Assessment of Prescription Adherence to Secondary Prevention Guideline Recommendations and Patient Adherence to Pharmacotherapy and Lifestyle Modifications in Acute Coronary Syndrome and Chronic Coronary Syndrome Patients.

BACKGROUND: Coronary artery diseases (CADs) contribute to the majority of deaths and disabilities worldwide. People who have suffered an acute myocardial infarction (AMI) are at a higher risk of having a further attack. Hence, prolonged secondary prevention is necessary following index myocardial infarction (MI) for long-term cardiovascular protection as it reduces the morbidity and mortality associated with reinfarction, improves the quality of life, and is cost-effective. METHODS: An observational, ambidirectional study was carried out in a tertiary care hospital for 6 months. A total of 200 patients above 18 years of age with a confirmed diagnosis of acute coronary syndrome (ACS) or chronic coronary syndrome (CCS) were included in the study. Prospective data were collected using a self-designed patient profile form and by interviewing patients in the cardiac outpatient department while retrospective data were collected from the medical records department of the hospital. RESULTS AND CONCLUSION: Sex-wise distribution showed that males and females constituted 79 and 21% of the study participants, respectively, while the age-wise distribution revealed that the majority of patients were in the age-group of 60 years and above (63.5%). Hypertension and diabetes mellitus were the most common comorbid conditions, while dyslipidemia was the least observed comorbidity. Prescription adherence to secondary prevention guideline recommendations was studied, which revealed that 26.5% of the prescriptions were adherent to all four guideline recommendations. On evaluating adherence to pharmacotherapy, the maximum proportion of patients demonstrated moderate adherence (45%).

Protective Effect of Standardized Extract of Passiflora incarnata Flower in Parkinson's and Alzheimer's Disease.

BACKGROUND: Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Flavonoids exert their antioxidant effects by neutralizing all types of oxidizing radicals including the superoxide and hydroxyl radicals. Passiflora incarnata Linn. (Passifloraceae) is an important plant used in Ayurveda for the treatment of various disorders of the CNS and is a rich source of flavonoids. AIM: In the present study, we investigated the antioxidant, antiparkinsonian, and memory enhancing activity of flavonoid rich n-butanol extract of P. incarnata flowers (BEPIF). MATERIALS AND METHODS: Antioxidant activity was assessed using DPPH and hydrogen peroxide scavenging assay. The antiparkinsonian activity was evaluated using haloperidol induced catalepsy and tacrine induced vacuous chewing movement and memory enhancing activity was assessed using elevated plus maze and object recognition test. STATISTICAL ANALYSIS: The results were analyzed by Analysis of Variance test followed by Dunnett's test. RESULTS: Administration of BEPIF decreased transfer latency on day 2 and 9 significantly in elevated plus maze test and showed a significant increase in discrimination index in the object recognition test which is suggestive of its cognitive improvement action. Pretreatment with BEPIF showed a significant reduction in the haloperidol induced catalepsy and the tacrine induced jaw movements which are suggestive of its antiparkinsonian activity. In DPPH and H2O2 scavenging assay, BEPIF exhibited significant free radical scavenging activity. CONCLUSIONS: It can be concluded that the butanolic extract of P. incarnata flowers has significant antiparkinsonian and cognition enhancing activity which may be associated with its antioxidant potential. Thus, P. incarnata flowers may be employed in treatment of dementia and parkinsonism.

A case-control study of risk factors for lung cancer in Mumbai, India.

In the year 2010, it is estimated that nearly 1.35 million new cases and 1.18 million deaths with lung cancer occurred. In India, among males, lung cancer rates vary across the country which has encouraged us to conduct a case-control study to study the risk factors. The present unmatched hospital-based case-control study conducted at Tata Memorial Hospital included subjects registered between the years 1997-99. There were 408 lung 'cancer cases' and 1383 'normal controls'. Data on age, tobacco habits, occupational history, dietary factors, tea, coffee were collected by the social investigators. Univariate and regression analysis were applied for obtaining the odds ratio for risk factors. In the study, cigarette smoking (OR=5.2) and bidi smoking (OR=8.3), as well as alcohol consumption (OR=1.8), demonstrated dose-response relationships with lung cancer risk. Among the dietary items, only red-meat consumption showed 2.2-fold significant excess risk. Consumption of milk showed a 60% reduction in risk; while coffee showed a 2-fold excess risk for lung cancer. In addition, exposure to use of pesticides showed a 2.5-fold significant excess risk for lung cancer.

Multiple growth factors regulate coronary embryonic vasculogenesis.

Mechanisms regulating coronary vascularization are not well understood. To test hypotheses regarding the influence of key growth factors and their interactions, we studied vascular tube formation (vasculogenesis) in collagen gels onto which quail embryonic ventricles were placed and incubated in the presence of growth factors or inhibitors. Vasculogenesis in this model is dependent on tyrosine kinase receptors, since tube formation was totally blocked by genestein. Tube formation was attenuated when anti-bFGF or anti-VEGF neutralizing antibodies were added to the medium and nearly completely inhibited when the both were added. The attenuation associated with anti-VEGF was due primarily to a decrease in assembly of endothelial cells, while that associated with bFGF was primarily due to a reduction in endothelial cells. Soluble tie-2, the receptor for angiopoietins, also had an inhibitory effect and, when added with either anti-bFGF or anti-VEGF, markedly attenuated tube formation. At optimal doses, tube formation was enhanced 6.5-fold by bFGF and 2.5-fold by VEGF over the controls. Each of these growth factors was dependent upon the other for optimal induction of tube formation, since neutralizing antibodies to one markedly reduced the potency of the other. VEGF potency was also markedly reduced when soluble tie-2 was added to the medium. Tube formation was virtually totally blocked by exogenous TGF-beta at doses > 1 ng/ml, while neutralizing TGF-beta antibodies enhanced tube formation 2-fold in the 30 ng-30 microg range. These data provide the first documentation of multiple growth factor regulation of coronary tube formation.

Growth suppression of intracranial xenografted glioblastomas overexpressing mutant epidermal growth factor receptors by systemic administration of monoclonal antibody (mAb) 806, a novel monoclonal antibody directed to the receptor.

A mutant epidermal growth factor receptor (variously called DeltaEGFR, de2-7 EGFR, or EGFRvIII) containing a deletion of 267 amino acids of the extracellular domain is frequently highly expressed in human malignant gliomas and has been reported for cancers of the lung, breast, and prostate. We tested the efficacy of a novel monoclonal anti-DeltaEGFR antibody, mAb 806, on the growth of intracranial xenografted gliomas in nude mice. Systemic treatment with mAb 806 significantly reduced the volume of tumors and increased the survival of mice bearing xenografts of U87 MG.DeltaEGFR, LN-Z308.DeltaEGFR, or A1207.DeltaEGFR gliomas, each of which expresses high levels of DeltaEGFR. In contrast, mAb 806 treatment was ineffective with mice bearing the parental U87 MG tumors, which expressed low levels of endogenous wild-type EGFR, or U87 MG.DK tumors, which expressed high levels of kinase-deficient DeltaEGFR. A slight increase of survival of mice xenografted with a wild-type EGFR-overexpressing U87 MG glioma (U87 MG.wtEGFR) was effected by mAb 806 concordant with its weak cross-reactivity with such cells. Treatment of U87 MG.DeltaEGFR tumors in mice with mAb 806 caused decreases in both tumor growth and angiogenesis, as well as increased apoptosis. Mechanistically, in vivo mAb 806 treatment resulted in reduced phosphorylation of the constitutively active DeltaEGFR and caused down-regulated expression of the apoptotic protector, Bcl-XL. These data provide preclinical evidence that mAb 806 treatment may be a useful biotherapeutic agent for those aggressive gliomas that express DeltaEGFR.

Central mucoepidermoid carcinoma--a case report.

The mucoepidermoid carcinoma (MEC) account for approximately 6-8 Percent of all salivary gland tumors. Central mucoepidermoid carcinoma of the jaws is rare. Following is a case report of central mucoepidermoid carcinoma which involves the ramus of the mandible. Origin of the central mucoepidermoid carcinoma is discussed.

VEGF and bFGF stimulate myocardial vascularization in embryonic chick.

We tested the hypothesis that early vascularization of the embryonic heart is enhanced after bolus injections of vascular, endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) into the vitelline vein before the onset of myocardial vasculogenesis (3.5 days, stage 21). Electron and light microscopy were utilized to obtain morphometric data. At stages 29 and 31, myocardial vessel volume or numerical density were higher in embryos injected with 50 ng bFGF than in the saline-injected controls. A VEGF injection increased vascular volume density at stage 29 and both volume and numerical, density at stage 31, bFGF, but not VEGF, was associated with an enhancement of the sinusoidal system (spongy layer of the ventricle) at stage 29. This effect disappeared by stage 31. In conclusion, 1) enhancement of bFGF or VEGF before myocardial vascularization increases vascular growth, but the initial effect of bFGF is greater; 2) the effects of these growth factors on vascular volume and numerical density are temporally dependent; and 3) bFGF, in addition to its effects on the coronary vasculature, influences ventricular modeling by apparently acting on myocytes as well as endothelial cells.

A thyroid hormone analog stimulates angiogenesis in the post-infarcted rat heart.

In view of the evidence that thyroid hormone administration has angiogenic effects on the hypertrophic myocardium, we tested the hypothesis that the capillary supply in the hypertrophic myocardium surviving infarction would be improved by administration of the thyroid hormone analog, diiodothyroproprionic acid (DITPA). We administered DITPA (MI-DITPA) or saline (MI-saline), s.c., to rats for 10 days following experimental infarction of the left ventricle (LV). Morphometric methods were used to assess capillarity and myocyte cross-sectional area in three regions of the left ventricle: (1) border (next to the scar of infarction); (2) adjacent (next to the border); and (3) remote (interventricular septum). Infarct size ranged from 20-85% of the LV free-wall, and both groups had similar mean infarct size. Capillary length density (LV) was significantly higher in the remote region of the treated group than in the MI-saline rats. LV in the border region, which experienced the most marked increase in cardiocyte cross-sectional area, was not significantly lower than in the other regions, indicating a more marked angiogenic response. In hearts with large infarcts (> or = 40%) LV in the border region was higher in the DITPA group than in the non-treated rats. In the MI-DITPA group, cardiocyte size in the border region was positively correlated with that of the other regions, which contrasts with the negative correlations noted for the MI-saline rats. These data suggest that DITPA therapy (1) may improve maximal perfusion potential of the hypertrophied myocardium surviving a myocardial infarction, and (2) is selectively effective in the border region of hearts with large infarcts.

Maxillary metastasis of osteosarcoma.

Osteosarcoma, either primary or metastatic, rarely involves the jaws. Though only a few cases of mandibular metastasis of osteosarcoma have been reported, only one case of et al maxillary involvement (Singh, 1978) has been reported. A case of 21 year old boy with metastasis of osteosarcoma to the right maxilla from primary osteosarcoma of the left femur is presented. The patient complained of pain and swelling in the left maxillary region which was earlier diagnosed as maxillary sinusitis on the basis of Water's sinus radiograph in a medical hospital. Further radiographic examination with the panoramic and intraoral periapical radiographs done by us and later by fine needle aspiration cytology led us to diagnose a secondary deposits of osteosarcoma.

Efficacies of ofloxacin, rifampin, and clindamycin in treatment of Staphylococcus aureus abscesses and correlation with results of an in vitro assay of intracellular bacterial killing.

We studied the efficacies of ofloxacin, rifampin, and clindamycin in a Staphylococcus aureus abscess model and seven antimicrobial regimens in an intracellular killing assay. Ofloxacin plus rifampin was the most effective regimen in the abscess model, and rifampin and ofloxacin were the most active regimens in the intracellular killing assay.

Does pulmonary airway inflammation relate to intercellular adhesion molecule (ICAM-1) in bronchoalveolar lavage specimens? A pilot study.

BACKGROUND: The objective of this study was to assess the value of intercellular adhesion molecule-1 (ICAM-1) levels in bronchoalveolar lavage (BAL) specimens. METHODS: BALs from 44 unselected patients undergoing routine diagnostic bronchoscopy with bronchoalveolar lavage were studied. Cell-free supernatants of the BAL specimens were frozen at -70 degrees C until tested. BAL ICAM-1 concentration was measured using enzyme immunoassay and degree of patient illness assessed by modified APACHE II scores. RESULTS: ICAM-1 in BAL fluid was positively correlated to the patient illness score (modified APACHE II) at a p value of 0.026. No such association was found between ICAM-1 levels and cigarette use or infection with pneumocystis carinii, although a few individuals in the smoker's group with pulmonary infection had 10-fold elevations of BAL ICAM-1. CONCLUSIONS: BAL ICAM-1 may relate to the pulmonary pathogenic process as supported by the association between modified APACHE II scores and ICAM-1 values. Specific pulmonary-related diagnosis and BAL ICAM-1 did not produce significant relationships in this study.

Coronary vascularization during development in the rat and its relationship to basic fibroblast growth factor.

OBJECTIVE: Our overall aims were to elucidate the temporal and spatial sequence of coronary vascularization during development in the rat, and to determine whether basic fibroblast growth factor expression corresponds to any phase of the vascularization process. METHODS: Immunohistochemical, histochemical, morphometric and in situ hybridization analyses were performed on prenatal and postnatal hearts of various ages. RESULTS: Coronary vascularization, which begins at embryonic day 13 (E13) with blood island-like structures in the epicardium, progresses from this layer toward the endocardium as indicated by a transmural gradient of vascular volume throughout the ventricles. Vascular smooth muscle first appears in E17 hearts at the time a capillary-like plexus coalesces and penetrates the aorta to form the main coronary arteries. These vessels maintain an anastomatic morphology and must undergo subsequent remodeling in order to assume adult branching characteristics. The early postnatal period is characterized by development of the arterial tree and the enzymatic differentiation of the arteriolar and venular ends of the capillary bed. Although bFGF is expressed both prenatally and postnatally, the highest mRNA expression was noted during the early period of vascularization (E14 and E15), and the early neonatal period (1-6 days) which corresponds to a period of substantial microvascular growth. CONCLUSIONS: Coronary vascularization follows a temporal sequence which includes transmural expansion of the capillary bed, arteriolar formation subsequent to vascular penetration of the aorta, and postnatal growth, differentiation, and remodeling. Since high levels of bFGF expression are correlated with key time points in coronary vascular growth, bFGF may play an important role in this process.

Azithromycin in an experimental Staphylococcus aureus abscess model.

We studied the efficacy and pharmacokinetics of azithromycin in a rabbit tissue-cage Staphylococcus aureus abscess model. A dosage of 15 mg/kg/day azithromycin was administered to rabbits with 24 h or 2 week old infected tissue cages and to uninfected controls. Concentrations of azithromycin were higher in the infected compared with the uninfected tissue cages. Azithromycin was effective in reducing the bacterial concentrations in both groups of infected tissue cages by approximately 3 log10 cfu/mL compared with untreated controls after 8 days of therapy. Fifty percent of the 24 h and 29% of the 2 week infected tissue cages became culture-negative.

Contribution of the host to test results in assays of Staphylococcus epidermidis.

From two human populations (one pediatric and one adult), clinically diagnosed with Staphylococcus epidermidis (S. epidermidis) sepsis of similar severity, bacteria were isolated from pre-antibiotic blood samples and evaluated for virulence. The LD50 of the bacteria in a mouse model was performed, with evaluation of animals dying acutely following intravenous S. epidermidis administration. More simple assays of virulence were also performed, including bacterial adherence to a fibrin clot and carbohydrate specific lectin binding. The eight pediatric-host S. epidermidis isolates required a significantly larger dose to produce lethality in dosed animals (LD50) when compared to the 20 adult-host S. epidermidis isolates. The fibrin clot assay, a test that has corroborated bacterial virulence in endocarditis models, did not differentiate the groups: all but one of the 28 isolates were well above the adherence seen with the ATCC control, suggesting endocarditis-producing potential. Glycocalyx (slime) from eight of the more virulent isolates showed reactivity with a glucose-specific biotinylated lectin which was lacking in other isolates. Necropsy of mice dying at 12 hr showed S. epidermidis strain differences in specific organ effects. Overall, this study demonstrates the utility of the LD50 to provide a highly sensitive quantification of bacterial virulence. Necropsy of test animals dying acutely has showed an apparent organ tropism of some of these isolates which are usually considered harmless commensals.

Bacterial characterization in Staphylococcus epidermidis septicemia.

An analysis of the in vitro characteristics of Staphylococcus epidermidis strains isolated from patients with true S. epidermidis septicemia was undertaken. From a potential population of 921 cultures from adult patients with coagulase-negative bacteremia, highly defined selective criteria limited the population to 20 patients with S. epidermidis sepsis, from whose blood cultures the study organisms were isolated. Another population of 11 S. epidermidis blood isolates, clinically determined to be contaminants, were tested as a control group. In vitro assays performed on all isolates included slime quantification, hydrophobicity, surface hexoses, and capsule presence. Murine spleen phagocytosis of intravenously administered isolates was measured in vivo. The assayed quantity of cell-associated bacterial hexose sugars positively correlated with organism virulence to the host (p = 0.02). This bacterial population was also low in slime but varied as to the presence of capsule and ease of phagocytosis. Permanent catheter-bearing patients' bacteria were somewhat more hydrophobic (p = 0.07). We conclude that in vitro assays can differentiate bacteremic cultures from contaminants and that the characteristic that best relates to host toxicity in these S. epidermidis isolates was bacterial cell surface-associated carbohydrate.

The effect of zinc on microbial growth and bacterial killing by cefazolin in a Staphylococcus aureus abscess milieu.

Microbial growth and antimicrobial bacterial killing are both diminished in abscesses. It was postulated that zinc depletion in abscesses, perhaps secondary to a neutrophil protein resembling calprotectin, may be partly responsible for these effects. In a rabbit tissue-cage abscess model, pooled abscess supernatant concentration of zinc was < 1.53 microM. The addition of 41.7 microM zinc had no effect on Staphylococcus aureus growth or the bacterial killing effect of cefazolin in serum. In abscess fluid supernatants, bacterial growth without antibiotic and bacterial killing by cefazolin were both enhanced by the addition of zinc. Fractionation of the abscess fluid with ultrafiltration membranes showed that these effects could be reproduced with the fraction between 30 and 50 kDa. These findings suggest that a protein in abscess fluid supernatants that resembles the neutrophil protein calprotectin may, through its zinc binding effects, inhibit microbial growth within an abscess but also inhibit the activity of bactericidal antibiotics.