Ancient Chinese Chariots

The Shang Dynasty or Yin Dynasty, according to traditional historiography, ruled in the Yellow River valley in the second millennium BC. Archaeological work at the Ruins of Yin (near modern-day Anyang), which has been identified as the last Shang capital, uncovered eleven major Yin royal tombs and the foundations of palaces and ritual sites, containing weapons of war and remains from both animal and human sacrifices.

The Tomb of Fu Hao is an archaeological site at Linux, the ruins of the ancient Shang Dynasty’s capital Yin, within the modern city of Anyang in Henan Province, China. Discovered in 1976, it was identified as the final resting place of the queen and military general Fu Hao. The artifacts unearthed within the grave included jade objects, bone objects, bronze objects, etc. These grave goods are confirmed by the oracle texts, which constitute almost all of the first handwritten records we possess of the Shang Dynasty. Below the corpse was a small pit holding the remains of six sacrificial dogs and along the edge lay the skeletons of human slaves, evidence of human sacrifice.

The Terracotta Army was discovered on 29 March 1974 to the east of Xi’an in Shaanxi. The terracotta soldiers were accidentally discovered when a group of local farmers was digging a well during a drought around 1.6 km (1 mile) east of the Qin Emperor’s tomb around Mount Li (Lichen), a region riddled with underground springs and watercourses. Experts currently place the entire number of soldiers at 8,000 – with 130 chariots (130 cm long), 530 horses, and 150 cavalry horses helping to ward off any dangers in the afterlife. In contrast, the burial of Tutankhamun yielded six complete but dismantled chariots of unparalleled richness and sophistication. Each was designed for two people (90 cm long) and had its axle sawn through to enable it to be brought along the narrow corridor into the tomb.

Excavation of ancient Chinese chariots has confirmed the descriptions of them in the earliest texts. Wheels were constructed from a variety of woods: elm provided the hub, rosewood the spokes, and oak the felloes. The hub was drilled through to form an empty space into which the tempered axle was fitted, the whole being covered with leather to retain lubricating oil. Though the number of spokes varied, a wheel by the fourth century BC usually had eighteen to thirty-two of them. Records show how elaborate was the testing of each completed wheel: flotation and weighing were regarded as the best measures of balance, but even the empty spaces in the assembly were checked with millet grains. One outstanding constructional asset of the ancient Chinese wheel was dishing. Dishing refers to the dish-like shape of an advanced wooden wheel, which looks rather take a flat cone. On occasion, they chose to strengthen a dished wheel with a pair of struts running from rim to rim on each of the hubs. As these extra supports were inserted separately into the felloes, they would have added even greater strength to the wheel. Leather-wrapped up the edge of the wheel aimed to retain bronze. Within a millennium, however, Chinese chariot-makers had developed a vehicle with shafts, the precursor of the true carriage or cart. This design did not make its appearance in Europe until the end of the Roman Empire.
Because the shafts curved upwards, and the harness pressed against a horse’s shoulders, not his neck, the shaft chariot was incredibly efficient. The halberd was also part of a chariot standard weaponry. This halberd usually measured well over 3 meters in length, which meant that a chariot warrior wielding it sideways could strike down the charioteer in a passing chariot. The speed of the chariot which was tested on the sand was quite fast. At speed, these passes were very dangerous for the crews of both chariots.

The advantages offered by the new chariots were not entirely missed They could see how there were literally the Warring States, whose conflicts lasted down the Qin unification of China. Qin Shi Huang was buried in the most opulent tomb complex ever constructed in China, a sprawling, city-size collection of underground caverns containing the evening the emperor would need for the afterlife. Even a collection of terracotta armies called Terra-Cotta Warriors was buried in it. The ancient Chinese, along with many cultures including ancient Egyptians, believed that items and even people buried with a person could be taken with him to the afterlife.

Stealth Forces in Weight Loss

The field of weight loss is like the ancient fable about blind men and the elephant. Each man investigates a different part of the animal and reports back, only to discover their findings are bafflingly incompatible.

A. The various findings by public-health experts, physicians, psychologists, geneticists, molecular biologists, and nutritionists are about as similar as an elephant’s tusk is to its tail. Some say obesity is largely predetermined by our genes and biology; others attribute it to an overabundance of fries, soda, and screen-sucking; still, others think we’re fat because of viral infection, insulin, or metabolic conditions we encountered in the womb. “Everyone subscribes to their own little theory,” says Robert Berkowitz, medical director of the Centre for Weight and Eating Disorders at the University Of Pennsylvania School Of Medicine. We’re programmed to hang onto the fat we have, and some people are predisposed to create and carry more fat than others. Diet and exercise help, but in the end, the solution

will inevitably be more complicated than pushing away the plate and going for a walk. “It’s not as simple as ‘Your fat because you’re lazy’ says Nikhil Dhurandhar, an associate professor at Pennington Biomedical Research Centre in Baton Rouge. “Willpower is not a prerogative of thin people. It’s distributed equally.”

B. Science may still be years away from giving us a miracle formula for fat loss. The hormone leptin is a crucial player in the brain’s weight-management circuitry. Some people produce too little leptin; others become desensitized to it. And when obese people lose weight, their leptin levels plummet along with their metabolism. The body becomes more efficient at using fuel and conserving fat, which makes it tough to keep the weight off. Obese dieters’ bodies go into a state of chronic hunger, a feeling Rudolph Leibel, an obesity researcher at Columbia University, compares to thirst. “Some people might be able to tolerate chronic thirst, but the majority couldn’t stand it”, says Leibel. “Is that a behavioral problem – a lack of willpower? I don’t think so.”

C. The government has long espoused moderate daily exercise – of the evening-walk or take-the-stairs variety – but that may not do much to budge the needle on the scale. A 150-pound person burns only 150 calories on a half-hour walk, the equivalent of two apples. It’s good for the heart, less so for the gut. “Radical changes are necessary,” says Deirdre Barrett, a psychologist at Harvard Medical School and author of Wasteland. “People don’t lose weight by choosing the small fries or talking a little walk every other day,” Barrett suggests taking a cue from the members of the Nation Weight Control Registry (NWCR), a self-selected group of more than 5,000 successful weight-losers who have shed diets an average of 66 pounds and kept it off 5.5 years. Some registry members lost weight using low-carb diets; some went low-fat; other eliminated refined foods. Some did it on their own; others relied on counseling. That said, not everyone can lose 66 pounds and not everyone needs to. The goal shouldn’t be getting thin, but getting healthy. It’s enough to whittle your weight down to the low end of your set range, says Jeffrey Friedman, a geneticist at Rockefeller University. Losing even 10 pounds vastly decreases your risk of diabetes, heart disease, and high blood pressure. The point is to not give up just because you don’t look like a swimsuit model.

D. The negotiation between your genes and the environment begins on day one. Your optimal weight, writ by genes, appears to get edited early on by conditions even before birth, inside the womb. If a woman has high blood sugar levels while she’s pregnant, her children are more likely to be overweight or obese, according to a study of almost 10,000 mother-child pairs. Maternal diabetes may influence a child’s obesity risk through a process called metabolic imprinting, says Teresa Hillier, an endocrinologist with Kaiser Permanente’s Center for Health Research and the study’s lead author. The implication is clear: Weight may be established very early on, and obesity largely passed from mother to child. Numerous studies in both animals and humans have shown that a mother’s obesity directly increases her child’s risk for weight gain. The best advice for moms-to-be: Get fit before you get pregnant. You’llReduce your risk of complications during pregnancy and increase your chances of having a normal-weight child.

E. It’s the $64,000 question: Which diets work? It got people wondering: Isn’t there a better way to diet? A study seemed to offer an answer. The paper compared two groups of adults: those who, after eating, secreted high levels of insulin, a hormone that sweeps blood sugar out of the bloodstream and promotes its storage as fat, and those who secreted less. Within each group, half were put on a low-fat diet and half on a low-glycemic-load diet. On average, the low-insulin-secreting group fared the same on both diets, losing nearly 10 pounds in the first six months — but they gained about half of it back by the end of the 18-month study. The high-insulin group didn’t do as well on the low-fat plan, losing about 4.5 pounds, and gaining back more than half by the end. But the most successful was the high-insulin-secretors on the low-glycemic-load diet. They lost nearly 13 pounds and kept it off.

F.  What if your fat is caused not by diet or genes, but by germs — say, a virus? It sounds like a sci-fi horror movie, but research suggests some dimension of the obesity epidemic may be attributable to infection by common viruses, says Dhurandhar. The idea of “infect obesity” came to him 20 years ago when he was a young doctor treating obesity in Bombay. He discovered that a local avian virus, SMAM-1, caused chickens to die, sickened with organ damage but also, strangely, with lots of abdominal fat. In experiments, Dhurandhar found that SMAM-1 -infected chickens became obese on the same diet as uninfected ones, which stayed svelte.

G. He later moved to the U.S. and onto a bona fide human virus, adenovirus 36 (AD-36). In the lab, every species of animal Dhurandhar infected with the virus became obese — chickens got fat, mice got fat, even rhesus monkeys at the zoo that picked up the virus from the environment suddenly gained 15 percent of their body weight upon exposure. In his latest studies, Dhurandhar has isolated a gene that, when blocked from expressing itself, seems to turn off the virus’s fattening power. Stem cells extracted from fat cells and then exposed to AD-36 reliably blossom into fat cells — but when stem cells are exposed to an AD-36 virus with the key gene inhibited, the stem cells don’t differentiate. The gene appears to be necessary and sufficient to trigger AD-36-related obesity, and the goal is to use the research to create a sort of obesity vaccine.