 logic components.
https://en.wikipedia.org/wiki/Baker_clamp

A: I'll keep it fairly simple. (And it is very similar to hacktastical's approach except that the input isn't DC-blocked and I've tied the input stage's emitters just slightly differently.) Consider the following:

simulate this circuit – Schematic created using CircuitLab
Personally, I'd put resistors in the emitters of the output BJTs to limit the output current. But I don't know what you are driving or care about, so I left them off for simplicity.

Just did a simulation to make sure I wasn't a complete idiot:

That includes a \$60\:\Omega\$ to \$100\:\Omega\$ source impedance, which is likely for any MCU pin drive, and also \$10\:\Omega\$ emitter resistors for the driver BJTs. (But a very light \$10\:\text{k}\Omega\$ load, as I'm just giving it a whirl for now.)

A: First, let's note that this circuit is never going to perform exceptionally well as-is. Without adding semiconductors, that is. I'll try and tweak it somewhat below, but it'd be much easier to use any of the fully symmetric architectures to achieve inherent symmetry. This circuit has asymmetry due to Q1 and Q2 having no complementary devices to work with.
The simulation was not set up correctly. Both the Offset and Ampltiude of V1 should be set to 3.3/2. Yes, such formulas can be used.

simulate this circuit – Schematic created using CircuitLab
Let's look at their base currents (timestep=10ns), with V(IN) and V(OUT) below them for timing reference:


Q3 never fully turns off - it has about 3uA flowing through the base in the off state. Q4 does turn off fully. But this isn't the problem.
Let's observe how those transistors are driven, then. Let's speed up the square wave a bit, and sweep R3 from 400ohm to 10kohm:

simulate this circuit

At 200kHz, R3 above about 5kohm makes the circuit too slow to switch. That's because Q2 is driven deep into saturation. So, to speed things up, generally R3 needs to be lower. The lower the value, the faster Q2 turns off, but also the slower it turns on. The asymmetry grows the deeper Q2 is driven into saturation. When Q2 operates in very light saturation, the turn-on and turn-off times become almost equal. Just below R3 of 500 ohms, Q2's turn-on and turn-off become equally quick at about 600ns.
We can now see if negative feedback might make things less sensitive. Let's set R3 to 1kohm, and add an emitter degeneration resistor.

simulate this circuit

We can see that for R3=1k, R8=120 gives a reasonable degree of symmetry without changing anything else. For R3=600, R8=40 is the limiting value:

We can also check the sensitivity to Q2's beta - it's insignificant across the range of beta=50 to 150.

Let's now add a bypass capacitor to Q2's input resistor R2:

simulate this circuit

The relationship is nonmonotonic: the minimal falling edge delay is for C1=100pF. Values lower or higher give higher delays. We're now solidly in the 0.3-0.5us propagation delay territory.
We can improve symmetry now by letting Q4 turn on faster, by lowering R6.

simulate this circuit

Best propagation delay symmetry is around R6=50k. We can now see if R5's value can be improved as well.
Let's choose R6=10k for fastest falling edge, and select R5 for equal rising edge delay:

Reasonable symmetry is achieved with R6=10k, R5=20k. We note that at lower R5/R6 values, there's a bit of a raised pedestal before the rising edge. We could get rid of it by slowing things down a bit.
We can also evaluate the performance when faced with varying capacitive loading, as expected in a more realistic model:

simulate this circuit
The behavior is reasonable across a range of load capacitances:

We can now guess that R1 will need a speed-up capacitor as well. Due to the time scales involved, we need to get the simulation time step down to 4ns to avoid numerical artifacts.
The optimized circuit looks as follows:

simulate this circuit
The propagation delay is below 0.1us, and is fairly symmetric:

The performance is quite acceptable at 100kHz, and should be well-suited for operation at 10kHz. The the rise/fall propagation delay will further vary up to 50ns due to Q3/Q4 beta mismatch. 50ns over 100us is about 0.05% duty cycle error due to mismatch, and it's relatively stable otherwise, so for any particular selection of components, it's a constant error term.
The load resistance can go a bit below 1kohm, but not much:

The various optimization steps are shown below:





A: Here's a version that uses a dual Sziklai driver (simulate it here):

This design will render the full duty cycle range and provide strong +/-12V drive.
How it works: the pre-driver pair emitters are biased to 3.3V/2. As the input swings above and below that threshold by +/- Vbe, it activates the upper or lower transistor. So the input signal requirement is 3.3V/2 +/- Vbe, or about 2.25V / 1.05V.
The 100pf cap provides some negative feedback to control the slew rate. The 100k resistor provides some hysteresis.
[A short postscript. The Level 2 charger pilot signal is 1kHz, 10-90% duty cycle. Design accordingly.]
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Production of reactive oxygen species, often by NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidases, plays a role in the signaling responses of cells to many receptor stimuli. Here, we describe the function of the calcium-dependent, nonphagocytic NADPH oxidase Duox1 in primary human CD4+ T cells and cultured T cell lines. Duox1 bound to inositol 1,4,5-trisphosphate receptor 1 and was required for early T cell receptor (TCR)–stimulated production of hydrogen peroxide (H2O2) through a pathway that was dependent on TCR-proximal kinases. Transient or stable knockdown of Duox1 inhibited TCR signaling, especially phosphorylation of tyrosine-319 of ζ chain–associated protein kinase of 70 kilodaltons (ZAP-70), store-operated entry of calcium ions (Ca2+), and activation of extracellular signal–regulated kinase. The production of cytokines was also inhibited by knockdown of Duox1. Duox1-mediated inactivation of Src homology 2 domain–containing protein tyrosine phosphatase 2 promoted the phosphorylation of ZAP-70 and its association with the Src family tyrosine kinase Lck and the CD3ζ chain of the TCR complex. Thus, we suggest that activation of Duox1, downstream of proximal TCR signals, generates H2O2 that acts in a positive feedback loop to enhance and sustain further TCR signaling.Welcome to Basil World! I'll explain the relevance of everything you see and hear.
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