Browsing by Author "Agarwal, S"

Now showing 1 - 20 of 187
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    ABO gene distribution in south-east region of Madhya Pradesh.
    (1981-12-01) Pradhan, P K; Sen, K; Agarwal, S; Kavishwar, K W
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    Acardiac acephalic monster.
    (1988-01-01) Sikka, M; Agarwal, S; Pradhan, S; Saxena, R
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    Accelerated platelet activation in Asian Indians with diabetes and coronary artery disease--The Chennai Urban Population Study (CUPS-13).
    (2006-09-11) Deepa, R; Mohan, V; Premanand, C; Rajan, V S; Karkuzhali, K; Velmurugan, K; Agarwal, S; Gross, M D; Markovitz, J
    AIM : To assess platelet activation in south Indian type 2 diabetic subjects with and without CAD. METHODS : Four groups of subjects were studied; Group 1 comprised of non-diabetic subjects without coronary artery disease (CAD) (n = 30). Type 2 diabetic subjects without CAD formed Group 2 (n = 30); Group 3 comprised of type 2 diabetic subjects with CAD (n = 30) and Group 4 consisted of non- diabetic subjects with CAD (n=14). CAD was diagnosed based on coronary angiographic evidence of severe double or triple vessel disease. Platelet activation was tested after an overnight fast in blood obtained from a bleeding wound at 1 minute post-incision (wound-induced activation) as well as venous blood stimulated in vitro with collagen, using whole blood flow cytometry. In subjects with CAD, aspirin was withdrawn for 7 days and nitrates for 24 hours. RESULTS: Collagen induced GP IIb/IIIa binding was significantly higher among diabetic subjects with (28.10 +/-19.89; p<0.05) and without CAD (21.02+/-19.62; p<0.05) and non-diabetic subjects with CAD (23.89+/-15.65; p<0.05) compared to non-diabetic subjects without CAD (11.69+/-13.69). Regression analysis showed collagen induced GP IIb/IIIa binding to be significantly associated with CAD [odds ratio (OR): 1.029, p = 0.025] and diabetes (OR: 1.037, p = 0.007). CONCLUSION: Increased platelet activation is seen in urban south Indians with diabetes and CAD.
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    Adamantinoma of the tibia.
    (1967-06-01) Agarwal, S; Manjrekar, P S; Koshal, K D; Prasad, U S
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    Adenoid cystic carcinoma of the cervix. A report of 7 cases.
    (1978-03-01) Lahiri, B; Agarwal, B M; Agarwal, S; Lahiri, V L
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    Alkaptonuria.
    (1989-11-01) Singh, B N; Mehrotra, S; Bhargava, B; Agarwal, S
    A case of alkaptonuria with its various sequelae in the form of ochronosis, ochronotic arthropathy, spondylitis and prostatic calculi is reported. The case is of interest as it presented with hepatocellular failure and hepatitis B surface antigenaemia.
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    Amino acid pattern in breast versus artificially fed babies.
    (1987-09-01) Misra, P K; Awasthi, S; Malik, G K; Saksena, P N; Agarwal, S
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    Anaemia of chronic renal failure.
    (1979-07-01) Agarwal, S; Mathur, M; Malhotra, K K; Das, K C; Sood, S K
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    Anetoderma secondary to lepromatous leprosy.
    (2001-01-01) Khandpur, S; Agarwal, S; Reddy, B S
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    Antiphospholipid Syndrome and Lupus Anticoagulant: Where do we stand today ?
    (Prathima Institute of Medical Sciences, 2024-01) Trivedi, S; Verma, S; Kaur, O; Agarwal, S; Singhal, U; Singh, MB
    Lupus Anticoagulant (LAC) is a group of auto antiantibodies that interfere with phospholipid dependent tests like Activated Partial Thromboplastin time (APTT) and dilute Russell Viper venom time (dRVVT) on in vitro basis. LA, anti cardiolipin antibodies (aCL) IgG/IgM, and anti-?2 glycoprotein I antibodies [a?2GPI]IgG/IgM are three diagnostic criteria for laboratory diagnosis of anti-phospholipid antibodies (aPL). The circulating aPLs in the clinical se?ng of hypercoagulability state or adverse pregnancy outcomes is termed as anti-phospholipid syndrome (APS). The laboratory diagnosis of APS is complicated, it includes constellation of tests like solid phase immunoassays for measurement of aCL and a ? 2GPI by and coagulation based assays for detection of LAC. LAC diagnosis is especially challenging in the se?ng of anti-coagulation therapy, numerous modifications to circumvent this interference have rendered success. The Thrombin generation assays [TGA] for LAC detection and estimation of LAC pathogenicity are available but are yet to be accepted as routine laboratory tests. The medley of assays like Enzyme-linked immunosorbent and chemiluminescent assays are available for detection of aCL and a?2GPI but due to the non-availability of universal calibrators and standards there is lack of harmonization between various solid phase assays. In this article we intend to highlight new recommendations of laboratory diagnosis of LAC with special emphasis on diagnosis in the se?ng of pregnancy and anti-coagulation. For risk assessment in APS other non-criteria aPL like as antidomain ?2 glycoprotein I and anti-phosphatidyl serine/prothrombin antibodies are under evaluation. There is an ongoing quest towards harmonization of detection of LAC, thus there has been succession of guidelines to meet the challenges and incorporate newly found knowledge every time, namely International Society for Thrombosis and Hematology- Scientific Standardization Commi?ee (ISTH-SSC) guidelines, followed by British Commi?ee for Standards in Hematology (BCSH), Clinical and Laboratory Standards Institute (CLSI) guidelines 2014 and finally guidelines/updates issued by ISTH- SSC in 2018
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    An approach towards understanding the genesis of sunlight-induced skin cancer.
    (1990-08-01) Chatterjee, S N; Agarwal, S; Bose, B
    The molecular basis of the sunlight-induced skin carcinogenesis has been elucidated. Of the two ultraviolet components of sunlight that reach the earth's surface the UV-B is known to be carcinogenic but the mode of action of UV-A, the predominant component of sunlight, is ill understood. Using the liposomes as a model system, it has been shown here that UV-A causes dose-dependent lipid peroxidation as estimated by measurements of conjugated dienes, lipid hydroperoxides, malondialdehydes and the fluorescent adducts (Schiff bases) produced by the reaction of MDA with glycine. Direct exposure to sunlight has also been shown to cause dose-dependent lipid peroxidation. The UV-A induced lipid peroxidation has also been shown to be dependent on dose rate. While the sodium formate, dimethyl sulphoxide, superoxide dismutase and EDTA do not have any significant effect, sodium azide, histidine, beta-carotene and dimethylfuran were shown to inhibit significantly the UV-A induced lipid peroxidation, thereby providing significant evidence of the involvement of singlet oxygen (1O2) as the initiating agent. The use of D2O in place of H2O as the liposome dispersing medium enhanced to great extent the UV-A induced lipid peroxidation, thereby lending additional support to the finding that singlet oxygen was the initiating agent. The possible mode of formation of 1O2 on exposure to UV-A was discussed. This study also highlighted the role of environmental factors on the sunlight-induced cutaneous damage. Finally, the relation between lipid peroxidation, DNA damage and carcinogenesis has been discussed in a way to suggest the possible link between sunlight exposure and causation of skin cancer.
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    Asphyxia neonatorum.
    (1973-12-01) Agarwal, S; Chopra, K; Gupta, S
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    Autoimmune hemolytic anaemia and foetal loss.
    (1977-10-01) Jain, S; Agarwal, S; Dash, S C; Grewal, K S
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    Benign vs malignant soft tissue neoplasms: Limitations of magnetic resonance imaging.
    (2010-07) Sen, J; Agarwal, S; Singh, S; Goel, S; Sen, R
    Aims: Various features have been described in the literature to differentiate benign from malignant lesions. The aim of the present study was to study the accuracy of each of these features and that of magnetic resonance imaging (MRI) in diagnosing malignant lesions. Materials and Methods: Fifty-five consecutive patients presenting with neoplastic (both benign and malignant) lesions diagnosed clinically and on ultrasound were studied and their MRI features were compared with the findings on surgical exploration and histopathologic examination. Results: There were 32 (58%) benign and 23 (42%) malignant masses. Malignant masses were more common in patients older than 20 years (83%), and these had symptoms of less than 6 months duration (75%), as against benign lesions. The swelling was painful in 8 malignant masses and these were more common in the upper limbs (61%). Various features of malignant lesions were size more than 5 cm in 83%, change in signal intensity from homogenous on T1-weighted images to heterogenous on T2-weighted images in 74%, irregular margins in 74%, and heterogenous contrast enhancement in 91%. The accuracy of these features was 76%, 58%, 78%, and 60%, respectively. Most benign and malignant lesions were intramuscular in location. A significant number (38%) of benign lesions were located in the intermuscular facial plane. Definitive diagnosis was made in 42% of the lesions. Conclusions: MRI is an excellent modality for evaluating soft tissue neoplasms; however, prediction of a specific diagnosis and differentiation of malignant and benign lesions is not always possible.
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    Bilateral proptosis with acute myeloid leukaemia.
    (1971-09-01) Ahmad, S H; Mishra, R K; Agarwal, S
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    Bilateral testicular biopsy--is it necessary?
    (1991-07-01) Sikka, M; Agarwal, S
    Bilateral testicular biopsies from 202 infertile males were examined to ascertain the differences in the degree of damage to the germinal epithelium on both sides. Depending on the histologic changes, the biopsies were divided into six groups. A significant difference in the morphology on both sides was seen only in 3% cases. The left and the right testes were equally damaged in cases with similar morphology.
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    Birth weight patterns in rural undernourished pregnant women.
    (2002-03-23) Agarwal, S; Agarwal, A; Bansal, A K; Agarwal, D K; Agarwal, K N
    OBJECTIVE: To study the birth weight pattern in chronic as well as currently undernourished pregnant women. DESIGN: Prospective study of rural pregnant women by following eligible women. SETTING: Two adjoining blocks of rural Varanasi. METHOD: 3700 pregnant women from rural areas of Varanasi for whom data for anthropometry, hemoglobin, dietary intake, birth weight, fundal height and abdominal girth at 16 +/- 2, 28 +/- 2 and 36 +/- 2 weeks of gestation were recorded. Outcome measure was birth weight pattern of newborns. RESULTS: Of the births, 7.2% were < 2250 g and 27.4% < 2500 g. The weekly birth weight increments in gestation 36-42 weeks were 5-53 g, only. The fundal height did not increase during 35-39 weeks of gestation (lower by 5 cm as compared to normal). Nutrition supplement in the third trimester significantly increased fundal height and abdominal girth. Fundal height below 24.5 cm at 28 weeks of gestation (1368 women) was associated with higher low birth weight deliveries. CONCLUSION: Birth weight and fundal height increments during later pregnancy are low in undernourished pregnant women. Fundal height < 24.5 cm at 28 weeks of gestation identified women with higher risk for lowbirth weight infants. The prevalence of low birth weight was 27.4% and of prematurity was 6.6%.