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Biomedical subjects

K Rao

Publications and source records attributed to K Rao.

At least 109 records · Page 6Linked to original sources
PubMed1989

Primary carcinoma of vagina with uterine prolapse.

Eleven cases of primary carcinoma of vagina were admitted in Kasturba Medical College Hospital during the last 10 years, of which 6 cases aged 44-72 years, were associated with 3rd degree uterine prolapse. All the patients attended the hospital in late stage in spite of having 3rd degree uterine prolapse. Blood stained discharge and ulceration on the prolapsed part, irreducible prolapse with urinary retention and marked oedema of local and surrounding tissues were the presenting symptoms. Lesion on the vagina varied in size from 5 cm to 15 cm. IVP in both the cases of irreducible prolapse and retention of urine revealed hydroureter and hydronephrosis bilaterally. X-ray chest revealed secondaries in one patient only. Histopathology of vaginal biopsy revealed well differentiated squamous cell carcinoma in 5 cases and undifferentiated squamous cell carcinoma in one. Since the patients were in late stage of malignancy and were inoperable, treatment with external telecobalt therapy was undertaken. One patient developed vesicovaginal fistula during the treatment period and another patient developed it at the end of telecobalt therapy.

Adult↗
PubMed1989

Platelet transfusion therapy in thrombocytopaenia of haematologic malignancies.

Thirty thrombocytopaenic patients of acute leukaemias and myelodysplastic syndrome were transfused platelets collected from ABO-matched donors using Haemonetics V30 and V50 blood processors. Twenty-seven patients had septicaemia and/or splenomegaly; 2 patients had disseminated intravascular coagulation (DIC). Pre-transfusion platelet count was 11.0 +/- 4.0 X 10(9)/L. The mean corrected count increments (CCI) 1 hour and 18 hours post-transfusion were 13.02 X 10(9)/L and 3.88 X 10(9)/L respectively, in the absence of DIC. Active bleeding stopped when platelet count was above 15.0 X 10(9)/L. There was no difference between the platelet yield from two blood processors.

Acute Disease↗
PubMed1988

Two genetic loci participate in the regulation by iron of the gene for the human transferrin receptor.

Iron regulation of the human transferrin receptor gene was examined in murine cells transformed with chimeric constructs containing the human transferrin receptor gene's promoter and either the structural gene for bacterial chloramphenicol acetyltransferase or the human transferrin receptor cDNA. The activity of the transferrin receptor gene's promoter with the heterologous indicator gene was found to be approximately equal to 3-fold higher in cells treated with the iron chelator desferrioxamine than in cells treated with the iron source, hemin. A higher degree of iron regulation was seen in the expression of the human transferrin receptor cDNA driven by its own promoter. The receptor cDNA under the control of the simian virus 40 early promoter was also iron-regulated. Several human transferrin receptor transcripts differing in their 3' end were produced in the murine cells regardless of the promoter used, with the shorter transcripts being relatively unregulated by iron. Deletion of cDNA corresponding to most of the 3' untranslated portion of the mRNA for the receptor ablated the iron regulation. We conclude that at least two genetic elements exist for the regulation of the transferrin receptor gene by iron. One has its locus in the DNA upstream of the transferrin receptor gene's transcription start site, and the other is dependent upon the integrity of the sequences in the 3' end of the gene.

Acetyltransferases↗
PubMed1988

Instability of neural xenografts placed in neonatal rat brains.

Embryonic mouse retinae placed in neonatal rat brains differentiate normally, form appropriate connections with the host brain, and may survive for longer than 1 year. However, such grafts are susceptible to rejection, either spontaneously or after challenge. Advanced spontaneous rejection of the transplant was identified in about 10% of the animals. In addition, two circumstances have been defined in which mouse retinal grafts can be subsequently induced to undergo rejection. One is following placement of a mouse skin graft on the flank of a rat that has received a retinal transplant in the brain, and the other is following removal of a host eye. After each of these procedures, the neural grafts become infiltrated with lymphocytes and undergo degeneration. It is proposed that this system may provide a useful approach not only for studying the immunology and genetics of neural transplantation, but also for examining the circumstances that precipitate the degenerative events associated with certain autoimmune diseases of the central nervous system.

Animals↗
PubMed1988

The promoter region of the human transferrin receptor gene.

Genomic DNA fragments corresponding to the promoter region of the human transferrin receptor were linked to either the full-length receptor cDNA or to the bacterial enzyme chloramphenicol acetyltransferase. These constructs were transfected into mouse and human cells, respectively. Gene expression was monitored 40-48 hours after transfection. Bal31 exonuclease was employed to produce 5' to 3' deletions of the promoter region. Deletion of DNA between -86 and -70 upstream of the receptor's mRNA start site resulted in a greater than 80% reduction in apparent promoter activity. DNA sequencing of the 150 bp upstream of the start site revealed that the promoter region contained several sequence elements more than 90% homologous to the consensus sequence for binding of the transcription factor Sp1. In addition, an 11 bp sequence identical to a segment of the enhancers of polyoma virus and adenovirus was located between -80 and -70. Internal deletions confirmed that this enhancer homologue was critical for full promoter activity. A 66 bp fragment encompassing the -80/-70 element augmented gene expression when the fragment was placed in either orientation upstream of the remainder of the transferrin receptor promoter.

Animals↗
PubMed1986

Vesical calculi associated with vesicovaginal fistulas: management considerations.

Vesical calculi were detected in 5 patients with a vesicovaginal fistula. Of these patients 3 had undergone unsuccessful repair of the fistula previously. The predisposing factors for vesical calculous formation in patients with a vesicovaginal fistula in whom urine leaks continuously into the vagina and urinary stasis does not occur in the bladder, as in patients with neurogenic bladder dysfunction or bladder outlet obstruction, are a foreign body (for example nonabsorbable suture material used during previous surgery), incrustation around an indwelling catheter and infection. The vesical calculus is removed transvaginally after enlarging the fistula by a vertical incision at the 6 o'clock position. The incised edges do not usually bleed because of fibrosis and scar formation, and they need not be approximated at that operation. Indwelling catheter drainage is not necessary after transvaginal cystolithotomy in this situation. This operation is preferable to suprapubic cystolithotomy, which may lead to more morbidity from urine leakage in the retropubic space and subsequent fibrosis, in addition to producing bladder scarring, hindering any future reconstructive surgery requiring the use of vesical flaps. Transvaginal cystolithotomy is contraindicated when the fistula is situated close to the bladder neck (for fear of damaging the bladder neck and the vesical continence mechanism) or when the stone is large. Repair of the fistula is undertaken after an interval of 3 months to allow for resolution of stone-induced edema and friability of the vesical wall.

Adult↗
PubMed1986

Exposure of K562 cells to anti-receptor monoclonal antibody OKT9 results in rapid redistribution and enhanced degradation of the transferrin receptor.

When the human erythroleukemia cell line K562 is treated with OKT9, a monoclonal antibody against the transferrin receptor, effects on receptor dynamics and degradation ensue. The apparent half-life of the receptor is decreased by greater than 50% as a result of OKT9 treatment. The transferrin receptor is also rapidly redistributed in response to OKT9 such that a lower percentage of the cellular receptors are displayed on the cell surface. OKT9 treatment also leads to a decrease in the total number of receptors participating in the transferrin cycle for cellular iron uptake. The reduction in iron uptake that results from the loss of receptors from the cycle leads to enhanced biosynthesis of the receptor. Receptors with bound OKT9 continue to participate in multiple cycles of iron uptake. However, OKT9 treatment appears to result in a relatively small increase per cycle in the departure of receptors from participation in iron uptake to a pathway leading to receptor degradation. Radiolabeled OKT9 is itself degraded by K562 cells and this degradation is inhibitable by leupeptin or chloroquine. In the presence of leupeptin, OKT9 treatment results in the enhanced intracellular accumulation of transferrin. Because the time involved in the transferrin cycle is shorter (12.5 min) than the normal half-life of the receptor (8 h), a small change in recycling efficiency caused by OKT9 treatment could account for the marked decrease in receptor half-life. In this paper the implications of these findings are discussed as they relate to systems in which receptor number is regulated by ligand.

Antibodies, Monoclonal↗
PubMed1986

Transcriptional regulation by iron of the gene for the transferrin receptor.

Treatment of K562 cells with desferrioxamine, a permeable iron chelator, led to an increase in the number of transferrin receptors. Increasing intracellular iron levels by treatment of cells with either human diferric transferrin or hemin lowered the level of the transferrin receptors. By using a cDNA clone of the human transferrin receptor, we showed that the changes in the levels of the receptor by iron were accompanied by alterations in the levels of the mRNA for the receptor. The rapidity of these changes indicated that the mRNA had a very short half-life. By using an in vitro transcriptional assay with isolated nuclei, we obtained evidence that this regulation occurred at the transcriptional level.

Cell Line↗
PubMed1986

Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells.

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

Cell Cycle↗
PubMed1986

Two-year longitudinal study of post-stroke mood disorders: comparison of acute-onset with delayed-onset depression.

Patients who developed post-stroke depression 3 to 24 months after hospital discharge (N = 21) were compared with patients who developed depression during hospitalization (N = 26) and patients who never developed depression over 24 months of follow-up (N = 15). During the acute hospitalization and at follow-up, the three groups were not significantly different in their demographic characteristics, neurological impairment, intellectual impairment, or quality of social support. The acute depression group, however, showed an increased correlation between impairment and depression from hospitalization to follow-up. Findings suggest that impairment does not produce depression, but, once depression occurs, it may interact with impairment to influence post-stroke recovery.

Acute Disease↗