.308 vs .30-06..still hands down is the .30-06 is better

Ballistics of the .308 vs. 30-06

Velocity 2700fps

Bullet Wt. .168gr

Sight in at 100Yds.

Bullet Coef. 0.495

Muz. Energy 2720

……Range……Velocity……….Drop……….. ToF………Energy
…………0………2700…………….0……. ……0………….2720
………100………2516………..2.74………0 .12………….2362
………200………2344……….11.00……..0. 24………….2050
………300………2180……….25.62……..0. 37………….1773
………400………2021……….47.59……..0. 52………….1524
………500………1870……….78.11……..0. 67………….1305
………600………1728……..118.59……..0.8 4………….1114
………700………1594……..170.74……..1.0 2……………948
………800………1470……..236.57……..1.2 1……………806
………900………1358……..318.45……..1.4 3……………688
…….1000………1259……….419.1……..1.6 6……………591

The above chart illustrates the common ballistics of any .30 cal rifle using the exact same bullet weight and velocity. Giving that the rifles fired from are the same brand and barrel leingth.

Example .308 taken right from Hornady reloading manual; A .168 gr. HPBT loaded with 44.3 grs. of RL-15 powder achieves about 2600fps.

Example .30-06 taken right from the Hornady reloading manual; A 168 gr HPBT loaded with 46.8 grs. of RL-15 achieves about 2600fps.

Where the difference exists is that you can load the .30-06 up a tad bit more with this powder to achieve the full 2700fps. The case is longer and allows for a little bit more powder to be used. Along with the ability of the .30-06 to effectively use .220 gr bullets where the .308 reloading data stops at .190gr.

Powders come in Flaked, Balled, and Tubular shapes, and with the Tubular powder one can more efficiently and effectively use this powder in the .30-06 to achieve the same ballistics listed above. Because the tubular powder takes more room in the case, and the .308 does not have quite as much room in the case as the .30-06.

So the advantage of .30-06 over the .308 is that one can load a few differing types of powder, and you can use more powder to achieve a slight higher velocity. But giving the same weights they both perform exactly the same under the same conditions and rifles.


more on BIO-Weaps

The values are estimates of the doses which have lethal effects on a 70kg man. Effective dosages of vapor are estimated for exposure durations of 2-10 minutes.
The effects of the nerve agents are mainly due to their ability to inhibit acetylcholinesterase throughout the body. Since the normal function of this enzyme is to hydrolyse acetylcholine wherever it is released, such inhibition results in the accumulation of excessive concentrations of acetylcholine at its various sites of action. These sites include the endings of the parasympathetic nerves to the smooth muscle of the iris, ciliary body, bronchial tree, gastrointestinal tract, bladder and blood vessels; to the salivary glands and secretory glands of the gastrointestinal tract and respiratory tract; and to the cardiac muscle and endings of sympathetic nerves to the sweat glands.

The sequence of symptoms varies with the route of exposure. While respiratory symptoms are generally the first to appear after inhalation of nerve agent vapor, gastrointestinal symptoms are usually the first after ingestion. Tightness in the chest is an early local symptom of respiratory exposure. This symptom progressively increases as the nerve agent is absorbed into the systemic circulation, whatever the route of exposure. Following comparable degrees of exposure, respiratory manifestations are most severe after inhalation, and gastrointestinal symptoms may be most severe after ingestion.

The lungs and the eyes absorb nerve agents rapidly. In high vapor concentrations, the nerve agent is carried from the lungs throughout the circulatory system; widespread systemic effects may appear in less than 1 minute.
•The earliest ocular effect which follows minimal symptomatic exposure to vapor is miosis. The pupillary constriction may be different in each eye. Within a few minutes after the onset of exposure, there also occurs redness of the eyes. Following minimal exposure, the earliest effects on the respiratory tract are a watery nasal discharge, nasal hyperaemia, sensation of tightness in the chest and occasionally prolonged wheezing
•Exposure to a level of a nerve agent vapor slightly above the minimal symptomatic dose results in miosis, pain in and behind the eyes and frontal headache. Some twitching of the eyelids may occur. Occasionally there is nausea and vomiting.
•In mild exposures, the systemic manifestations of nerve agent poisoning usually include tension, anxiety, jitteriness, restlessness, emotional lability, and giddiness. There may be insomnia or excessive dreaming, occasionally with nightmares.
•If the exposure is more marked, the following symptoms may be evident: headache, tremor, drowsiness, difficulty in concentration, impairment of memory with slow recall of recent events, and slowing of reactions. In some casualties there is apathy, withdrawal and depression.
•With the appearance of moderate systemic effects, the casualty begins to have increased fatiguability and mild generalised weakness which is increased by exertion. This is followed by involuntary muscular twitching, scattered muscular fasciculations and occasional muscle cramps. The skin may be pale due to vasoconstriction and blood pressure moderately elevated.
•If the exposure has been severe, the cardiovascular symptoms will dominate and twitching (which usually appear first in the eyelids and in the facial and calf muscles) becomes generalised. Many rippling movements are seen under the skin and twitching movements appear in all parts of the body. This is followed by severe generalised muscular weakness, including the muscles of respiration. The respiratory movements become more laboured, shallow and rapid; then they become slow and finally intermittent.
•After moderate or severe exposure, excessive bronchial and upper airway secretions occur and may become very profuse, causing coughing, airway obstruction and respiratory distress. Bronchial secretion and salivation may be so profuse that watery secretions run out of the sides of the mouth. The secretions may be thick and tenacious. If the exposure is not so overwhelming as to cause death within a few minutes, other effects appear. These include sweating, anorexia, nausea and heartburn. If absorption of nerve agent has been great enough, there may follow abdominal cramps, vomiting, diarrhea, and urinary frequency. The casualty perspires profusely, may have involuntary defecation and urination and may go into cardiorespiratory arrest followed by death.
•If absorption of nerve agent has been great enough, the casualty becomes confused and ataxic. The casualty may have changes in speech, consisting of slurring, difficulty in forming words, and multiple repetition of the last syllable. The casualty may then become comatose, reflexes may disappear and generalised convulsions may ensue. With the appearance of severe central nervous system symptoms, central respiratory depression will occur and may progress to respiratory arrest.
•After severe exposure the casualty may lose consciousness and convulse within a minute without other obvious symptoms. Death is usually due to respiratory arrest requires prompt initiation of assisted ventilation to prevent death. If assisted ventilation is initiated , the individual may survive several lethal doses of a nerve agent.
•If the exposure has been overwhelming, amounting to many times the lethal dose, death may occur despite treatment as a result of respiratory arrest and cardiac arrhythmia. When overwhelming doses of the agent are absorbed quickly, death occurs rapidly without orderly progression of symptoms.
Nerve agent poisoning may be identified from the characteristic signs and symptoms. If exposure to vapor has occurred, the pupils will be very small, usually pin-pointed. If exposure has been cutaneous or has followed ingestion of a nerve agent in contaminated food or water, the pupils may be normal or, in the presence of severe systemic symptoms, slightly to moderately reduced in size. In this event, the other manifestations of nerve agent poisoning must be relied on to establish the diagnosis. No other known chemical agent produces muscular twitching and fasciculations, rapidly developing pin-point pupils, or the characteristic train of muscarinic, nicotinic and central nervous system manifestations.
The rapid action of nerve agents call for immediate self treatment. Unexplained nasal secretion, salivation, tightness of the chest, shortness of breath, constriction of pupils, muscular twitching, or nausea and abdominal cramps call for the immediate intramuscular injection of 2 mg of atropine, combined if possible with oxime.


with the outbreak here in the U.S. Im talking about Bio-weaps

Nerve Agents

The nerve agents are a group of particularly toxic chemical warfare agents. They were developed just before and during World War II and are related chemically to the organophosphorus insecticides. The principle agents in this group are:

  • GA – tabun
  • GB – sarin
  • GD – soman
  • GF – cyclosarin
  • VX – methylphosphonothioic acid

The “G” agents tend to be non-persistent whereas the “V” agents are persistent. Some “G” agents may be thickened with various substances in order to increase their persistence, and therefore the total amount penetrating intact skin. At room temperature GB is a comparatively volatile liquid and therefore non-persistent. GD is also significantly volatile, as is GA though to a lesser extent. VX is a relatively non-volatile liquid and therefore persistent. It is regarded as presenting little vapor hazard to people exposed to it. In the pure state nerve agents are colorless and mobile liquids. In an impure state nerve agents may be encountered as yellowish to brown liquids. Some nerve agents have a faint fruity odor.

  • GB and VX doses which are potentially life-threatening may be only slightly larger than those producing least effects. Death usually occurs within 15 minutes after absorption of a fatal VX dosage.
  • Although only about half as toxic as GB by inhalation, GA in low concentrations is more irritating to the eyes than GB. Symptoms appear much more slowly from a skin dosage than from a respiratory dosage. Although skin absorption great enough to cause death may occur in 1 to 2 minutes, death may be delayed for 1 to 2 hours. Respiratory lethal dosages kill in 1 to 10 minutes, and liquid in the eye kills almost as rapidly

To all those responsible for the Charlie Hebdo attack I hope you can read this!

To all those responsible for the Charlie Hebdo attack.

Well done guys, you really showed us. You showed us what will happen to us if we dare criticize the warped creed you espouse. You proved, beyond all doubt, that yours is a just and noble crusade, and we will certainly refrain from criticising your virtuous cause in future.

Well, actually, we might renege on that last promise.

Journalists – be they scribes, broadcasters or satirists; print, TV, online – are duty-bound to report the truth and highlight injustice wherever it arises. It is what we do the job for (believe me, it is not the money). Sickening events such as the event that occurred on 7 January only harden our resolve to confront and denounce the atrocities you perpetrate, in the name of a creed that rejects you.

It is reported that you shouted “Allahu Akbar” as you massacred a roomful of innocent designers at Charlie Hebdo’s offices, so you must think you are advancing the cause of Islam. But real Muslims, the overwhelming majority of Muslims, despise you. They think the same as the rest of us, that you are just pathetic low-lives who need to kill defenceless people to dredge some meaning from your importance.

Killing people who criticise you will not make their criticism go away. In fact, it will only throw an even harsher spotlight on your crimes, and on the human rights abuses inflicted by extremist zealots the world over.

Activists, aid organisations, counter-extremism groups… all will receive a spike in subscriptions and goodwill through what you have done today. So, in reality, you have achieved precisely the opposite of your stated aim.


Could Pairs been prevented?

The one effective response to such attacks would be to change foreign policy, which has helped to create precisely the terrorism that it now abhors. ISIS has grown in Iraq and Syria as a consequence of the failed wars there. The instability created in Iraq as a result of western intervention, the backing of a sectarian and oppressive government by the occupiers, and the current air strikes which are helping to win support for ISIS, have all contributed to the strengthening of this organisation. ISIS has received weapons and money from the Saudis and Qataris, has grabbed weapons provided by the west for other anti Assad groups, and has received material support from Turkey.

These are precisely the western allies — Turkey also being a Nato member — who sign up for the ‘war on terror’ but practice something different. The interventions they supported have greatly increased instability, for example in Libya where the British and French led bombing in 2011 continues to result in bitter civil war and conflict.

The prediction made by, among others, former head of MI5 Eliza Manningham-Buller that the war on Iraq would lead to a much greater threat of terrorism has unfortunately proved to be the case.

In recent years France, under presidents Sarkozy and Hollande, has played an increasing role in these interventions.

That the wars are all blamed on Muslims ignores the fact that the Libyan groups and ISIS are of course in large part fighting other Muslims. The refugees coming out of Syria, left on crewless boats to sink or swim in the Mediterranean, are also Muslims.

The consequences of the wars, with hundreds of thousands dead and many more refugees, have incensed people around the world. The large marjorities in western countries who have opposed these interventions have been ignored by their warmongering governments.

Muslims have also faced a growing level of racism and prejudice, see in the rise of far right parties, the restrictions on Muslim dress, the infringements of civil liberties, and the branding of all Muslims as somehow extremists or proto terrorists.

In France, there is a very strong far right party in the shape of the Front National, and the country has legislated some of the worst restrictions on Muslims — for example over wearing the hijab. In Germany, the anti Islamic Pergida demonstrations have linked Muslims to crime. Levels of racism in Britain have grown, focussed both on immigrants and on Muslims.

The latest attack will lead to a greater backlash and greater levels of Islamophobia. But it is not Muslims who are the problem but the foreign policies that have helped create terrorism. That is what needs to change.


Something to think on! When did modern infantry combat tactics evolve?

When did modern infantry combat tactics evolve? What I mean is during the 1860-65 Civil war and the following Indian campaigns the army was still using Napoleonic tactics of everybody standing rank and file and shooting at each other. They wore bright colored uniforms with shiny brass buttons that gleamed in the sun and gave your position away, etc… Fast forward to WW1, some 50 years later and everybody was dug into trenches with earth tone uniforms and steel helmets using cover and concealment tactics. Was it purely the new use of crew served machine guns that changed the tactics or was it a gradual change from the late 1800s into the early 1900s? It just seems like a radical change of tactics in a short amount of time, like they through away the rule book and started over again.