Biomedical subjects

S Byahatti

Publications and source records attributed to S Byahatti.

4 recordsLinked to original sources

PubMed1999

New aspects in the histopathology of the cochlear aqueduct in children.

OBJECTIVE: To study the histoanatomy and pattern of growth of the cochlear aqueduct in children of different ages. BACKGROUND: Since Du Verney described the cochlear aqueduct in 1684, its form, pattern of growth, patency, and function have been controversial. As most of the previous studies of the aqueduct were performed on adults, none had looked at its pattern of growth from the neonate to 9 years of age. In addition, previous histologic studies had suggested an age-dependent patency, but recent investigations had not statistically correlated patency with age. METHOD: Histologic sections of 137 temporal bones from 79 infants and children were studied by light microscopy. From this group, we selected 32 temporal bones from 18 infants, newborn to 9 years (average age 9.1 months, median 0.5 months), in whom the entire length of the cochlear aqueduct was visible on one histologic section. We measured the width of the orifices at the scala tympani (external aperture) and the subarachnoid space (internal aperture) and the length of the aqueduct, and noted the contents of the lumen. RESULTS: The measurements of the cochlear aqueduct were: length 4.19 mm (range 1.7-10.7 mm), width of the external aperture 435 microm (range 225-869 microm), width of the internal aperture 1,323 microm (range 699-2344 microm), mean diameter of the narrowest part (isthmus) 138 microm (range 68-244 microm), intraluminal mononucleated cells 6%, and erythrocytes 15%. CONCLUSIONS: Our findings demonstrate that, in the newborn, the cochlear aqueduct is short and patent. After birth, the duct lengthens significantly primarily by growth of the medial periosteal portion. There was no statistically significant change in the diameter of the external and internal apertures and the isthmus with age. With one exception, the cochlear aqueduct was always present and patent.

Adult↗

PubMed1998

Inactivation of p53 and amplification of cyclin D1 correlate with clinical outcome in head and neck cancer.

The authors have investigated whether genetic abnormalities in two genes, loss of heterozygosity (LOH) of p53 and amplification of the cyclin D1 gene, correlate with clinical outcome in 56 matched pairs of blood and tumor from patients with squamous cell carcinoma of the head and neck (SCCHN). Frequency of p53 LOH was 47.4%, of cyclin D1 amplification 33.9%, and of both abnormalities together 23.7%. p53 LOH was associated with T4 (P = 0.003) and stage IV (P = 0.015) tumors. Cyclin D1 amplification was associated with recurrences and/or metachronous tumors (P = 0.007). The total number of p53 and cyclin D1 abnormalities (scored as zero, one, and two) show a pattern that seems to be additive; the increase in the number of these abnormalities is associated with a proportional increase in the frequency of T4, stage IV, presence of recurrences and/or metachronous tumors, and possibly a proportional decrease in the disease-free interval in the sample. The association of the markers with recurrences and/or metachronous tumors persists if the tumor stage effect is mathematically removed. The combined analysis of the p53 and cyclin D1 abnormalities seems to be more informative than either of them individually and may have predictive value in SCCHN.

Carcinoma, Squamous Cell↗

PubMed1997

The cochlear aqueduct in pediatric temporal bones.

The cochlear aqueduct is a bony channel which contains the fibrous periotic duct and connects the perilymphatic space of the basal turn of the cochlea with the subarachnoid space of the posterior cranial cavity. Previous histological studies suggested that patency depended on age, whereas a more recent study showed no statistical correlation between age and patency. To clarify patency in pediatric cochlear aqueducts, we selected 21 temporal bones from 12 infants and children, varying in age from birth to 9 years, in which the cochlear aqueduct was fully visible on one histological section. Photographs were taken for documentation and the length and width of the orifice of the external aperture of the aqueduct at the scala tympani were measured and followed to the internal aperture at the subarachnoid space. The lumen of the duct was examined for mononucleated cells, blood cells and fibrous tissue. Measurements revealed that the mean length of the cochlear aqueduct was 4.6 mm (range, 2.4-10.7 mm), mean width of the external aperture was 484 microm (range, 225-869 microm), and mean width of the internal aperture was 1293 microm (range, 699-2344 microm). The mean diameter of the narrowest part (isthmus) was 151 microm (range, 75-244 microm). In all temporal bones the cochlear aqueduct was patent, with one exception. This latter temporal bone was from a 2-month-old girl with multiple intralabyrinthine anomalies, with the missing cochlear aqueduct believed to be due to an aplasia. Our results support prior measurements of the cochlear aqueduct and demonstrate a short and patent cochlear aqueduct in newborns. With growth, a significant increasing length of the duct was found.

Aging↗

PubMed1990

Base changes at position 792 of Escherichia coli 16S rRNA affect assembly of 70S ribosomes.

To investigate the function of base 792 of 16S rRNA in 30S ribosomes of Escherichia coli, the wild-type (adenine) residue was changed to guanine, cytosine, or uracil by oligonucleotide-directed mutagenesis. Each base change conferred a unique phenotype on the cells. Cells containing plasmid pKK3535 with G792 or T792 showed no difference in generation time in LB broth containing ampicillin, whereas cells with C792 exhibited a 20% increase in generation time in this medium. To study the effect on cell growth of a homogeneous population of mutant ribosomes, the mutations were cloned into the 16S rRNA gene on pKK3535 carrying a spectinomycin-resistance marker (thymine at position 1192), and the cells were grown with spectinomycin. Cells containing G792 or C792 showed 16% and 56% increases in generation time, respectively, and a concomitant decrease in 35S assimilation into proteins. Cells with T792 did not grow in spectinomycin-containing medium. Maxicell analyses indicated decreasing ability to form 70S ribosomes from 30S subunits containing guanine, cytosine, or uracil at position 792 in 16S rRNA. It appeared that C792-containing 30S ribosomes had lost the ability to bind initiation factor 3.

Base Sequence↗