In vitro evaluation of medicinal plant extracts against Pestalotiopsis mangiferae

A serious leaf-spot disease of Mangifera indica was noted during the last 10 years in Satpura plateau of India. On the basis of characteristic symptoms and cultural characters, the pathogen was identified as Pestalotiopsis mangiferae which is hitherto not reported from Satpura plateau of India. Screening of 17-medicinal plants against the test pathogen revealed 14 antimycotic whereas 3-plants, viz., Argemone mexicana, Caesalpinia bonducella, and Casia fistula acclerated the growth of the pathogen. The maximum activity was shown by Eucalyptus globulus (88%) and Catharanthus roseus (88%) followed by Ocimum sanctum (85.50%), Azadirachta indica (84.66%), Ricinus communis (75%) and Lawsonia inermis (74.33%) while the minimum activity was exhibited by Jatropha curcas (10%).     

Modelling of hydrolysis controlled anaerobic digestion

A mathematical model of anaerobic digestion has been developed which considers the process as occurring through hydrolysis followed by a sequence of steps which have been considered together as a pseudo-first order process. The Michaelis-Menten equation has been modified to incorporate variable enzyme concentration. An immobilized reactor has been designed, fabricated and operated on cowdung feed to obtain data for estimating the model parameters by non-linear regression. These model parameters were used to predict the performance of the reactor and good agreement between experimental and predicted values was observed. The model was further tested satisfactorily on data from the literature. From the parameters estimated it was concluded that hydrolysis was the slowest stage and that the mass transfer of hydrolytic enzyme from microbe to bulk was the rate controlling step in this stage. The hydrolysis reaction, represented by a modified Michaelis-Menten equation, was reduced to first order in bulk enzyme concentration and zero order in substrate concentration thereby emphasizing the significance of bulk enzyme concentration.     

Current status of neonatal screening for congenital adrenal hyperplasia

Randomized trials are the optimal approach for evaluations of treatment efficacy but may not always be feasible. We study the adequacy of the case-control design in evaluating efficacy in a situation where the investigated therapy, namely the administration of magnesium sulfate for the prevention of eclampsia in patients with preeclampsia, has a suspected strong protective effect. A total of 66 cases of eclampsia were ascertained from among deliveries occurring between 1977 and 1992 at two hospitals in Houston, Texas. Randomly selected preeclamptic controls were matched to cases based on hospital and month of delivery. Magnesium sulfate administration prior to seizure occurrence had a strong protective effect against eclampsia in patients with preeclampsia (OR, 0.02; 95% CI, 0.01-0.05). This protective effect remained when controls were stratified by the degree of severity of preeclampsia (mild-to-moderate OR, 0.03, 95% CI, 0.01-0.09 and severe OR, 0.005; 95% CI, 0.0005-0.04) and when cases were stratified by the timing of the first seizure (antepartum and intrapartum seizures OR, 0.01; 95% CI, 0.003-0.05 and postpartum seizures OR, 0.03; 95% CI, 0.005-0.15). The effect also remained after adjustment for other important predictors in a multivariate logistic regression model (OR, 0.11; 95% CI, 0.03-0.38). The results of this study are in support of a recent randomized trial on the efficacy of magnesium sulfate as a prophylactic agent against eclampsia. Although there are serious potential sources of bias in this study, the magnitude of the protective effect of magnesium sulfate minimizes the likelihood that this effect can be explained by bias. Observational studies could be appropriate complements or alternatives to randomized trials in situations where a strong treatment effect is expected.     

Perforin-dependent neurologic injury in a viral model of multiple sclerosis

In this study we demonstrate perforin-mediated cytotoxic effector function is necessary for viral clearance and may directly contribute to the development of neurologic deficits after demyelination in the Theiler's murine encephalomyelitis virus (TMEV) model of multiple sclerosis. We previously demonstrated major histocompatability complex (MHC) class I-deficient (beta2m-deficient) mice with an otherwise resistant genotype develop severe demyelination with minimal neurologic disease when chronically infected with TMEV. These studies implicate CD8(+) T cells as the pathogenic cell in the induction of neurologic disease after demyelination. To determine which effector mechanisms of CD8(+) T cells, granule exocytosis or Fas ligand expression, play a role in the development of demyelination and clinical disease, we infected perforin-deficient, lpr (Fas mutation), and gld (Fas ligand mutation) mice with TMEV. Perforin-deficient mice showed viral persistence in the CNS, chronic brain pathology, and demyelination in the spinal cord white matter. Perforin-deficient mice demonstrated severely impaired MHC class I-restricted cytotoxicity against viral epitopes, but normal MHC class II-restricted delayed-type hypersensitivity responses to virus antigen. Despite demyelination, virus-infected perforin-deficient mice showed only minimal neurologic deficits as indicated by clinical disease score, activity monitoring, and footprint analysis. Perforin- and MHC class II-deficient mice (with functional CD8(+) T cells and perforin molecules and an H-2(b) haplotype) had comparable demyelination and genotype, however, only the latter showed severe clinical disease. Gld and lpr mice demonstrated normal TMEV-specific cytotoxicity and maintained resistance to TMEV-induced demyelinating disease. These studies implicate perforin release by CD8(+) T cells as a potential mechanism by which neurologic deficits are induced after demyelination.     

Coercive and voluntary referrals: how ethnic minority adults get into mental health treatment

The relationship of oxidative stress with maximum life span (MLSP) in different vertebrate species is reviewed. In all animal groups the endogenous levels of enzymatic and non-enzymatic antioxidants in tissues negatively correlate with MLSP and the most longevous animals studied in each group, pigeon or man, show the minimum levels of antioxidants. A possible evolutionary reason for this is that longevous animals produce oxygen radicals at a low rate. This has been analysed at the place where more than 90% of oxygen is consumed in the cell, the mitochondria. All available work agrees that, across species, the longer the life span, the lower the rate of mitochondrial oxygen radical production. This is true even in animal groups that do not conform to the rate of living theory of aging, such as birds. Birds have low rates of mitochondrial oxygen radical production, frequently due to a low free radical leak in their respiratory chain. Possibly the low rate of mitochondrial oxygen radical production of longevous species can decrease oxidative damage at targets important for aging (like mitochondrial DNA) that are situated near the places of free radical generation. A low rate of free radical production can contribute to a low aging rate both in animals that conform to the rate of living (metabolic) theory of aging and in animals with exceptional longevities, like birds and primates. Available research indicates there are at least two main characteristics of longevous species: a high rate of DNA repair together with a low rate of free radical production near DNA. Simultaneous consideration of these two characteristics can explain part of the quantitative differences in longevity between animal species.     

An application of SPRT for detecting change point in a reliability growth model

The monotone likelihood ratio property of the gamma distribution is used to detect the change point in reliability growth model. Wald's Sequential Probability Ratio Test (SPRT) is applied to regulate the reliability of the gamma failure model. The Operating Characteristic and Average Sample Number functions are also discussed.     

Network Protocol Development with nsclick

Ad hoc network protocols are often developed, tested and evaluated using simulators. However, when the time comes to deploy those protocols for use or testing on real systems the protocol must be reimplemented for the target platform. This usually results in two, completely separate code-bases that must be maintained. Bugs which are found and fixed under simulated conditions must also be fixed separately in the deployed implementation, and vice versa. There is ample opportunity for the two implementations to drift apart, possibly to the point where the deployed and simulated version have little actual resemblance to each other. Testing the deployed version may also require construction of a testbed, a potentially time-consuming and expensive endeavor. Even if constructing an actual testbed is feasible, simulators are very useful for running large, repeatable scenarios for tasks such as protocol evaluation and regression testing. Furthermore, since the implementation may require modification of the kernel network stack, there's a good chance that a particular implementation may only run on specific versions of specific operating systems. To address these issues, we constructed the nsclick simulation environment by embedding the Click Modular Router inside of the popular ns-2 network simulator. Routing protocols may be implemented as Click graphs and easily moved between simulation and any operating system supported by Click. This paper describes the design, use, validation and performance of nsclick.