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Biomedical subjects

R Bova

Publications and source records attributed to R Bova.

At least 19 recordsLinked to original sources
PubMed2006

Modulation of BDNF and TrkB expression in rat hippocampus in response to acute neurotoxicity by diethyldithiocarbamate.

In this study, we examined the expression profile of brain-derived neurotrophic factor (BDNF) and its receptor TrkB in adult rat hippocampus following acute administration of diethyldithiocarbamate (DDTC), a neurotoxic compound which was previously shown to induce microglia activation and cell death. Semiquantitative RT-PCR analysis detected significant variations of BDNF mRNA levels in whole hippocampus homogenates, with a peak at 24h after DDTC injection. Increased BDNF protein expression was demonstrated by immunohistochemistry in various hippocampal subfields. The most relevant increase was observed in the hilus of the dentate gyrus where BDNF levels at 120h were found to be almost four times those of basal levels. Full-length TrkB (TrkB.FL) encoding mRNA was also shown to undergo an earlier increase in the hippocampus of DDTC-treated rats. TrkB immunostaining with an antibody binding both full-length and truncated (TrkB.T) isoforms was found to increase at 120h in the hippocampal CA2 and CA3 regions. These results demonstrate that DDTC modulates the expression of BDNF and its receptor in the adult rat hippocampus and suggest a possible involvement of this neurotrophin in the protective response to DDTC-induced neuronal damage.

Animals↗
PubMed1998

BDNF and trkB mRNAs oscillate in rat brain during the light-dark cycle.

In this study, we investigated whether in basal conditions the different functional states occurring during a 24-h cycle are reflected by the expression of brain-derived neurotrophic factor (BDNF) and its receptor, trkB, in rat cerebral cortex and hippocampus. Using semiquantitative RT-PCR assay, the levels of both BDNF and trkB mRNAs were found to undergo significant variation in a 24-h period. The strongest variation was detected in the hippocampus, where the ratio between maximum and minimum levels was about 3.5 and 17.5 for BDNF and trkB, respectively. These findings provide the first evidence that, in the absence of any experimental manipulation, the expression of a neurotrophin and its receptor undergoes diurnal oscillation, possibly related to the physiological variations of the activity level.

Animals↗
PubMed1998

Appendicitis in HIV-positive patients.

BACKGROUND: The aim of the present study was to review the experience of appendicitis in human immunodeficiency virus (HIV)-positive patients. METHODS: A retrospective analysis of all HIV-positive patients operated on for suspected acute appendicitis during a 10-year period at St Vincent's Hospital was performed. These patients were compared to a group of 60 age- and sex-matched patients with no HIV risk factors who were operated on during the same time period. RESULTS: On presentation the clinical findings were similar in both groups, with two notable exceptions. No HIV-positive patient had an elevated white cell count. The present study demonstrated a significant delay in presentation of the HIV-positive group to the Emergency Department, possibly explaining the higher appendiceal perforation rate in this group. There were no cases of HIV-related diseases mimicking acute appendicitis. There was no mortality, and morbidity was higher in the seropositive group. CONCLUSIONS: HIV-positive patients with a history suggestive of acute appendicitis should not be treated differently from the normal population. Morbidity and mortality can be minimized by prompt surgical treatment.

Acute Disease↗
PubMed1997

Partial 9p monosomy in a girl with a tdic(9p23;13p11) translocation, minor anomalies, obesity, and mental retardation.

We report on a case with a partial monosomy for the regions 9p23 --> pter and 13p11 --> pter as a result of a de novo translocation (9p23;13p11). The patient, a 16-year-old girl, has mental deficiency, obesity, and minor anomalies, including trigonocephaly, hypertelorism and a short, broad neck. Cytogenetic and microsatellite marker analysis allowed us to assign the breakpoint to the chromosomal region 9p23, flanked by the markers D9S144 and D9S157. In an attempt to establish a phenotype-genotype correlation, the clinical manifestations present in our patient are compared to those with partial 9p monosomy and breakpoint in p23, referred to in the literature.

Abnormalities, Multiple↗
PubMed1996

From Pitt-Rogers-Danks syndrome to Wolf-Hirschhorn syndrome and back?

Apparently normal chromosomes without a molecular 4p16.3 deletion were found in a patient with a Wolf-Hirschhorn syndrome (WHS) phenotype. During a 10-year-period of observation he consistently presented with typical facial appearance, moderate to severe mental retardation, normal physical development with normal head circumference. Genetic results and the relatively mild clinical manifestations suggest that a diagnosis of Pitt-Rogers-Danks syndrome (PRDS) may be more likely in this patient. If WHS and PRDS will ultimately prove to be caused by haploinsufficiency of the same gene in 4p16, non-deleted patients such as the present one will be good candidates for the search of point mutations in such putative gene.

Abnormalities, Multiple↗
PubMed1995

Bacteriophage T4 gene 28.

The complete nucleotide sequence of bacteriophage T4D gene 28 has been determined. Gene 28 product is a structural component of the viral baseplate for which an enzymatic activity has also been proposed.

Amino Acid Sequence↗
PubMed1991

Molecular biology of hepatocellular carcinoma and hepatitis B virus association.

The involvement of the hepatitis B virus in the pathogenesis of hepatocellular carcinoma was initially suggested on the basis of epidemiological studies. In recent years several kinds of experimental evidence have supported this hypothesis; however, the role played by hepatitis B virus in hepatocarcinogenesis still needs to be elucidated. Several groups of researchers are presently involved in establishing whether hepatitis B virus makes a specific genetic contribution to carcinogenesis or predisposes to neoplastic transformation by causing chronic inflammation and cell regeneration. A comprehensive examination of the data available in the literature suggests that the two hypotheses may not be mutually exclusive.

Animals↗
PubMed1990

Molecular study of parental origin of extra chromosome 21 in regular and de novo translocation trisomies.

The parental origin of the extra chromosome 21 (or extra 21q) was determined in seven informative families with a Down syndrome (DS) child by using molecular polymorphisms. Five DS patients had regular trisomy, one a de novo 14/21 translocation and another a de novo 21/21 translocation or isochromosome 21q. In four families with regular trisomy, the extra chromosome was of maternal origin, and in one family it was paternally derived. In the two families with a de novo aberration, both the 14/21 translocation and 21/21 rearrangement originated during maternal meiosis. For a better evaluation of the stage of meiotic error and the occurrence of crossovers between nondisjoined chromosomes, the regional map position of four of the nine informative DNA markers, used in this study, was refined, leading to useful localizations in both centromeric and distal regions. Recombination events were found in two families with regular trisomy, one occurring between chromosomes 21 that failed to disjoin at maternal meiosis I, the other prior to a paternal meiosis II nondisjunction.

Blotting, Southern↗
PubMed1990

Pericentric inversion of chromosome 9: prevalence in 300 Down syndrome families and molecular studies of nondisjunction.

The incidence of Down syndrome (DS) families where one of the parents is an heterozygous carrier of pericentric inversion of the heterochromatic region of chromosome 9-inv(9) (qh) - was determined in 3 independent groups of 100 families each. The total number of 17 such families found in the sample is significantly greater than the expected number of 5.73 for a sample of non-DS families of equal size. Consequently, the statistical association of the presence of inv (9) (qh) in one parent with the birth of a DS offspring, and the correlative 3-fold increased risk of a DS child for such families, seem to be demonstrated. A study of the origin of nondisjunction, using restriction fragment length polymorphism (RFLP) segregation analysis with a sufficient number of chromosome 21 specific probes, has provided complete information in 7 of 8 available families. Although the statistical interpretation of the results is not straightforward, due to the small size of the sample, the observed data do not contradict the assumption that the presence of inv (9) (qh) in a parent increases, by a factor of about 3, the chance that the offspring will inherit an extra chromosome 21 from that parent. Nevertheless, gathering further data appears desirable because stronger evidence would have relevance both for clinical implications and for the understanding of the function of heterochromatin, particularly with respect to meiotic and mitotic processes.

Chromosome Inversion↗
PubMed1990

Acrocentric chromosome double NOR is not a risk factor for Down syndrome.

Jackson-Cook et al. (American Journal of Human Genetics 37:1049-1061, 1985) predicted a high risk of Down syndrome (DS) children for parents carrying a double NOR on acrocentric chromosomes. Hassold et al. (Human Genetics 76:381-384, 1987) could not confirm Jackson-Cook et al.'s findings, thus casting doubts on their conclusions. We studied the NORs of 1) 60 parents of 30 unselected DS subjects; 2) 30 unselected healthy subjects without trisomic offspring, who asked for chromosome analysis; and 3) 100 slides randomly chosen among 1,000 prepared by routine standard techniques and belonging to subjects who were chromosomally normal. By applying rigorously established techniques and scoring criteria we found 4 subjects (6.7%) with strictly defined double NORs (dNORs) in the DS parents sample, 2 subjects (6.7%) in the first control sample, and 3 (3%) in the second control sample. No significant difference among the observed frequencies of dNORs in the 3 samples could be demonstrated. Therefore, our data do not support Jackson-Cook et al.'s statements on the association of dNOR carrier status with DS offspring and on a highly increased risk of meiotic nondisjunction of chromosome 21 for a dNOR carrier parent. A tentative interpretation of the apparently contrasting cytogenetic findings would indicate that sampling and assignment biases are the main causes of this discrepancy.

Case-Control Studies↗
PubMed1988

Symmetric transcription of bacteriophage T4 base plate genes.

Dot-blot and Northern-blot experiments, using strand-specific RNA probes, show that part of the bacteriophage T4 DNA that codes for six of the base plate structural genes (gp 51, 27, 28, 29, 48 and 54), is transcribed in vivo from both DNA strands. The r DNA strand transcripts contain sequences which are translated into structural proteins. Antisense l strand RNA is about 100 fold less abundant than RNA molecules transcribed from the r DNA strand.

Blotting, Northern↗
PubMed1988

Purification of T47D human progesterone receptor and immunochemical characterization with monoclonal antibodies.

In order to obtain steroid-independent probes for human progesterone receptor (PR), the A [88-93 kilodalton (kDa)] and B (109-119 kDa) forms of PR from T47D human breast cancer cells were partially purified and used to generate a series of 14 monoclonal antibodies. Initially, unoccupied PR was isolated from cytosol extracts by steroid affinity chromatography, followed by chromatography on diethylaminoethyl Bio-Gel. The partially pure (3-15%) PR consisted of two steroid-binding components that migrated at 89 kDa and 109 kDa in reducing sodium dodecyl sulfate gels after being photoaffinity labeled with the synthetic progestin [3H]R5020. Two unique monoclonal antibodies to PR were derived from a male Lewis rat immunized with this material. One of these antibodies (JU601) was coupled to Sepharose 4B and used to purify T47D nuclear PR for additional immunizations. Highly purified (30-70%) PR migrated as 93 kDa and 119 kDa progestin-binding proteins in sodium dodecyl sulfate gels. In all, thirteen monoclonal antibodies were obtained that recognized epitopes shared by both receptor forms. One mouse immunoglobulin G (KC146) was completely specific for the larger B form. Interestingly, the epitope for this antibody was present on all PRs tested, including the B form of PR from chicken oviduct, whereas nine other antibodies recognized only human PR and the remaining four cross reacted with rabbit PR. With the exception of the JU145 and JU601 rat immunoglobulin Ms, all antibodies appeared to be completely specific for the A or B forms of PR. Each recognized the cytosol and nuclear forms of occupied as well as unoccupied PR. Although the relationship between B and A was not established, it is clear that an amino-terminal region of B is not present in A, and that a significant portion of A and B are either identical or very similar in amino acid sequence.

Antibodies, Monoclonal↗
PubMed1984

Estradiol and progesterone receptors in malignant gastrointestinal tumors.

Estradiol and progesterone receptors were assayed in tumors from 79 patients with primary colorectal and 56 patients with stomach adenocarcinomas. Eighteen of 79 colorectal cancers contained estradiol receptor, while 34 specimens were positive for progesterone receptor. In stomach cancer, the positive samples were 8 for estradiol and 14 for progesterone receptors. In both types of tumors, the Kd was in the range of 10(-10) M for estradiol and 10(-9) M for progesterone receptor, respectively. In colorectal adenocarcinomas, the presence of progesterone receptor seems to be partially correlated to the presence of estradiol receptor while, in stomach tumors, this correlation is lost. The positivity of at least one receptor in colorectal cancers is higher in the female sex. The contrary occurs for stomach cancer. Sucrose gradient centrifugation showed that cytoplasmic estradiol receptor of stomach cancer sedimented at 8S or 4 to 5S at low ionic strength. The isoelectric point of stomach cancer estradiol receptor is 6.5.

Adenocarcinoma↗