Intra-operative fluorescence angiography is reproducible and reduces the rate of anastomotic leak after colorectal resection for cancer: a prospective case-matched study.

AIM: Intra-operative fluorescence angiography (IOFA) with indocyanine green provides information on tissue perfusion that may help prevent an anastomotic leak (AL). The aim of this study was to assess the impact of IOFA on outcomes after left-sided colonic or low anterior resection with anastomosis for colorectal cancer. METHODS: All patients with left-sided colonic or rectal cancer, operated between June 2017 and December 2018, were prospectively included. IOFA has been routinely implemented since May 2018. Reproducibility of IOFA, after a 1:1 matching for relevant clinical risk factors of AL, was studied in patients with IOFA (IOFA+) and without IOFA (IOFA-). Outcomes were compared in terms of postoperative events such as clinically relevant AL as the primary end-point. RESULTS: In the IOFA+ group, changing of the initially planned colon transection due to inadequate perfusion occurred in five out of 46 patients (10.9%). Agreement between intra-operative assessment and postoperative blind review of IOFA was deemed strong (Cohen's kappa index 0.893, 95% CI 0.788-0.998, P < 0.001). Among 111 patients, 42 matched patients were included in each group. There was significantly more clinically relevant AL in the IOFA- group compared to the IOFA+ group (16.7% vs 2.4%, P = 0.026) involving significantly more anastomotic dehiscence which required re-intervention (19% vs 2.4%, P = 0.014). Additionally, more descending colon ischaemia/necrosis was observed in the IOFA- group compared with the IOFA+ group (9.5% vs 0%, P = 0.040). CONCLUSION: In this prospective case-matched study, IOFA decreased the occurrence of clinically relevant AL due to necrosis of the descending colon or anastomosis. Upon blind review, perfusion assessment using IOFA was reproducible.

Inflammatory appendix mass in patients with acute appendicitis: CT diagnosis and clinical relevance.

The purpose of our study was to analyze the clinical relevance of computerized tomography (CT) in providing the diagnosis of inflammatory appendix mass (IAM) in patients with acute appendicitis. The CT images of 134 patients were reviewed. Two groups of patients were made according to the presence (group 1; n = 21) or the absence (group 2; n = 113) of IAM. Clinical signs of patients, CT features, complications at surgery, and histological examinations were noted. Inter-observer agreement was assessed by using kappa statistics. Twenty-one patients presenting with CT features of IAM were diagnosed. An excellent inter-observer agreement (κ = 0.94) was assessed for the diagnosis of IAM. No significant statistical difference in the age distribution was observed between patients with IAM (mean age 55) and patients without (mean age 45) (p = 0.2232). No clinical sign showed a statistically significant association with the presence of IAM (p = 0.707) or with complication encountered at surgery (p = 0.180). Delay to CT examination was 5.4 days in patients presenting with CT features of IAM and of 1.7 days for patients presenting without (p = 0.0001). Conversely to acute appendicitis complicated by simple perforation (p = 0.153) or peri-appendicular abscess (p = 0.501), acute appendicitis presenting with IAM showed a statistically significant association with complications encountered at surgery (p = 0.0003) and the need for conversion to open surgery (p = 0.001). Performing CT in complicated acute appendicitis provides the diagnosis of IAM. Distinction of IAM appeared to be of clinical relevance, since immediate surgery in IAM was statistically associated with surgical complications and conversion to open surgery in our study.

Pre-irradiation of mouse mammary gland stimulates cancer cell migration and development of lung metastases.

BACKGROUND: In most patients with breast cancer, radiotherapy induces inflammation that is characterised by an increase of promigratory factors in healthy tissues surrounding the tumour. However, their role in the emergence of the migration phenotype and formation of metastases is still unclear. METHODS: A single mammary gland of BALB/c mice was irradiated with four doses of 6 Gy given at a 24-h interval. After the last session of irradiation, treated and control mammary glands were either collected for quantification of promigratory and proinflammatory factors or were implanted with fluorescent ubiquitination-based cell cycle indicator (FUCCI)-expressing mouse mammary cancer D2A1 cells. The migration of cancer cells in the mammary glands was monitored by optical imaging. On day 21, mammary tumours and lungs were collected for histology analyses and the quantification of metastases. RESULTS: Pre-irradiation of the mammary gland increased by 1.8-fold the migration of cancer cells, by 2-fold the quantity of circulating cancer cells and by 2.4-fold the number of lung metastases. These adverse effects were associated with the induction of interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2). CONCLUSION: The emergence of the metastasis phenotype is believed to be associated with the accumulation of mutations in cancer cells. Our results suggest an alternative mechanism based on promigratory factors from irradiated mammary glands. In clinic, the efficiency of radiotherapy could be improved by anti-inflammatory agents that would prevent the stimulation of cancer cell migration induced by radiation.

Radiation-enhancement of MDA-MB-231 breast cancer cell invasion prevented by a cyclooxygenase-2 inhibitor.

BACKGROUND: Recent evidences support that radiation can promote the invasion of cancer cells. As interactions between cancer cells and surrounding stromal cells can have an important role in tumour progression, we determined whether an irradiation to fibroblasts can enhance the invasiveness of breast cancer cells. The role of cyclooxygenase-2 (COX-2), an inflammatory enzyme frequently induced by radiotherapy, was investigated. METHODS: Irradiated 3T3 fibroblasts were plated in the lower compartment of invasion chambers and used as chemoattractant for non-irradiated human breast cancer cell MDA-MB-231, which are oestrogen receptor negative (ER(-)) and the oestrogen receptor positive (ER(+)) MCF-7 cells. Stimulation of COX-2 expression in irradiated 3T3 cells was measured by a semi-quantitative qPCR and western blot. Capacity of the major product of COX-2, the prostaglandin E2 (PGE(2)), to stimulate the production of the matrix metalloproteinase-2 (MMP-2) and cancer cell invasion were assessed with a zymography gel and invasion chambers. RESULTS: Irradiation (5 Gy) of 3T3 fibroblasts increased COX-2 expression and enhanced by 5.8-fold the invasiveness of non-irradiated MDA-MB-231 cells, while their migration was not modified. Addition of the COX-2 inhibitor NS-398 completely prevented radiation-enhancement of cancer cell invasion. Further supporting the potential role of COX-2, addition of PGE(2) has increased cancer cell invasion and release of MMP-2 from the MDA-MB-231 cells. This effect of radiation was dependant on the expression of membrane type 1 (MT1)-MMP, which is required to activate the MMP-2, but was not associated with the ER status. Although irradiated fibroblasts stimulated the invasiveness of MDA-MB-231 ER(-) cells, no enhancement was measured with the ER(+) cell line MCF-7. CONCLUSIONS: Radiation-enhancement of breast cancer cell invasion induced by irradiated 3T3 fibroblasts is not dependant on the ER status, but rather the expression of MT1-MMP. This adverse effect of radiation can be prevented by a specific COX-2 inhibitor.

Emergency surgery for obstructing colonic cancer: a comparison between right-sided and left-sided lesions.

PURPOSE: Few studies compare management and outcomes of obstructive colonic cancer, depending on the tumor site. We aim to evaluate the differences in patient characteristics, tumor characteristics, and outcomes of emergency surgery for obstructive right-sided versus left-sided colonic cancers. METHODS: Between 2000 and 2009, 71 consecutive patients had an emergency colectomy following strict and clear definition of obstruction in a single institution. We retrospectively analyzed pre, per, and postoperative data that were prospectively collected. RESULTS: There were 31 and 40 patients in the right and left group, respectively. Patients aged over 80 were more frequent in the right group (p = 0.03). At operation, ileocecal valve was less often competent in the right group (p = 0.03). The one-stage strategy was more frequent in the right group (p = 0.008). Patients in the right group had a higher rate of nodes invasion (p = 0.04). One- and two-year mortality rate in the right group had a tendency to be higher. CONCLUSIONS: Patients presenting with a right obstructive colonic cancer are older, have a more advanced locoregional disease, and are more often treated in a one-stage strategy than patients with a left obstructive tumor.

Acute appendicitis: Factors associated with inconclusive ultrasound study and the need for additional computed tomography.

PURPOSE: To identify variables associated with inconclusive ultrasound examination and the need for further abdominopelvic computed tomography (CT) examination for the diagnosis of acute appendicitis. MATERIALS AND METHODS: A total of 105 adult patients with acute appendicitis were included. There were 55 patients (38 men, 17 women; mean age, 23±9 [SD] years; range: 15-58 years) with a diagnosis of acute appendicitis using ultrasound alone and 50 patients (30 men, 20 women; mean age, 31±14 [SD] years; range: 16-83 years) who required further CT. Demographic, clinical, and biological criteria and appendix location were compared between the two groups to search for variables associated with the need of further CT. RESULTS: Patients who required further CT were older (31.1±14 [SD] years) and had a greater body mass index (BMI) (26.7±4.3 [SD]kg/m2) than those who did not require CT (23±9 [SD] years and 22.9±3.4 [SD]kg/m2), respectively (P<0.01). A greater proportion of patients with complicated acute appendicitis was observed in patients who required further CT (9/50; 18%) than in those who had only ultrasound (1/55; 2%) (P=0.012). Atypical appendix location was more frequent in patients who required CT (19/50; 36%) than in those who had only ultrasound (6/55; 11%) (P<0.001). There were no significant differences regarding gender, inflammatory syndrome and hours of imaging (on call vs. working hours) between the two groups. CONCLUSION: Advanced age, high BMI, atypical appendix location, and complicated appendicitis are associated with inconclusive ultrasound and the need for further CT to diagnose acute appendicitis.

Combined Treatment of a Gallbladder Volvulus with a Common Bile Duct Obstruction.

Gallbladder volvulus is a rare disease and can lead to an acute cholecystitis. We report the case of an elderly woman with a gallbladder volvulus, diagnosed at CT scan and treated by surgery and endoscopic sphincterotomy.

In vivo enhancement of genomic instability in minisatellite sequences of mouse C3H/10T1/2 cells transformed in vitro by X-rays.

The level of genomic instability was determined during tumor development in vivo. Genomic rearrangements, a marker of genomic instability, was measured in mouse C3H/10T1/2 cells transformed in vitro by X-rays with a DNA fingerprinting assay. Three transformed clones isolated from type III foci were divided into two groups. Cells from the first group were injected s.c. into syngeneic and nonimmunosuppressed C3H mice. After 3 to 5 months, the tumors were excised, and the neoplastic cells were isolated and subcloned. Cells from the second group were incubated in vitro for 25 passages (about 6 months) to approximate the number of cell divisions occurring in the tumor, and then they were subcloned. DNA was extracted from subclones grown in vitro and in vivo and analyzed with the DNA fingerprinting assay. A high frequency of genomic rearrangements (50-100%) was found in subclones derived from tumors that arose in vivo, whereas the frequency was very low (< 10%) among subclones passaged in vitro, suggesting that genetic instability may be enhanced by factors present in the C3H mouse. In one clone (F-17) genomic instability appeared to be activated and down regulated. The high frequency of instability found in tumor cell subclones did not appear to result from an in vivo selection of a more tumorigenic subpopulation of cells present in the original clone prior to injection in the animal. This enhancement of genomic instability occurring in vivo could be required to complete the process of transformation to tumorigenicity and allow the neoplastic cells to adapt to a new environment.

Genomic rearrangements in mouse C3H/10T1/2 cells transformed by X-rays, UV-C, and 3-methylcholanthrene, detected by a DNA fingerprint assay.

Genomic rearrangements occurring in C3H/10T1/2 cells transformed by X-rays were examined with a DNA fingerprint assay. Four multilocus and multiallele probes were employed (M, X, H10, and H16) that detect different families of minisatellite sequences dispersed throughout the genome. Genomic rearrangements were detectable only with probe M. This specificity may be explained by a genomic instability owing to a specific sequence or structure of DNA recognized by probe M. Genomic rearrangements were detected in 5 of 12 type III foci transformed by 600 cGy of X-rays and in all clones isolated from a previously transformed clone exposed to a second dose of 600 cGy and recloned. The latter data suggest that the stage of transformation and the occurrence of genomic rearrangement induced by X-rays may be related. An intensity shift or a complete deletion of band 2 was common to these X-ray-induced clones, as well as to clones transformed by UV-C (1 of 5) or 3-methylcholanthrene (4 of 6). This band did not hybridize to probes for the retinoblastoma gene RB or for p53. We hypothesize that the loss of band 2 may reflect a significant genetic change in the transformation of 10T1/2 cells, perhaps representing the inactivation of a tumor suppressor gene other than RB or p53. Additional rearrangements occurred in X-ray-transformed clones; these rearrangements were not observed with the other carcinogens. Aside from the changes in band 2, however, no specific pattern of genomic rearrangement was associated with X-ray transformation, and the presence or absence of rearrangements did not correlate with tumorigenicity in syngeneic nonimmunosuppressed C3H mice.

The ability of staurosporine to modulate pancreatic acinar cell desensitization by TPA, carbamylcholine and caerulein.

The implication of protein kinase C in the phenomenon of pancreatic acinar cell desensitization to carbamylcholine, caerulein and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was investigated using a potent PKC inhibitor, staurosporine. At a concentration of 1 microM, staurosporine caused a maximum 64% inhibition of amylase release from rat pancreatic acini stimulated by 100 nM TPA. At 100 nM, staurosporine reduced by 50 to 55% amylase secretion elicited by maximal concentrations of carbamylcholine or caerulein without affecting their potency. Staurosporine was also able to prevent completely desensitization by TPA of the subsequent secretory response to carbamylcholine and caerulein. Furthermore, staurosporine also totally prevented desensitization by caerulein of the subsequent secretory response to caerulein. In contrast, staurosporine only partially prevented desensitization by carbamylcholine of the subsequent secretory response to carbamylcholine. These results indicate that staurosporine is a potent inhibitor of protein kinase C as it inhibited the secretory response to carbamylcholine, caerulein and TPA. They also suggest that desensitization of the secretory response induced by TPA and caerulein used a common pathway involving protein kinase C activation. Finally, desensitization by carbamylcholine is more complex as it is only partially prevented at staurosporine; therefore, protein kinase C activation seems to be one of the factors involved.

Antioxidants to prevent bovine neutrophil-induced mammary epithelial cell damage.

Activated neutrophils are able to produce a large quantity of bactericidal molecules such as reactive oxygen species that have been associated with tissue damage in several inflammation models. The protective effects of antioxidants in a context of neutrophil-induced damage to mammary epithelial cells were first evaluated in vitro using a coculture model of activated bovine neutrophils and a bovine mammary epithelial cell line (MAC-T cells). Cell damage was determined by quantifying the release of lactate dehydrogenase by MAC-T cells in culture medium. Morphological observation of cells stained with acridine orange was used to visualize the extent of cell damage. When incubated with neutrophils activated by lipopolysaccharides and phorbol 12-myristate 13-acetate, MAC-T cells released large amounts of lactate dehydrogenase indicating significant cell damage. The addition of dimethylthiourea or bathocuproine disulfonic acid did not reduce the damage whereas catechin, deferoxamine or glutathione ethyl ester significantly reduced neutrophil-induced cytotoxicity in a dose-dependent manner. The effect of deferoxamine, an iron chelator, on the growth of Escherichia coli and the ability of bovine neutrophils to phagocytose these bacteria were then assessed in vitro. Our data showed that deferoxamine did not interfere with the phagocytic activity of neutrophils but inhibited growth of the bacteria. Overall, our results suggest that antioxidants may be effective tools for protecting mammary tissue against neutrophil-induced oxidative stress during bovine mastitis.

Mesenteric panniculitis: still an ambiguous condition.

PURPOSE: To study the possible relationship between mesenteric panniculitis (MP) visible on computed tomography (CT) and the presence of an underlying neoplastic disease. PATIENTS AND METHODS: A retrospective analysis of 158 patients with CT examinations that revealed the presence of MP was performed. CT images were analyzed by two different radiologists using morphological criteria validated in the radiological literature. The presence, frequency and type of neoplastic lesions associated with MP were assessed. RESULTS: MP was asymptomatic in 96/158 patients (61%). Fat halo sign and pseudocapsule were visible on CT in 89/158 (56%) and 93/158 (59%) patients, respectively. Underlying neoplastic disease was present in 88/158 patients (56%). The neoplastic diseases most often associated with MP were lymphoma (28%), melanoma (18%), colorectal cancer (15%) and prostate cancer (13%). CONCLUSION: MP has typical CT appearance and is associated with underlying neoplastic disease in 56% of patients. Such levels of association might suggest that MP may be considered as a paraneoplastic condition. Hence, incidental depiction of MP on CT in a patient without known neoplastic disease should incite radiologists to further scrutinize CT examination for presence of synchronous neoplastic lesions.

DNA damage induced by catecholestrogens in the presence of copper (II): generation of reactive oxygen species and enhancement by NADH.

Certain estrogen metabolites are involved in carcinogenesis and the development of resistance to methotrexate (MTX). In this study, we determined whether these well-established biological effects correlate with the relative efficiency of several estrogen metabolites to induce DNA strand breaks in the presence of copper, and investigated the potential enhancing effect of reduced nicotinamide adenine dinucleotide (NADH). DNA strand breaks induced by estradiol metabolites were measured by the conversion of supercoiled phage phiX-174 RF1 DNA to open circular and linear forms. The most active catecholestrogens were the 4-hydroxy derivatives, which produced about 2.5 times more DNA double strand breaks than the 2-hydroxy derivatives, while estradiol and 16alpha-hydroxyestrone were inactive. In addition, our results show that 4-hydroxyestradiol (4-OHE2) at physiological concentrations was capable of exhibiting DNA cleaving activity. The formation of these catecholestrogen-induced DNA strand breaks was associated with the utilization of oxygen and the generation of H2O2, because catalase inhibited the DNA cleaving activity of 4-OHE2. Interestingly, we also observed that NADH enhanced the induction of DNA strands breaks by 4-OHE2/Cu(II), probably by perpetuating the redox cycle between the quinone and the semiquinone forms of the catecholestrogen. In conclusion, this study demonstrated that the relative efficiency of 2-, and 4-hydroxyestrogen in carcinogenesis and for the enhancement of MTX resistance correlates with their relative capability to induce DNA strand breaks. In order to inhibit these estrogen-mediated biological effects, it may be important to develop different strategies to block the production of reactive oxygen species by the catecholestrogen-redox cycle.

Thiols can either enhance or suppress DNA damage induction by catecholestrogens.

The estrogen metabolites catecholestrogens (or hydroxyestrogens) are involved in carcinogenesis and the development of resistance to methotrexate. This induction of drug resistance correlates with the relative efficiency of catecholestrogens in the generation of reactive oxygen species (ROS) and the induction of DNA strand breaks. Although antioxidants can neutralize ROS, the generation of these reactive species by catecholestrogens can be enhanced by electron donors like NADH. Therefore, this study was undertaken to determine the ability of different thiol agents (GSH, NAC, DTT, DHLA) to either inhibit or enhance the level of DNA damage induced by the H(2)O(2) generating system 4-hydroxyestradiol/Cu(II). Our results show that GSH, DTT, and DHLA inhibited the induction of the 4-hydroxyestradiol/Cu(II)-mediated DNA damage, with GSH showing the best potential. In contrast, the GSH precursor NAC at low concentrations was able to enhance the level of oxidative damage, as observed with NADH. NAC can reduce Cu(II) to Cu(I) producing the radical NAC&z.rad;, which can generate the superoxide anion. However, the importance of this pathway appears to be relatively minor since the addition of NAC to the 4-hydroxyestradiol/Cu(II) system generates about 15 times more DNA strand breaks than NAC and Cu(II) alone. We suggest that NAC can perpetuate the redox cycle between the quinone and the semiquinone forms of the catecholestrogens, thereby enhancing the production of ROS. In conclusion, this study demonstrates the crucial importance of the choice of antioxidant as potential therapy against the negative biological effects of estrogens.

In vitro reversion of transformed phenotype in mouse C3H/10T1/2 cells.

Spontaneous tumor regression is still one of the most puzzling events in human cancer. A cell culture model of malignant transformation designed to permit the study of this phenomenon in vitro was applied to examine reversion and re-expression of the transformed phenotype in two X-ray transformed mouse 10T1/2 cell clones. By alternating cell passages at low and high seeding density, the expression of cell contact inhibition and tumorigenic capacity were both reverted and restored. Growth of non-transformed wild-type cells was not affected by seeding density. This reversion of the transformed phenotype was associated with a modification in genomic 5-methylcytosine content. Initially, the transformed clones were hypomethylated, as occurs in most human tumors. After only four passages at low seeding density, the phenotype was reverted to that of non-transformed 10T1/2 cells and genomic 5-methylcytosine content was significantly increased to levels measured in non-transformed C3H/10T1/2 mouse cells. Thus, hypomethylation induced by ionizing radiation was not a permanent feature of malignantly transformed 10T1/2 cells. Although genomic 5-methylcytosine content returned to normal levels during low density passaging, the methylation pattern of the c-myc gene specifically was not associated with cell passages either at low or high seeding density. In an attempt to identify genes involved in this process, expression of the tumor suppressor gene p53 was measured. Western blot analysis failed to detect any correlation between expression of p53 protein and reversion of the transformed phenotype. The results of this study indicate that the transformed phenotype is not permanently associated with the malignant transformation of C3H/1OT1/2 cells, and can be modulated by growth conditions in vitro. We propose that modulation of genomic 5-methylcytosine levels may be involved in this process.

Carbamylcholine and phorbol esters desensitize muscarinic receptors by different mechanisms in rat pancreatic acini.

Pretreatment of rat pancreatic acini with phorbol 12-myristate, 13-acetate (PMA), a protein kinase C (PK-C) activator, caused the desensitization of carbamylcholine (CBC)-induced amylase release in a concentration- and time-dependent fashion. The less potent phorbol-12, 13-dibutyrate (PDBu) also provoked a desensitization, but the inactive 4-alpha-phorbol-12,13-didecanoate had no effect. PMA or PDBu also significantly reduced subsequent amylase release induced by caerulein or secretin in contrast to CBC, which only reduced amylase release induced by CBC or secretin. Preincubation of acini with PMA did not lead to a decrease in PMA or A23187-stimulated amylase release. A 3 h resting period did not restore the desensitization induced by PMA or PDBu. Pretreatment with PMA did not cause changes in muscarinic receptor high- and low-affinity populations as observed with CBC pretreatment. The PK-C inhibitor H-7 completely prevented the desensitization induced by PDBu but not that induced by CBC. TMB-8, another PK-C inhibitor, also completely prevented the desensitization induced by PDBu but only partially that induced by CBC. These results suggest that phorbol esters can induce desensitization of muscarinic receptor-stimulated amylase release by a different mechanism than that involved in muscarinic agonist-induced desensitization.

Biological activities of phthalocyanines--XI. Phototoxicity of sulfonated aluminum naphthalocyanines towards V-79 Chinese hamster cells.

The phototoxicity of sulfonated aluminum naphthalocyanines towards V-79 Chinese hamster cells is investigated. The disulfonated naphthalocyanine exhibits similar photostability, but better cell penetrating properties than the tetrasulfonated dyes. The capacity of the naphthalocyanines to generate singlet oxygen is comparable to that of the corresponding phthalocyanines. However, in contrast to the phthalocyanine dyes, the sulfonated aluminum naphthalocyanines show very little phototoxicity towards the V-79 cells, suggesting close association with non-vital cell constituents or extensive formation of photoinactive adducts and aggregates.

Sulfonated phthalimidomethyl aluminum phthalocyanine: the effect of hydrophobic substituents on the in vitro phototoxicity of phthalocyanines.

The photocytotoxicity of sulfonated phthalimidomethyl aluminum phthalocyanine, a more hydrophobic photosensitizer as compared to phthalocyanine substituted with sulfonate groups only, was investigated. Inclusion of 1-2 phthalimidomethyl groups into disulfonated aluminum phthalocyanine, resulted in increased partition coefficients between n-octanol and water, and a six-fold increase in both cellular uptake and photocytotoxicity towards Chinese hamster lung fibroblast cells (line V-79). Reducing the number of phthalimidomethyl groups, or increasing the degree of sulfonation, lead to a decrease in the partition coefficient, cellular uptake, and phototoxicity. The quantum yield of singlet oxygen was comparable for all dyes tested in this series, indicating that no significant change in this photophysical parameter resulted from phthalimidomethylation. These results suggest that the addition of 1-2 phthalimidomethyl groups to disulfonated aluminum phthalocyanine improves cellular uptake, but, as the relative efficiency of cell killing was not effected, the intracellular distribution on photosensitive molecules may not be modified.

A retrospective study of equine infectious anemia based on the canadian control program.

Equine infectious anemia in Canada was reviewed for the period January 1976 to December 1981. The human and ecological factors prevailing in Canada are deemed instrumental with respect to the evolution of the disease. The natural spread of the disease on a large scale has not been influenced by the Federal program. Reactors with signs of the disease are important for it's propagation. The author underlines the necessity of cooperation with private practising veterinarians to control it.

Cirrhotic and malignant ascites: differential CT diagnosis.

OBJECTIVES: To assess the diagnostic accuracy of the different computed tomography (CT) signs for differentiating between malignant and cirrhotic ascites. MATERIALS AND METHODS: We performed a retrospective study of 102 CT scans in adults, distributed into two groups based on the cirrhotic or malignant etiology of their ascites. The CT signs studied were ascites volume and relative distribution between the greater peritoneal cavity (GPC) and the omental bursa (OB), the density of the ascites, the thickness of the gallbladder wall, the thickness of the parietal peritoneum and its degree of enhancement, and tethered-bowel sign. RESULTS: The CT signs associated with malignant ascites were: presence of fluid in the omental bursa (P=0.003), thickening of the peritoneum its degree of enhancement (P=0.005), increased density of the ascites (P=0.01), and loss of mobility of bowel loops in the ascites (P=0.001). There was no difference in gallbladder wall thickness between the two groups. CONCLUSION: The CT scan can play a role in diagnosing malignant ascites. We confirm the usefulness of the indirect signs composed of distribution of ascites fluid, thickening and enhancement of the parietal peritoneum, and loss of mobility of the bowel loops in the ascites.