Giant maxillary gingival fibromatosis.

We present a case of both unusual pathology and severity - giant maxillary gingival fibromatosis - and discuss the disease and its management, accompanied by clinical imaging. This represents an overlap between maxillofacial and oral surgery, and may present as demonstrated in this case.

N-terminal cleavage fragment of glycosylated Gag is incorporated into murine oncornavirus particles.

Glycosylated Gag (Glycogag) is a transmembrane protein encoded by murine and feline oncornaviruses. While the protein is dispensible for virus replication, Glycogag-null mutants of a neurovirulent murine oncornavirus are slow to spread in vivo and exhibit a loss of pathogenicity. The function of this protein in the virus life cycle, however, is not understood. Glycogag is expressed at the plasma membrane of infected cells but has not been detected in virions. In the present study we have reexamined this issue and have found an N-terminal cleavage fragment of Glycogag which was pelleted by high-speed centrifugation and sedimented in sucrose density gradients at the same bouyant density as virus particles. Its association with virions was confirmed by velocity sedimentation through iodixanol, which effectively separated membrane microvesicles from virus particles. Furthermore, the apparent molecular weight of the virion-associated protein was different from that of the protein extracted from the plasma membrane, suggesting some level of specificity or selectivity of incorporation.

Correlation between intestinal metaplasia of the gastric cardia and gastroesophageal reflux disease.

BACKGROUND/AIMS: IMC (intestinal metaplasia of the cardia) has been a subject of great interest, given the rapidly increasing incidence of adenocarcinoma in this location, over the past two decades. Whether this histological alteration is a consequence of gastroesophageal reflux disease, or a manifestation of an H. pylori-related multifocal atrophic gastritis, is unclear. Furthermore, whether IMC should be considered a premalignant lesion of gastric cardia is still unknown. We performed a prospective study in order to determine the prevalence of IMC in patients presenting for elective esophagogastric-duodenal endoscopy and to evaluate a potential association between IMC and some clinical, endoscopic and histological variables. METHODOLOGY: Biopsy specimens were taken from 105 unselected patients undergoing routine diagnostic endoscopy. Eight biopsies were taken from different sides, for histological evaluation: 1 above and 3 below the squamocolumnar junction, 2 from gastric fundus and 2 from gastric antrum. All specimens were stained with hematoxylin and eosin-Alcian blue and modified Giemsa to facilitate the detection of H. pylori. RESULTS: Eighty-six patients (50 males, 36 females) with a mean age of 46.5 years (range: 23-75 years), were included in the study. Twenty-one (24.5%) were found to have IMC; 4 (19%) of these had concomitant low-grade dysplasia of the cardiac mucosa. IMC was associated with: males (P = 0.04), endoscopic diagnosis of esophagitis (P = 0.02), histological diagnosis of esophagitis (P = 0.008), mucosa of the cardiac type (P = 0.02), chronic carditis (P = 0.002) and dysplasia (P = 0.04). There was no correlation with: age, reflux symptoms, activity of carditis, H. pylori infection of the cardia and intestinal metaplasia of the distal gastric mucosa. CONCLUSIONS: IMC is common in our area. It is associated with endoscopic and histological changes of gastroesophageal reflux disease, but not with H. pylori infection of the cardia. Although 19% of patients presented concomitant dysplasia (of low grade), long-term follow-up studies will be necessary to assess the effective risk of IMC for cancer transformation.

Increased expression of MIP-1 alpha and MIP-1 beta mRNAs in the brain correlates spatially and temporally with the spongiform neurodegeneration induced by a murine oncornavirus.

The chimeric murine oncornavirus FrCas(E) causes a rapidly progressive paralytic disease associated with spongiform neurodegeneration throughout the neuroaxis. Neurovirulence is determined by the sequence of the viral envelope gene and by the capacity of the virus to infect microglia. The neurocytopathic effect of this virus appears to be indirect, since the cells which degenerate are not infected. In the present study we have examined the possible role of inflammatory responses in this disease and have used as a control the virus F43. F43 is an highly neuroinvasive but avirulent virus which differs from FrCas(E) only in 3' pol and env sequences. Like FrCas(E), F43 infects large numbers of microglial cells, but it does not induce spongiform neurodegeneration. RNAase protection assays were used to detect differential expression of genes encoding a variety of cytokines, chemokines, and inflammatory cell-specific markers. Tumor necrosis factor alpha (TNF-alpha) and TNF-beta mRNAs were upregulated in advanced stages of disease but not early, even in regions with prominent spongiosis. Surprisingly there was no evidence for upregulation of the cytokines interleukin-1 alpha (IL-1 alpha), IL-1 beta, and IL-6 or of the microglial marker F4/80 at any stage of this disease. In contrast, increased levels of the beta-chemokines MIP-1 alpha and -beta were seen early in the disease and were concentrated in regions of the brain rich in spongiosis, and the magnitude of responses was similar to that observed in the brains of mice injected with the glutamatergic neurotoxin ibotenic acid. MIP-1alpha and MIP-1beta mRNAs were also upregulated in F43-inoculated mice, but the responses were three- to fivefold lower and occurred later in the course of infection than was observed in FrCas(E)-inoculated mice. These results suggest that the robust increase in expression of MIP-1 alpha and MIP-1 beta in the brain represents a correlate of neurovirulence in this disease, whereas the TNF responses are likely secondary events.

EsophaCoil for palliation of dysphagia in unresectable oesophageal carcinoma: short- and long-term results.

BACKGROUND AND AIM: Few reports have shown that EsophaCoil is an effective and safe prosthesis for palliation of malignant oesophageal dysphagia. A single centre experience using this type of prosthesis is reported. PATIENTS AND METHODS: Between January 1995 and September 2000, 42 consecutive patients, 41 with unresectable oesophageal cancer and one with oesophageal stenosis secondary to lung cancer, were treated with 44 EsophaCoils (2 patients received 2 stents). Tumours were located in lower third of oesophagus and/or gastric cardia in 22 cases, in middle third in 18 and in upper third in 2. Mean stricture length was 5.3 cm. Implantation was performed on hospitalized patients. RESULTS: EsophaCoil placement was successful all 44 times and was followed by complete expansion of the prostheses. There were no major procedure-related complications or deaths. Dysphagia score improved from mean of 2.9 to 1.3 within 24 hours of stent implantation. Median hospital stay was 2.7 days. Late complications occurred in 14 patients (34.2%): 3 migrations into stomach, 7 tissue overgrowth, 2 late perforations and 2 food impactions. Mean survival time was 4.2 months (range 1-10). CONCLUSIONS: In our experience, full expansion of EsophaCoil was achieved in all cases. This result, was associated with high incidence of retrosternal pain. Relief of dysphagia score was identical to that obtained with other types of Self-Expanding Metal Stent. Coil design prevented tumour ingrowth and allowed retrieval of three migrated stents. Mean survival time was similar to that reported in larger series using different types of Self-Expanding Metal Stent.

Brain infection by neuroinvasive but avirulent murine oncornaviruses.

The chimeric murine oncornavirus FrCas(E) causes a rapidly progressive noninflammatory spongiform encephalomyelopathy after neonatal inoculation. The virus was constructed by the introduction of pol-env sequences from the wild mouse virus CasBrE into the genome of a neuroinvasive but nonneurovirulent strain of Friend murine leukemia virus (FMuLV), FB29. Although the brain infection by FrCas(E) as well as that by other neurovirulent murine retroviruses has been described in detail, little attention has been paid to the neuroinvasive but nonneurovirulent viruses. The purpose of the present study was to compare brain infection by FrCas(E) with that by FB29 and another nonneurovirulent virus, F43, which contains pol-env sequences from FMuLV 57. Both FB29 and F43 infected the same spectrum of cell types in the brain as that infected by FrCas(E), including endothelial cells, microglia, and populations of neurons which divide postnatally. Viral burdens achieved by the two nonneurovirulent viruses in the brain were actually higher than that of FrCas(E). The widespread infection of microglia by the two nonneurovirulent viruses is notable because it is infection of these cells by FrCas(E) which is thought to be a critical determinant of its neuropathogenicity. These results indicate that although the sequence of the envelope gene determines neurovirulence, this effect appears to operate through a mechanism which does not influence either viral tropism or viral burden in the brain. Although all three viruses exhibited similar tropism for granule neurons in the cerebellar cortex, there was a striking difference in the distribution of envelope proteins in those cells in vivo. The FrCas(E) envelope protein accumulated in terminal axons, whereas those of FB29 and F43 remained predominantly in the cell bodies. These observations suggest that differences in the intracellular sorting of these proteins may exist and that these differences appear to correlate with neurovirulence.

Increased neurovirulence of polytropic mouse retroviruses delivered by inoculation of brain with infected neural stem cells.

Following intraperitoneal (IP) inoculation of neonatal mice, the polytropic recombinant murine leukemia virus (MuLV), Fr98, induces a severe brain disease characterized by ataxia, seizures and death. In contrast, no apparent clinical neurological disease is seen after IP infection with Fr54, a polytropic MuLV differing from Fr98 in its envelope gene sequences. In the brain both Fr98 and Fr54 infect primarily capillary endothelial cells and microglia. However, the level of microglial infection by Fr98 is twofold higher than by Fr54, which might account for the difference in neurovirulence. In the present study, in order to test directly whether an increase in the number of microglia infected by Fr54 would be sufficient to induce clinical disease, we attempted to increase the level of Fr54 in the brain by changing the route of infection. After intraventricular inoculation with Fr54-infected neural stem cells (clone C17.2), a well-established vehicle for delivery of viruses and genes to the brain, mice became ataxic and died 4 weeks postinfection. In these mice induction of brain disease was correlated with a higher level of viral antigen in the cerebrum and an increase in the number of infected microglial cells in all brain regions examined compared with mice inoculated IP. In contrast, mice inoculated with neural stem cells infected with an ecotropic nonneurovirulent murine leukemia virus, FB29, developed no clinical disease in spite of evidence for widespread infection of microglia in brain. Since the main differences between Fr54 and FB29 are in the SU (gp70) region of the envelope gene, this region is most likely to account for the differences in induction of CNS disease seen in the current experiments.

Mapping of a neurovirulence determinant within the envelope protein of a polytropic murine retrovirus: induction of central nervous system disease by low levels of virus.

Murine leukemia virus (MuLV) clone Fr98 is a recombinant polytropic virus that causes neurological disease characterized by ataxia in susceptible mouse strains. The envelope gene of Fr98 has been previously shown to encode at least two separate neurovirulence determinants. In the present study, the determinant encoded within the EcoRI/AvrII fragment of the envelope gene was further defined. In these experiments, neurovirulence was associated with a change from a serine to an arginine at position 195 and a glycine to an alanine at position 198 within the envelope protein. Neurovirulent and nonvirulent virus clones, which differed only at these two amino acid residues, showed no difference in the type or location of cells infected. Furthermore, equivalent levels of viral p30 capsid protein were detected in the brains of mice infected with either the neurovirulent or nonvirulent virus clones. These results were consistent with the interpretation that the envelope protein of the neurovirulent virus differed from that of the nonvirulent virus by having a greater toxic effect on central nervous system function.

Endoscopic treatment of postoperative colonic strictures using an achalasia dilator: short-term and long-term results.

BACKGROUND AND STUDY AIMS: Endoscopic dilation has proven to be a valid therapeutic alternative to surgery for treating postoperative anastomotic colonic strictures. The authors here evaluate retrospectively the short and long-term clinical results obtained in such patients by pneumatic dilation. PATIENTS AND METHODS: From March 1986 to December 1993, 18 patients who had undergone surgery for colorectal cancer were treated for a postoperative symptomatic stricture. Four patients had undergone a left hemicolectomy and 14 an anterior resection. The strictures had a diameter of less than 2 mm, and a length ranging from 5 to 29 mm. The dilations were performed using a 30-40 mm pneumatic dilator for achalasia. The clinical results were classified in relation to the abdominal symptomatology reported by the patients, and were evaluated in the short term (one week) and long term (mean follow-up: 39 months). RESULTS: Seventeen of the 18 patients underwent a total of 45 dilating sessions; one patient was excluded because a recurrence was diagnosed at the suture line. Five patients had a single dilating session; eight patients had two sessions, and four patients had a mean of 4.5 sessions. Two complications were observed: a punctiform bowel perforation and one transient mucosal bleeding. Immediate symptomatic relief was achieved in all cases, and good long-term clinical results were achieved in 16 patients (94.1%). CONCLUSIONS: Endoscopic dilation with an achalasia balloon has proved to be safe and simple to perform, and allowed us to obtain good short-term and long-term clinical results. This type of dilation may be considered the first-line therapeutic approach for symptomatic benign colonic anastomotic strictures.

[Esophageal achalasia: its ambulatory treatment by balloon dilatation]. / Acalasia esofagea: trattamento ambulatoriale mediante dilatazioni pneumatiche.

We report immediate and late clinical results achieved in 33 patients with achalasia treated with pneumatic dilation as an outpatient procedure. Thirty patients were seen before any therapy and 3 following a failed esophagomyotomy. All patients were submitted to clinical, radiological and manometric evaluation before treatment: six of them belonged to Adams' class I, 19 to class II and 8 to class III. The dilations were performed with Microvasive Regiflex System (30-35-40. mm.). The average number of dilations per patient was 1.4; one dilation was performed in 25 patients, 2 dilations in 6, and three dilation in two. The patients after the dilation were controlled for a maximum period of 3 hours before being discharged from the outpatient facilities. No complications, worthy of note, was related to the procedures. The clinical results were subdivided in four classes according to Vantrappen's schema. Ten days--immediate results--after the first dilation excellent-good results were obtained in 26 patients (78.8%); moderate results in four (12.1%) and poor results in three (9.1%). The mean LES pressure, evaluated in 15 out of 25 cases fell from 37.6 mmHg. Before treatment to a value of 16.2 mmHg after treatment (p < 0.005). Of the 30 patients followed for an average period of 30.6 months (2-82)--late results--excellent-good results were obtained in 24 (80%), moderate results in 4 (13.3%) and poor in 2 (6.7%). In conclusion the clinical results, of our study, repeat those published in a previous prospective evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)