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ENCYCLOPEDIA OF RADIO ELECTRONICS AND ELECTRICAL ENGINEERING
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Converter for powering household equipment

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Encyclopedia of radio electronics and electrical engineering / Chargers, batteries, galvanic cells

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As you know, nickel-cadmium (Ni-Cd) batteries have a "memory": not being discharged to a voltage of 1 V, they cannot accept a full charge. Therefore, in the most advanced chargers [1,2, 3], each such battery is preliminarily discharged to the specified voltage. The discharge device is also the basis of battery capacity meters [XNUMX].

On fig. 1 shows a schematic diagram of a device that discharges a Ni-Cd battery with a capacity of up to 2 ... 3 Ah to a voltage of UG1 \u1d 4 V in automatic mode. Through the resistor R2 and the collector-emitter section of the open transistor VT1, the battery is discharged with a CURRENT Idis = (UG3 - UK2 us VT4) / R1,1 (at a battery voltage of 2 V, Unas \ l-0,3 = 4 V and a resistance of resistor R8,2 equal to 100 ohms - approximately 4 mA). If desired, by replacing RXNUMX with a resistor of less resistance (and, accordingly, with more power dissipation), the discharge current can be increased.

Converter for powering household equipment

As you can see, the voltage of the battery UG1 is connected to the non-inverting input of the comparator DA1, and an exemplary voltage of 1 V is applied to its inverting input from the engine of the tuning resistor R6. As long as the battery voltage exceeds Uo6p by more than 40 μV (40 μV - Upit / kus - the area of ​​\u554b\u9bthe linear, "non-comparator" mode of operation of the K1SAZ), the output voltage of the UBblx comparator is almost equal to the supply voltage (pin 2 is connected to an open collector of its output transistor, closed in this mode). Almost the same voltage is present at the emitter of the transistor VT2, which creates a current IbVT2 "(UvyX - 2UEB) / R4,8 = XNUMX mA in the base of the transistor VTXNUMX, sufficient to keep it in deep saturation mode.

When the battery voltage drops to (UG1 + 40 μV) < Uo6p, the situation changes dramatically: Uout becomes close to 0, transistors VT1 and VT2 close, and the discharge of battery G1 stops. The opened transistor VT3 turns on the HL1 LED (end of discharge signal), and the bias voltage UR6-R10 (Upit-UK10KacVT3-UHL3) / R1-9B is supplied to the resistor R0,08. Thus, the introduced positive feedback organizes the hysteresis mode of operation of the comparator, which eliminates its frequent switching. Of course, UR10 can be smaller (for this, it is enough to reduce the resistance of the resistor R10). Instead of the KT3102EM (VT1) and KT3107D (VT3) indicated in the diagram, other low-power transistors of the corresponding structure with a static current transfer coefficient h21e ≥ 50 can be used in the device. The requirements for the VT2 transistor are somewhat stricter: with h21e ≥ 50 ... 100, it must have a voltage saturation Uke us no more than 0,2 ... 0,3 V. With an increase in the discharge current, it may be necessary to slightly reduce the resistance of the resistor R2. Let's replace the AL307KM LED with any other.

The printed circuit board of the device (Fig. 2) is made of double-sided foil fiberglass. The foil on the side of the parts is used as a common wire, the places for soldering the leads of the parts and wires to it are shown in black squares (before being put in place, pins 2 and 6 of the DA1 chip are bent at a right angle). To avoid short circuits, the foil in the immediate vicinity of the holes for the leads of parts that cannot be connected to a common wire must be removed (this can be done both by etching and by countersinking the edges of the holes after etching).

Converter for powering household equipment

Establishing a properly assembled device comes down to setting the required reference voltage at pin 4 of DA1. The most convenient way to do this is with a digital voltmeter (both its accuracy and high input resistance are needed): by connecting a voltmeter to the trimmer resistor R6 engine, set 0rev = 1 V + UR10 if the HL1 LED is on, or Uo6p = 1 V if it is off . You can also use a conventional voltmeter, controlling the voltage on the battery being discharged: at UG1 = 1 V, the slider of the resistor R6 (previously installed in the upper - according to the diagram - position) is slowly turned until the LED turns on and left in this position.

The process of discharging the battery can be considered complete already at the first turns on of the HL1 LED (the voltage on the battery without load is partially restored, but only to a value of 1 V + UR10, after which the discharge circuit is turned on again). The continuous glow of HL1 indicates that the EMF of the battery does not exceed 1 V + UR10.

Discharging the battery, especially in forced mode, is quite fast. Therefore, all the cells of the rechargeable battery (in modern equipment there are usually no more than three or four of them) can be discharged sequentially, one after the other, without much loss of time.

Literature

  1. Shamis V. Charging device. - Radio, 1992, No. 10, p. 18, 19.
  2. Demenev M. Koroleaa I. "Intelligent" charger. - Radio, 2002, No. 1, p. 38, 39, 42.
  3. Stepenov B. Battery capacity meter. - Radio, 2002, No. 7, p. 38, 39.

Author: Yu.Vinogradov, Moscow

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How to recover lost memories 07.06.2015

Most often, when they talk about amnesia, they mean its anterograde or retrograde variety. It is easy to distinguish them: anterograde amnesia - a violation of memory about what happened after the onset of the disease; retrograde - impaired memory of what happened before the onset of the disease. Both can happen to a person due to a brain injury, or due to severe stress, or due to a severe neurological disease (for example, Alzheimer's syndrome). Obviously, the specific cause of amnesia is that some neurons related to recording and storing information, for some reason, stop working as they should. But what is the essence of these problems? Some (and most) defend the hypothesis that information is simply lost from neural circuits so that it cannot be recovered. Others believe that we are dealing with an access problem here, that the information is still in the brain store, but it has become blocked, and we cannot get to it.

Apparently, the hypothesis of blocked access is still true - the results of the experiments of Susumu Tonegawa and employees of his laboratory at the Massachusetts Institute of Technology speak in its favor. Tonegawa himself received the Nobel Prize in 1987 for the discovery of the genetic principle of the formation of antibody diversity, but then switched to cellular memory mechanisms. And here he and his colleagues achieved outstanding success. So, for example, just last year they released several papers in which they described how the brain remembers the sequence of events and how working memory is corrected when we suddenly realize that we did something wrong. Finally, in their Nature paper last year, they talked about reprogramming emotional memory: by influencing hippocampal neurons, the researchers were able to literally turn bad memories into good ones.

In 2012, Tonegawa's group was able to confirm the existence of engram cells in the hippocampus (one of the main memory centers). An engram is understood as a trace left by a stimulus; if we talk about neurons, then a repeated signal - a sound, a smell, a certain environment, etc. - should provoke some physical and biochemical changes in them. If the stimulus is then repeated, then the "trace" is activated, and the cells in which it is present will recall the entire memory from memory. In other words, our engram ("key") neurons are responsible for accessing the recorded information, and in order for them to work themselves, they must be affected by a key signal. But, in addition, such cells must be able to somehow preserve traces of stimuli. In practice, this means that intercellular synapses should be strengthened between engram cells: the stronger they are, the more reliable the signal will pass between them, the stronger the neurons will remember a certain stimulus. However, until recently, there were no experimental confirmations here - no one knew whether specific biochemical changes actually occur in such neurons associated with the memorization of a stimulus.

The researchers used the same methods of optogenetics that allowed them to confirm the very existence of "key" cells a few years ago. Recall that the essence of optogenetics is that a neuron introduces a photosensitive protein that forms an ion channel in the cell membrane: a light signal opens the channel, ions are redistributed on both sides of the membrane, and the neuron either "turns on" or "falls asleep", depending on what is needed in a particular experience. First, they found cells in the hippocampus of mice that turned on memories when they themselves were activated by light. These cells, as the authors of the work write in their article in Science, really strengthened intercellular connections - in other words, they together formed a neural switch, which, on a signal, opened access to a certain block of information. Increased intercellular contact means that the cell needs more proteins that serve the synapse, that is, everything rests on the process of protein biosynthesis. Synthesis in neurons was turned off with an antibiotic, and this was done immediately after the mouse memorized something. Synapses in this case remained fragile, and, most importantly, the mouse could not remember anything the next day when it was exposed to the same stimulus that was active during training. It turned out a real retrograde amnesia - the memory of what happened before the antibiotic treatment disappeared, and it was impossible to restore it with the help of ordinary stimuli.

But the same engram cells that were supposed to respond to a key stimulus and that were silent due to weakened synapses carried optogenetic modifications. And now, if they were activated with the help of a light pulse, then the memory of the animals returned. If we discard the details about special switch cells, synapses and protein synthesis, it turns out that neuroscientists restored memory with the help of a light flash to the brain.

But the emphasis should still be placed on engram neurons, no matter how strange their name may seem for unusual hearing. Previously, Tonegawa's laboratory was able to show that not just one cell is responsible for turning on memory, but a neural circuit of several such neurons. Based on the new data, the researchers propose the following diagram of how memory is organized in the brain of mammals (and, perhaps, in general, in most animals with a central nervous system). Its main point is that different structures are responsible for storing and activating memory - groups of engram cells take care of other neural circuits that store blocks of information, and activation neurons can in some sense be compared with librarians lending out books on demand. Moreover, the relationship between activation neurons and storage neurons can be different, for example, one activating network can act on several memory units at once, and specific relationships between those and others still need to be studied properly.

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