Safe disposal of infectious waste--Indian perspective.
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Color↗
Biomedical subjects
N Taneja
Publications and source records attributed to N Taneja.
Spread of cholera with newer clones of Vibrio cholerae O1 El Tor, serotype inaba, in India.
During 2004 and 2005, cholera was recorded in 15 states of India, with 7 outbreaks. The newly emerged Vibrio cholerae O1 Inaba had a different antibiogram and ribotype, different pulsotypes, and different mutations in the wbeT gene. Due to the absence of serogroup O139, the Inaba serotype may have acquired the potential to affect the population at large.
Anti-Bacterial Agents↗
Hospital environment contamination with Gram-negative bacteria is as common and important as that with Gram-positive bacteria in an overloaded tertiary care hospital in India.
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Bacterial Infections↗
Hydrogen peroxide fogging in an overcrowded tertiary care referral centre: some practical queries.
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Air Conditioning↗
Nosocomial outbreak of diarrhoea by enterotoxigenic Escherichia coli among preterm neonates in a tertiary care hospital in India: pitfalls in healthcare.
An outbreak of watery diarrhoea accompanied by low-grade fever and weight loss in 16 preterm neonates (age range 2-20 days) admitted to a neonatal intensive care unit (NICU) over four days in August 2000 is reported. Escherichia coli having similar antibiograms were identified on routine bacterial stool cultures in 14 (87.5%) neonates and none of the other known enteropathogens were detected. An investigation was undertaken to trace the source of infection. Surveillance cultures of swabs from the utensils used to prepare milk feed, culture of the formula feed and all items handled by one particular cook yielded growth of E. coli as did culture of his hand swabs and faecal sample. The causative agent was identified as enterotoxigenic E. coli (ETEC) as toxin production could be demonstrated by reverse passive latex agglutination in all the strains of E. coli isolated both from the infected neonates and the source of infection. The outbreak was effectively controlled by appropriate therapy and institution of proper measures of hygiene after identification of the source of infection.
Animals↗
Imipenem resistance in nonfermenters causing nosocomial urinary tract infections.
Nonfermenting gram-negative bacilli (nonfermenters) have emerged as important nosocomial pathogens causing opportunistic infections in immunocompromised hosts. These organisms show high level of resistance to b-lactam agents, fluoroquinolones and aminoglycosides. Imipenem is a carbapenem antibiotic, which can be very useful for treatment of infections caused by nonfermenters. Eighty-five nonfermenters causing nosocomial UTI were tested for MIC to imipenem by agar dilution method. Resistance to other antimicrobial agents was compared between imipenem sensitive (S) and resistance (R) groups. Overall 36.4% of nonfermenters were resistant to imipenem. Forty two percent of P. aeruginosa and 18.5% of Acinetobacter baumanii were imipenem resistant. Other nonfermenters showed variable resistance, resistance in Alcaligenes spp. being very high. More than 70% of the nonfermenters were resistant to ceftazidime, gentamicin and ciprofloxacin. Piperacillin and amikacin had the best in vitro susceptibility. No significant difference was found in the antibiotic susceptibility profile among imipenem sensitive (S) or resistant (R) strains.
Anti-Bacterial Agents↗
Irradiation of mitochondria initiates apoptosis in a cell free system.
The ability to modulate the sensitivity of mammalian cells to ionizing radiation (IR) (e.g. using chemotherapeutics) is dependent on our understanding of the primary target and biochemical pathway that leads to IR-induced apoptosis. We demonstrate using a cell free assay that irradiation of mitochondria is a primary event that initiates IR-induced apoptosis. IR results in loss of mitochondrial membrane potential, opening of the permeability transition pore (PTP) and the release of cytochrome c (cyto c). Apaf-1 and ATP were required to initiate apoptosis upon release of cyto c from mitochondria. The importance of mitochondrial events in the initiation of IR-induced apoptosis was also supported by the observation that inhibition of caspase-9 by the over-expression of dominant negative mutants resulted in the inhibition of IR-induced apoptosis. In contrast, inhibition of caspase-8 had only a minor impact on IR-induced apoptosis. Over-expression of Bcl-X(L) inhibited the initiation of IR-induced apoptosis due to its ability to prevent the loss of mitochondrial membrane potential, PTP opening and cytochrome c release. In a cell free assay for apoptosis, mitochondria as well as cytosol derived from Bcl-X(L) over-expressing cells were less efficient at supporting apoptosis in response to IR suggesting multiple roles for Bcl-X(L) in the regulation of apoptosis.
Adenosine Triphosphate↗
Flavobacters as urinary tract pathogens--case report.
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Adolescent↗
Prevention of postoperative infections in ophthalmic surgery.
Postoperative endophthalmitis is a serious, vision-threatening complication of intraocular surgery. Better instrumentation, surgical techniques, prophylactic antibiotics and better understanding of asepsis have significantly reduced the incidence of this complication. Postoperative endophthalmitis may occur as an isolated event or as a cluster infection. Topical antibiotics, preoperative periocular preparation with povidone-iodine combined with a sterile operating room protocol significantly reduce the incidence of isolated postoperative endophthalmitis. The role of antibiotics in the irrigating fluid and subconjunctival antibiotics remains controversial. Cluster infections on the other hand are more likely to occur due to the use of contaminated fluids/viscoelastics or a breach in operating room asepsis. Prevention of postoperative endophthalmitis requires strict adherence to operating room norms, with all involved personnel discharging their assigned roles faithfully.
Administration, Topical↗
Erythromycin in pityriasis rosea: A double-blind, placebo-controlled clinical trial.
BACKGROUND: The study stemmed from an incidental observation of improvement in 2 patients with pityriasis rosea while receiving erythromycin. OBJECTIVE: The purpose of the study was to evaluate the efficacy of erythromycin in patients with pityriasis rosea. METHODS: A double-blind, placebo-controlled clinical study was performed in an outpatient setting in a major hospital. Ninety patients over a period of 2 years were alternatively assigned to treatment group or placebo group. Patients in the treatment group received erythromycin in divided doses for 14 days. The response was categorized as complete response, partial response, or no response. All patients were followed up for 6 weeks. RESULTS: Both groups were comparable with regard to age at presentation, sex, and average duration of disease at the time of reporting to the clinic. Upper respiratory tract infection before the appearance of skin lesions was reported in 68.8% of all patients. Complete response was observed in 33 patients (73.33%) in the treatment group and none in the placebo group (P <.0001). CONCLUSION: Oral erythromycin was effective in treating patients with pityriasis rosea.
Administration, Oral↗
A caspase-resistant form of Bcl-X(L), but not wild type Bcl-X(L), promotes clonogenic survival after ionizing radiation.
Bcl-2 and Bcl-X(L) belong to a family of proteins overexpressed in a variety of human cancers which inhibit apoptosis in response to a number of stimuli including chemotherapeutic agents and ionizing radiation. To better understand the role of these polypeptides in modulating the response of cancer cells to ionizing radiation we used cell lines that were engineered to overexpress the two polypeptides. Although Bcl-2 and Bcl-X(L) overexpression resulted in inhibition of radiation-induced apoptosis, it did not result in enhanced clonogenic survival. Consistent with this was the observation that Bcl-2 and Bcl-X(L) protected cells from DNA fragmentation, loss of mitochondrial membrane potential, and caspase activation for up to 72 hours after irradiation. Beyond 72 hours, there was a rapid loss in the ability of Bcl-2 and Bcl-X(L) to inhibit these markers of apoptosis. When Bcl-X(L) was analyzed at 72 hours after irradiation and beyond, a rapid accumulation of a 16-kDa form of Bcl-X(L) was observed. To test the hypothesis that cleavage of the 29-kDa form of Bcl-X(L) by caspases to a 16-kDa polypeptide results in its inability to inhibit apoptosis beyond 72 hours, we constructed a cell line that overexpressed a caspase-resistant form of Bcl-X(L) (Bcl-X(L)-deltaloop). Cells overexpressing Bcl-X(L)-deltaloop were resistant to apoptosis beyond 72 hours after irradiation and did not contain the 16-kDa form at these time points. In addition, Bcl-X(L)-deltaloop overexpression resulted in enhanced clonogenic survival compared with control or Bcl-X(L) overexpressing cells. These results provide a molecular basis for the observation that expression of Bcl-2 or Bcl-X(L) is not a prognostic marker of tumor response to cancer therapy.
Apoptosis↗
Effects of tea polyphenols and flavonoids on liver microsomal glucuronidation of estradiol and estrone.
Administration of 0.5 or 1% lyophilized green tea (5 or 10 mg tea solids per ml, respectively) as the sole source of drinking fluid to female Long-Evans rats for 18 days stimulated liver microsomal glucuronidation of estrone, estradiol and 4-nitrophenol by 30-37%, 15-27% and 26-60%, respectively. Oral administration of 0.5% lyophilized green tea to female CD-1 mice for 18 days stimulated liver microsomal glucuronidation of estrone, estradiol and 4-nitrophenol by 33-37%, 12-22% and 172-191%, respectively. The in vitro addition of a green tea polyphenol mixture, a black tea polyphenol mixture or (-)-epigallocatechin gallate inhibited rat liver microsomal glucuronidation of estrone and estradiol in a concentration-dependent manner and their IC50 values for inhibition of estrogen metabolism were approximately 12.5, 50 and 10 microg/ml, respectively. Enzyme kinetic analysis indicates that the inhibition of estrone glucuronidation by 10 microM (-)-epigallocatechin gallate was competitive while inhibition by 50 microM (-)-epigallocatechin gallate was noncompetitive. Similarly, several flavonoids (naringenin, hesperetin, kaempferol, quercetin, rutin, flavone, alpha-naphthoflavone and beta-naphthoflavone) also inhibited rat liver microsomal glucuronidation of estrone and estradiol to varying degrees. Naringenin and hesperetin displayed the strongest inhibitory effects (IC50 value of approximately 25 microM). These two hydroxylated flavonoids had a competitive mechanism of enzyme inhibition for estrone glucuronidation at a 10 microM inhibitor concentration and a predominantly noncompetitive mechanism of inhibition at a 50 microM inhibitor concentration.
Animals↗
Ionizing radiation stimulates a Grb2-mediated association of the stress-activated protein kinase with phosphatidylinositol 3-kinase.
The stress-activated protein (SAP) kinases are induced by tumor necrosis factor, oncoproteins, and UV light. The present studies demonstrate that ionizing radiation (IR) activates p54 SAP kinase. IR-induced activation of SAP kinase is associated with binding to the SH2/SH3-containing adaptor protein Grb2. This interaction is mediated by the SH3 domains of Grb2 and the proline-rich sequence PPPKIP in the carboxy-terminal region of SAP kinase. We also demonstrated that SAP kinase and the p85 alpha-subunit of phosphatidylinositol (PI) 3-kinase form a complex in irradiated cells. The results indicate that this complex involves binding of the p85 alpha subunit of PI 3-kinase to the SH2 domain of Grb2. The functional role of linking SAP kinase to PI 3-kinase is further supported by the finding that wortmannin, an inhibitor of PI 3-kinase, stimulates SAP kinase activity. These results suggest that the cellular response to IR may include regulation of SAP kinase by a PI 3-kinase-dependent signaling pathway.
Adaptor Proteins, Signal Transducing↗
Activation of serine/threonine protein kinases and early growth response 1 gene expression by tumor necrosis factor in human myeloid leukemia cells.
The early growth response 1 (EGR-1) gene is induced by mitogenic and differentiating signals in diverse cell types. The present studies have examined the effects of TNF-alpha on the induction of EGR-1 expression in human myeloid leukemia cells and the potential cytoplasmic signaling cascades that transduce TNF-induced signals to the nucleus. The results demonstrate that treatment of HL-60 cells with TNF is associated with the transient induction of the EGR-1 gene. The results also demonstrate that TNF treatment is associated with activation of the serine/threonine kinase, pp90rsk, which acts upstream to EGR-1 gene induction. Partial purification of pp90rsk by affinity chromatography demonstrated an increase in S6 peptide phosphorylation in response to TNF treatment. Because TNF activates sphingomyelin hydrolysis, we also studied the effects of sphingomyelinase (SMase) on induction of EGR-1 and pp90rsk. The results demonstrate that SMase also activates pp90rsk and induces EGR-1 gene expression. Previous work has demonstrated that mitogen-activated protein (MAP) kinase activates pp90rsk. The present studies further show that treatment with TNF or SMase is associated with induction of both the pp42/44 MAP and the related Jun kinases. Induction of pp42/44 MAP kinase activity is temporally related to activation of pp90rsk and the EGR-1 gene. These findings support the involvement of an MAP kinase/pp90rsk/EGR-1 cascade in the response of myeloid leukemia cells to TNF.
Amino Acid Sequence↗
Overexpression of Bcl-XL by cytotoxic drug exposure confers resistance to ionizing radiation-induced internucleosomal DNA fragmentation.
Acquired resistance to diverse chemotherapeutic agents has been associated with overexpression of the P-glycoprotein. We have selected human U-937 cells for clones resistant to the cytotoxic agents doxorubicin (U-A20) and vincristine (U-V20). The results demonstrate that P-glycoprotein-positive U-A20 and U-V20 cells exhibit resistance to inducers of internucleosomal DNA fragmentation. Although parental U-937 cells responded to ionizing radiation with the DNA laddering characteristic of physiological cell death, the drug-resistant lines were insensitive to this effect. The U-A20 and U-V20 clones were also resistant to endonucleolytic DNA cleavage associated with exposure to tumor necrosis factor or ceramide. Previous work has demonstrated that physiological cell death is inhibited by overexpression of the Bcl-2 protein. However, analysis of Bcl-2 revealed similar levels in the parental and drug-resistant cells. In contrast, we show that U-A20 and U-V20 cells overexpress the Bcl-2-related protein, Bcl-xL. Moreover, studies with a U-937 cell line transfected with a Bcl-XL expression vector confirm resistance to ionizing radiation-induced DNA fragmentation and cell killing. These findings suggest that, unlike Bcl-2, Bcl-XL may be constitutively overexpressed as a result of selection for cytotoxic drug resistance and that Bcl-XL participates in an acquired form of multimodality resistance to chemotherapeutic agents and radiation.
Base Sequence↗
Genetic heterogeneity in true hermaphrodites. A report of two cases.
True hermaphrodites are identified from the presence of ambiguous genitalia with both ovarian and testicular tissue. Two cases presented below had a 46,XX chromosome pattern, cryptorchidism and undescended testes. Both cases showed an absence of secondary sexual characteristics and presence of bilateral breasts and a uterus. The gonads in case 1 were an ovotestis and testis (left side) and in case 2 were an ovary and testis (right side). Case 1 was analyzed for a sex-determining region on the Y chromosome (SRY) and was negative. Phenotypic, gonadal and molecular studies suggest that 46,XX true hermaphroditism is a genetically heterogeneous condition.
Adolescent↗