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a total of 67 mulberry accessions have been conserved in vitro and 238 accessions have been successfully cry preserved .
शहतूत की कुल 67 नई प्रजातियों को परखनलियों में संरक्षित किया गया और 238 को सफलतापूर्वक क्रायोप्रिजर्व किया गया ।
preliminary data indicate that high doses of ribavirin are necessary to inhibit sars-cov-2 in vitro.
प्रारंभिक आँकड़ों से संकेत मिलता है कि कृत्रिम परिवेशीय sars-cov-2 के संदमन के लिए रिबाविरिन की उच्च खुराकें आवश्यक हैं।
the advent of new techniques made it possible to bring about mutations in vitro by deliberate design instead of blind chance .
इन नयी तकनीकों के आगमन से शरीर के बाहर किसी पात्र में उत्परिवर्तन करना संभव हो गया हैz तथा ऐसा करना कोई संयोग से होने वाली घटना नहीं हे . यह किसी योजनाबद्ध तरीके से करवाया जा सकता है .
when the recombination in vitro between vehicle and passenger dna is completed , the recombinant dna must be introduced into he host cell where it can replicate .
शरीर के बाहर वाहन तथा यात्री डी . एन . ए . का पुनर्मिलासप पूरा होने के बाद यह आवश्यक हो जाता है कि इस पुनर्मिलापी डी . एन . ए . को किसी ऐसी आतिथेयी कोशिका में प्रविष्ट कराया जाये जहां वह अपनी प्रतिकृति का निर्माण कर सकता है .
studies carried out at sree chitra tirunal institute for medical sciences and technology , trivandrum , using an in vitro cell culture model to evaluate the response of adult rat cardiac fibroblasts to hypoxia ;
श्री चित्रा तिरूनल आयुर्विज्ञान और प्रौद्योगिकी संस्थान , तिरूवनंतपुरम में वयस्क चूहे के हृदय की फाइब्रोब्लास्ट की हाइपोक्सिया के प्रति प्रतिक्रिया के आकलन के लिए परखनली में कोशिका संवर्धन मॉडल में इस्तेमाल से अध्ययन किए गए ,
sars-cov and mers-cov can survive in vitro for 48 hours in a dry environment and up to 5 days under 20 °c and 40%-50% humidity.
sars-cov और mers-cov कृत्रिम परिवेशीय शुष्क वातावरण में 48 घंटे और 20 °c से कम और 40%-50% आद्रता पर 5 दिन तक जीवित रह सकता है।
inputs and services - soil health : good quality seeds , disease free planting material , including in - vitro cultured propagules and soil health enhancement hold the key to raising small farm productivity .
भूमि की देखभाल हेतु सेवाएँ और निवेश - अच्छी गुणवत्ता के बीज , रोगमुक्त रोपण सामग्री - जिसमें हरित गृह में उगाए बीज - और मिट्टी की गुणवत्ता को बढ़ाकर छोटे खेतों की उत्पादकता बढ़ाई जाएगी ।
duchenne muscular dystrophy, a severe type of muscle weakness that usually begins at an early age and worsens quickly, may soon have a new strategy of treatment through genetic regulation. there is no known cure for duchenne muscular dystrophy. treatments usually aim to control symptoms to improve quality of life. sandeep eswarappa, assistant professor indian institute of science (iisc), bengaluru one of the 21 recipients of this year’s swarnajayanti fellowship of the department of science and technology (dst), government of india proposes to supress the disease-causing premature stop codon or the genetic process that initiates these diseases. he is trying to bring about the suppression through translational readthrough, a gene regulatory principle found in humans, yeasts, bacteria and drosophila which takes place with the variation of the genetic code. prof. sandeep’s group has been developing strategies to induce translational readthrough across genetic diseases caused by non-sense mutations --a change in dna that causes a protein to terminate or end its translation earlier than expected. they were successful in achieving this in vitro in case of thalassemia and are working on other disease models. this research work has been published in the scientific journal ‘biochemistry’ recently. with the swarna jayanti fellowship, they will extend it to duchenne muscular dystrophy. if successful, this project may lead to novel therapeutics for the treatment of genetic diseases like thalassemia, duchenne muscular dystrophy, haemophilia. in case of any protein formation genetic information present in the genome is first transcribed into an mrna, which in turn is translated into a protein. protein synthesis or translation is executed by macromolecular machinery called ribosomes. ribosomes start this process at a specific location on an mrna called ‘start codon’ and terminate at a stop signal called ‘stop codon’. in case of diseases with nonsense mutations, such mutations result in premature stop signal in mrna often resulting in non-functional truncated protein. prof. sandeep eswarappa’s laboratory at iisc has shown that in certain mrnas, under certain conditions, translating ribosomes misread the stop signal and continue till they encounter another stop signal. in this translational readthrough process, a longer protein is synthesized with an extension. this extension might change the properties of the protein. the experiments carried out by his group have revealed that such long proteins can have different localization, stability and function. “the knowledge we have already gained from our experiment have opened an unexpected avenue to treat genetic diseases caused by non-sense mutations like duchenne muscular dystrophy, haemophilia and so on,” said prof. sandeep.
duchenne muscular dystrophy, a severe type of muscle weakness that usually begins at an early age and worsens quickly, may soon have a new strategy of treatment through genetic regulation. there is no known cure for duchenne muscular dystrophy. treatments usually aim to control symptoms to improve quality of life. sandeep eswarappa, assistant professor indian institute of science (iisc), bengaluru one of the 21 recipients of this year’s swarnajayanti fellowship of the department of science and technology (dst), government of india proposes to supress the disease-causing premature stop codon or the genetic process that initiates these diseases. he is trying to bring about the suppression through translational readthrough, a gene regulatory principle found in humans, yeasts, bacteria and drosophila which takes place with the variation of the genetic code. prof. sandeep’s group has been developing strategies to induce translational readthrough across genetic diseases caused by non-sense mutations --a change in dna that causes a protein to terminate or end its translation earlier than expected. they were successful in achieving this in vitro in case of thalassemia and are working on other disease models. this research work has been published in the scientific journal ‘biochemistry’ recently. with the swarna jayanti fellowship, they will extend it to duchenne muscular dystrophy. if successful, this project may lead to novel therapeutics for the treatment of genetic diseases like thalassemia, duchenne muscular dystrophy, haemophilia. in case of any protein formation genetic information present in the genome is first transcribed into an mrna, which in turn is translated into a protein. protein synthesis or translation is executed by macromolecular machinery called ribosomes. ribosomes start this process at a specific location on an mrna called ‘start codon’ and terminate at a stop signal called ‘stop codon’. in case of diseases with nonsense mutations, such mutations result in premature stop signal in mrna often resulting in non-functional truncated protein. prof. sandeep eswarappa’s laboratory at iisc has shown that in certain mrnas, under certain conditions, translating ribosomes misread the stop signal and continue till they encounter another stop signal. in this translational readthrough process, a longer protein is synthesized with an extension. this extension might change the properties of the protein. the experiments carried out by his group have revealed that such long prote “the knowledge we have already gained from our experiment have opened an unexpected avenue to treat genetic diseases caused by non-sense mutations like duchenne muscular dystrophy, haemophilia and so on,” said prof. sandeep.
Última actualización: 2021-03-15
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