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A Fuertes

Publications and source records attributed to A Fuertes.

At least 19 recordsLinked to original sources
PubMed1999

Hepatitis C virus-related fibrosing cholestatic hepatitis after cardiac transplantation: is azathioprine a contributory factor?

We report a patient who acquired hepatitis C virus (HCV) infection at cardiac transplantation, developing fibrosing cholestatic hepatitis (FCH) with early liver failure and a fatal outcome. FCH is a recently described clinicopathological entity characterized by a cholestatic pattern of serum liver enzyme abnormalities, a progressive course leading to liver failure, and a pathological picture defined by periportal fibrosis, neutrophilic infiltrates and signs of histological cholestasis. Although it was initially described secondary to hepatitis B virus infection, it has also been recently related to HCV infection. Some histopathological features consistent with azathioprine hepatotoxicity like cholestasis, perisinusoidal fibrosis, veno-subocclusive lesions and nodular regenerative hyperplasia were also observed in this case. Therefore, a direct cytopathic effect of HCV and the concurrent pathogenic role of azathioprine hepatotoxicity may be involved in the development of this complication of transplantation.

Azathioprine↗
PubMed1999

Function search in a large transcription factor gene family in Arabidopsis: assessing the potential of reverse genetics to identify insertional mutations in R2R3 MYB genes.

More than 92 genes encoding MYB transcription factors of the R2R3 class have been described in Arabidopsis. The functions of a few members of this large gene family have been described, indicating important roles for R2R3 MYB transcription factors in the regulation of secondary metabolism, cell shape, and disease resistance, and in responses to growth regulators and stresses. For the majority of the genes in this family, however, little functional information is available. As the first step to characterizing these genes functionally, the sequences of >90 family members, and the map positions and expression profiles of >60 members, have been determined previously. An important second step in the functional analysis of the MYB family, through a process of reverse genetics that entails the isolation of insertion mutants, is described here. For this purpose, a variety of gene disruption resources has been used, including T-DNA-insertion populations and three distinct populations that harbor transposon insertions. We report the isolation of 47 insertions into 36 distinct MYB genes by screening a total of 73 genes. These defined insertion lines will provide the foundation for subsequent detailed functional analyses for the assignment of specific functions to individual members of the R2R3 MYB gene family.

Arabidopsis↗
PubMed1998

More than 80R2R3-MYB regulatory genes in the genome of Arabidopsis thaliana.

Transcription factors belonging to the R2R3-MYB family contain the related helix-turn-helix repeats R2 and R3. The authors isolated partial cDNA and/or genomic clones of 78 R2R3-MYB genes from Arabidopsis thaliana and found accessions corresponding to 31 Arabidopsis genes of this class in databanks, seven of which were not represented in the authors' collection. Therefore, there are at least 85, and probably more than 100, R2R3-MYB genes present in the Arabidopsis thaliana genome, representing the largest regulatory gene family currently known in plants. In contrast, no more than three R2R3-MYB genes have been reported in any organism from other phyla. DNA-binding studies showed that there are differences but also frequent overlaps in binding specificity among plant R2R3-MYB proteins, in line with the distinct but often related functions that are beginning to be recognized for these proteins. This large-sized gene family may contribute to the regulatory flexibility underlying the developmental and metabolic plasticity displayed by plants.

Amino Acid Sequence↗
PubMed1998

Clinical, virological, and histologic evolution of hepatitis C virus infection in liver transplant recipients.

We designed a prospective study to assess the time course and evolution of hepatitis C virus (HCV) infection in 152 patients who underwent a liver transplantation (LT) in our institution. Forty-four recipients (29%) were infected by HCV after transplantation: 40 who developed recurrent infection after LT and four who acquired infection during or after LT. No differences were found in survival actuarial rates at 1, 2, and 4 years after transplantation for patients infected by HCV vs. noninfected ones. Graft hepatitis occurred in 66% of HCV-infected recipients: 18 developed chronic active hepatitis (10 of them with intense fibrosis) and 2 developed cirrhosis during the follow-up. Infection by the HCV-1b genotype was found in 79% of the infected recipients and in 100% of those in whom histologic evolution was worst. Fourteen grafts were lost in 44 HCV-infected recipients, in comparison with 12 in 108 HCV-negative patients (P = .007), mostly because of chronic rejection. HCV infection did not affect life expectancy in the midterm follow-up for LT patients. However, it was often associated with the occurrence of early and severe graft hepatitis and with a higher incidence of graft loss due to chronic rejection.

Adult↗
PubMed1998

Fibrosing cholestatic hepatitis in hepatitis C virus-infected renal transplant recipients.

Severe hepatitis C virus (HCV)-related fibrosing cholestatic hepatitis leading to early liver failure has been reported only exceptionally. Of 259 HCV-infected renal transplant (RT) patients in one hospital unit, four (1.5%) are described, representing the first series of this particular post-RT disease. Patient mean age was 55.7 yr. Three were men. All had pretransplant, hepatitis B surface antigen-negative and were anti-HCV antibodies positive. Three of them showed pretransplant mild liver enzyme abnormalities, and all received kidneys from HCV-negative donors. All were on steroids, cyclosporine, and azathioprine (AZA). The clinical pattern appeared early after RT (mean, 11.5 mo). In three patients, hyperbilirubinemia (6.5 to 20 mg/dl) and high alkaline phosphatase levels (428 to 859 IU/L) were observed. Also, in all subjects, high gamma glutamyl transpeptidase levels (639 to 4270 IU/L), mild aspartate aminotransferase and alanine aminotransferase abnormalities, and serum HCV RNA were observed. Liver biopsy revealed diffuse fibrosis, leukocyte infiltrates, and different degrees of cholestasis, with typical signs of HCV hepatitis in only one patient. Two patients developed subfulminant liver failure and died 2 and 3 mo after biopsy, respectively. One patient also suffered hepatic failure, receiving a liver transplant. The fourth is alive on dialysis awaiting a combined kidney and liver transplant. It is concluded that fibrosing cholestatic hepatitis is a new, early, and severe complication after RT in HCV(+) patients, which appears in patients with ongoing HCV infection under AZA therapy, despite a nonaggressive immunosuppressive protocol. Both HCV and AZA could play a concurrent role in the pathogenesis of this severe complication after RT.

Adult↗
PubMed1997

Membranous glomerulonephritis associated with hepatitis C virus infection in renal transplant patients.

BACKGROUND: Hepatitis C virus (HCV) infection has been described in association with various types of glomerular diseases, usually type I membranoproliferative glomerulonephritis and rarely membranous glomerulonephritis (MGN). In this article, we describe the first series of MGN exhibited in renal transplant patients and associated with HCV infection. METHODS: From January 1980 to December 1994, 2045 kidney transplantations were performed in our renal transplant units. A retrospective analysis demonstrated an overall 20% prevalence of HCV virus-positive patients; 409 transplanted patients were HCV positive (ELISA and RIBA). RESULTS: Fifteen patients developed an allograft MGN (3.66%) 24 months after renal transplantation. MGN appeared in the form of significant proteinuria (>1.5 g/24 h) with stable renal function. In all cases, graft biopsy demonstrated a thickening of the capillary wall, subepithelial electron-dense deposits, and IgG and C3 diffuse granular deposits along the basal membrane. Ten cases were considered de novo, two cases were considered recurrent MGN, and three cases were considered undetermined because the primary renal disease was chronic glomerulonephritis. All patients showed negative antinuclear antibodies and cryoglobulins, normal complement, and negative rheumatoid factors. During follow-up (an average of 2 years), 12 patients developed a progressive worsening of renal function, with increased serum creatinine and persistent proteinuria; 8 of the 12 patients returned to dialysis. Of the remaining three cases, two patients showed partial remission of nephrotic syndrome after high doses of steroids, and one patient persisted with stable renal function and proteinuria (<2 g/24 h.). CONCLUSIONS: In summary, HCV is preferentially associated with MGN in renal transplant patients, rather than with membranoproliferative glomerulonephritis as in the normal adult population. MGN associated with HCV infection has a similar clinical picture and outcome to posttransplant idiopathic de novo MGN, with persistent massive proteinuria and progressive deterioration of renal function.

Adult↗
PubMed1997

A single residue substitution causes a switch from the dual DNA binding specificity of plant transcription factor MYB.Ph3 to the animal c-MYB specificity.

Transcription factor MYB.Ph3 from Petunia binds to two types of sequences, MBSI and MBSII, whereas murine c-MYB only binds to MBSI, and Am305 from Antirrhinum only binds to MBSII. DNA binding studies with hybrids of these proteins pointed to the N-terminal repeat (R2) as the most involved in determining binding to MBSI and/or MBSII, although some influence of the C-terminal repeat (R3) was also evident. Furthermore, a single residue substitution (Leu71 --> Glu) in MYB.Ph3 changed its specificity to that of c-MYB, and c-MYB with the reciprocal substitution (Glu132 --> Leu) essentially gained the MYB.Ph3 specificity. Molecular modeling and DNA binding studies with site-specific MYB.Ph3 mutants strongly supported the notion that the drastic changes in DNA binding specificity caused by the Leu --> Glu substitution reflect the fact that certain residues influence this property both directly, through base contacts, and indirectly, through interactions with other base-contacting residues, and that a single residue may establish alternative base contacts in different targets. Additionally, differential effects of mutations at non-base-contacting residues in MYB.Ph3 and c-MYB were observed, reflecting the importance of protein context on DNA binding properties of MYB proteins.

Amino Acid Sequence↗
PubMed1997

Influence of viral genotype and level of viremia on the severity of liver injury and the response to interferon therapy in Spanish patients with chronic C infection.

BACKGROUND: We wanted to investigate the influence of viral genotype on the severity of liver injury and response to interferon and whether the level of viremia differs in accordance with genotype, severity of liver disease, and response to interferon in patients with hepatitis C virus (HCV) infection. METHODS: We studied 118 patients with HCV-related liver disease. HCV genotypes were determined with a line probe assay, and serum HCV RNA levels with a competitive reverse transcription polymerase chain reaction assay. RESULTS: HCV type 1b was the most prevalent genotype (88%). It was present in 100% of cirrhotic patients, with or without hepatocellular carcinoma (HCC), but only in 78% of patients with chronic hepatitis (P < 0.001). The response to interferon was better in patients infected with non-1b HCV genotypes (P = 0.002). In a multivariate analysis non-1b HCV genotypes and a low hepatic fibrosis correlated with a favorable response to interferon. Among patients with chronic hepatitis those infected with HCV type 1b were older (P < 0.001), and age was the only independent factor associated with HCV type 1b. Viremia levels differed neither between genotypes nor in response to interferon and was significantly lower in patients with cirrhosis and HCC. CONCLUSIONS: HCV 1b was associated with more severe liver disease and a worse response to interferon therapy. Non-1b genotypes and a lower liver fibrosis were the only independent predictors of a favorable response to interferon. Levels of HCV viremia differed neither among different genotypes nor in response to interferon and decreased with advanced liver disease.

Aged↗
PubMed1995

[Prevalence and sequelae of childhood sexual abuse in Spain].

The aim of this research was to determine the prevalence of sexual abuse in Spain and its long and short effects. A representative sample of Spanish society was studied (N = 1.821) through proportional stratified random sampling. Data were obtained by interview (Personal History of Sexual Abuse), carried out in the subjects home and by means of a Self Reporting Questionnaire (S.R.Q.), which the interviewer gave the subject to be returned by post. The results show a high prevalence of sexual abuse prior to age 17 (15% of males and 22% of females) with short-term effects (lack of trust, disgust, fear, hostility towards the aggressor, shame, anxiety, etc.) and in long-term a greater tendency towards mental health problems (F = 7.7; p < .01), as well as other problems throughout the life cycle (running away from home, school failure, sexual dissatisfaction, drug-taking, etc.). The high prevalence and the clear long and short effect make prevention programs and help for the victims advisable.

Acting Out↗