Model: Chandar/sv-subject-based-matryoshka-mpnet-base
Author: Chandar
Pipeline: sentence-similarity
Library: sentence-transformers
Tags: sentence-transformers, safetensors, mpnet, sentence-similarity, feature-extraction, generated_from_trainer, dataset_size:1124250, loss:MatryoshkaLoss, loss:CoSENTLoss, arxiv:1908.10084, arxiv:2205.13147, base_model:microsoft/mpnet-base, base_model:finetune:microsoft/mpnet-base, model-index, endpoints_compatible, region:us
Base models (finetune): id: microsoft/mpnet-base
Card metadata: tags: sentence-transformers, sentence-similarity, feature-extraction, generated_from_trainer, dataset_size:1124250, loss:MatryoshkaLoss, loss:CoSENTLoss
base_model: microsoft/mpnet-base
widget: source_sentence: channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire
an action potential.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic
cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be
accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be
degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the
presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that
are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades
acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that
release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and
unbind to postsynaptic receptors.
Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine — CNS and/or
PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or
PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric
acidCNS
Neuropeptide Substance P, endorphins CNS and/or
PNS
Table 35.2
Electrical Synapse
While electrical synapses are fewer in number than chemical synapses, they are found in all nervous
systems and play important and unique roles. The mode of neurotransmission in electrical synapses is
quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic
membranes are very close together and are actually physically connected by channel proteins forming
gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the
ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction
pores.
There are key differences between chemical and electrical synapses. Because chemical synapses
depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there
is an approximately one millisecond delay between when the axon potential reaches the presynaptic
terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this
signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which
is important for synapses involved in key reflexes), and some electrical synapses are bidirectional.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important
for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the
thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.
Signal Summation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron,
but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic
neuron to be sufficiently depolarized to fire an action potential. This process is calledsummation and
occurs at the axon hillock, as illustrated inFigure 35.16. Additionally, one neuron often has inputs
from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs
and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the
postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together,
synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system
is not transmitted as important information.
1004 CHAPTER 35 | THE NERVOUS SYSTEM
This content is available for free at http://cnx.org/content/col11448/1.9
sentences: 7.2 
CHAPTER 
Moray Offshore Renewables Limited - Environmental Statement  
Telford, Stevenson and MacColl Offshore Wind Farms and Transmission Infrastructure 
 
 
Section 3 – Offshore Generating Station Impact Assessment 7-51 
Table 7.2-10 Qualitative Assessment for Species not Modelled and Without Defined Surrogates Based 
on Potential Magnitude of Effects and Receptor Sensitivities 
Species 
Potential 
Magnitude of 
Effect 
Sensitivity of Receptor Magnitude 
of Effect 
Sandeels Small 
 Important prey species; and 
 Known to be present in the Moray Firth area.  The results 
of the site specific survey undertaken, however, 
suggest that within the three proposed wind farm sites 
there are not extensive areas supporting important 
sandeel populations.  Substrate specific. 
Medium 
Elasmobranchs Small 
 Most species are of conservation Importance; 
 Generally more prevalent in the north and west of 
Scotland than in the Moray Firth; and 
 Some with nursery grounds defined in the proposed 
sites (spurdog, spotted ray and thornback ray). 
Low-
Medium 
River and Sea 
Lamprey Small 
 Conservation importance; and 
 Potentially transiting the site during migration (lack of 
detailed information on migration). 
Medium 
Anglerfish Small 
 Commercially important; and 
 High intensity nursery area in the sites. 
Medium 
Haddock Small to 
Medium 
 Commercially important; and 
 Nursery grounds in the area and spawning grounds in 
the proximity of the proposed sites, however 
comparatively large. 
Low 
European Eel Small to 
Medium 
 Conservation importance; and 
 Potentially transiting the site during migration (lack of 
detailed information on migration). 
Medium 
Sprat Medium 
 Important as prey species; and 
 Spawning and nursery grounds in the area, however 
these are comparatively large. 
Low- 
Medium 
Life Stages of Limited Mobility 
7.2.5.47 Life stages of limited mobility such as larvae, and in the case of European eel, their 
juvenile form (glass eels), will not be able to avoid areas where the highest noise 
levels are reached during construction, assum ing they drift through the proposed 
wind farm sites .  Although there is limited information on the effect of piling noise to 
date on early life stages of fish, research recently carried out by the Institute for 
Marine Resources and Ecosystem Studies (IMARES) (Bolle et al., 2011) suggests that 
the assumption of 100 % of larvae mortality within a radius of 1,000  m around a piling 
site (used in the Appropriate Assessment of Dutch offshore wind farms) is too 
conservative.  Bolle et al ., (2011) found no significant effects in the larval stages 
analysed at the highe st exposure level (cumulative SEL = 206  dB re 1µPa 2s) which 
represented 100 pulses at a distance of 100  m from piling.  It is recognised that the 
results, based on sole ( Solea solea) larvae, should not be extrapolated to fish larvae 
in general as inter -specific differences in vulnerability to sound exposure may exist .  
The findings, however suggest that larval mortality would only occur within a few, 168 7.17. Ferromagnetism
0
0.5
1
1.5
10−6 ρ/χ (kg m−3)
0 300 600 900 1200 1500
T(K)
Figure 7.11: Plot ofρ/χ(where ρis the mass density) versus temperature for gadolinium above
its Curie temperature. The curve is (apart from some slight departures at high temperatures) a
straight-line, in accordance with the Curie-Weiss law. The intercept of the line with the temperature
axis givesTc =310 K. The metal becomes ferromagneticbelow 289 K. Data from S. Arajs, and
R.V . Colvin, J. appl. Phys.32, 336S (1961).
Here, r /nequal1. Hence, deduce that
S ∞= a
1 −r,
assuming that 0<r <1.
7.2 Let
I(n) =
∫ ∞
0
xn e−αx2
dx.
Demonstrate that
I(n) =−∂I(n −2)
∂α .
Furthermore, show that
I(0) =
√
π
2 α1/2
(see Exercise 2.2), and
I(1) = 1
2 α., 416 10 Spontaneous Symmetry Breaking
10.9 The Goldstone Theorem
So far, we have only discussed the simplest of all symmetry groups, namelyG = Z2,
which is both ﬁnite and abelian. Although it will not change our picture of SSB ,
for the sake of completeness (and interest to foundations) we also present a brief
introduction to continuous symmetries, culminating in the Goldstone Theorem and
the Higgs mechanism (which at ﬁrst sight contradict each other and hence require a
very careful treatment). The former results when the broken symmetry groupG is a
Lie group, whereas the latter arises when it is an inﬁnite-dimensional gauge group.
Let us start with the simple case G = SO(2), acting on R2 by rotation. This
induces the obvious action on the classical phase space T ∗R2, i.e.,
R(p,q)=( Rp,Rq), (10.300)
cf. (3.94), as well as on the quantum Hilbert space H = L2(R2), that is,
uRψ(x)= ψ(R−1x). (10.301)
Let us see what changes with respect to the action of Z2 on R considered in §10.1.
We now regard the double-well potentialV in (10.11) as anSO(2)-invariant function
on R2 through the reinterpretation ofx2 as x2
1 +x2
2. This is theMexican hat potential.
Thus the classical Hamiltonianh(p,q)= p2/2m+V (q), similarly with p2 = p2
1 + p2
2,
is SO(2)-invariant, and the set of classical ground states
E0 = {(p,q) ∈T ∗R2 |p = 0,q2 = a2} (10.302)
is the SO(2)-orbit through e.g. the point (p1 = p2 = 0,q1 = a,q2 = 0). Unlike the
one-dimensional case, the set of ground states is now connected and forms a cir-
cle in phase space, on which the symmetry group SO(2) acts. The intuition behind
the Goldstone Theorem is that a particle can freely move in this circle at no cost
of energy. If we look at mass as inertia, such motion is “massless”, as there is no
obstruction. However, this intuition is only realized in quantum ﬁeld theory. In quan-
tum mechanics, the ground state of the Hamiltonian (10.6) (now acting onL2(R2))
remains unique, as in the one-dimensional case. In polar coordinates (r,φ) we have
h¯h = −¯h2
2m
(∂2
∂r2 + 1
r
∂
∂r + 1
r2
∂2
∂φ2
)
+V (r), (10.303)
with V (r)= 1
4 λ(r2 −a2)2. With
L2(R2) ∼= L2(R+) ⊗ℓ2(Z) (10.304)
under Fourier transformation in the angle variable, this becomes
h¯hψ(r,n)=
(
−¯h2
2m
(∂2
∂r2 + 1
r
∂
∂r −n2
r2
)
+V (r)
)
ψ(r,n). (10.305), source_sentence: channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire
an action potential.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic
cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be
accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be
degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the
presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that
are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades
acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that
release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and
unbind to postsynaptic receptors.
Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine — CNS and/or
PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or
PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric
acidCNS
Neuropeptide Substance P, endorphins CNS and/or
PNS
Table 35.2
Electrical Synapse
While electrical synapses are fewer in number than chemical synapses, they are found in all nervous
systems and play important and unique roles. The mode of neurotransmission in electrical synapses is
quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic
membranes are very close together and are actually physically connected by channel proteins forming
gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the
ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction
pores.
There are key differences between chemical and electrical synapses. Because chemical synapses
depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there
is an approximately one millisecond delay between when the axon potential reaches the presynaptic
terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this
signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which
is important for synapses involved in key reflexes), and some electrical synapses are bidirectional.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important
for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the
thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.
Signal Summation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron,
but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic
neuron to be sufficiently depolarized to fire an action potential. This process is calledsummation and
occurs at the axon hillock, as illustrated inFigure 35.16. Additionally, one neuron often has inputs
from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs
and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the
postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together,
synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system
is not transmitted as important information.
1004 CHAPTER 35 | THE NERVOUS SYSTEM
This content is available for free at http://cnx.org/content/col11448/1.9
sentences: 517
The components of orbital angular momentum do not commute with H.
[H,Lz] = icγ4[γjpj,xpy − ypx] = ¯hcγ4(γ1py − γ2px)
The components of spin also do not commute with H.
Σ z = [γ1,γ2]
2i = γ1γ2
i
[H,Sz] = [ H,¯h
2 Σ z] = c¯h
2 [γ4γjpj,γ1γ2] = c¯h
2 pj[γ4γjγ1γ2 − γ1γ2γ4γj]
= c¯h
2 pj[γ4γjγ1γ2 − γ4γ1γ2γj] = c¯h
2 pjγ4[γjγ1γ2 − γ1γ2γj] = ¯hcγ4[γ2px − γ1py]
However, the helicity, or spin along the direction of motion does commute.
[H,⃗S· ⃗ p] = [ H,⃗S] · ⃗ p= ¯hcγ4⃗ p× ⃗ γ· ⃗ p= 0
From the above commutators [ H,Lz] and [ H,Sz], the components of total angular momentum
do commute with H.
[H,Jz] = [ H,Lz] + [ H,Sz] = ¯hcγ4(γ1py − γ2px) + ¯hcγ4[γ2px − γ1py] = 0
The Dirac equation naturally conserves total angular momentum but not conserve the orbital
or spin parts of it.
We will need another conserved quantity for the solution to the Hyd rogen atom; something akin to
the ± in j = ℓ± 1
2 we used in the NR solution. We can show that [ H,K] = 0 for
K = γ4⃗Σ · ⃗J− ¯h
2 γ4.
It is related to the spin component along the total angular momentu m direction. Lets compute the
commutator recalling that H commutes with the total angular momentum.
H = icγ4⃗ γ· ⃗ p+ mc2γ4
[H,K] = [ H,γ4](⃗Σ · ⃗J− ¯h
2 ) + γ4[H,⃗Σ] · ⃗J
[H,γ4] = ic[γ4⃗ γ· ⃗ p,γ4] = 2 ic⃗ γ· ⃗ p
[H,Σ z] = 2 cγ4[γ2px − γ1py][
H,⃗Σ
]
= −2cγ4⃗ γ× ⃗ p
[H,K] = 2 ic(⃗ γ· ⃗ p)(⃗Σ · ⃗J− ¯h
2 ) − 2c⃗ γ× ⃗ p· ⃗J
⃗ p· ⃗L = 0
⃗J = ⃗L+ ¯h
2
⃗Σ
[H,K] = 2 c
(
i(⃗ γ· ⃗ p)(⃗Σ · ⃗J) − ⃗ γ× ⃗ p· ⃗J− i¯h
2 (⃗ γ· ⃗ p)
), 289
19.7 Homework 7
1. A particle is in the state ψ= R(r)
(√
1
3 Y21 + i
√
1
3 Y20 −
√
1
3 Y22
)
. Find the expected values of
L2, Lz, Lx, and Ly.
2. A particle is in the state ψ= R(r)
(√
1
3 Y11 + i
√
2
3 Y10
)
. If a measurement of the xcomponent
of angular momentum is made, what are the possilbe outcomes and wh at are the probabilities
of each?
3. Calculate the matrix elements ⟨Yℓm1 |Lx|Yℓm2 ⟩ and ⟨Yℓm1 |L2
x|Yℓm2 ⟩
4. The Hamiltonian for a rotor with axial symmetry is H =
L2
x+L2
y
2I1
+ L2
z
2I2
where the I are constant
moments of inertia. Determine and plot the eigenvalues of H for dumbbell-like case that
I1 >>I2.
5. Prove that ⟨L2
x⟩ = ⟨L2
y⟩ = 0 is only possible for ℓ= 0.
6. Write the spherical harmonics for ℓ≤ 2 in terms of the Cartesian coordinates x, y, and z.
7. A particle in a spherically symmetric potential has the wave-funct ion ψ(x,y,z ) = C(xy+ yz+
zx)e−αr2
. A measurement of L2 is made. What are the possible results and the probabilities
of each? If the measurement of L2 yields 6¯h2, what are the possible measured values of Lz
and what are the corresponding probabilities?
8. The deuteron, a bound state of a proton and neutron with ℓ= 0, has a binding energy of -2.18
MeV. Assume that the potential is a spherical well with potential of −V0 for r <2.8 Fermis
and zero potential outside. Find the approximate value of V0 using numerical techniques., 1. Introduction and Fundamental Principles 
 
 13
        
For a free particle like that found in a monatomic gas, the partition function1 is (see 
also section 11.1b) 
 Vh
)mkT2()T(U 3
23
π=    ,                                       (1.1.19) 
 
where V is the specific volume of the gas, m is the mass of the particle, and T is the 
kinetic temperature. Replacing dlnU/dlnT in equation (1.1.18) by its value obtained 
from equation (1.1.19), we get the familiar relation 
 
NkT2
3E =     ,                                            (1.1.20) 
 
which is only correct if T is the kinetic temperature. Thus we arrive at a self-
consistent solution if the parameter T is to be identified with the kinetic temperature. 
 
 The situation for a photon gas in the presence of material matter is somewhat 
simpler because the matter acts as a source and sinks for photons. Now we can no 
longer apply the constraint dN = 0. This is equivalent to adding lnα2= 0  (i.e., α2 = 1) 
to the equations of condition. If we let β2 = 1/(kT) as we did with the Maxwell-
Boltzmann statistics, then the appropriate  solution to the B ose-Einstein formula 
[equation (1.1.15)] becomes   
1e
1
n
N
)kT(h
i
−
= ν ,                                            (1.1.21)   
where the photon energy wi has been replaced by hν. Since two photons in a volume 
h3 can be distinguished by their state of polarization, the number of phase space 
compartments is 
 n = (2/h3)dx1dx2dx3dp1dp2dp3                                 (1.1.22) 
 
 We can replace the rectangular form of the momentum volume dp1dp2dp3, by 
its spherical counterpart 4πp2dp and remembering that the momentum of a photon is 
hν/c, we get 
ν
−
πν= ν d
1e
1
c
8
V
dN
)kT(h3
2
     .                            (1.1.23) 
Here we have replaced Ni with dN. This assumes that the number of particles in any 
phase space volume is small compared to the total number of particles. Since the 
energy per unit volume dEν is just hν dN/V, we get the relation known as Planck's 
law or sometimes as the blackbody law:, source_sentence: channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire
an action potential.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic
cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be
accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be
degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the
presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that
are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades
acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that
release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and
unbind to postsynaptic receptors.
Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine — CNS and/or
PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or
PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric
acidCNS
Neuropeptide Substance P, endorphins CNS and/or
PNS
Table 35.2
Electrical Synapse
While electrical synapses are fewer in number than chemical synapses, they are found in all nervous
systems and play important and unique roles. The mode of neurotransmission in electrical synapses is
quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic
membranes are very close together and are actually physically connected by channel proteins forming
gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the
ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction
pores.
There are key differences between chemical and electrical synapses. Because chemical synapses
depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there
is an approximately one millisecond delay between when the axon potential reaches the presynaptic
terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this
signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which
is important for synapses involved in key reflexes), and some electrical synapses are bidirectional.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important
for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the
thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.
Signal Summation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron,
but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic
neuron to be sufficiently depolarized to fire an action potential. This process is calledsummation and
occurs at the axon hillock, as illustrated inFigure 35.16. Additionally, one neuron often has inputs
from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs
and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the
postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together,
synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system
is not transmitted as important information.
1004 CHAPTER 35 | THE NERVOUS SYSTEM
This content is available for free at http://cnx.org/content/col11448/1.9
sentences: Figure 42.21The spleen is similar to a lymph node but is much larger and filters blood instead of
lymph. Blood enters the spleen through arteries and exits through veins. The spleen contains two
types of tissue: red pulp and white pulp. Red pulp consists of cavities that store blood. Within the
red pulp, damaged red blood cells are removed and replaced by new ones. White pulp is rich in
lymphocytes that remove antigen-coated bacteria from the blood. (credit: modification of work by
NCI)
42.3 | Antibodies
By the end of this section, you will be able to:
• Explain cross-reactivity
• Describe the structure and function of antibodies
• Discuss antibody production
An antibody, also known as an immunoglobulin (Ig), is a protein that is produced by plasma cells after
stimulation by an antigen. Antibodies are the functional basis of humoral immunity. Antibodies occur in
the blood, in gastric and mucus secretions, and in breast milk. Antibodies in these bodily fluids can bind
pathogens and mark them for destruction by phagocytes before they can infect cells.
Antibody Structure
An antibody molecule is comprised of four polypeptides: two identical heavy chains (large peptide units)
that are partially bound to each other in a “Y” formation, which are flanked by two identical light chains
(small peptide units), as illustrated inFigure 42.22. Bonds between the cysteine amino acids in the
antibody molecule attach the polypeptides to each other. The areas where the antigen is recognized on
the antibody are variable domains and the antibody base is composed of constant domains.
In germ-line B cells, the variable region of the light chain gene has 40 variable (V) and five joining
(J) segments. An enzyme called DNA recombinase randomly excises most of these segments out of the
gene, and splices one V segment to one J segment. During RNA processing, all but one V and J segment
are spliced out. Recombination and splicing may result in over 106 possible VJ combinations. As a result,
each differentiated B cell in the human body typically has a unique variable chain. The constant domain,
which does not bind antibody, is the same for all antibodies.
CHAPTER 42 | THE IMMUNE SYSTEM 1233, 156
Access to the bus used by AS-I is made using the master/slave mode, which may be 
inserted with a PLC or a PC, or else, using a Gateway. The Gateway works like a trans-
lator from an upper protocol into the bus AS-I. There are Gateways for all main proto-
cols. In the AS-I network it is necessary to plan the presence of a dedicated feeder that 
supplies a specific voltage in order to transmit the data. Specific equipment, found on 
the market, allows an address to be assigned it. Each slave may handle a maximum of 
4 inputs and 4 outputs, and the maximum number of slaves is 31.
– Protocol according to EN 50295 standards
– Master/slave structure 
– Maximum transmission speed: 167 Kbit/sec
– Maximum number of slaves: 31
– Line connection 
– Maximum bus distance: 100 m
                                                          
         187 
 
 
 
 
AS-Interface ( AS-I ) 
 
                                                   
 
Il sistema AS -I ( Actuator Sensor Interface ) nasce nel 1994 ed è una rete di 
comunicazione progettata per il  solo collegamento di dispositivi industrial i quali 
sensori e attuatori. La semplicità del protocollo consente di integrare in un unico cavo 
non schermato sia i segnali di comando che l’alimentazione ai nodi. E’ un cavo di 
colore giallo con una forma particolare ed è diventato il simbolo di questo p rotocollo. 
Il collegamento del cavo avvie ne per perforazione di isolante.  Gli spilli presenti sul 
connettore prelevano il segnale senza bisogno togliere la guaina al filo. La 
configurazione geometrica del cavo impedisce l’inversione di polarità. Se il cavo  ha 
una lunghezza superiore a 100m è necessario inserire un repeater  che porta la 
lunghezza della rete a 300m. La massima portata del cavo giallo è di 2 A, se il 
consumo delle elettrovalvole dovesse superare quel valore si  deve aggiungere un 
secondo cavo di colore nero che porta il 24Vcc alle uscite. Anche questo cavo utilizza 
la stessa tecnica di cablaggio. 
 
 
                                      
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
         187 
 
 
 
 
AS-Interface ( AS-I ) 
 
                                                   
 
Il sistema AS -I ( Actuator Sensor Interface ) nasce nel 1994 ed è una rete di 
comunicazione progettata per il  solo collegamento di dispositivi industrial i quali 
sensori e attuatori. La semplicità del protocollo consente di integrare in un unico cavo 
non schermato sia i segnali di comando che l’alimentazione ai nodi. E’ un cavo di 
colore giallo con una forma particolare ed è diventato il simbolo di questo p rotocollo. 
Il collegamento del cavo avvie ne per perforazione di isolante.  Gli spilli presenti sul 
connettore prelevano il segnale senza bisogno togliere la guaina al filo. La 
configurazione geometrica del cavo impedisce l’inversione di polarità. Se il cavo  ha 
una lunghezza superiore a 100m è necessario inserire un repeater  che porta la 
lunghezza della rete a 300m. La massima portata del cavo giallo è di 2 A, se il 
consumo delle elettrovalvole dovesse superare quel valore si  deve aggiungere un 
secondo cavo di colore nero che porta il 24Vcc alle uscite. Anche questo cavo utilizza 
la stessa tecnica di cablaggio. 
 
 
                                      
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
30 V + Dates
24 V aux.
Profiled cable
Contact
Electromechanical AS-interface
Pneumatic Guide_GB.indd   156 15/04/2015   08:47:37, "The	caverns	in	Carniola	and	Carinthia,	in	which	the	blind	
Proteus
	and	so
many	other	blind	animals	live,	belong	geologically	to	the	Jurassic
formation;	and	although	we	do	not	exactly	know	when	for	example	the
Proteus
	first	entered	them,	the	low	organization	of	this	amphibian	certainly
indicates	that	it	has	been	sheltered	there	for	a	very	long	period	of	time,	and
that	thousands	of	generations	of	this	species	have	succeeded	one	another	in
the	caves.
"Hence	there	is	no	reason	to	wonder	at	the	extent	to	which	the	degeneration
of	the	eye	has	been	already	carried	in	the	
Proteus
;	even	if	we	assume	that	it
is	merely	due	to	the	cessation	of	the	conserving	influence	of	natural
selection."
[103]
Let	me	first	note	a	strange	oversight	on	the	part	of	Prof.	Weismann.	He	points
out	that	the	caverns	in	question	belong	to	the	Jurassic	formation:	apparently
intending	to	imply	that	they	have	an	antiquity	related	to	that	of	the	formation.
But	there	is	no	such	relation,	except	that	the	caverns	cannot	be	older	than	the
formation.	They	may	have	originated	at	any	period	since	the	containing	strata
were	deposited;	and	they	may	be	therefore	relatively	modern.	But	passing	over
this,	and	admitting	that	the	
Proteus
	has	inhabited	the	caverns	for	an	enormous
period,	what	is	to	be	said	of	the	fact	that	their	eyes	have	not	disappeared	entirely,
as	Prof.	Weismann	contends	they	should	have	done	had	the	inheritance	of	the
effects	of	disuse	been	all	along	operative?	There	is	a	very	sufficient	answer—the
rudimentary	eyes	are	not	entirely	useless.	It	seems	that	when	the	
underground
streams	it	inhabits	are	unusually	swollen,	some	individuals	of	the	species	are
carried	out	of	the	caverns	into	the	open	(being	then	sometimes	captured).	It	is
also	said	that	the	creatures	shun	the	light;	this	trait	being,	I	presume,	observed
when	it	is	in	captivity.	Now	obviously,	among	individuals	carried	out	into	the
open,	those	which	remain	visible	are	apt	to	be	carried	off	by	enemies;	whereas,
those	which,	appreciating	the	difference	between	light	and	darkness,	shelter
themselves	in	dark	places,	survive.	Hence	the	tendency	of	natural	selection	is	to
prevent	the	decrease	of	the	eyes	beyond	that	point	at	which	they	can	distinguish
between	light	and	darkness.	Thus	the	apparent	anomaly	is	explained.
Let	me	suggest,	as	another	possible	reason	for	persistence	of	rudimentary	organs,
that	the	principle	of	economy	of	growth	will	cause	diminution	of	them	only	in
proportion	as	their	constituents	are	of	value	for	other	uses	in	the	organism;	and
that	in	many	cases	their	constituents	are	practically	valueless.	Hence	probably, source_sentence: channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire
an action potential.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic
cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be
accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be
degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the
presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that
are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades
acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that
release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and
unbind to postsynaptic receptors.
Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine — CNS and/or
PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or
PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric
acidCNS
Neuropeptide Substance P, endorphins CNS and/or
PNS
Table 35.2
Electrical Synapse
While electrical synapses are fewer in number than chemical synapses, they are found in all nervous
systems and play important and unique roles. The mode of neurotransmission in electrical synapses is
quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic
membranes are very close together and are actually physically connected by channel proteins forming
gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the
ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction
pores.
There are key differences between chemical and electrical synapses. Because chemical synapses
depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there
is an approximately one millisecond delay between when the axon potential reaches the presynaptic
terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this
signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which
is important for synapses involved in key reflexes), and some electrical synapses are bidirectional.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important
for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the
thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.
Signal Summation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron,
but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic
neuron to be sufficiently depolarized to fire an action potential. This process is calledsummation and
occurs at the axon hillock, as illustrated inFigure 35.16. Additionally, one neuron often has inputs
from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs
and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the
postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together,
synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system
is not transmitted as important information.
1004 CHAPTER 35 | THE NERVOUS SYSTEM
This content is available for free at http://cnx.org/content/col11448/1.9
sentences: 167
9.7.5 1D Model of a Molecule Derivation *
ψ(x) =



eκx x< −d
A(eκx + e−κx) −d<x<d
e−κx x>d
κ=
√
−2mE
¯h2 .
Since the solution is designed to be symmetric about x= 0, the boundary conditions at −dare the
same as at d. The boundary conditions determine the constant A and constrain κ.
Continuity of ψ gives.
e−κd = A
(
eκd+ e−κd)
A= e−κd
eκd+ e−κd
The discontinuity in the ﬁrst derivative of ψ at x= d is
−κe−κd− Aκ
(
eκd − e−κd)
= − 2maV0
¯h2 e−κd
−1 − Aeκd − e−κd
e−κd = − 2maV0
κ¯h2
−1 − eκd− e−κd
eκd+ e−κd = − 2maV0
κ¯h2
2maV0
κ¯h2 = 1 + eκd− e−κd
eκd+ e−κd
2maV0
κ¯h2 = 1 + tanh( κd)
We’ll need to study this transcendental equation to see what the a llowed energies are.
9.7.6 1D Model of a Crystal Derivation *
We are working with the periodic potential
V(x) = aV0
∞∑
n=−∞
δ(x− na).
Our states have positive energy. This potential has the symmetry that a translation by the lattice
spacing a leaves the problem unchanged. The probability distributions must th erefore have this
symmetry
|ψ(x+ a)|2 = |ψ(x)|2,
which means that the wave function diﬀers by a phase at most.
ψ(x+ a) = eiφψ(x), 7.5 Quadratic Dispersion 181
Group delay (or group velocity) essentially tracks the center of the pulse.
In our derivation we have assumed that the phase delayk(ω)·∆r could be well-
represented by the first two terms of the expansion (7.33). While this assumption
gives results that are often useful, higher-order terms can also play a role. In
section 7.5 we’ll find that the next term in the expansion controls the rate at which
the pulse spreads as it travels. We should also note that there are times when the
expansion (7.33) fails to converge (when ω0 is near a resonance of the medium),
and the above expansion approach is not valid. We’ll analyze pulse propagation
in this sticky situation in section 7.6.
7.5 Quadratic Dispersion
A light pulse traversing a material in general undergoes dispersion when different
frequency components propagate with different phase velocities. As an example,
consider a short laser pulse traversing an optical component such as a lens or
window, as depicted in Fig. 7.8. The short light pulse can broaden in time8 with
the different frequency components becoming separated (often called stretching
or chirping). If absorption (and surface reflections) can be neglected, then the
amplitude of E(r,ω) does not change – only its phase changes – and the power
spectrum (7.21) remains unaltered.
Continuing our example of a short pulse traversing a piece of glass, we assume
that the pulse travels in the ˆz-direction. We place r0 at the start of the glass where
we assign z = 0, so that k ·∆r = kz . We take the Fourier transform of pulse at z = 0
to determine the amplitudes and phases of the plane waves involved.
To find the waveform at the new position z (where the pulse presumably has
just exited the glass), we must adjust the phase of each plane wave by the factor
kz and take the inverse Fourier transform accruing to (7.31). Again, the function
k (ω) must be specified. Typically, the functional form of n (ω) spoils any chance
of doing the integral analytically. And as before, we will resort to the expansion
(7.33), but this time we will keep an additional term:
k (ω) z ∼= k0 z +v−1
g (ω−ω0) z +α(ω−ω0)2 z +··· (7.39)
where
k0 ≡ k (ω0) = ω0n (ω0)
c (7.40)
v−1
g ≡ ∂k
∂ω
¯¯
¯
¯
ω0
= n (ω0)
c + ω0n′ (ω0)
c (7.41)
α ≡ 1
2
∂2k
∂ω2
¯¯¯
¯
ω0
= n′ (ω0)
c + ω0n′′ (ω0)
2c (7.42)
Unfortunately, even after resorting to the expansion we won’t be able to per-
form the inverse Fourier transform except for very specific initial pulses. However,
8See J. D. Jackson, Classical Electrodynamics, 3rd ed., Sect. 7.9 (New York: John Wiley, 1999)., Chapter 8
Coherence Theory
Coherence theory is the study of correlations that exist between different parts
of a light field. Temporal coherenceindicates a correlation between fields offset
in time, E(r, t) and E(r, t −τ). Spatial coherence has to do with correlations be-
tween fields at different spatial locations, E(r, t) and E(r +∆r, t). Because light
oscillations are too fast to resolve directly, we usually need to study optical co-
herence using interference techniques. In these techniques, light from different
times or places in the light field are brought together at a detection point. If
the two fields have a high degree of coherence, they consistently interfere either
constructively or destructively at the detection point. If the two fields are not
coherent, the interference at the detection point rapidly fluctuates between con-
structive and destructive interference, so that a time-averaged signal does not
show interference.
You are probably already familiar with two instruments that measure coher-
ence: the Michelson interferometer, which measures temporal coherence, and
Young’ s two-slit interferometer, which measures spatial coherence. Your pre-
liminary understanding of these instruments was probably gained in terms of
single-frequency plane waves, which are perfectly coherent for all separations in
time and space. In this chapter, we build on that foundation and derive descrip-
tions that are appropriate when light with imperfect coherence is sent through
these instruments. We also discuss a practical application known as Fourier spec-
troscopy (Section 8.4) which allows us to measure the spectrum of light using a
Michelson interferometer rather than a grating spectrometer.
8.1 Michelson Interferometer
Beam
Splitter
Detector
Figure 8.1 Michelson interferome-
ter.
A Michelson interferometer employs a 50:50 beamsplitter to divide an initial
beam into two identical beams and then delays one beam with respect to the
other before bringing them back together (see Fig. 8.1). Depending on the relative
path difference d (round trip by our convention) between the two arms of the
system, the light can interfere constructively or destructively in the direction of
the detector. The relative path difference d introduces a time delay τ, defined by
203, source_sentence: channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire
an action potential.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic
cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be
accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be
degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the
presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that
are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades
acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that
release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and
unbind to postsynaptic receptors.
Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine — CNS and/or
PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or
PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric
acidCNS
Neuropeptide Substance P, endorphins CNS and/or
PNS
Table 35.2
Electrical Synapse
While electrical synapses are fewer in number than chemical synapses, they are found in all nervous
systems and play important and unique roles. The mode of neurotransmission in electrical synapses is
quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic
membranes are very close together and are actually physically connected by channel proteins forming
gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the
ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction
pores.
There are key differences between chemical and electrical synapses. Because chemical synapses
depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there
is an approximately one millisecond delay between when the axon potential reaches the presynaptic
terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this
signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which
is important for synapses involved in key reflexes), and some electrical synapses are bidirectional.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important
for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the
thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.
Signal Summation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron,
but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic
neuron to be sufficiently depolarized to fire an action potential. This process is calledsummation and
occurs at the axon hillock, as illustrated inFigure 35.16. Additionally, one neuron often has inputs
from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs
and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the
postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together,
synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system
is not transmitted as important information.
1004 CHAPTER 35 | THE NERVOUS SYSTEM
This content is available for free at http://cnx.org/content/col11448/1.9
sentences: WHERESELENIUMPOISONING
IncertainportionsoftheNorthCentralgreatplains,plantsabsorbenoughsele-niumfromthesoiltoinjureanimalsthatfeeduponthem.Thepoisoningmayresultinaslowdiseaseknownas"blindstaggers"oras"alkalidisease",oritmaybequicklyfatal.Asaresultoftheselenium,thejointsoftheleg-bonesbecomebadlyeroded.Thehoofsdevelopabnormalitiesordropoff.Locomotionisimpaired.Theeffectoftheseleniumper-sists,fortheanimalsdonotusuallyrecoverevenifre-movedfromsucharegionandfedagoodrationOCCURSironisanessentialconstituentofthehemoglobin(seepage205).Coppercompoundsaregenerallypoisonoustomostkindsofprotoplasm;yetforsomespeciescopperisnecessaryinsmallamounts.Copperisanessentialelementinthebluishoxygen-carrierhemocyaninofthekingcrabandthelobster.InsomeoftheWesternstatesthesoilcontainstheelementselenium.Thiselementispresentalsoinplantsgrowinginsuchsoil,althoughitdoesnotappeartoaffecttheminanyway.Butanimalsthatfeeduponsuchplantsareoftenseriouslypoisoned(seeillustrationopposite).Inotherregionsvariationintheamountoffluorineinthesoilmaybeimportanttous.Theelementfluorine,whichisverywidelybutunevenlydistributed,seemstoplayaroleintheassimilationofcalciumandphosphorus,andsoaffectstheformationoftheteeth.Astudyof7000girlsandboysofhigh-schoolageinvariousmiddleandsouthwesternstatesbroughtoutthefactthattherewasmuchmoretoothdecay,orcaries^incommunitieswhosewatersupplieswerefreeoffluorinethanincommunitiesusingwaterwith0.5ormorepartsfluorinepermillionpartswater.Thus,thepopulationofacertainpartofTexas,DeafSmithCounty,wasfoundtohaveanexceptionallylownumberofdecayedteeth;andthisrelativefreedomfromdentalcariesisasso-ciatedwithmorethanusualamountsoffluorineinthelocalwaters.Inotherregionsunusualamountsoffluorineinthesoilandsoilwatersapparentlybringaboutthedevelopmentof"mottledteeth"amongthechildrenlivingthere.Nobodywantsblotchyteeth,butnobodywantscaries102, 16.5 | Eukaryotic Post-transcriptional Gene
Regulation
By the end of this section, you will be able to:
• Understand RNA splicing and explain its role in regulating gene expression
• Describe the importance of RNA stability in gene regulation
RNA is transcribed, but must be processed into a mature form before translation can begin. This
processing after an RNA molecule has been transcribed, but before it is translated into a protein, is called
post-transcriptional modification. As with the epigenetic and transcriptional stages of processing, this
post-transcriptional step can also be regulated to control gene expression in the cell. If the RNA is not
processed, shuttled, or translated, then no protein will be synthesized.
RNA splicing, the first stage of post-transcriptional control
In eukaryotic cells, the RNA transcript often contains regions, called introns, that are removed prior to
translation. The regions of RNA that code for protein are called exons (Figure 16.10). After an RNA
molecule has been transcribed, but prior to its departure from the nucleus to be translated, the RNA is
processed and the introns are removed by splicing.
Figure 16.10 Pre-mRNA can be alternatively spliced to create different proteins.
CHAPTER 16 | GENE EXPRESSION 435, INDEX 275
Senescence
1
, 27-30,46,7078
theoiietiof,43f>0
Senilechangesinneivecells,27-29
Senilityat,causeofdeath,1011
inplants,44,71,75
SepiK.rniia,231,282
Seitna,252,258
Meium,influenceontissuecultme,
70,77
Se\organs,107,IOS,111,121-125,
217219
Sexualiepioduction,3741
Shell,J, 20,27
Skeletalsyhtem,107,108,112,127,
128
skin,107,H)8,no,112,331,132
Slonakei,,T I?,212,213,218,228,
2U7
Sloiopolhki,B, 33,2(>7
Snow,12 C,179-383,225,267
Softeningofthe-hiain,231,2.12
Soma,40
Somaticcella,ranmntalityof,5878
Span,174,175
Spiegelberg,W, 87
Spmtuahsm,18-20
Spleen,61
Sponges,62
Statine,174,175
Stomach,M,217-210,207
Stenuntomum,35,36
Sievenflon,THC.,206-208,2(>7
Stillbirths,205
$ ongyloocnt')otuspitrpmnIus,55,
56
HummaiyofreaultH,223-227
f-hxi'vivorfiluplinesofDrosophilo,
188,192,195
SyphihH,123
Table,life,70-82
Tempeiatuic,208-217
Tethehn,70,220222
Tbeoiiesofdeath,4350
Theoiyofpopulationgiowtli,249
Thyioulgland,01
Tissuecnltmet Ditto,5878
Tianaplantationoftumois,04,(51
TubeicuIomH,101,204,208,230,2!1,
238
Tuiuoiti.uihpliinlation,61, 65
Typhoidfcvei,230,2,11,2.J5,2,'iO
UnitedStates,giowtliol,2502,12,
254-257
Li'iostylayiandis,72
VanBuien,GII, 11J,2UO
Variation,genetic,190
Veneiwildiseases,123,124
VeilmlHt,PF,249,2(57
Verwoin,M,,44,207
Vienna,245,246
Voumoll,217
Wallei,AD,216,207
Walwoith,BH,152,267
War,243
Wedekmd,33,267
Weiimann,A, 26,43,65,207
Wlialc,longevityof,22
Wilaon,HV,62,267
Wittalom,99
Woodruff,LL,30,33,72,73,267,
268
Woodn,FA, 38,3,208
Yellowfever,240,21-2
Young,TTO,,23-25,268
pipeline_tag: sentence-similarity
library_name: sentence-transformers
metrics: cosine_accuracy, cosine_accuracy_threshold, cosine_f1, cosine_f1_threshold, cosine_precision, cosine_recall, cosine_ap, cosine_mcc
model-index: name: SentenceTransformer based on microsoft/mpnet-base
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name: Binary Classification
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Created: 2025-07-25 02:32:44