Biomedical subjects
Publications and source records attributed to S Sen.
A 5-year-old girl presented with a large swelling measuring 50 x 35 mm in the left upper lid. The mass was firm to hard in consistency. Fine-needle aspiration showed a few spindle-shaped cells arranged in clusters. The mass was excised in toto and the histopathological examination revealed dermatofibroma, which is an extremely rare condition affecting the eyelid.
Numeric aberrations in chromosomes, referred to as aneuploidy, is commonly observed in human cancer. Whether aneuploidy is a cause or consequence of cancer has long been debated. Three lines of evidence now make a compelling case for aneuploidy being a discrete chromosome mutation event that contributes to malignant transformation and progression process. First, precise assay of chromosome aneuploidy in several primary tumors with in situ hybridization and comparative genomic hybridization techniques have revealed that specific chromosome aneusomies correlate with distinct tumor phenotypes. Second, aneuploid tumor cell lines and in vitro transformed rodent cells have been reported to display an elevated rate of chromosome instability, thereby indicating that aneuploidy is a dynamic chromosome mutation event associated with transformation of cells. Third, and most important, a number of mitotic genes regulating chromosome segregation have been found mutated in human cancer cells, implicating such mutations in induction of aneuploidy in tumors. Some of these gene mutations, possibly allowing unequal segregations of chromosomes, also cause tumorigenic transformation of cells in vitro. In this review, the recent publications investigating aneuploidy in human cancers, rate of chromosome instability in aneuploidy tumor cells, and genes implicated in regulating chromosome segregation found mutated in cancer cells are discussed.
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A case of unilateral salpingitis caused by Enterobius vermicularis presenting as a painful adnexal mass in a 28-year-old woman is reported.
It is well known that uraemia affects skeletal muscle metabolism. This has been attributed to a variety of causes, including anaemia, vitamin D, carnitine deficiency and hyperparathyroidism. The aim of this study was to ascertain whether 99Tcm-sestamibi leg scintigraphy is useful in the evaluation of skeletal muscle metabolism and the monitoring of treatment response in uraemic myopathy. Forty patients with chronic renal failure and 24 normal controls underwent examination. Fifteen patients with chronic renal failure received erythropoietin treatment. 99Tcm-sestamibi leg scintigraphy was performed in all subjects and in 15 patients after therapy. The calf-to-ankle uptake ratio was calculated by semi-quantitative analysis and normalized to lean body mass. The normalized uptake ratios were significantly different between patients and controls. After erythropoietin therapy, there was a significant increase in the normalized uptake ratios compared with pre-therapy. Our results suggest that 99Tcm-sestamibi leg scintigraphy is useful in the assessment of muscle metabolic abnormalities and the effect of treatment in uraemic myopathy.
OBJECTIVE: In the present study, we attempted to complete the hemodynamic assessment of propranolol response in cirrhotics with esophageal varices at high risk of bleeding, in one sitting, so as to identify nonresponders at the earliest. Some noninvasive indicators of this response were also evaluated. METHODS: Hepatic venous pressure gradient (HVPG) was measured in 33 such cases (18 nonbleeders, 15 bleeders) before and 90 min after an oral dose of 80 mg propranolol, and reduction by > or =20% taken as responder. RESULTS: Twenty-two patients (66.67%) responded (HVPG reduction > or =26%), whereas 11 (33.33%) did not (HVPG reduction < or =6%). Postdrug HVPG between responders and nonresponders showed a significant difference (p < 0.001). Neither baseline HVPG (p > 0.1), baseline CI (p = 0.665), nor baseline stroke volume index (p > 0.1) could predict responder status. Difference of HVPG reduction (percent) between bleeders (21.49 +/- 35.53) and nonbleeders (40.58 +/- 23.95) approached, but did not reach, statistical significance (p = 0.076). However, logistic regression showed this difference to be significant (p = 0.026). Age of responders was found to be significantly lower than that of nonresponders (p approximately equals 0.05). During a follow-up of 9-38 months, only one of 22 responders (on propranolol) had an episode of variceal bleed. None in whom HVPG fell to < or = 12 mm Hg bled. CONCLUSION: The study suggests that single-sitting hemodynamic assessment of acute response to high-dose oral propranolol clearly differentiates between responders and nonresponders. Moreover, it appears that prior history of variceal bleeding and old age negatively influences the effect of propranolol.
Ascorbic acid during oxidation in vitro can generate H2O2 which induces non-disulphide covalent cross-linking of coincubated oxyhemoglobin. The cross-linking phenomenon mediated by H2O2 takes place possibly without the involvement of hydroxyl radicals as evident from the failure of radical scavengers like mannitol and dimethyl sulphoxide as well as metal-chelator, to inhibit the process. This pro-oxidant effect of ascorbic acid may have physiological significance in red blood cells in vivo.
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BACKGROUND: Diagnosis of Budd-Chiari syndrome (BCS) is often missed unless its possibility has been kept in mind. Obstruction of inferior vena cava (IVC) is reportedly the most frequent cause of BCS in Afro-Asian variety. AIM: An attempt was made to classify BCS (in an eastern Indian population) etiopathologically. PATIENTS AND METHODS: Thirty consecutive cases of BCS presenting over a period of five years were included. Following a thorough physical examination, necessary investigations (including coagulation profile, ultrasonography (with Doppler study) of hepatobiliary tract, hepatic vein and IVC angiography (n = 22) and liver biopsy (n = 26, including autopsy in two cases) were performed. RESULTS: Mean age at presentation was 32.7 +/- 10.36 years (range 12-60 years) with M:F = 21:9. Clinical presentations included, hepatomegaly in 28 (93.3%), ascites in 27 (90%), splenomegaly in 15 (50%), pain in abdomen in 26 (86.6%), jaundice in 10 (33.3%), back veins in 20 (66.6%) and gastrointestinal bleeding in three (10%) cases. Amongst the total of 30 patients, four, six and 20 cases presented as fulminant, acute and chronic BCS respectively. Twenty four cases of BCS could be diagnosed by ultrasonography alone, while the remainder required angiography for diagnosis. IVC and hepatic vein angiography revealed membranous obstruction in nine, partial stricture of IVC in six, and IVC and/or hepatic vein block in others. The etiopathological nature in 30 cases were as follows: idiopathic membranous obstruction in nine (30%), hepatocellular carcinoma in six (20%), idiopathic stricture in six (20%) cases and one case (3.3%) each of the following: cholangiocarcinoma, renal cell carcinoma, chronic pancreatitis, hydatid cyst in liver, protein S deficiency, oral contraceptive use, nephrotic syndrome (with antithrombin III deficiency), polycythemia rubra vera and chronic lymphatic leukemia. CONCLUSION: Idiopathic membranous obstruction and stricture of IVC are the commonest cause of BCS in the eastern part of India. Hepatocellular carcinoma is also a common cause, presenting in the fulminant form. Ultrasonography may be a helpful screening test for BCS, but IVC and hepatic vein catheterisation is essential for a complete work up of these patients.
[formula: see text] The biological relevance and irresistible synthetic challenge of compounds containing the diaryl ether linkage encourages the development of new methodologies targeted toward this structural subunit. The syntheses of diaryl ethers 2 using a benzannulation strategy that formally involves a [3 + 2 + 1] cycloaddition between aryloxy-substituted Fischer carbenes 1 and alkynes are described. This methodology provides a neutral near ambient temperature formation of diaryl ethers.
In order to assess the prognostic value of silent myocardial ischemia in acute myocardial infarction after thrombolysis and early coronary angiography (14-48 h after start of thrombolysis) including percutaneous transluminal coronary angioplasty, if indicated, 126 patients underwent 24 h-Holter-monitoring in the early postinfarction period. The 24 h-Holter-recording was initiated directly after early coronary intervention (40+/-11 h after onset of symptoms). Of the 126 patients initially eligible for the study 29 had to be excluded from further analysis for clinical or methodical reasons. Of the remaining 97 patients, 10 (10%) had silent ischemia (group A) and 87/97 (90%) patients showed no significant ST-segment alterations. Both groups did not significantly differ from each other with regard to baseline clinical characteristics, severity of coronary artery disease and frequency of successful percutaneous transluminal coronary angioplasty. The left ventricular ejection fraction showed a trend towards lower values in patients with than in those without silent ischemia (47+/-15% vs. 55+/-13%, p=0.07). When both silent ischemia and left ventricular ejection fraction <40% were present, a subset of patients at high risk for cardiac death could be identified (specificity: 98%, positive predictive accuracy: 75%). By Kaplan-Meier analysis, significantly more cardiac deaths occurred in group A than in group B (30% vs. 6%, p<0.01) during the three-year follow-up (950+/-392 days) after acute myocardial infarction. Regarding the cardiac events during long-term follow-up (emergency percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, non-fatal reinfarction, and cardiac death) there was no significant difference between both groups (30% vs. 18%, NS). In conclusion, Holter monitor-detected silent ischemia in the subacute phase of myocardial infarction after thrombolysis followed by early delayed coronary intervention occurs in 10% of the patients indicating either a residual ischemia in the infarcted zone despite a combined reperfusion strategy or a remote ischemic potential in case of multivessel disease. In this small selected group of infarct patients too, silent ischemia is to be considered as an important non-invasive parameter to predict cardiac death during long-term follow-up and provides valuable complementary information to left ventricular dysfunction, a well established prognostic marker in the postinfarction period.
The myocardium's response to increased stress or load is not stereotyped. Differences have been observed in the heart's molecular composition and performance characteristics when exposed to stress. Myosin isoforms gradually change during development of hypertrophy, whereas collagen levels change only during the chronic phase of hypertrophy. Cardiac hypertrophy can regress if treated with antihypertensive drugs, but the myocardium of the post-hypertrophic heart no longer has the same composition as it did before hypertrophy. In rat studies of the effects of antihypertensive drugs on cardiac functional reserve, captopril showed a regression of hypertrophy associated with a lower baseline stroke volume and, after dobutamine stress, a dose-dependent rise in stroke volume. In untreated rates captopril showed no change in stroke volume. In hydralazine-treated rats, there was no change in reserve after dobutamine stress, whereas propranolol treatment resulted in partial regression and a slight change in stroke volume. Overall, our data suggests that development of hypertension and hypertrophy plays a role in changes in the molecular structure of the myocardium, especially during the chronic phase of hypertrophy and heart failure. This complex process cannot be explained by one factor but involves a combination of factors. Identification of each factor would be of importance for the development of appropriate therapeutic agents.
Resistance to isoniazid (INH), a frontline, antituberculosis drug, presents a major problem in the chemotherapy of tuberculosis. Although several targets of INH have been identified, the mechanism of INH resistance remains incompletely understood. This report demonstrates that INH accumulation in Mycobacterium smegmatis is enhanced both upon addition of both a proton motive force (pmf) uncoupler, carbonylcyanide m-chlorophenylhydrazone (CCCP), and upon addition of ortho-vanadate, an inhibitor of ATP-dependent efflux pumps. Both the Deltapsi and DeltapH components of the pmf are likely to be involved as judged by the effects of valinomycin and nigericin, respectively. Reserpine, an inhibitor of the human MDR1 P-glycoprotein, enhances INH accumulation in a manner similar to o-vanadate. Verapamil, a calcium channel blocker, also enhances INH uptake. Taken together, the results provide evidence of the involvement of both pmf- and ATP-dependent extrusion systems in INH efflux in M. smegmatis, making it important to evaluate the role of such systems in INH resistance in pathogenic mycobacteria.
Ophthalmoscopically guided intraocular fine-needle aspiration biopsy (FNAB) under general anesthesia was performed in three suspected cases of retinoblastoma (Rb). The first case presented with uveitis and the second with unusual radiological features. The third case had classical clinical features of bilateral Rb but the parents refused enucleation. After a cytologic diagnosis of retinoblastoma, two cases were subjected to enucleation and a histologic confirmation was obtained. The present article discusses the technique of guided intraocular FNAB and its limitations as well as utility in the preoperative diagnosis of retinoblastoma (Rb). The authors are of the opinion that FNAB should be considered a viable diagnostic option in selected cases of leucocoria when conventional investigative modalities prove inconclusive or for tissue diagnosis when a patient of suspected Rb refuses enucleation.
We report a 9-month-old infant with a torted ovarian cyst who presented with an acute consumptive coagulopathy (CC) with lethal outcome. That ischemic tissue can act as a trigger for a CC is well-known, but we did not find any report of a torted ovarian cyst causing a coagulopathy in the pediatric literature. This potential complication constitutes one more reason for the prompt surgical removal of torted ovarian cysts in infants.
A 0.7-ns molecular dynamics simulation of the DNA-EcoRI complex in a 7.0-A solvent shell indicated a stable behavior of the system. No significant evaporation or smearing of the solvent's outer boundary occurred. The structure and the intermolecular interactions were found to be well maintained during the simulation. The interaction pattern in the simulation was found to be very similar to that in the crystal structure. Most of the specific interactions between the DNA and the protein were found to be enhanced in the simulation compared to that in the crystal structure as a result of improved interaction geometry. The nonspecific interactions were found to be stronger than the specific ones. The specific interactions between the N7 atoms of Gua(4) or Ade(5) or Ade(6) and the protein were found to be present over almost the entire time of the simulation, whereas hydrogen bonds involving the amino groups of the Ade(5) and Ade(6) with the protein were found to be relatively weaker, with lower probability and shorter lifetime. The time evolution of the root mean square deviations of the DNA and the protein were highly correlated even at the later part of the simulation, showing the tight binding between them. Several long-lived water bridges were found between the DNA backbone atoms and the protein and also between the two protein monomers, which increased the overall stability of the complex. The two protein monomers were found to interact strongly with each other. The energy of the DNA kink deformation was estimated as approximately 31 kcal/mol.
Molecular dynamics simulations and free energy calculations of the wild-type EcoRI-DNA complex and several variants have been performed in aqueous solvent. In general, he theoretical estimations of the free energy differences (DeltaDeltaA) qualitatively agree well with the corresponding experimental data. The modifications which were experimentally found unfavorable compared to the wild-type complex were also found to be so in theoretical estimates. The mutant where the amino group of the base Ade(6) was replaced by a hydrogen atom eliminating one H-bond between the DNA and the protein, was experimentally found to be more stable than the wild-type complex. It was speculated that the modification also caused a structural relaxation in the DNA making DeltaDeltaA favorable. Our theoretical estimate yields a positive DeltaDeltaA in this case, but the difference is small, and no significant local structural relaxation was observed. The major H-bonds between the DNA and the protein in the wild-type complex are found to be maintained in the different mutants although the specific and non-specific interaction energies between the interacting the DNA bases and the protein residues are different in different mutants. The interaction pattern of the other nearby nucleotides are significantly influenced by each modification. Thus, the alteration of the non-specific interactions may also play an indirect role in determining the specificity of the complex. The interaction of the Gua(4) of the DNA with the protein is found to be most sensitive to any alteration in the recognition site. Because Gua(4) is the nucleotide closest to the scissile bond, this extra sensitivity seems to play an important role in altering the functional activity of the complex.
BACKGROUND: Stroke is occasionally associated with ECG repolarization changes including ST depression. Recent evidence suggests a neurogenic contribution to these abnormalities in stroke patients. Animal studies implicate the insular cortex in cardiovascular control. We describe a patient with a left insular infarct and without cardiac or coronary artery disease, who developed ST depression indicating a neurogenic etiology. CASE DESCRIPTION: A 48 year-old female, with no risk factors for stroke, developed sudden expressive aphasia. MRI brain showed an infarct in the left insular cortex. Twenty-four hour Holter monitoring on the third day revealed transient ST depression more than 1.5 mm, which was not reproducible on subsequent monitoring. Transesophageal echo-cardiography (TEE) was normal. She had no cardiac symptoms and serial ECGs, cardiac enzymes (CKMB) and adenosine thallium scan were normal. To-date, there had been no cardiac events like congestive heart failure or myocardial ischemia. CONCLUSION: These findings suggest neurogenic ST depression is related to the left insular infarct in view of the normal adenosine thallium scan, non-reproducibility and evanescence of the ST segment changes and lack of associated cardiac symptoms. When neurogenic ST depression is combined with underlying coronary artery disease, it may adversely influence cardiac outcome after stroke.