg-Gly-Asp-Ser (GRGDS), which competes for the binding of fibronectin to its cell receptors and inhibits the adhesion of endothelial cells to substrates, arrested the elongation of developing microvessels causing regression and inhibition of angiogenesis. Conversely, Gly-Arg-Gly-Glu-Ser (GRGES), which lacks the RGD sequence, had no inhibitory effect. These data support the hypothesis that fibronectin promotes angiogenesis and suggest that developing microvessels elongate in response to fibronectin as a result of an adhesion-dependent migratory recruitment of endothelial cells that does not require increased cell proliferation.

The purpose of this study was to investigate the vasoformative behavior in vitro of the native intimal endothelium of the rat aorta. To visualize the intimal surface directly, thoracic aortas were everted using a procedure that sequestered adventitial cells and possible remnant microvessels of periaortic soft tissues inside the aortic tube. Everted aortas embedded in collagen gel and cultured under serum-free conditions generated branching microvessels by a process of sprouting from the aortic intima. The newly formed microvessels originated from patches of activated intimal endothelial cells, which had survived the mechanical damage of the eversion procedure. Activated endothelial cells crawled over each other and engaged in lumen formation forming bilayers or multilayers of cells which became the source of sprouting histotypic microvessels. The endothelium of the newly formed microvessels was positive for factor VIII-related antigen and was partially surrounded by periendothelial cells which expressed alpha-smooth muscle actin. The results of this study indicate that the intimal endothelium of the rat aorta has considerable functional plasticity and can switch to a vasoformative phenotype in response to changes in the surrounding extracellular matrix environment.

The role of collagen in microvascular growth was investigated using the aortic ring model of angiogenesis. Collagen production by vasoformative outgrowths in plasma clot culture of rat aorta was either stimulated with ascorbic acid or inhibited with the proline analogue cis-hydroxyproline. Microvessels proliferating in the absence of ascorbic acid supplements became ecstatic and developed large lumina. In contrast, newly formed microvessels in the presence of ascorbic acid remained small and maintained thin lumina throughout the angiogenic process. Biochemical studies demonstrated enhanced collagen production and deposition in cultures treated with ascorbic acid. Ultrastructural studies of these cultures showed a marked increase in newly formed interstitial collagen in the perivascular matrix and in regions of the plasma clot containing nonendothelial mesenchymal cells. Small microvessels with thin lumina similar to the ones observed in ascorbic acid-treated plasma clot cultures were obtained by growing aortic explants in gels of interstitial collagen in the absence of ascorbic acid. Inhibition of collagen production with the proline analogue cis-hydroxyproline had a marked anti-angiogenic effect in both plasma clot and collagen gel cultures. The anti-angiogenic effect of cis-hydroxyproline was abolished by adding L-proline to the culture medium, thereby restoring normal metabolism. These results support the hypothesis that angiogenesis is regulated by collagen production and suggest that the size of newly formed microvessels is influenced by the degree of collagenization of the extracellular matrix.

This study was designed to evaluate the effect of the synthetic peptide Gly-Arg-Gly-Asp-Ser (GRGDS) on angiogenesis in serum-free collagen gel culture of rat aorta. The GRGDS peptide contains the amino acid sequence Arg-Gly-Asp (RGD), which has been implicated as a recognition site in interactions between extracellular matrix (ECM) molecules and cell membrane receptors. RGD-containing synthetic peptides are known to inhibit attachment of endothelial cells to substrates, but their effect on angiogenesis has not been fully characterized. Aortic explants embedded in collagen gel in the absence of GRGDS generated branching microvessels through a process of endothelial migration and proliferation. Addition of GRGDS to the culture medium caused a marked inhibition of angiogenesis. In contrast, GRGES, a control peptide lacking the RGD sequence, failed to inhibit angiogenesis. The inhibitory effect of GRGDS was nontoxic and reversible. The angiogenic activity of aortic explants previously inhibited with GRGDS could be restored by incubating the cultures in GRGDS-free medium. These findings suggest that angiogenesis is an anchorage-dependent process that can be inhibited by interfering with the attachment of endothelial cells to the ECM. It also indicates that synthetic peptides can be used as probes to study the mechanisms by which the ECM regulates angiogenesis.

We report here that rings of rat aorta embedded in gels of fibrin or collagen and cultured in MCDB 131, an optimized growth medium for microvascular endothelial cells, generate branching microvessels in the absence of serum or other soluble protein supplements. The angiogenic response is self-limited and can be quantitated by counting the newly formed microvessels daily in the living cultures. The microvascular growth curves are characteristic for each gel. Growth of microvessels in collagen gel peaks at the end of the 1st week and is followed by a rapid regression in the 2nd week. Fibrin gels, as compared with collagen, stimulate angiogenesis by 170%, support growth during the 2nd week, and protect the newly formed microvessels from early regression. Angiogenesis is inhibited by adding hydrocortisone to the culture medium. Conversely, a 230% stimulation of angiogenesis is obtained when aortic rings are cultured in collagen gels floating in serum-free medium conditioned by sarcoma 180 cells. Our results demonstrate that: (a) angiogenesis can be obtained reproducibly in serum-free culture; (b) serum-free culture is a sensitive method for testing the inhibitory or stimulatory effects of soluble or matrix factors on angiogenesis; (c) the aortic ring model can be used as a quantitative assay for the study of angiogenesis under chemically defined culture conditions.

In 1986 Grayston and coworkers termed TWAR (or Taiwan Acute Respiratory) a new strain of Chlamydia which has still not received an exact taxonomic classification. In fact, whereas initially the TWAR strain was classified as C. psittaci because of its oval-shaped, glycogen free, dense inclusions, recent studies on the immunological analysis, DNA analysis and ultrastructural morphology, would seem to indicate that TWAR is a new Chlamydial species, whose proposed name as C. pneumonia. TWAR is mainly responsible for respiratory syndrome varying in gravity from a slight form to pneumonia, and is liable to give rise to epidemic forms; in addition, more recently, certain Authors have postulated its involvement in the pathogenesis of ischemic cardiopathy.

Rings of rat aorta cultured in Matrigel, a reconstituted gel composed of basement membrane molecules, gave rise to three-dimensional networks composed of solid cellular cords and occasional microvessels with slitlike lumina. Immunohistochemical and ultrastructural studies showed that the solid cords were composed of endothelial sprouts surrounded by nonendothelial mesenchymal cells. The angiogenic response of the aortic rings in Matrigel was compared to that obtained in interstitial collagen, fibrin, or plasma clot. Morphometric analysis demonstrated that the mean luminal area of the microvascular sprouts and channels was significantly smaller in Matrigel than in collagen, fibrin, or plasma clot. The percentage of patent microvessels in Matrigel was also markedly reduced. Autoradiographic studies of 3H-thymidine-labeled cultures showed reduced DNA synthesis by developing microvessels in Matrigel. The overall number of solid endothelial cords and microvessels was lower in Matrigel than in fibrin or plasma clot. A mixed cell population isolated from Matrigel cultures formed a monolayer in collagen or fibrin-coated dishes but rapidly reorganized into a polygonal network when plated on Matrigel. The observation that gels composed of basement membrane molecules modulate the canalization, proliferation, and organization into networks of vasoformative endothelial cells in three-dimensional cultures supports the hypothesis that the basement membrane is a potent regulator of microvascular growth and morphogenesis.

A model for the study of angiogenesis in vitro is described. Rat aortas, cultured in a tridimensional matrix of clotted chick plasma, gave rise to luxuriant outgrowth of vascular channels. We studied this process with light microscopic, radioautographic, and ultrastructural techniques. On the 2nd d of culture, endothelial cells sprouted from the intima of the aorta and its collateral branches into the surrounding clot, forming solid cellular cords. A complex vascular network was established within the 1st wk by spindly, poorly differentiated endothelial cells. At this stage cells were migrating, branching, and proliferating in a longitudinal fashion (labeling index: 67.4% +/- 7.7). Lumens, when present, appeared as slitlike spaces enclosed with junctional complexes. By the end of the 2nd wk the migratory activity decreased and proliferation occurred mostly in a cross-sectional plane, with formation of large patent lumens (labeling index: 48% +/- 3.1). Vascular channels were lined by prominent endothelial cells rich in rough endoplasmic reticulum, polysomes, mitochondria. Golgi apparatuses, and coated vesicles. Cells were enveloped with a ruthenium red positive layer, particularly abundant on the luminal surface and in the interendothelial space. A discontinuous basal lamina was present along the abluminal side. At 28 d the labeling index was reduced to 2.25% +/- 0.9. The still viable endothelium exhibited numerous microfilaments and microtubules, decreased cytoplasmic organelles, and increased pinocytotic activity. This experimental model, histophysiologic gradient culture, provides us with a new tool for the study of vascular morphogenesis, angiogenesis dependent growth of tumors, and neoplastic intravasation.

Throughout the animal kingdom the Chlamydiae are among the most common and ancient pathogens, but only in the 1966 they were classified by Page in the same genus because of different nosological pictures that they cause, while more recently were identified as bacteria. Chlamydiae have been divided into two species: C. trachomatis and C. psittaci. In 1986 Grayston et al. proved the etiological role of a "new chlamydial strain", named TWAR (Taiwan-Acute Respiratory), in human pneumonia and bronchitis; TWAR is distinguishable from other Chlamydiae and possibly represents a new entity. The Chlamydiae are non-motile, metabolically poor bacteria, completely lacking of any enzimatic system for energy production (ATP) and for this reason are obligate intracellular parasites; they poses group-specific, species-specific and type-specific antigens. Four series of surface proteins were identified as responsible for their pathogenic properties, while many Authors consider a particular lipopolysaccharidical acid, group antigen, as a real LPS. These bacteria poses an unique developmental cycle with production of two type of particles different for metabolic and infecting characters: elementary body and reticulate body. The Chlamydiae have a broad spectrum of host. They cause persistent or chronic infections and their survival is insured by the elementary body. The Chlamydiae stimulate the humoral and the cellular-mediate immunity system and are capable of survival in the monocytes and macrophages.

Electron microscopy and autoradiography with 3H-thymidine have been employed to study the cellular dynamic of intimal thickening occurring in the rabbit carotid artery after selective endothelial injury. The results obtained suggest that migration of SMC of the tunica media rather than proliferation is the key event in the development of the intimal thickening.

Serious infections due to hospital-transmitted Staphylococcus epidermidis strains have become more and more important and frequent. Therefore, a need for typing methods which characterize St. epidermidis strains for epidermiological purpose is increasing. Only a few data are available for the phage typing of those strains and the aim of our paper has been to set them up.

Fire fighters' respiratory organs, circulatory system and muscular system are often exposed to considerable risks. In fact in addition to the most obvious external stress causes (heat, humidity, O2 decrement, CO2 increment, emotional stress) these workers use heavy equipments and carry people or things. Furthermore always present is the risk of poisoning by inhalation of toxic combustion gas of the fire atmosphere.

The composition of the extracellular matrix of developing microvessels in plasma clot cultures of rat aorta was studied with light and electron immunohistochemical techniques using affinity-purified antibodies against fibronectin, laminin, and collagen Types I, III, IV, and V. The extracellular matrix of solid endothelial sprouts in young cultures consisted of a delicate fibrillary network of fibronectin and Type V collagen and of patchy amorphous deposits of laminin and Type IV collagen. Rare fibrils of collagen Types I and III were also observed. Fibronectin stained intensely and appeared to be the predominant component of the provisional subendothelial matrix during vascular sprouting. As the cultures aged, laminin and Type IV collagen accumulated in the subendothelial space, forming a continuous feltwork around the newly formed microvessels. Patent microvessels were also surrounded by discontinuous deposits of fibronectin and by increased amounts of collagen Types I, III, and V. Ultrastructural studies revealed positive immunostaining for fibronectin, laminin, and collagen Types IV and V in the endoplasmic reticulum and in putative secretory vesicles, indicating active synthesis and secretion of these molecules by the endothelial cells. These observations indicate that the microvascular extracellular matrix undergoes significant dynamic changes during capillary development. The different composition and structural organization of the extracellular matrix at various stages of angiogenesis may have important effects on endothelial behavior and capillary morphogenesis.

The nervous system of a primitive Coelenterate (Chlorohydra viridissima) has been studied using ultrastructural and histochemical techniques. The authors confirm the ultrastructural pattern of nerve cells described by Lentz and coworkers. Reserpine treatment fails to induce any reduction of catechol- and indoleamine content visible to histochemical observation. In vivo treatment with tetanus toxin does not induce behavioural changes and no specific binding of toxin is revealed by immunocytological analysis. This suggests that neuron tetanus toxin receptor sites are absent in hydra. Hydra nerve cells must therefore be considered as extremely primitive elements, which the Authors consider to support the hypothesis of neurons having originated as a gradual differentiation of myoepithelial cells, as proposed by Pantin (1956) and by Passano (1963).

Bovine capillary endothelial cells (BCEC), cultured in suspension on a rotary shaker, formed aggregates ranging from 50 to 300 micron in diameter. In plasma clot these aggregates sprouted in multiple directions and gave rise to vascular channels. Aggregates of the squamous cell carcinoma line of rat bladder NBT-II-81, cultured in plasma clot, formed solid spheroids that grew slowly by expansion. When cultured together with BCEC, however, NBT-II-81 infiltrated the plasma clot extensively. The tumor cells, after establishing contacts with the vascular channels, spread into the fibrin meshwork using the subendothelial space as their path of propagation. Endothelial cells that were separated from the surrounding matrix by invading tumor cells degenerated, leaving behind channels lined only by neoplastic epithelium. The adhesive properties of the subendothelial matrix were studied by seeding NBT-II-81 cells on dishes coated with the extracellular matrix produced by BCEC. Tumor cells attached readily and in large numbers to dishes coated with the subendothelial matrix. In contrast they attached poorly to dishes coated with fibrin. We conclude that the spread of carcinoma cells into plasma clot is markedly enhanced by endothelial channels, developed in the absence of blood flow. The production of a highly adhesive extracellular matrix by the capillary endothelium during angiogenesis may represent an important element in the preferential growth of the tumor along the vascular route.

150 Pseudomonas aeruginosa strains, isolated from pathological samples (urine, faeces, sputum, etc.) of affections developed in cancerous patients have been studied. In vitro, with two different inocula, activities of some cephalosporins--ceftazidime, cefotaxime, cefoperazone--have been compared with those of gentamicin, carbenicillin and tobramycin. Ceftazidime, among the antibiotics tested, has been the most active against Pseudomonas aeruginosa strains.

Rings of rat aorta cultured in plasma clots gave rise to microvascular networks. Scanning electron microscopy revealed that, in most cultures, the newly formed microvessels communicated with an endothelial-lined chamber which had developed around the aorta. The endothelial cells lining the wall of this chamber were elongated and frequently overlapped each other forming unicellular or multicellular bridges. The endothelium also produced solid bands and webs which spanned wide regions of the periaortic chamber and of the aortic lumen. Solid endothelial ropelike structures overran the openings of the newly formed vascular channels and connected the outer wall of the chamber with the aortic ring. Webs were composed of branching cords of spiraling endothelial cells with or without collagenized cores. Webs and bands formed as a result of the extensive surface remodeling of the fibrin clot by developing endothelial channels. These structures are reminiscent of the intimal bands and webs which develop in human blood vessels as a late sequela of the organization of thromboemboli.

The intima of the elastic arteries undergoes progressive thickening with aging under hemodynamic stress. The earliest changes in humans have been recorded soon after birth, but rare intrauterine fetal cases are on record. We studied a case of intimal thickening that occurred during fetal life in the aorta of the hypervolemic partner of a pair of twins afflicted with placental transfusion syndrome. These in utero changes suggest that intimal thickening of elastic arteries may also occur any time during fetal life if the walls of these vessels are exposed to factors known to cause endothelial damage.

The Chlamydia trachomatis (C.t.) causes trachoma, inclusion conjunctivitis, lymphogranuloma venereum and it is the more frequent responsible of sexually transmitted infections; in fact, only in the United States, 3-4 million of people suffer from these infections each year. Besides, there are many secondary infections that may cause sterility in man and woman. Risk factors, for venereal infections owed to C.t., are related to the number of sexual partners, age, socioeconomics status and sexual preference. More frequently, the C.t. infects persons that begin sexual activity earlier, those who have many sexual partners and an higher level of education. The direct diagnosis for detecting C.t. can be performed with the citologic test, cell culture, direct immunofluorescence and enzyme immuno-assay. Although, the cell culture is the technique of choice, at present the immunofluorescence and enzyme immuno-assay are the methods preferred because of rapidity and esecution. The indirect diagnosis can be achieved by the complement fixation, indirect immunofluorescence and enzyme immuno-assay tests. In this case, excluding the complement fixation test not more reliable, the method of choice depends, above all, upon the kind of infection in progress. Tetracycline, erythromycin, rifampicin and cloramphenicol are considered the treatment of choice.

A syntetic review of data about the free coagulase and the clumping factor has been made. The importance of the test, the different methods, the possible reasons of mistake are discussed.

Extraction of sea urchin eggs and embryos with Triton X-100 generated a cytoskeletal framework (CSK) composed of a cortical filamentous network and an internal system of filaments associated with ribosomes. The CSK contained only 10-20% of the cellular protein, RNA, and lipid. A specific subset of proteins was enriched in the CSK. Several lines of evidence suggest that mRNA is a component of the CSK of both eggs and embryos. First, the CSK contained poly(A) sequences which hybridized with [3H]poly(U). Second, the CSK contained polyribosomes. Finally, RNA extracted from the CSK showed translational activity in an in vitro system. The nonhistone messages present in the CSK were qualitatively similar to those solubilized by detergent, as determined by separation on polyacrylamide gels of the products of in vitro translation. In the unfertilized egg, most mRNA was present as nonpolyribosomal messenger ribonucleoprotein complexes which, along with monoribosomes, were efficiently extracted by Triton X-100. The converse was found in blastulae, as most of the mRNA was present as polyribosomes associated with the CSK, although monoribosomes were still efficiently extracted by detergent. These results indicate a correlation between the activation of protein synthesis in eggs and the association of polyribosomes with the CSK.

The Authors carried out a research on 22 strains of Staphylococcus, isolated from pathological specimens, studying the free coagulase and the clumping factor with human, pig and rabbit plasma and two types of anticoagulant, citrate and heparine. The results are discussed test by test and in relation one to another.

The present study was performed to determine the immediate (hours) and long-term (28-day) effects of angioplasty-balloon dilatation on arterial wall diameter, histology, response to vasoconstrictors, and passive mechanics. Dilated left iliac arteries of New Zealand rabbits were compared to control, right iliac arteries. In the immediate studies, dilation increased arteriographic diameter by 32%, denuded the endothelium, stretched and may have lysed smooth muscle cells, decreased arterial wall thickness, and increased passive stress and incremental elastic modulus. The dilated arteries failed to contract to norepinephrine or potassium chloride. In contrast, 28 days after dilation, arteriographic diameter had returned to normal, an intimal thickening had formed, passive stress and the incremental elastic modulus had decreased to below normal, and the arteries contracted, but to only 53% to 67% of control. Angioplasty had no long-term effect on arterial sensitivity (EC50) to potassium chloride or serotonin but did produce a decreased sensitivity (6X) to norepinephrine. These studies demonstrate that the effects of dilatation of the normal artery are partially reversible, suggest that restenosis after angioplasty is more likely to be due to intimal proliferation than increased arterial stiffness, and suggest that vasospasm of arteries after long-term recovery from the dilation is more likely to be mediated by serotonin than by norepinephrine.

To investigate the role played by developing microvessels in the spread of tumors, segments of rat aorta were cultured with aggregates of NBT-II-81, a cell line derived from squamous cell carcinoma of rat bladder. Aortic rings cultured in plasma clot gave rise to microvascular networks composed of branching endothelial channels. Aggregates of carcinoma in contract with fibrin clot alone grew slowly and by expansion. When the proliferating branching endothelial sprouts and channels contacted the tumor aggregates, the pattern of neoplastic growth changes abruptly, as carcinoma cells infiltrated the fibrin clot, migrating and proliferating in periendothelial location. Some vascular channels were disrupted and permeated by cords of invading tumor cells. Ultrastructural studies revealed intimate associated between invading epithelial cells and endothelial cells. Focal fusion of the endothelial basal lamina with the basal lamina of the tumor cells was observed. Our results demonstrate that angiogenesis in vitro, ie., in absence of active circulation, markedly enhanced the spread of a carcinoma in plasma clot and modified its pattern of growth. This indicates that other vascular-related factors beside nutritional gradients from the circulation attract tumor cells along endothelial paths.

94 strains of Pseudomonas aeruginosa, isolated from hospitalized patients, were typed with serological and pyocinic methods, also testing their sensitivity to 6 antibiotics. The serological method allowed for the typing of almost all the strains (98.9%), (the 0-11 serotype was the most frequent -23.4%-) vs. 80.6% by the pyocinic method. Among those tested, ceftazidime was the most active antibiotic, against the P. aeruginosa strains examined.

Following the discovery of Legionella pneumophila as the cause of an epidemic of pneumonia at an American Legion Convention in Philadelphia, a group of related bacteria were recognized as additional human pathogens. This newly established bacteria genus, Legionella, includes the agents of Legionnaires' Disease, Pittsburgh pneumonia and several related infections. A number of researches have been performed in the past few years about these bacteria; many of these data are here summarized to give an idea of the most important characteristics of Legionella and of the diseases they cause.

Segments of rat thoracic duct cultured in plasma clot or in collagen gel produced microvascular and fibroblastic outgrowths. Lymphaticlike channels (LLC) with a highly attenuated endothelium, which was barely visible by light microscopy, were found in 8 out of 25 cultures (32%). Serial histologic sections revealed that the endothelium of the LLC was continuous with the intimal endothelium of the thoracic duct and was therefore of lymphatic origin. In addition to the LLC, vascular channels lined by a thick endothelium with hump-shaped, cross-sectional profiles were found in 10 cultures (40%). These channels were indistinguishable from the microvessels of blood vascular origin that formed in parallel cultures of rat aorta or periductal adipose tissue and were termed hematiclike channels (HLC). Contrary to the LLC, the HLC did not originate from the lymphatic endothelium of the thoracic duct. The frequent association of the HLC with the adventitia of the thoracic duct and with the surrounding adipose tissue suggested that they probably developed from the hematic microvessels of the periductal soft tissues.

The production of the five classes of immunoglobulins represents the highest grade of the various system of defence the man puts in act against the microbial attack. So bacteria fight in several levels across the different stages of human antibodies synthesis processes and action, trying for cancelling the effect. Therefore, a more exact definition of the mechanisms of bacterial actions against human immunoglobulins would permit us to intervene in a more efficacious way in favour of defence powers of the human organism. In this way we could improve the knowledge of the bacterial damage process, increase the means of human immunization, and our therapy attempts. We analyzed therefore in this study the different defence mechanisms that bacteria use against human immunoglobulins. Bacteria can avoid "a priori" or divert antibodies formation, by synthesis of surface structural identical to components of the host. Bacteria can stop or hinder transmission of antigenic message working against the phagocytosis mechanisms. Bacteria can stop or lessen antibodies synthesis process. Bacteria can avoid specific contact with antibodies, especially, by masking the microbial surface. Bacteria can change their superficial structures to avoid antibodies action. Bacteria can destroy antibodies by synthesis of protease activity capable of hydrolyzing globulins.