Punjab Da Puttar

At just 2ft 9in, Indian muscleman Aditya 'Romeo' Dev is the world's smallest bodybuilder. Pint-sized Romeo is well-known in his hometown of Phagwara, India - for his ability to lift 1.5kg dumbbells - despite his overall 9kg body weight. Every day, crowds flock to the local gym to the see the mini-muscleman in training.Unlike many dwarfs, Romeo is well proportioned, with a head circumference of 15in and a chest measurement of 20in.
Romeo said: "I've been training as a bodybuilder for the last two years and by now I think I must be the strongest dwarf in the world. "I have always been fit but since I started working out, I have become famous for my strength. "My size has never stopped me. I train with dumbbells and do aerobics and dance. People are always pleased to see me. I have been invited on TV shows and dance on stage."
His trainer Ranjeet Pal spents hours helping his 19-year-old protege build his small muscles to perfection. "Because of his small size, I don't assign him hard exercises. But Romeo trains more or less the same as anyone else and he's much more determined.
"When he first started, I insisted he did a month of basic exercises like aerobics, push-ups and basic gymnastics to prepare his body."After that, I made lightweight dumbbells and taught him basic weight-lifting exercises to shape his biceps and triceps. His size and his weight were taken care of so that he never hurt himself." Determined Romeo is hoping to have an entertainment career after performing in many local TV shows. He said: "I earn good money through my dance and bodybuilding shows but being rich doesn't interest me. "My dream is to travel a lot - I want to perform in London with my idol, Jazzy-B."

Human Infertility May Be Explained By Evolutionary Phenomenon In Mice

Scientists at the University of Liverpool have found that field mice have evolved a unique way of ensuring faster fertilisation, a phenomenon which could explain some cases of infertility in humans.

The team, in collaboration with Charles University, Prague, found that field mice sacrifice some of their immunity protection in favour of a more rapid fertilisation process. This occurs due to the absence of a protein, called CD46. Present in both animals and humans, it helps protect the body's cells from attack by its immune system. Over time, field mice have lost the ability to produce this protein, resulting in instability of a cap-like structure, called the acrosome, present over the head of the sperm.

This instability allows the acrosome to be shed from the sperm head to create a new surface essential for sperm to be capable of fusing with an egg. This is a natural process that can take days to occur in humans, but field mice have developed a way in which this can occur rapidly.

Immunologist, Professor Peter Johnson, explains: "Field mice have traded the production of an immunologically important protein in favour of this faster fertilization process in order to compete with other mice more successfully. Female mice produce multiple eggs and if there are a lot of male mice competing for her, then it is an advantage to an individual mouse for its sperm to react quickly in order to beat other male competitors to fertilisation."

"By improving our understanding of defects in CD46 we may improve treatments for infertility in men. Humans normally produce a single egg each month and there is no evolutionary necessity to develop rapid sperm reaction to egg fertilisation. The process is therefore much slower and so any defect in CD46 could result in sperm being destabilised too early.

"Interestingly the rapid reaction caused in mice is similar to that in IVF treatment in humans where the acronome is artificially expelled from the sperm head before it is introduced to the egg to speed up the fertilisation process. Field mice appear to do this naturally."

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Evolution

Chicken Soup For The Soul- TGIF

Why Cells That Become Sperm And Ova Can't Copy Their Own Genes

Researchers in Kobe, Japan, and Montreal, Canada, have uncovered a previously unknown mechanism which causes embryonic germ cells -- which later develop into sperm or ova -- to go through a period of "transcriptional silence," during which information from the cell's DNA cannot be copied. Without this important phase, unique to cells of this type, an organism produces sterile offspring.

The study was conducted by a team led by Dr. Akira Nakamura at the RIKEN Center for Developmental Biology (CDB) in Kobe and by Dr. Paul Lasko, Chair of McGill University's Department of Biology. Their results were published in January, 2008, in the journal Nature.

"A fundamental characteristic of embryonic germ cells in all organisms is that they don't transcribe their own genes for a certain time during embryonic development," Dr. Lasko explained. "They are transcriptionally silent; that's what makes them special. It's not fully understood why this is the case, but if that silencing doesn't happen, then the germ cells don't work. They don't migrate correctly and they don't make their way into the gonads."

Dr. Nakamura was a post-doctoral fellow in Dr. Lasko's lab in the mid-1990s when they co-discovered the Polar Granule Component (PGC) gene in drosophila, commonly known as the fruit fly. If the mother fly lacks PGC, her offspring will be unable to produce germ cells. Initially, Dr. Lasko said, they discovered that the PGC gene produced an RNA, but they did not believe it produced any proteins. Using current technology, Dr. Nakamura discovered that PGC does indeed produce a protein which regulates Transcription Elongation Factor B (TEF-B), the genetic machinery that expresses proteins.

"It's a very small, 71-amino acid protein," Dr. Lasko explained. "The average length of a protein is about 400 to 500 amino acids, so this is extremely small. Back when we did the initial research, there weren't very many genes known that encoded such a short protein. The significance of this is that Nakamura has shown that this little protein seems to be the key regulator that keeps gene expression shut off in germ cells."

Mutant fruit flies without the ability to produce the protein produce sterile offspring which produce no sperm or eggs.

"What the study argues is that this regulation of TEF-B might be very important for germ cell development in a variety of organisms. That's something people will want to look at in mammals," Dr. Lasko said.