Monday, 14 July 2014

BILL ADONGO



LIFE TIME:
Bill Adongo (1983-present) is a Ghanaian physician even though he has never been in medical field. He is not only the last person to describe the mechanical events of the coordinate function and the cell function but the last to transform the mechanical events of the coordinate function and the cell function. He is a master of sciences and regarded as one of the most intelligent physiologist of all time. He is known by his functional model and below is copy of his model.


FUNCTIONAL MODEL
MECHANICAL RELATION OF CARDIAC CYCLE
During excitation-contraction coupling in cardiac muscle, calcium released from the sorcoplasmic reticulum is the major source of the increased cytosolic calcium. The signal for this release of extracellular calcium diffusing into the cell across voltage sensitive calcium channels in the T tubules. This process described triggers a recurring cardiac cycle of arterial and ventricular contractions and relations.
They key cause of the mechanical events of the cardiac cycle is the pressure and volume changes. These events are the period of ventricular contraction ejection, called systole and the period of ventricular relaxation and blood filling, diastole. The divisions of the systole and diastole for simplicity may show only one atrium and ventricles are also shown. In these subdivisions, they ventricles are contraction but all valves in the heart are closed and no blood can be ejected. This process is termed isovolumetric ventricular contraction since the ventricular volume, the process would be constant.
The analogous isovolumetric ventricular is contracted by an isovolumetric skeletal-muscle, the muscle develops tension, but does not shorten. The relationship between membrane potential changes and contraction in a ventricular muscle cell occurs, making the refraction period to last as long as the contraction. The inability of the heart to generate tetanic contraction is the result of the period which the refractory lasts. One rising pressure in the aorta and pulmonary trunk, the aortic and pulmonary valves open and the ventricular ejection period of systole occurs. The volume of blood ejected from each ventricle during systole is termed the stroke volume (SV) and the volume of blood pumped by each ventricle per minute is called cardiac output (CO).
During brief phase of isovolumetric ventricular contraction ends when the rapid at first and later lapers off, the amount of blood remaining after ejection is termed as end-systolic volume (ESV). The amount of blood in the ventricle at the end of diastole is called end-diastolic volume (EDV). The formula which I produced for the cardiac cycle is;


Stroke Volume= 4(end-diastolic X end-systolic ) / (end-diastolic – end-systolic)

Moreover, rhythmical beating of the heart at rate of approximately 100 beats/min usually occur when nervous or hormonal influences on sinoatrical node occur. The effects of sympathetic and parasympathetic nerve stimulation on the pacemaker potential of an sinoatrical-node cell, realized that parasympathetic stimulation not only reduce the slope of the pacemaker potential to be more negative before the pacemaker potential begins. The relationship between heart rate (HR), Cardiac output (CO), end-diastolic volume (EDV) and end-systolic volume (ESV) is mechanism which is given as;

CO= 4(heart rate X end-diastolic X end-systolic) / (end-diastolic – end-systolic)


Contractility which is defined as the strength of contraction at any given end-diastolic volume at end-systolic volume is the increase force of contraction and stroke volume resulting from sympathetic-nerve stimulation or epinephrine is independent of a change in end-systolic ventricular volume. At contractility, the ejection fraction (EF), which I defined as the ratio of ends systolic (ESV) to four times end-diastolic volume minus end-systolic volume is;


Ejection fraction = end-systolic/(4Xend-diastolic volume – end-systolic volume)

LUNG CAPACITIES MECHANISM
The volume of air into the lungs during inspiration is approximately equal to the volume leaving on the subsequent expiration and this is termed as tidal volume. Lung volumes and capacities are usually recorded on a spirometer, an apparatus for measuring inspired and expired volumes. When the subject inspires, the pen moves up; with expiration, it moves down. The capacities are the sums of two or more lung volumes. These measurements are usually diagnostic tools for treating with obstractive lung diseases typically have force expiratory volume in 1s, in which the person takes a maximal inspiration and then exhales maximally as fast as possible.
The total ventilation per minute, which is the minute ventilation (MV) is a ratio of four times respiration rate (RR), times aveololar ventilation (AV) to respiration times dead space (DS) plus aveololar ventilation (AV).


MV= 4(respire rate times dead space X aveololar vent) / (respire rateXdead space + aveololar vent)

Thus, the volume of fresh air entering the aveoli during each inspiration equals the volume of air in the anatomic dead space minus the tidal volume(TV). The total volume of fresh air entering the aveoli per minute is termed aveololar ventilation.


Aveololar ventilation = 4(respire rate X tidal volumeXdead space) / (tidal volume– dead space)

CELL FUNCTION
DIFFUSION MODEL
The amount of material crossing a surface in a unit of time is known as Flux. This one-way flux of glucose from compartment 1 of a cell to compartment 2 of a cell depends on the concentration of glucose in compartment 1 of a cell. Here, molecules initially concentration in one region of a solution will, due to their random thermal motion, undergo at net movement from the region of higher to the region of lower concentration-that is, they will diffuse until they become distributed throughout the solution. The two one-way fluxes occurring during the diffusion of solute across a boundary and the net flux, which is the difference between the two one-way fluxes. The increase in intracellular concentration as a substance diffuses from a constant extracellular concentration until diffusion equilibrium is reached across plasma membrane of a cell. As with all diffusion processes the net flux (F) of material across the membrane is from the region of higher concentration to region of lower concentration. The magnitude of the net flux is proportional to the difference in concentration across the membrane (Co - Ci), the surface area of the membrane and the permeability constant Kp.

Kp= net flux/4[1/(area times low concentration) – 1/(area times higher concentration)]


DIFFUSION OF IRONS IN THE BLOODSTREAM
In our blood stream, the area of red cells are permeable to potassium irons in the sense that these irons continuously from the plasma into the red cells, or move continuously are interested in studying permeability as a means of eventually division method which I believed and think can be used to determine the rates of permeability involved in introducing an amount of radioactive potassium 42K into the blood to act as a tracer. Usually, all of radioactive potassium is in the plasma, but over time, some of it passes through the red cells and the amount left in the plasma is measured by listing periodic blood samples.