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1  sex is commonly regarded as an evolutionary dead end.
2 y breaking or reversed as the cell reaches a dead end.
3 s for logic operations is not engaged into a dead end.
4 ene products and is considered a replicative dead end.
5 isexuality in vertebrates is an evolutionary dead-end.
6 subsequent core fusion within 20 s) and half dead-end.
7 e accurate choices between live channels and dead ends.
8 flux and preventing the formation of pathway dead ends.
9 tes away from states that are photosynthetic dead ends.
10 sign principle for future power grids: avoid dead ends.
11 ominant selfing constitutes an "evolutionary dead end."
12 ation of nanos1 after fertilization requires Dead-end 1 (Dnd1), a vertebrate-specific germline RNA-bi
13                          Here we report that Dead-End 1 (Dnd1), an RNA-binding protein required for p
14         It thereby induces the assembly of a dead-end 3' processing complex, blocking mRNA 3' cleavag
15  length lipid chains, as well as a synthetic dead-end acceptor analogue, we have also shown that MurG
16 t converted to product by DEBS module 2 form dead-end acyl-enzyme intermediates.
17 ion of the oxyanion intermediate to form the dead-end adduct is more thermodynamically favored than m
18 rolysis may arise through the formation of a dead-end ADP:GroEL:ATP:GroES complex.
19 of pre-existing monomeric IgG1 nuclei into a dead-end aggregate, rather than through macromolecular c
20    Initial velocity, product inhibition, and dead-end analog inhibition studies with the AcH4-21 and
21                                          The dead-end analog inhibitor H3-20 K14A was competitive ver
22 uct CoA behaves in a manner identical to the dead-end analogue desulfo-CoA, suggesting an E:alpha-ket
23     2-Amino-6-heptenoic acid was chosen as a dead-end analogue of L-AASA and is competitive vs AASA,
24 alpha-Ketoglutarate (alpha-Kg) serves as the dead-end analogue of L-glutamate and is competitive vs L
25                                              Dead-end analogues of alpha-ketoglutarate were used to o
26 ate (OAA), pyruvate, and glutarate behave as dead-end analogues of lysine, which suggests that the ly
27 glyoxylic acid, and L-ornithine were used as dead-end analogues of saccharopine and showed competitiv
28 d oxalylglycine serve as lysine and alpha-Kg dead-end analogues, respectively, and are uncompetitive
29 rticularly in cancer, have been fraught with dead ends and context-specific functions.
30 that tree-like connection schemes--so-called dead ends and dead trees--strongly diminish stability.
31 ithout allowing interconversions between the dead-end and open complexes.
32                                   The use of dead-end and product inhibition and solvent-isotope effe
33                               Two-substrate, dead-end and product inhibition data, using analogues of
34                                   The use of dead-end and product inhibition, the solvent isotope eff
35                              In contrast, a 'dead-end' antibody sublineage unable to neutralize these
36         Addition of a trans diene leads to a dead-end as the trans intermediates have insurmountable
37 ese instances, the diploid males are genetic dead ends because they are inviable or sterile.
38     Hybridization is not a mere reproductive dead end but has been suggested to play a central role i
39 tes that the inverse is also true: repairing dead ends by addition of a few transmission lines substa
40 ed the model's applicability for an infused, dead-end cavity or a non-infused joint during cyclical m
41  a means to control the colloid transport in dead-end channels by introducing a solute gradient.
42 he transport of colloidal particles into the dead-end channels can be either enhanced or completely p
43                     Transport of colloids in dead-end channels is involved in widespread applications
44 circular Ty1 DNA, which is comparable to the dead-end circular products that arise during retroviral
45 l was not an alternative substrate but was a dead end competitive inhibitor versus tryptamine and an
46 ic analysis, product inhibition studies, and dead-end competitive inhibition studies is most consiste
47                           N-Benzylglycine, a dead-end competitive inhibitor with respect to N-methyl-
48  dNTP binding affinity as measured using the dead end complex formation.
49 rate inhibition by formation of an E.ADP.APS dead end complex.
50 es at PcopA in the absence of nucleotides: a dead-end complex and an open complex, constituting a bra
51 a(max) approximately 350 nm is assigned as a dead-end complex between the enzyme-persulfide and a sec
52 ors versus nitroethane due to formation of a dead-end complex between the oxidized enzyme and the pro
53 ing, incorporation into primer/template, and dead-end complex formation in the presence of the next d
54     This latter structure likely simulates a dead-end complex in the reaction mixture.
55         With the fast substrate D-arginine a dead-end complex of the reduced enzyme and the substrate
56  both E.NADPH and E.NADP(+), only the latter dead-end complex shows significant inhibition of the ste
57  values if unphosphorylated SK and RR form a dead-end complex that prevents SK autophosphorylation.
58 tide phosphate (E.NADP(+)) to form a ternary dead-end complex that prevents turnover in the steady st
59 pressor form reinforces the dominance of the dead-end complex to repress transcription, and the holo-
60 cts that the self-enhancing formation of the dead-end complex transforms the network into a largely i
61  concluded that Ca(2+)-ATPase is locked in a dead-end complex upon binding TG with an affinity of <1
62              The free reduced enzyme forms a dead-end complex with nitroethane, with a K(ai) value of
63  X-ray crystal of the AldC C291A mutant in a dead-end complex with octanal and NAD(+) reveals an apol
64                             In contrast, the dead-end complex with terreic acid is open, is free of U
65            The crystal structure of the MurA dead-end complex with terreic acid revealed that the qui
66 mB, holo(haem)CcmE binds to CcmC in a stable dead-end complex, indicating high affinity binding of ha
67 hat sorbinil binds to E.NADP(+) to produce a dead-end complex, the so-called sorbinil trap, which pre
68 hosphorylated SK EnvZ and the RR OmpR form a dead-end complex.
69 versus P-DME, consistent with formation of a dead-end complex.
70 with formation of an enzyme-NADP(+)-AcAc-CoA dead-end complex.
71 CoA, suggesting an E:alpha-ketoglutarate:CoA dead-end complex.
72  a result of formation of the E.PAP.naphthol dead-end complex; formation of the complex is corroborat
73 gma factor for sigma(F) forms a long-lived, "dead-end" complex with its anti-anti-sigma factor and AD
74  cycloaddition requires dissociation of the (dead-end) complex.
75 both E-MgADP-FAK-tide and E-MgATP-P-FAK-tide dead-end complexes form.
76 ects of ppGpp to drive formation of inactive dead-end complexes formed by RNA polymerase at the ArgX
77 utL-E32K mutation is due to the formation of dead-end complexes in which the MutL-E32K protein is una
78 s between topoisomerase I and DNA can become dead-end complexes that lead to cell death.
79 M, Ala), suggesting that this compound forms dead-end complexes with multiple enzyme states.
80 -competent orientation or form high-affinity dead-end complexes, both RT/NNRTI/DNA complexes being un
81 g that self-fertilization is an evolutionary dead end conflates two distinct claims: the transition f
82      Imaging experiments in vivo reveal that Dead end-containing vesicles are associated with recycli
83 s such as DNA polymerase beta (Polbeta) form dead-end, covalent intermediates in vitro during attempt
84 s from the complexity of intra-, inter-, and dead-end cross-linked peptide mixtures.
85 et of unique interpeptide, intrapeptide, and dead-end cross-linked products that provides protein str
86  as well as the array of inter-, intra-, or "dead-end"-cross-linked peptides that may be generated fr
87 lt: the chemically reasonable formation of a dead-end cysteine-cofactor adduct when NAD+ was in the "
88 2 represents a long road traveled, with many dead-ends, disappointments, and delays.
89                                    Zebrafish dead end (dnd) mRNA is specifically expressed in primord
90                       This phenomenon termed dead-end docking has not been investigated until now.
91 ction for this acceptor complex in mediating dead-end docking.
92 onovalent oxyanion dissociation constants of dead end E.MgATP.oxyanion complexes were all increased.
93 nal oxyanion.) Chlorate and perchlorate form dead-end E.MgATP.oxyanion complexes.
94 es a rapid equilibrium random mechanism with dead-end EAP and EBQ complexes.
95 es a rapid equilibrium random mechanism with dead-end EAP and EBQ complexes.
96 brium random mechanism with the formation of dead-end EAP and EBQ complexes.
97  a new protein design algorithm based on the dead-end elimination (DEE) algorithm, which we call iMin
98           A popular method is to combine the dead-end elimination (DEE) and A* tree search algorithms
99                                              Dead-End Elimination (DEE) is a powerful algorithm capab
100                                          The dead-end elimination (DEE) theorems are powerful tools f
101                          We further derive a dead-end elimination (DEE)-based criterion for pruning c
102 heorem for the identification of the GMEC is Dead-End Elimination (DEE).
103 (GA); self-consistent mean field (SCMF); and dead-end elimination (DEE).
104                                          The dead-end elimination and A( *) search algorithms were us
105 FASPR lies in the optimal combination of the dead-end elimination and tree decomposition with a well
106   The method we use is based on a variety of dead-end elimination methods and the recently discovered
107                The algorithm is based on the dead-end elimination procedure that makes it possible to
108 lizes a physically based force-field and the Dead-End Elimination theorem to compute sequences that a
109                                              Dead-end elimination was used to identify global minimum
110 OLPROBITY score of 2.71 A (77th percentile), dead-end elimination with the polarizable AMOEBA force f
111                               Beginning from dead-end elimination, we derive the first algorithm, to
112  this reaction is complicated by a competing dead-end equilibrium to form the thiolate complex (Fe(II
113 ecies transmission episodes can be singular, dead-end events or can result in viral replication and s
114 er, how nonselected T cells proceed in their dead-end fate is not clear.
115                      We present an automated dead-end filling (DEF) approach, which is derived from t
116 exits from the oral cavity, (2) conventional dead-end filters that sieve particles from water exiting
117 al agent, as demonstrated by both short-term dead-end filtration and long-term cross-flow filtration
118                                    Long-term dead-end filtration experiments for 1 week reveal a high
119                              By operation in dead-end filtration mode using the model virus MS2 (diam
120                                              Dead-end filtration was carried out using 10(7) and 10(8
121 , are significant drawbacks of conventional 'dead end' filtration.
122 missible, hence representing an evolutionary dead-end for the pathogen.
123 ound obstacles and extricate themselves from dead-ends (for reviews, see [1-3]).
124 se systemic infections are presumed to be a "dead-end" for P. aeruginosa and to have no impact on tra
125 diffusive zones adjacent to flow paths or in dead-end fractures.
126    In this study, we isolated the tambaqui's dead end gene (dnd) homolog (tdnd) and used it as a mole
127                               The Drosophila dead end gene is expressed in fusion cells, and encodes
128              These results indicate that the Dead end GTPase plays an important role in trafficking m
129 hanolamine lipid composition, productive and dead-end hemifusion account for 65% of all fusion events
130 ue virus infections are generally considered dead-end hosts for transmission because they do not reac
131          Our findings question the status of dead-end hosts in the WNV transmission cycle and may par
132 FV is readily zoonotic, humans may represent dead-end hosts.
133 pecies can vary from important reservoirs to dead-end hosts.
134 tem and apparently results from formation of dead-end HR DNA intermediates.
135 ly, this therapeutic "paradigm" has led to a dead end, illustrated by the failure of all randomized t
136 xpression of a constitutively active form of Dead end in S2 cells reveals that it influences the stat
137         Some of these channels lead to tiny, dead-ends in the state space: the persistence of complex
138 elded both promising leads and disappointing dead ends, indicating the multifactored and complex natu
139 pread zoonosis which in nature exhibits both dead-end infections and varying levels of sustained tran
140  pandemics such as COVID-19; in other cases, dead-end infections or smaller epidemics result.
141 alvin-Benson-Bassham cycle in higher plants, dead-end inhibited complexes of Rubisco must constantly
142 sphate carboxylase/oxygenase (Rubisco) forms dead-end inhibited complexes while binding multiple suga
143 g synergism was associated with formation of dead-end inhibited ternary complexes.
144 te initial velocity, product inhibition, and dead end inhibition experiments, which elucidated an ord
145                                  Product and dead-end inhibition analyses revealed that nicotinamide
146                                              Dead-end inhibition and ITC experiments revealed that AA
147                                              Dead-end inhibition by 2'-adenosine monophosphate (2'AMP
148 plots for product inhibition by NADH and the dead-end inhibition by 3-acetylpyridine adenine dinucleo
149 ate kinetic results of substrate titrations, dead-end inhibition by AMP and lumichrome, and product i
150                                  Product and dead-end inhibition data indicated that enzymatic phosph
151         Thus, initial velocity, product, and dead-end inhibition data were consistent with a di-iso p
152                                  Product and dead-end inhibition data with DCIP were consistent with
153  results of initial velocity and product and dead-end inhibition experiments indicate that PRMT1 util
154                                  Product and dead-end inhibition patterns indicate that binding of am
155                                  Product and dead-end inhibition patterns indicated a random sequenti
156                                              Dead-end inhibition studies are also consistent with the
157           Two-substrate kinetic analysis and dead-end inhibition studies for 5alpha-DHP reduction and
158 he results of initial velocity, product, and dead-end inhibition studies indicate that cPRMT5 uses a
159 he results of initial velocity, product, and dead-end inhibition studies indicate that methylation by
160 al velocity studies, product inhibition, and dead-end inhibition studies indicate that MtIPMS follows
161    Initial velocity, product inhibition, and dead-end inhibition studies indicate the kinetic mechani
162    Initial velocity, product inhibition, and dead-end inhibition studies provided assignments of the
163               Initial velocity, product, and dead-end inhibition studies showed the kinetic mechanism
164 the normal reaction (alphaKG to isocitrate), dead-end inhibition studies suggest that wild-type IDH1
165                         Initial velocity and dead-end inhibition studies support an ordered sequentia
166 sequential mechanism is also corroborated by dead-end inhibition studies using analogues of AASA, L-g
167                                              Dead-end inhibition studies were used to investigate the
168 g-pong bi-bi mechanism; however, product and dead-end inhibition studies with cytochrome c(3+) were c
169                                              Dead-end inhibition studies with the substrate analogues
170 of initial velocity, product inhibition, and dead-end inhibition studies, the reaction is shown to be
171    The mechanism is supported by product and dead-end inhibition studies.
172 eased based on initial velocity, product and dead-end inhibition studies.
173 rythroleukemia cells, Dnmt1, exhibits potent dead-end inhibition with a single-stranded nucleic acid
174        Initial velocity, product inhibition, dead-end inhibition, and equilibrium binding studies ind
175                                          The dead end inhibitor analog cyclolaudenol was competitive
176                                          The dead end inhibitor analog desulfo-CoA was competitive ve
177 sence of products and in the presence of the dead end inhibitor sulfite are most consistent with a se
178 yl-L-alanine in the absence or presence of a dead-end inhibitor (pyrrole-2-carboxylate) indicate that
179                                          The dead-end inhibitor analog desulfo-CoA was competitive ve
180    beta-Fluoropyruvate was investigated as a dead-end inhibitor for pyruvate.
181                               Desulfo-CoA, a dead-end inhibitor, also demonstrated simple competitive
182 but supports no kinase activity, acting as a dead-end inhibitor.
183 s in the absence and presence of product and dead end inhibitors in both reaction directions.
184                      We utilized product and dead end inhibitors of prenylcysteine lyase to probe the
185 omplex mechanism, and the response of SAT to dead-end inhibitors indicates a random order for the add
186 agnitude of the inhibition constants for the dead-end inhibitors may provide insight into the catalyt
187 dy state kinetics of AKT1 in the presence of dead-end inhibitors supported the finding and suggested
188 procal plots, in the presence and absence of dead-end inhibitors, argues that interconversion of tern
189 ocity studies in the absence and presence of dead-end inhibitors, suggests random addition of NAD and
190 ined using fosmidomycin and dihydro-NADPH as dead-end inhibitors.
191 TP substrates were varied in the presence of dead-end inhibitors.
192  an increased tendency for the catalytically dead-end intermediate compound III to form.
193       A high-resolution reconstruction of a "dead-end" intermediate at 3.6 angstrom allowed us to vis
194 alpha5 or beta3, stable, partially degraded, dead end intermediates accumulated within the cells.
195 ded DNA invading strand, which may represent dead end intermediates of homologous recombination in vi
196 r program, SQID-XLink, searches all regular, dead-end, intra and inter cross-linked peptides simultan
197                                 In addition, dead-end, intra-, and inter-cross-linked peptides can be
198 on on solvent accessibility of lysine sites, dead end iqPIR cross-linked products can provide protein
199                                              Dead-end JNK inhibitors were then used to differentiate
200 t into how homing endonucleases may escape a dead-end life cycle in a population of saturated target
201 groups multiplied the opportunities for many dead-end lineages to iteratively evolve developmental ho
202    Many fluid-transporting epithelia possess dead-end, long, and narrow channels opening in the direc
203        The structure suggests a noncovalent, dead-end mechanism of inhibition.
204 ansported intracellularly and reduced to the dead-end metabolite xylitol.
205                                       Hence, dead-end metabolites and blocked reactions can arise tha
206 ing reactions that are indirectly related to dead-end metabolites but of biological importance to the
207 iJR904 model, for instance, about 42% of the dead-end metabolites were fixed by our proposed method.
208 ent of information gaps for E. coli, such as dead-end metabolites.
209 l of four intermolecular cross-links and two dead-end modifications were identified using IRCX and LC
210 asexuality is supposed to be an evolutionary dead end, morphological, cytogenetic, and genomic data s
211 cyanobacteria are widely regarded as trophic dead-ends mostly inedible for zooplankton, but substanti
212 der binding combined with the formation of a dead-end mRNA-Hfq complex causes high concentrations of
213 of the enzyme, because of the formation of a dead-end N-5 formylflavin adduct, is more than 100-fold
214 ly capture ~500 single cells inside isolated dead-end nanoliter compartments using simple pipette inj
215                      The maternal RNAs vasa, dead end, nanos1, and daz-like all become localized to t
216 lass of germ plasm components, which include dead end, nanos1, and vasa RNAs, are initially present i
217 n of weak adaptability drives species into a dead end of evolution.
218                 The recalls of reactions and dead ends of DEF reach around 73% and 86%, respectively.
219 ed prion forming capability and representing dead ends of the prion replication cycle.
220 he presence and type (i.e., inter, intra, or dead-end) of the cross-linked products to be readily det
221 The non-swapped oligomers likely represent a dead-end offshoot of the amyloid pathway and must dissoc
222 tribution of carbonate minerals that form in dead-end one-dimensional diffusion-limited zones that ar
223 ed that this empty capsid was an off-pathway dead end or at best served for storage of pentameric sub
224 Any obvious problems in the network, such as dead end or disconnected reactions, can, therefore, be s
225 indicate that the enzyme may be resistant to dead-end organophosphate aging reactions that permanentl
226 ate model which describes the time course of dead-end, partial HA ultrafiltration.
227 mation of Co(4)(CO)(12) is not necessarily a dead end pathway in the Co(2)(CO)(8)-catalyzed Pauson--K
228 y converts Mtb's methylcitrate cycle into a "dead end" pathway that sequesters tricarboxylic acid (TC
229  is achieved by removing trapped regions and dead-end pathways using a simple algorithm.
230 ut and leading to the formation of apparent "dead-end" pathways.
231 e formation of the experimentally observed ''dead-end'' phosphohistidine product (PDB Code = 1V0W ).
232 lly unstable, the reactions proceeded via a "dead-end" polymerization mechanism, and only low to mode
233    Importantly, it is shown that addition of dead-end pores increases tortuosity in proportion to the
234 sity decrease in ischemic brain slices where dead-end pores were partially occluded by large macromol
235 ipolar cycloaddition, while the formation of dead-end prenylated flavin mononucleotide cycloadducts o
236 tected thiols can undergo isomerization to a dead-end product (a 4-methylcoumarin-3-yl thioether) upo
237 te, the dinitrosyl complex is converted to a dead-end product after the dissociation of the proximal
238      The hydroquinone detected in vitro is a dead-end product most likely resulting from chemical or
239 of 0.2 to 0.8 V using acetic acid, a typical dead-end product of glucose or cellulose fermentation.
240 ast for bovine enterovirus, but are either a dead-end product or direct precursor into which viral RN
241 b forms in vivo, it will not accumulate as a dead-end product.
242 g that this is a true intermediate and not a dead-end product.
243 epine and 10,11-dihydroxy carbamazepine as a dead-end product.
244 et, rather than promote the formation of the dead-end product.
245  susceptible to Cannizzaro reduction to give dead end products.
246               Based on the identification of dead-end products (i.e., a cross-link modification conta
247  cells, suggesting that these RNAs represent dead-end products normally destined for decay by TbDSS-1
248 strate that these immature particles are not dead-end products of assembly, but progress into mature
249 grated viral genomes are largely considered "dead-end products" of reverse transcription.
250 stream from the PPT is predicted to generate dead-end products.
251 dentified as both intermediates and apparent dead-end products.
252 s to the 3' exon of the precursor, producing dead-end products.
253  can be ascribed to the presence of inactive dead-end promoter complexes with features similar to tho
254 S strongly, and these oligomers rapidly form dead-end protofilaments.
255 quent to substrate binding by formation of a dead-end quaternary complex consisting of enzyme, coenzy
256 DNA and inhibits TAR-induced self-priming, a dead-end reaction that competes with minus-strand transf
257                                              Dead-end reactions with oxidized folate are avoided by t
258 ity benefits the bacteria because males are "dead ends" regarding bacterial transmission, and their a
259 y that creates connected pathways as well as dead-end regions.
260 This method is capable of finding indirectly dead-end-related reactions with biological importance fo
261 pid release of tight-binding inhibitors from dead-end ribulose-bisphosphate carboxylase/oxygenase (Ru
262                                  Analyses of dead end RNAi and mutant embryos reveal that the lumen f
263 not undergo reductive elimination meaning a "dead-end route".
264                                     Standard dead-end sample filtration is used to improve sample pur
265 mber of operations required to eliminate the dead-ending segments and segment pairs grows quadratical
266    Although often considered as evolutionary dead ends, selfing taxa may make an important contributi
267 er, this pathway represents a thermodynamic "dead end" since the radical pairs generated by homolysis
268                                 By contrast, dead-end species tend to be disulfide-insecure, in that
269 as des[26-84] and des[58-110] are metastable dead-end species that preferentially reshuffle.
270 bserved incomplete chains are non-obligatory dead-end species, in that their formation is not mandato
271                                Thus, it is a dead-end species, neither oxo group acceptance nor e(-)-
272 nsfer, respectively, than previously studied dead-end species.
273 at can misfold to form an aggregation-prone, dead-end species.
274 to distinguish on-pathway intermediates from dead-end species.
275 ation of this four-coordinate cob(II)alamin "dead-end" species in the His759Gly variant illustrates t
276 CF3)3], are stable and unreactive, remaining dead-end spectators throughout the coupling process.
277           Most emerging infections result in dead-end "spillover" events in which a pathogen is trans
278 ggregates or inclusion bodies that represent dead-end static structures.
279                                 Evolutionary dead-end strategies are characterized by short-term prod
280                   Here, I detail a real-time dead-end strategy associated with the behavioural traits
281 er promote the formation of a nonproductive "dead-end" ternary complex, protected the lid from trypsi
282 ction loops sequentially while isolating or "dead-ending" the remaining nonactive loops.
283 that functional locationism is a theoretical dead end; their proposed mechanistic framework is a firs
284 ion, from trapping pathogens in evolutionary dead ends, through slowing or inhibiting the process of
285 in forms of conformational freedom, and also dead ends to further saturation.
286 whether nuclear eIF4E also binds nascent but dead-end transcripts is unclear.
287          An SmTK crystal was soaked with the dead end transition state analog (TSA) components tauroc
288                                        Using dead-end ultrafiltration (UF) and batch ozonation tests,
289 ent, permeate flux and permeate yield, using dead-end ultrafiltration.
290 , to fill gaps by finding the most efficient dead-end utilization paths in a constructed quasi-endosy
291                             We characterized dead-end vesicles using a combination of membrane capaci
292  Munc18-2 or SNAP-25 reduced the fraction of dead-end vesicles.
293 nts, indicating they were permanently docked dead-end vesicles.
294 sing open-syntaxin increased the fraction of dead-end vesicles.
295 nes incubated with anti-GAPDH and Rab2 form "dead end" vesicles that are unable to transport and fuse
296 th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the
297 melanogaster to retreat when it encounters a dead-end, we identified a pair of ascending neurons, the
298 ny of these interspecies transfer events are dead end, where transmission is confined only to the ani
299                 In between are ancestors and dead ends, which functionally correspond to stem and non
300  be mathematically shown to be inconsistent (dead-ending) with the globally optimal alignment.

 
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