- End replication problem in eukaryotes accounts for loss of 20 base pairs per cell division.
- Oxidative stress accounts for loss of 50-100 base pairs per cell division.
What are the symptoms of heat rash?
- Heat rash does not go away on its own within a few days.
- You develop an infection in an area where you recently had heat rash.
How can I prevent heat rash?
- Allen’s Law – Allen
- Artificial Parthenogenesis – Loeb
- Axial Gradient theory – Child
- Bergman’s Rule – Bergman
- Biogenetic Law – Earnst Haeckel (1868)
- Biological Species Concept – Earnst Mayer
- Biogenesis Theory – Developed by F. Redi
- Chromosomal Theory of Inheritance – Sutton and Boveri
- Theory of natural selection – Charles Darwin
Anaerobic release of energy
Pure culture of Bacteria
Towrt and De Herelle (1915)
Saffermann and Morris
First description of cell (RBC)
Jan Swammerdam (1658)
Robert Hooke (1665)
Schleiden and Schwann
Robertis and Francis
Paleviz et. al (1975)
Ribosomes (Animal cell)
Astral rays and spindle
F.H.C. Crick (1918)
Willstartter and Fisher
C.A. Macmunn (1886)
Citric Acid cycle
Hans A. Krebs
Double Helical Structure of DNA
Watson and Crick
Biological Synthesis of DNA with template
biological synthesis of DNA without template
Extra embryonic membranes
Fertilization in plants
Gaseous exchange in blood
Genetic defects in human
Sir Archibald Garrod
Giant Salivary gland chromosomes
Beylis and Starling
Issacs and Linderman
Insulin use for treatment of diabetics
Rediscoverer of Mendelism
Correns, Hugo de Vries and Tschmark
Farmer and Moore
Hugo de Vries
Meishcher called it ‘Nuclein’
Karl E. Von Baer
Omnis cellula e cellula
Edward and Lewis
Garner and Allard
Park and Bigginis (1960)
Protoplasm Physical basis of life
Measuring gaseous exchange manometry
Locating DNA in cell
Avena curvature test
Teminism (Reverse Transcription)
Synthesis of urea
Obtained crystals of virus
International Women day
World Handicaps day
World Forest day
World Tuberculosis day
World Health day
World Earth day
International Sun day (Non-conventional Energy sources day)
World Red Cross day
World No Tobacco Day
World Environment day
World Population Day
Hiroshima and Nagasaki Day
Malaria day (mosquito day)
Blood Donation Day
World Animal Day
World habitat Day
World Food Day
World Diabetes Day
World AIDS Day
National Pollution Prevention Day
World conservation Day
International Day for Biological Diversity
- Abdul Qadir Khan Research Laboratories
- Energy Conservation Cell (ENERCON), Islamabad
- Drainage Research Institute of Pakistan (DRIP), Hyderabad
- Forestry Institute, Peshawar
- Ghulam Ishaq Khan Institute of Advanced Science and Technology, Tarbella
- Geological Survey of Pakistan, Rawalpindi
- Irrigation, Drainage, and Flood Control Research Council, Islamabad
- National Center for Technology Transfer (NCTT), Islamabad
- National Institute of Health (NIH), Islamabad
- Nuclear Institute of Agricultural Biology (NIAB), Faisalabad
- Pakistan Agricultural Research Council (PARC), Islamabad
- Pakistan Arts Council
- Pakistan Atomic Energy Commission (PAEC), Islamabad
- Pakistan Council of Industrial and Scientific Research (PCSIR)
- Pakistan Science Foundation (PSF), Islamabad
- Pakistan Health Research Council (PHRC), Islamabad
- Silicon Institute of Technology, Islamabad
- Space and Upper Atmosphere Research Council (SUPPARCO), Karachi
Har Gobind Khorana was born of Hindu parents in Raipur, a little village in Punjab, which is now part of eastern Pakistan. The correct date of his birth is not known; that shown in documents is January 9th, 1922. He is the youngest of a family of one daughter and four sons. His father was a «patwari», a village agricultural taxation clerk in the British Indian system of government. Although poor, his father was dedicated to educating his children and they were practically the only literate family in the village inhabited by about 100 people.
Har Gobind Khorana attended D.A.V. High School in Multan (now West Punjab); Ratan Lal, one of his teachers, influenced him greatly during that period. Later, he studied at the Punjab University in Lahore where he obtained an M. Sc. degree. Mahan Singh, a great teacher and accurate experimentalist, was his supervisor.
Khorana lived in India until 1945, when the award of a Government of India Fellowship made it possible for him to go to England and he studied for a Ph. D. degree at the University of Liverpool. Roger J. S. Beer supervised his research, and, in addition, looked after him diligently. It was the introduction of Khorana to Western civilization and culture.
Khorana spent a postdoctoral year (1948-1949) at the Eidgenössische Technische Hochschule in Zurich with Professor Vladimir Prelog. The association with Professor Prelog molded immeasurably his thought and philosophy towards science, work, and effort.
After a brief period in India in the fall of 1949, Khorana returned to England where he obtained a fellowship to work with Dr. (now Professor) G. W. Kenner and Professor (now Lord) A. R. Todd. He stayed in Cambridge from 1950 till 1952. Again, this stay proved to be of decisive value to Khorana. Interest in both proteins and nucleic acids took root at that time.
A job offer in 1952 from Dr. Gordon M. Shrum of British Columbia (now Chancellor of Simon Fraser University, British Columbia) took him to Vancouver. The British Columbia Research Council offered at that time very little by way of facilities, but there was «all the freedom in the world», to use Dr. Shrum's words, to do what the researcher liked to do. During the following years, with Dr. Shrum's inspiration and encouragement and frequent help and scientific counsel from Dr. Jack Campbell (now Head of the Department of Microbiology at the University of British Columbia), a group began to work in the field of biologically interesting phosphate esters and nucleic acids. Among the many devoted and loyal colleagues of this period, there should, in particular, be mention of Dr. Gordon M. Tener (now a Professor in the Biochemistry Department of the University of British Columbia), who contributed much to the spiritual and intellectual well-being of the group.
In 1960 Khorana moved to the Institute for Enzyme Research at the University of Wisconsin. He became a naturalized citizen of the United States. As of the fall of 1970 Khorana has been Alfred P. Sloan Professor of Biology and Chemistry at the Massachusetts Institute of Technology.
Har Gobind Khorana was married in 1952 to Esther Elizabeth Sibler, who is of Swiss origin. Esther brought a consistent sense of purpose into his life at a time when, after six years' absence from the country of his birth, Khorana felt out of place everywhere and at home nowhere. They have three children: Julia Elizabeth (born May 4th, 1953), Emily Anne (born October 18th, 1954), and Dave Roy (born July 26th, 1958).
Most adults carry multiple herpesviruses. Following the initial acute infection, these viruses establish life-long infections in their hosts and cause cold sores, keratitis, genital herpes, shingles, infectious mononucleosis, and other diseases. Some herpesviruses can cause cancer in man. During the latent phase of infection, the viruses remain dormant for long periods of time, but retain the capacity to cause occasional reactivations, that may lead to disease. A study published on June 30th in PLOS Pathogens suggests that attacking herpesvirus DNA with CRISPR/Cas9 genome editing technology can suppress virus replication and, in some cases, lead to elimination of the virus.
The CRISPR/Cas9 system targets specific DNA sequences and induces clean cuts across both strands of the DNA. In mammalian cells, such cuts are flagged and quickly repaired by an emergency repair system called NHEJ (for non-homologous end-joining). NHEJ is efficient but not very accurate and often results in insertion or deletion of a few DNA bases at the repair site. Because DNA is read in codons of three bases at a time, such small changes in critical positions often destroy the function of the respective gene and its protein product.
Robert Jan Lebbink, from the University Medical Center in Utrecht, The Netherlands, and colleagues reasoned that CRISPR/Cas9 could target and mutate latent herpesvirus DNA in infected human cells and so potentially prevent herpesvirus-associated diseases. To test this, the researchers devised specific guide (g)RNAs—sequences that are complementary to vital parts of the viral genome and function as 'molecular addresses'. These gRNAs, combined with the 'molecular scissors' part of the CRISPR/Cas9 system, should induce specific cuts and subsequent mutations in the herpesvirus DNA, and so cripple the viruses.
In their systematic approach, the researchers looked at three different members of the herpesvirus group: herpes simplex virus type 1 (HSV-1) causing cold sores and herpes keratitis; human cytomegalovirus (HCMV), the most common viral cause of birth defects (when the virus is transmitted from mother to fetus); and Epstein-Barr virus (EBV) causing infectious mononucleosis and multiple types of cancer.
Working with lymphoma cells latently infected with EBV, the researchers showed that introduction of gRNAs that target specific EBV DNA sequences can introduce mutations at the targeted sites. Such mutations can eliminate essential functions of the virus as well as de-stabilize the viral DNA molecules. Consistent with this, the researchers report that by using two different gRNAs targeting an essential EBV gene, they can induce loss of over 95% of EBV genomes from the host cells.
During latent infection, HCMV genomes exist as circular DNA molecules in the nucleus of host cells. Upon virus reactivation, HCMV replication proceeds slowly. With appropriate gRNAs, the researchers found that CRISPR/Cas9 editing can efficiently impair HCMV replication. However, they also observed emergence of escape variants that bypass CRISPR/Cas9 editing, suggesting that simultaneous editing at multiple critical sites in the HCMV genome is necessary to avoid the development of resistant genomes.
Compared to HCMV, HSV-1 multiplies much faster. When the researchers tested various gRNAs targeting different essential HSV-1 genes in conjunction with CRISPR/Cas9, they found that many of them were able to reduce virus replication. When they combined two of those gRNAs, thereby simultaneously targeting two essential genes, they were able to completely suppress HSV-1 replication. On the other hand, they were unable to induce editing during the latent phase, i.e. when the viral DNA was not actively multiplying.
"We observed highly efficient and specific clearance of EBV from latently infected tumor cells and impairment of HSV-1 and HCMV replication in human cells", the researchers summarize. They go on to say, "although CRISPR/Cas9 was inefficient at directing genome engineering of quiescent HSV-1, virus replication upon reactivation of quiescent HSV-1 was efficiently abrogated using anti-HSV-1 gRNAs". Their results, they hope, "may allow the design of effective therapeutic strategies to target human herpesviruses during both latent and productive infections."