Практика

Космологическое красное смещение

Роберт С. Фрициус

Русский перевод Сарычева Ю.

Введение.

Когда мы используем закон красного смещения Хаббла для того, чтобы вычислять расстояния до отдаленных галактик, мы делаем так согласно предположению, что первоначальный свет, приходя к нам за тысячи миллионов лет, испускался, по существу, на тех же самых длинах волн, какие наблюдаются в локальных современных эквивалентных звездных процессах. Исходя из такого основополагающего предположения, мы можем выдвинуть гипотезу о некотором механизме типа Эффекта Доплера (изменение сигнала в зависимости от скорости источника), чтобы сдвинуть спектр света в область менее энергетических, но более длинных волн, которые мы обнаруживаем. Кажущиеся размеры и выход мощности излучения квазаров, как в настоящее время определено при использовании жизнеспособной идеи красного смещения, кажется, готовы потрясти самые основы физики. Эта статья предлагает новую гипотезу, использующую закономерность космологического красного смещения, которая может оставить основы физики незатронутыми или, по крайней мере, изменит их только слегка.

Галактическая плотность, зависящая от электрического заряда.

Если галактики — конденсаты изначального космического “бульона”, то их материальные плотности должны увеличиваться со временем. В предлагаемой статье выдвигается гипотеза о том, что унитарный электрический заряд пропорционален локальной галактической материальной плотности (концентрации). То есть, электрический заряд любого данного электрона или протона связан с общим количеством других протонов, электронов, и т. д., которые находятся достаточно близко, чтобы влиять на это через прямые электродинамические элементарные взаимодействия. Расстояние пяти световых лет может быть достаточным для нашего оценочного предела для прямых электродинамических влияний. Эта гипотеза выдвинута с использованием теоремы угасания, где заряженные частицы, находящиеся в среде, абсорбируют и заново излучают энергию электромагнитного поля, таким образом, гася первоначальную энергию.

Предполагается, что если унитарный электрический заряд в пределах галактик увеличивался в течение космологических веков, то сила электрических взаимодействий между атомными ядрами и их электронами, составляющими эти галактики, также увеличивалась. Размеры атомов должны уменьшаться, а энергии их электронов на орбитах должны увеличиваться как побочный эффект основного галактического процесса конденсации.

http://n-t.ru/tp/ns/kks.htm

Упражнение 4

Сделайте письменный перевод следующего научного текста в соответствии с требованиями стиля.

What You Need to Know. What You Can Do.

The Nature of Cancer

Introduction

Cancer types number more than 100. Cancer begins inside a cell — the basic building block of all living things. Normally, when the body needs more cells, older cells die off. Younger cells then divide to form new cells, replacing those that died. When cancer develops, however, the orderly process of producing new cells breaks down. Even when new cells are not needed cells continue to divide, forming a growth or extra mass of cells called a tumor^¹⁴. Over time, changes may take place in tumor cells that cause them to invade and interfere with the function of normal tissues^¹⁵.

Figure 1. An alteration in growth-promoting genes, known as oncogenes, can signal the cell to divide out of control. An alteration in tumor suppressor genes will, rather than repair the DNA or eliminate the injured cells, allow cells with damaged DNA to continue their uncontrolled growth.

Tumor development takes many years, and even more years pass before the tumor is detected. By that time, the tumor has often spread to other parts of the body. People exposed to carcinogens from smoking cigarettes, for example, generally do not develop detectable cancer for 20 to 30 years.

Much evidence suggests that permanent genetic changes are responsible for tumor development. These can be inherited, or acquired throughout a lifetime. Scientists have identified more than 300 altered genes that can play a role in tumor development. An alteration in growth-promoting genes, known as oncogenes^¹⁶, for example, can signal the cell to divide out of control, similar to having a gas pedal stuck to the floorboard. On the other hand, an alteration in tumor suppressor genes^¹⁷, which normally serve as brakes for dividing cells will, rather than repairing the DNA or eliminating the injured cells, allow cells with damaged DNA to continue dividing.

One explanation for the fact that cancer occurs more frequently in older people may be that, for a tumor to develop, a cell must acquire several gene alterations that accumulate as we age. As the graph below illustrates, less than 0.1 percent of the total number of cancer cases in the United States occur in people under the age of 15, whereas nearly 80 percent occur in people age 55 or older.

Figure 2. Cancer cases by age in the United States.

Types of Tumors

Tumors are classified as either benign or malignant. Benign tumors^¹⁸ are not cancerous and do not spread to other parts of the body.

A malignant tumor ^¹⁹can metastasize — a process during which cancer cells escape from the tumor, enter the bloodstream or lymphatic system^²⁰, and spread to nearby parts of the body and eventually to sites far away from the original tumor. Some benign tumors may, over time, become malignant tumors. The development of malignant tumors involves many steps taking place over several years. The earlier a tumor is detected, the less likely it will have spread to other parts of the body. In the past 25 years, enormous progress has been made in defining the molecular events that take place as a normal cell becomes malignant and the critical genes thought to be involved. For more information, see resources listed as “General Cancer Information^²¹”.

Most cancers are named for the organ or type of cell in which they begin to grow, such as lung, stomach, breast, or colon cancer. Some of the names for other cancers, however, are less clear. Melanoma^²² is a cancer of cells in the skin, eyes, and some other tissues, known as melanocytes, that make pigment. Leukemias^²³ are cancers of the blood cells, and lymphomas^²⁴ are cancers that develop in the lymphatic system. The most common cancers in the U.S are carcinomas^²⁵. Carcinomas are cancers that develop in the tissue that lines the surfaces of certain organs, such as the lung, liver, skin, or breast. This tissue is called epithelial tissue. Cancers that develop in the epithelial tissue of specific organs are called, for example, carcinoma of the lung, or carcinoma of the breast. Another group of cancers is sarcomas^²⁶: these arise from cells in bone, cartilage, fat, connective tissue, and muscle.

Key Points

When cancer develops, the orderly process of producing new cells breaks down. Cells continue to divide when new cells are not needed, and a growth or extra mass of cells is formed, known as a tumor.
The development of a tumor takes many years, and even more years until a tumor is detected, and it has spread to other parts of the body.
Much evidence suggests that permanent changes in our genes are responsible for tumor development.
One explanation for the fact that cancer occurs more frequently in older people may be that for a tumor to develop, a cell must acquire several gene alterations that accumulate as we age.
Tumors are classified as either benign or malignant. Benign tumors are not cancer and do not spread to other parts of the body.
A malignant tumor can metastasize — that is, its cells can escape from the tumor, enter the bloodstream or lymphatic system, and spread to nearby parts of the body and eventually to sites far away from the original tumor.
Most cancers are named for the organ or type of cell in which they begin to grow, such as lung, stomach, breast, or colon cancer.

Agency for Toxic Substances and Disease Registry

http://www.atsdr.cdc.gov

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