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A Nouri

Publications and source records attributed to A Nouri.

At least 37 records · Page 2Linked to original sources

[Neonatal hemoperitoneum].

PATIENTS AND RESULTS: A series of four cases observed in the department of pediatric surgery in Monastir between 1990 and 1998 are reported. The diagnosis was made in the two first days of life. The clinical features associated paleness, shock and abdominal distension. Ultrasonography revealed that the hemoperitoneum was associated with liver hematoma in three cases and with retroperitoneal hematoma in two cases. Three infants required emergency hemostatic laparotomy. The fourth was stabilized by initial resuscitation. One infant died at the age of six months following subarachnoid hemorrhage and subdural hematoma. No complication occurred in the three remaining patients. CONCLUSION: The pathogeny, clinical features and treatment of the hemoperitoneum in the newborn are discussed. The authors stress preventive measures, the only way to decrease the incidence of this neonatal complaint.

Hematoma↗

A comprehensive approach to mapping the interacting surfaces of murine amphotropic and feline subgroup B leukemia viruses with their cell surface receptors.

Because mutations in envelope glycoproteins of retroviruses or in their cell surface receptors can eliminate function by multiple mechanisms, it has been difficult to unambiguously identify sites for their interactions by site-directed mutagenesis. Recently, we developed a gain-of-function approach to overcome this problem. Our strategy relies on the fact that feline leukemia virus subgroup B (FeLV-B) and amphotropic murine leukemia virus (A-MLV) have closely related gp70 surface envelope glycoproteins and use related Na(+)-dependent phosphate symporters, Pit1 and Pit2, respectively, as their receptors. We previously observed that FeLV-B/A-MLV envelope glycoprotein chimeras spliced between the variable regions VRA and VRB were unable to use Pit1 or Pit2 as a receptor but could efficiently use specific Pit1/Pit2 chimeras. The latter study suggested that the VRA of A-MLV and FeLV-B functionally interact with the presumptive extracellular loops 4 and 5 (ECL4 and -5) of their respective receptors, whereas VRB interacts with ECL2. We also found that FeLV-B gp70 residues F60 and P61 and A-MLV residues Y60 and V61 in the first disulfide-bonded loop of VRA were important for functional interaction with the receptor's ECL4 or -5. We have now extended this approach to identify additional VRA and VRB residues that are involved in receptor recognition. Our studies imply that FeLV-B VRA residues F60 and P61 interact with the Pit1 ECL5 region, whereas VRA residues 66 to 78 interact with Pit1 ECL4. Correspondingly, A-MLV VRA residues Y60 and V61 interact with the Pit2 ECL5 region, whereas residues 66 to 78 interact with Pit2 ECL4. Similar studies that focused on the gp70 VRB implicated residues 129 to 139 as contributing to specific interactions with the receptor ECL2. These results identify three regions of gp70 that interact in a specific manner with distinct portions of their receptors, thereby providing a map of the functionally interacting surfaces.

Amino Acid Sequence↗

Sodium-dependent neutral amino acid transporter type 1 is an auxiliary receptor for baboon endogenous retrovirus.

The baboon endogenous retrovirus (BaEV) belongs to a large, widely dispersed interference group that includes the RD114 feline endogenous virus and primate type D retroviruses. Recently, we and another laboratory independently cloned a human receptor for these viruses and identified it as the human sodium-dependent neutral amino acid transporter type 2 (hASCT2). Interestingly, mouse and rat cells are efficiently infected by BaEV but only become susceptible to RD114 and type D retroviruses if the cells are pretreated with tunicamycin, an inhibitor of protein N-linked glycosylation. To investigate this host range difference, we cloned and analyzed NIH Swiss mouse ASCT2 (mASCT2). Surprisingly, mASCT2 did not mediate BaEV infection, which implied that mouse cells might have an alternative receptor for this virus. In addition, elimination of the two N-linked oligosaccharides from mASCT2 by mutagenesis, as substantiated by protein N-glycosidase F digestions and Western immunoblotting, did not enable it to function as a receptor for RD114 or type D retroviruses. Based on these results, we found that the related ASCT1 transporters of humans and mice are efficient receptors for BaEV but are relatively inactive for RD114 and type D retroviruses. Furthermore, elimination of the two N-linked oligosaccharides from extracellular loop 2 of mASCT1 by mutagenesis enabled it to function as an efficient receptor for RD114 and type D retroviruses. Thus, we infer that the tunicamycin-dependent infection of mouse cells by RD114 and type D retroviruses is caused by deglycosylation of mASCT1, which unmasks previously buried sites for viral interactions. In contrast, BaEV efficiently employs the glycosylated forms of mASCT1 that occur normally in untreated mouse cells.

3T3 Cells↗

Cellular and species resistance to murine amphotropic, gibbon ape, and feline subgroup C leukemia viruses is strongly influenced by receptor expression levels and by receptor masking mechanisms.

Chinese hamster ovary (CHO) cells are resistant to infections by gibbon ape leukemia virus (GALV) and amphotropic murine leukemia virus (A-MLV) unless they are pretreated with tunicamycin, an inhibitor of N-linked glycosylation. These viruses use the related sodium-phosphate symporters Pit1 and Pit2, respectively, as receptors in nonhamster cells, and evidence has suggested that the corresponding transporters of CHO cells may be masked by tunicamycin-sensitive secreted inhibitors. Although the E36 line of Chinese hamster cells was reported to secrete the putative Pit2 inhibitor and to be sensitive to the inhibitory CHO factors, E36 cells are highly susceptible to both GALV and A-MLV in the absence of tunicamycin. Moreover, expression of E36 Pit2 in CHO cells conferred tunicamycin-independent susceptibilities to both viruses. Based on the latter results, it was suggested that E36 Pit2 must functionally differ from the endogenous Pit2 of CHO cells. To test these ideas, we analyzed the receptor properties of CHO Pit1 and Pit2 in CHO cells. Surprisingly, and counterintuitively, transfection of a CHO Pit2 expression vector into CHO cells conferred strong susceptibility to both GALV and A-MLV, and similar overexpression of CHO Pit1 conferred susceptibility to GALV. Thus, CHO Pit2 is a promiscuous functional receptor for both viruses, and CHO Pit1 is a functional receptor for GALV. Similarly, we found that the natural resistance of Mus dunni tail fibroblasts to subgroup C feline leukemia viruses (FeLV-C) was eliminated simply by overexpression of the endogenous FeLV-C receptor homologue. These results demonstrate a novel and simple method to unmask latent retroviral receptor activities that occur in some cells. Specifically, resistances to retroviruses that are caused by subthreshold levels of receptor expression or by stoichiometrically limited masking or interference mechanisms can be efficiently overcome simply by overexpressing the endogenous receptors in the same cells.

Amino Acid Sequence↗

[Primary vesicoureteral reflux: report of 100 pediatric observations].

In this study, the authors have reported 100 cases of primary vesico-ureteral reflux (VUR) which occurred over a 7-year period. Patient age at presentation ranged from 1 month to 13 years, with a mean age of 3 years and 5 months. Overall, a higher rate of reflux was observed in the female population (63%) which was particularly evident after the age of 3 years, but with a male predominance during the first 12 months of life. In the majority of cases, the diagnosis of VUR was made following diagnosis and investigation of urinary infection (UI). A high level of UI was the most frequent sign of VUR (87% of cases), while in 6% of cases this disorder was diagnosed during the investigation of an uropathy which was found to be complex in all subjects. An analysis of 143 ureteral reflux units (URU) showed that VUR was pathological only in 17% of cases, and that the reflux grade was I, II, III and IV in 47.4, 28.14, 11.11 and 2.34% of cases respectively. DMSA scintigraphy in 38 patients showed signs of nephropathy in 24 cases, i.e., 14 scars and a decrease in kidney size in 9 cases, and an absence of fixation for one grade IV reflux. Forty subjects with 56 reflux units (34 grade I, II and 22 grade III, IV) were treated by antibiotic prophylaxis, with a positive outcome in 85% of cases in children under 2 years of age, compared to 40% for children aged over 2 years. Only 7 patients were treated by teflon endoscopic injection, and in one case a further injection was required; 21 patients with 30 reflux units were treated by surgery at a mean age of 4 years. In conclusion, VUR is a fairly common disorder, which is frequently detected via an IU; its potential gravity is associated with the risk of subsequent nephropathy.

Adolescent↗

Cloning and characterization of a cell surface receptor for xenotropic and polytropic murine leukemia viruses.

Xenotropic and polytropic murine leukemia viruses (X-MLVs and P-MLVs) cross-interfere to various extents in non-mouse species and in wild Asian mice, suggesting that they might use a common receptor for infection. Consistent with this hypothesis, the susceptibility of some wild mice to X-MLVs has been mapped to the P-MLV receptor locus at the distal end of mouse chromosome 1. In this study, we report the isolation and characterization of a cDNA for the human X-MLV cell surface receptor (X-receptor) by using a human T lymphocyte cDNA library in a retroviral vector. The predicted X-receptor contains 696 amino acids with multiple hydrophobic potential membrane-spanning sequences and with weak homologies to the yeast proteins SYG1, of unknown function, and PHO81, which has been implicated in a system that regulates transport of inorganic phosphate. Expression of the X-receptor in Chinese hamster ovary cells, which are substantially resistant to P-MLVs and to X-MLVs, made them susceptible to both of these virus groups. The mouse homologue of the X-receptor was mapped by hybridization to the distal end of chromosome 1 at the same position as the P-MLV receptor gene Rmc1. These results strongly support the hypothesis that a common gene encodes the receptors for X-MLVs and P-MLVs, with the human X-receptor preferentially mediating X-MLV infections and the homologous protein of inbred mice mediating only P-MLV infections. We propose that X-MLVs and P-MLVs comprise a single family of retroviruses that have coevolved in response to diversification in X-receptor genes of the host.

Amino Acid Sequence↗

Polymorphisms of the cell surface receptor control mouse susceptibilities to xenotropic and polytropic leukemia viruses.

The differential susceptibilities of mouse strains to xenotropic and polytropic murine leukemia viruses (X-MLVs and P-MLVs, respectively) are poorly understood but may involve multiple mechanisms. Recent evidence has demonstrated that these viruses use a common cell surface receptor (the X-receptor) for infection of human cells. We describe the properties of X-receptor cDNAs with distinct sequences cloned from five laboratory and wild strains of mice and from hamsters and minks. Expression of these cDNAs in resistant cells conferred susceptibilities to the same viruses that naturally infect the animals from which the cDNAs were derived. Thus, a laboratory mouse (NIH Swiss) X-receptor conferred susceptibility to P-MLVs but not to X-MLVs, whereas those from humans, minks, and several wild mice (Mus dunni, SC-1 cells, and Mus spretus) mediated infections by both X-MLVs and P-MLVs. In contrast, X-receptors from the resistant mouse strain Mus castaneus and from hamsters were inactive as viral receptors. These results suggest that X-receptor polymorphisms are a primary cause of resistances of mice to members of the X-MLV/P-MLV family of retroviruses and are responsible for the xenotropism of X-MLVs in laboratory mice. By site-directed mutagenesis, we substituted sequences between the X-receptors of M. dunni and NIH Swiss mice. The NIH Swiss protein contains two key differences (K500E in presumptive extracellular loop 3 [ECL 3] and a T582 deletion in ECL 4) that are both required to block X-MLV infections. Accordingly, a single inverse mutation in the NIH Swiss protein conferred X-MLV susceptibility. Furthermore, expression of an X-MLV envelope glycoprotein in Chinese hamster ovary cells interfered efficiently with X-MLV and P-MLV infections mediated by X-receptors that contained K500 and/or T582 but had no effect on P-MLV infections mediated by X-receptors that lacked these amino acids. In contrast, moderate expression of a P-MLV (MCF247) envelope glycoprotein did not cause substantial interference, suggesting that X-MLV and P-MLV glycoproteins interfere nonreciprocally with X-receptor-mediated infections. We conclude that P-MLVs have become adapted to utilize X-receptors that lack K500 and T582. A penalty for this adaptation is a reduced ability to interfere with superinfection. Because failure of interference is a hallmark of several exceptionally pathogenic retroviruses, we propose that it contributes to P-MLV-induced diseases.

Amino Acid Sequence↗

A sodium-dependent neutral-amino-acid transporter mediates infections of feline and baboon endogenous retroviruses and simian type D retroviruses.

The type D simian retroviruses cause immunosuppression in macaques and have been reported as a presumptive opportunistic infection in a patient with AIDS. Previous evidence based on viral interference has strongly suggested that the type D simian viruses share a common but unknown cell surface receptor with three type C viruses: feline endogenous virus (RD114), baboon endogenous virus, and avian reticuloendotheliosis virus. Furthermore, the receptor gene for these viruses has been mapped to human chromosome 19q13.1-13.2. We now report the isolation and characterization of a cell surface receptor for this group of retroviruses by using a human T-lymphocyte cDNA library in a retroviral vector. Swiss mouse fibroblasts (NIH 3T3), which are naturally resistant to RD114, were transduced with the retroviral library and then challenged with an RD114-pseudotyped virus containing a dominant selectable gene for puromycin resistance. Puromycin selection yielded 12 cellular clones that were highly susceptible to a beta-galactosidase-encoding lacZ(RD114) pseudotype virus. Using PCR primers specific for vector sequences, we amplified a common 2.9-kb product from 10 positive clones. Expression of the 2.9-kb cDNA in Chinese hamster ovary cells conferred susceptibility to RD114, baboon endogenous virus, and the type D simian retroviruses. The 2.9-kb cDNA predicted a protein of 541 amino acids that had 98% identity with the previously cloned human Na+-dependent neutral-amino-acid transporter Bo. Accordingly, expression of the RD114 receptor in NIH 3T3 cells resulted in enhanced cellular uptake of L-[3H]alanine and L-[3H]glutamine. RNA blot (Northern) analysis suggested that the RD114 receptor is widely expressed in human tissues and cell lines, including hematopoietic cells. The human Bo transporter gene has been previously mapped to 19q13.3, which is closely linked to the gene locus of the RD114 receptor.

3T3 Cells↗

[Primary psoas abscess in children: 6 cases].

BACKGROUND: Primary psoas abscess is very rare in childhood; its diagnosis and treatment can be improved by the use of recent imaging techniques. PATIENTS: Six children, aged 11 months to 10 years (mean: 51 months) were admitted from January 1987 to 15 December 1993 because they suffered mainly from fever, lumbar pain and/or homolateral flexed hip. Examination showed a painful inguinal mass in five patients and hyperleucocytosis in all. X-rays showed disappearance of the external limit of psoas in two patients; ultrasonography showed enlarged psoas in all, associated with hypoechogenic mass in two and without echo in four patients. CT scan showed the abscess in all cases, permitting a needle aspiration for bacteriological studies: Staphycococcus aureus was present in five cases. Drainage of the abscess by CT-guided percutaneous catheter was performed in two patients. Surgical drainage was performed in three including one for whom percutaneous catheter drainage did not succeed. The two other patients were only given antibiotics. CONCLUSION: CT-guided needle aspiration to establish presence and nature of fluid collection is a well established technique that may be extended to treatment of psoas abscesses.

Child↗

[Thoraco-abdominal digestive duplication].

The authors report a case of a thoraco-abdominal duplication of the foregut, observed in a 10-year old boy. Thoraco-abdominal duplication is an expression of notochordodysraphia, as it is frequently associated with vertebral malformations. Barium meal, ultrasonography and CT-Scan should provide a preoperative diagnosis. One-stage total excision in a single stage is mandatory in order to treat the symptoms and avoid the risks of further progression.

Cardia↗

[Neonatal testicular ischemic necrosis without torsion, associated with antithrombin III deficit].

There have been few reports of neonatal ischemic necrosis of the testis without torsion of the spermatic cord, which may be caused either by compression in utero or by transient torsion of the spermatic cord resolving spontaneously before surgery. The patient reported herein developed an inflammatory swelling of the right scrotum and an ecchymotic plaque over the left thigh at four days of age. Ischemic necrosis of the right testis without torsion was found upon surgery. When the patient was ten days of age, he developed an inflammatory swelling in the left scrotum; ischemic necrosis of the left testis without torsion was again found upon surgery. Thrombosis of the spermatic vessels was suspected. Postoperatively, ecchymotic and necrotic skin lesions developed, followed by pulmonary embolism and cerebral thrombosis. Outcome was fatal. Hematologic tests in the neonate and his parents established the diagnosis of inherited antithrombin III deficiency. Ischemic necrosis of the testes was thus probably due to hypercoagulability. No similar cases have been reported to date.

Antithrombin III Deficiency↗

[Abdominal cystic lymphangioma in children].

Cystic lymphangioma is a rare tumour (6% of benign tumours in children), frequently situated in the cervical or axillary region and exceptionally intraabdominal. It arises due to a congenital defect in the connection of the primary lymphatic channels with the central collecting system. It presents clinically either in the form of a pseudo-appendix or pseudo-ascites syndrome or in the form of an abdominal tumour with or without compression of adjacent structures. It can now be easily diagnosed by ultrasonography. Treatment is well defined and consists of surgical resection of the isolated lymphangioma or associated with the adjacent intestine, depending on the site of the tumour. It has a good prognosis.

Abdominal Neoplasms↗

Partial splenectomy in sickle cell syndromes.

Partial splenectomy was carried out in four children with homozygous sickle cell disease and eight children with sickle cell beta thalassaemia. It was performed in order to preserve splenic contribution to the host defence against infections while suppressing hypersplenism or the risk of recurrence of acute splenic sequestration. Indications for this surgical operation were acute splenic sequestration (n = 1), hypersplenism (n = 5), and acute splenic sequestration and hypersplenism (n = 6). Surgery was uneventful in 11 patients. A significant reduction of blood requirements and a significant decrease of the number of hospitalisations/patient/year were observed after splenectomy. No recurrence of hypersplenism or acute splenic sequestration occurred and no severe infection was noticed during the follow up period after surgery (mean (SD) 4.2 (2.8) years; range 6 months-7 years). Mean haemoglobin concentration and leucocyte and platelet counts increased after surgery. The benefit of partial splenectomy compared with total splenectomy to treat acute splenic sequestration or hypersplenism in sickle cell disease is discussed.

Child↗

[A case of esophageal duplication discovered in a newborn].

A case of esophageal duplication discovered in the neonatal period is reported and discussed. This infrequent malformation (9% of all childhood mediastinal tumors) is an entoblastic duplication of the digestive tract and is often accompanied with spinal malformations. The duplication may be either cystic or tubular; the latter form usually opens into the normal esophagus. The most common clinical manifestations are respiratory symptoms caused by compression. The diagnosis, suggested by the findings on the plain chest film and osephageal opacification, is confirmed by the ultrasound examination and, above all, the CT scan. The treatment of this malformation is surgical. Reconstruction may be difficult but overall results and prognosis are excellent.

Abnormalities, Multiple↗