Estimation of Stature from Arm Span in Medical Students of Maharashtra, India.

BACKGROUND: Stature can be estimated from body parameters in dead and mutilated bodies using regression equation or multiplication factor. However, regression equations and multiplication factors are specific for the region only and can't be used in all population. AIM: To formulate regression equation and multiplication factor for the estimation of stature from arm span (AS) for a region in Maharashtra, India. SUBJECTS AND METHODS: It was a cross-sectional study, did over a period of 2 years, from October 2011 to September 2013. Four hundred students of three Government medical colleges of Maharashtra, aged 18-24 years were enrolled in the study. Stature and AS were measured and subjected to statistical analysis. Unpaired t-test and simple linear regression were used. RESULTS: Stature and AS of 400 medical students (219 males and 181 females) were measured. Subjects were divided into six groups depending upon age. Simple regression equation and multiplication factor for male and female and for each age group were derived for estimation of stature. We found correlation coefficient (R) of 0.89 in male and 0.90 in female using simple regression, which shows strong correlation between stature and AS. CONCLUSION: Mean stature and AS of male were more than female with statistical significance. Stature can be accurately estimated from AS using simple regression equation or multiplication factor.

Molecular characterization of intergeneric hybrid between Aspergillus oryzae and Trichoderma harzianum by protoplast fusion.

AIMS: Protoplast fusion between Aspergillus oryzae and Trichoderma harzianum and application of fusant in degradation of shellfish waste. METHODS AND RESULTS: The filamentous chitinolytic fungal strains A. oryzae NCIM 1272 and T. harzianum NCIM 1185 were selected as parents for protoplast fusion. Viable protoplasts were released from fungal mycelium using enzyme cocktail containing 5 mg ml(-1) lysing enzymes from T. harzianum, 0.06 mg ml(-1) ß-glucuronidase from Helix pomatia and 1 mg ml(-1) purified Penicillium ochrochloron chitinase in 0.8 mol l(-1) sorbitol as an osmotic stabilizer. Intergeneric protoplast fusion was carried out using 60% polyethylene glycol as a fusogen. At optimum conditions, the regeneration frequency of the fused protoplasts on colloidal chitin medium and fusion frequency were calculated. Fusant showed higher rate of growth pattern, chitinase activity and protein content than parents. Fusant formation was confirmed by morphological markers, viz. colony morphology and spore size and denaturation gradient gel electrophoresis (DGGE). CONCLUSIONS: This study revealed protoplast fusion between A. oryzae and T. harzianum significantly enhanced chitinase activity which ultimately provides potential strain for degradation of shellfish waste. Consistency in the molecular characterization results using DGGE is the major outcome of this study which can be emerged as a fundamental step in fusant identification. SIGNIFICANCE AND IMPACT OF THE STUDY: Now it is need to provide attention over effective chitin degradation to manage shrimp processing issues. In this aspect, ability of fusant to degrade shellfish waste efficiently in short incubation time revealed discovery of potential strain in the reclamation of seafood processing crustacean bio-waste.

Optimization of medium for indole-3-acetic acid production using Pantoea agglomerans strain PVM.

AIMS: To optimize the medium components for the production of indole-3-acetic acid (IAA) by isolated bacterium Pantoea agglomerans strain PVM. METHODS AND RESULTS: Present study deals with the production of an essential plant hormone IAA by a bacterial isolate P. agglomerans strain PVM identified by 16S rRNA gene sequence analysis. The medium containing 8g l(-1) of meat extract and 1g l(-1) of l-tryptophan (precursor) at optimum pH 7, 30°C and 48-h incubation gave the maximum production of IAA (2·191 g l(-1) ). Effect of IAA synthesized on in vitro root induction in Nicotiana tobacum (leaf) explants was compared with that of control. IAA was characterized by high-performance thin-layer chromatography, high-performance liquid chromatography and gas chromatography-mass spectroscopy. CONCLUSIONS: Pantoea agglomerans strain PVM was a good candidate for the inexpensive and utmost production of IAA in short period, as it requires simple medium (meat extract and l-tryptophan). SIGNIFICANCE AND IMPACT OF THE STUDY: The present report first time showed the rapid, cost-effective and maximum production of IAA. No reports are available on the optimization of particular medium components for the production of IAA. This study demonstrates a novel approach for in vitro root induction in N. tobacum (leaf) explants.

Communal action of microbial cultures for Red HE3B degradation.

The consortium PMB11 consisting of three bacterial species, originally isolated from dye contaminated soil was identified as Bacillus odysseyi SUK3, Morganella morganii SUK5 and Proteus sp. SUK7. The consortium possessed the ability to decolorize various textile dyes as well as mixtures of dyes. PMB11 could decolorize Red HE3B (50 mg l(-1)) with 99% of decolorization within 12 h in nutrient broth, while in mineral medium it could decolorize up to 97% within 24h. Induction in the activities of various oxidative and reductive enzymes indicates the involvement of these enzymes in decolorization. Biodegradation of the dye was monitored using UV-vis spectroscopy, HPLC and FTIR analysis. The Red HE3B degradation pathway was proposed by GC-MS analysis. Various metabolites formed after the degradation were identified as 2,5-diaminobenzene 6-aminotriazine, aniline 2-sulfate, aniline 3-sulfate, 2-amino 5-chlorotriazine and naphthalene. Phytotoxicity studies revealed that metabolites formed after degradation were significantly less toxic in nature.

Evaluation of the efficacy of a bacterial consortium for the removal of color, reduction of heavy metals, and toxicity from textile dye effluent.

A microbial consortium DAS consisting three bacterial sp. originally obtained from dye contaminated sites of Solapur, India was selected because it was capable of decolorizing textile effluent and dye faster than the individual bacteria under static conditions. Identification of the isolates by 16S rRNA techniques revealed the isolates to be Pseudomonas species. The concerted metabolic activity of these isolates led to complete decolorization of textile effluent as well as Reactive Orange 16 (100 mg l(-1)) within 48-h at pH 7 and 30 degrees C. Studies involving Reactive Orange 16 (RO16) dye were carried with the bacterial consortium DAS to elucidate the mechanism of biodegradation. Induction of the laccase and reductase enzyme during RO16 decolorization indicated their role in biodegradation. The biodegradation of RO16 was monitored by using IR spectroscopy, HPLC and GC-MS analysis. Cytotoxicity, genotoxicity and phytotoxicity studies carried out before and after decolorization of the textile effluent revealed the nontoxic nature of the biotreated sample.

Ecofriendly biodegradation and detoxification of Reactive Red 2 textile dye by newly isolated Pseudomonas sp. SUK1.

The aim of this work is to evaluate textile dyes degradation by novel bacterial strain isolated from the waste disposal sites of local textile industries. Detailed taxonomic studies identified the organisms as Pseudomonas species and designated as strain Pseudomonas sp. SUK1. The isolate was able to decolorize sulfonated azo dye (Reactive Red 2) in a wide range (up to 5 g l(-1)), at temperature 30 degrees C, and pH range 6.2-7.5 in static condition. This isolate also showed decolorization of the media containing a mixture of dyes. Measurements of COD were done at regular intervals to have an idea of mineralization, showing 52% reduction in the COD within 24h. Induction in the activity of lignin peroxidase and azoreductase was observed during decolorization of Reactive Red 2 in the batch culture, which represented their role in degradation. The biodegradation was monitored by UV-vis, IR spectroscopy, HPLC. The final product, 2-naphthol was characterized by GC-mass spectroscopy. The phytotoxicity study revealed the degradation of Reactive Red 2 into non-toxic product by Pseudomonas sp. SUK1.

Biodegradation of Reactive Blue 59 by isolated bacterial consortium PMB11.

Morphologically different, three bacterial strains, capable of decolorizing Reactive Blue 59 were isolated from dye effluent contaminated soil sample, collected from Ichalkaranji, India. The individual bacterial strains viz. Bacillus odysseyi SUK3, Morganella morganii SUK5 and Proteus sp. SUK7 decolorized Reactive Blue 59 (50 mg l(-1)) completely within 60, 30, 24 h, respectively, while the bacterial consortium PMB11 of these strains required 3 h for the complete decolorization. The decolorization was confirmed by UV-Vis spectroscopy. Further, the biodegradation of Reactive Blue 59 in to different metabolites was confirmed by High performance liquid chromatography and Fourier transform infrared spectroscopy analysis. Significant increase in the activity of aminopyrine N-demethylase (AND) in the individual as well consortium cells, obtained after decolorization showed involvement of AND in the decolorization process. Phytotoxicity studies, revealed the nontoxic nature of the degraded metabolites of Reactive Blue 59 indicating effectiveness of bacterial consortium PMB11 for the treatment of textile effluent containing Reactive Blue 59.

Biodegradation of reactive textile dye Red BLI by an isolated bacterium Pseudomonas sp. SUK1.

A novel bacterial strain capable of decolorizing reactive textile dye Red BLI is isolated from the soil sample collected from contaminated sites of textile industry from Solapur, India. The bacterial isolate was identified as Pseudomonas sp. SUK1 on the basis of 16S rDNA analysis. The Pseudomonas sp. SUK1 decolorized Red BLI (50 mg l(-1)) 99.28% within 1h under static anoxic condition at pH range from 6.5 to 7.0 and 30 degrees C. This strain has ability to decolorize various reactive textile dyes. UV-Vis spectroscopy, FTIR and TLC analysis of samples before and after dye decolorization in culture medium confirmed decolorization of Red BLI. A significant increase in the activities of aminopyrine N-demethylase and NADH-DCIP reductase in cells obtained after decolorization indicates involvement of these enzymes in the decolorization process. Phytotoxicity testing with the seeds of Sorghum vulgare and Phaseolus mungo, showed more sensitivity towards the dye, while the products obtained after dye decolorization does not have any inhibitory effects.

Effects of dextromethorphan on dopamine dependent behaviours in rats.

Dextromethorphan, a noncompetitive blocker of N-methyl-D- aspartate (NMDA) type of glutamate receptor, at 7.5-75 mg/kg, ip did not induce oral stereotypies or catalepsy and did not antagonize apomorphine stereotypy in rats. These results indicate that dextromethorphan at 7.5-75 mg/kg does not stimulate or block postsynaptic striatal D2 and D1 dopamine (DA) receptors. Pretreatment with 15 and 30 mg/kg dextromethorphan potentiated dexamphetamine stereotypy and antagonised haloperidol catalepsy. Pretreatment with 45, 60 and 75 mg/kg dextromethorphan, which release 5-hydroxytryptamine (5-HT), however, antagonised dexamphetamine stereotypy and potentiated haloperidol catalepsy. Apomorphine stereotypy was not potentiated or antagonised by pretreatment with 7.5-75 mg/kg dextromethorphan. This respectively indicates that at 7.5-75 mg/kg dextromethorphan does not exert facilitatory or inhibitory effect at or beyond the postsynaptic striatal D2 and D1 DA receptors. The results are explained on the basis of dextromethorphan (15-75 mg/kg)-induced blockade of NMDA receptors in striatum and substantia nigra pars compacta. Dextromethorphan at 15 and 30 mg/kg, by blocking NMDA receptors, activates nigrostriatal dopaminergic neurons and thereby potentiates dexampetamine stereotypy and antagonizes haloperidol catalepsy. Dextromethorphan at 45, 60 and 75 mg/kg, by blocking NMDA receptors, releases 5-HT and through the released 5-HT exerts an inhibitory influence on the nigrostriatal dopaminergic neurons with resultant antagonism of dexampetamine stereotypy and potentiation of haloperidol catalepsy.

Decolourization of azo dye methyl red by Saccharomyces cerevisiae MTCC 463.

Saccharomyces cerevisiae MTCC 463 decolourizes toxic azo dye, methyl red by degradation process. Methyl red (100mgl(-1)) is degraded completely within 16min in plain distilled water under static anoxic condition, at the room temperature. Effect of physicochemical parameters (pH of medium, composition of medium, concentration of cells, concentration of dye, temperature and agitation) on methyl red decolourization focused the optimal condition required for decolourization. Biodegradation (fate of metabolism) of methyl red in plain distilled water was found to be pH dependent. Cells of Saccharomyces cerevisiae could degrade methyl red efficiently up to 10 cycles in plain distilled water. Analysis of samples extracted with ethyl acetate from decolourized culture flasks in plain distilled water (pH 6.5) and at pH 9 using UV-VIS, TLC, HPLC and FTIR confirm biodegradation of methyl red into several different metabolites. A study of the enzymes responsible for the biodegradation of methyl red in the control and cells obtained after decolourization in plain distilled water (pH 6.5) and at pH 9 showed different levels of the activities of laccase, lignin peroxidase, NADH-DCIP reductase, azoreductase, tyrosinase and aminopyrine N-demethylase. A significant increase in the activities of lignin peroxidase and NADH-DCIP reductase was observed in the cells obtained after decolourization in plain distilled water (pH 6.5), however cells obtained at pH 9 shows increased activities of azoreductase, tyrosinase, lignin peroxidase and NADH-DCIP reductase. High efficiency to decolourize methyl red in plain distilled water and low requirement of environmental conditions enables this yeast to be used in biological treatment of industrial effluent containing azo dye, methyl red.

Biotransformation of malachite green by Saccharomyces cerevisiae MTCC 463.

In recent years, use of microbial biomass for decolourization of textile industry wastewater is becoming a promising alternative in which some bacteria and fungi are used to replace present treatment processes. Saccharomyces cerevisiae MTCC 463 decolourized the triphenylmethane dyes (malachite green, cotton blue, methyl violet and crystal violet) by biosorption, showing different decolourization patterns. However, malachite green decolourized by biosorption at the initial stage and further biodegradation occurred, about 85% in plain distilled water within 7 h, and about 95.5% in 5% glucose medium within 4 h, under aerobic conditions and at room temperature. Decolourization of malachite green depends on various conditions, such as concentration of dye, concentration of cells, composition of medium and agitation. HPLC, UV-VIS, FTIR and TLC analysis of samples extracted with ethyl acetate from decolourized culture flasks confirmed the biodegradation of malachite green into several metabolites. A study of the enzymes responsible for the biodegradation of malachite green in the control and cells obtained after decolourization showed the activities of laccase, lignin peroxidase, NADH-DCIP reductase, malachite green reductase and aminopyrine N-demethylase in control cells. A significant increase in the activities of NADH-DCIP reductase and MG reductase was observed in the cells obtained after decolourization, indicating a major involvement of reductases in malachite green degradation.

Involvement of central serotonergic systems in dextromethorphan-induced behavioural syndrome in rats.

Dextromethorphan, a noncompetitive blocker of the N-methyl-D-aspartate (NMDA) type of glutamate receptor, at 45, 60 and 75 mg/kg, ip doses induced a behavioural syndrome characterised by reciprocal forepaw treading, lateral head-weaving, hind-limb abduction and flat body posture. Such type of behavioural syndrome is induced by 8-hydroxy-2- (di-n-propylamino) tetralin (8-OH-DPAT) by directly stimulating the central postsynaptic 5-hydroxytryptamine (5-HT, serotonin) receptors of the 5-HT1A type. Pretreatment with buspirone (5, 10 mg/kg, ip) and l-propranolol (10, 20 mg/kg, ip) antagonised the behavioural syndrome induced by 8-OH-DPAT and dextromethorphan. Pretreatment with p-chlorophenylalanine (100 mg/kg/day x 4 days) antagonised the behavioural syndrome induced by dextromethorphan and dexfenfluramine but had no significant effect on 8-OH-DPAT induced behavioural syndrome. This indicates that dextromethorphan induces the behavioural syndrome by releasing 5-HT from serotonergic neurons with resultant activation of the postsynaptic 5-HT1A receptors by the released 5-HT. Pretreatment with fluoxetine (10 mg/kg, ip) significantly potentiated the behavioural syndrome induced by dextromethorphan and 5-hydroxytryptophan but significantly antagonised dexfenfluramine induced behavioural syndrome. This indicates that dextromethorphan releases 5-HT by a mechanism which differs from that of dexfenfluramine. Dextromethorphan may be releasing 5-HT by blocking the NMDA receptors and thereby counteracting the inhibitory influence of l-glutamate on 5-HT release.

Effects of pentazocine on dopamine-dependent behaviours in mice.

Pentazocine, a kappa opioid receptor agonist, induced catalepsy in mice suggesting thereby that it might possess postsynaptic striatal D 2 dopamine (DA) receptor blocking activity. However, our other findings, that pentazocine pretreatment did not antagonise the cage climbing behaviour induced by the directly acting DA agonist apomorphine in mice and actually potentiated the stereotyped behaviour induced by the indirectly acting DA agonist methamphetamine in mice, indicate that pentazocine does not possess postsynaptic striatal and mesolimbic D 2 DA receptor blocking activity. Pretreatment with naloxone, an antagonist of opioid receptors, antagonised pentazocine-induced catalepsy. This suggests the possible involvement of opioid mechanisms in the induction of catalepsy by pentazocine in mice.

Involvement of dopaminergic mechanisms in racemate pentazocine induced stereotyped behaviour in rats.

Racemate pentazocine was found to induce stereotyped behaviour (SB) in rats. Pretreatment with haloperidol and alpha-methyl-p-tyrosine significantly antagonised dl-pentazocine induced SB. This indicates that dl-pentazocine induces SB by releasing dopamine (DA) from the nigrostriatal and mesolimbic dopaminergic neurones with resultant activation of the postsynaptic striatal and mesolimbic D2 DA receptors by the released DA. However, pretreatment with naloxone failed to significantly modify dl-pentazocine induced SB indicating thereby that opioid mechanisms are not involved in the DA releasing action of dl-pentazocine. Our findings are explained on the basis of recent reports that the d-isomer of pentazocine releases DA by stimulating sigma receptors located on the nigrostriatal and mesolimbic dopaminergic neurones.

Thalidomide in lepra reaction (ENL) in lepromatous leprosy patients.

Six male bacteriologically highly positive patients of lepromatous leprosy with ENL reaction not adequately controlled by conventional antireaction drugs were put on thalidomide 400 mg per day in four divided doses. Reaction was controlled between 13th to 18th day of therapy. There was no change in the bacteriological status. Liver functions, renal functions and hemogram were normal before therapy and remained unaltered at the end of treatment. Apart from fatigue, drowsiness and occassional constipation, thalidomide had no adverse effect. Control of ENL reaction by thalidomide in these patients is probably due to its immunosuppressive effect, more likely by its stablising action on lysosomes.

Effects of naloxone on methamphetamine and apomorphine stereotypy and on haloperidol catalepsy in rats.

Pretreatment with the opiate antagonist naloxone, at 1.25-5 mg/kg, increased the intensity of methamphetamine stereotypy, had no effect (over a range of 0.3125-5 mg/kg) on apomorphine stereotypy, and antagonized haloperidol catalepsy in rats at 1.25-5 mg/kg. It is suggested that naloxone, by blocking the opiate receptors located on the nigro-striatal and mesolimbic dopamine (DA) nerve terminals, releases the DA systems from endogenous inhibition, presumably caused by endogenous opiate systems, and thereby potentiates methamphetamine stereotypy and antagonizes haloperidol catalepsy. However, the possibility that naloxone might have affected methamphetamine stereotypy and haloperidol catalepsy by modulating the activity of the central noradrenergic and GABAergic systems, which are reported to influence dopaminergically mediated behaviours, also needs to be considered.

Involvement of histaminergic mechanisms in the cataleptogenic effect of morphine in mice.

Intraperitoneally administered morphine induced catalepsy in mice. Morphine pretreatment however, failed to antagonize apomorphine-induced cage climbing behaviour thereby ruling out the possibility of its possessing DA receptor blocking activity. Pretreatment with L-histidine, a precursor of histamine, and atropine, potentiated the cataleptic effect of morphine whilst pretreatment with chlorcyclizine, an H1 receptor blocker, and naloxone, a morphine antagonist, antagonized morphine-catalepsy. Pretreatment with metiamide, an H2 receptor blocker, and methysergide, a 5-HT antagonist, did not significantly alter the cataleptic effect of morphine. The results with L-histidine and chlorcyclizine suggest an involvement of central histaminergic mechanisms in the cataleptogenic effect of morphine in mice. Further, as the cataleptic effect of morphine was also antagonized by naloxone it appears that the interaction of morphine with the central histaminergic mechanisms is mediated through specific opiate receptors.