| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-124 |
Sentence |
denotes |
Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia. |
| T1 |
0-124 |
Sentence |
denotes |
Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia. |
| T2 |
125-266 |
Sentence |
denotes |
In 2001, the first author of this paper reported that schizophrenia is associated with an increased frequency of the haptoglobin (Hp)-2 gene. |
| T2 |
125-266 |
Sentence |
denotes |
In 2001, the first author of this paper reported that schizophrenia is associated with an increased frequency of the haptoglobin (Hp)-2 gene. |
| T3 |
267-364 |
Sentence |
denotes |
The precursor of Hp-2 is zonulin, a molecule that affects intercellular tight junction integrity. |
| T3 |
267-364 |
Sentence |
denotes |
The precursor of Hp-2 is zonulin, a molecule that affects intercellular tight junction integrity. |
| T4 |
365-512 |
Sentence |
denotes |
Recently, we reported increased plasma IgA/IgM responses to Gram-negative bacteria in deficit schizophrenia indicating leaky gut and gut dysbiosis. |
| T4 |
365-512 |
Sentence |
denotes |
Recently, we reported increased plasma IgA/IgM responses to Gram-negative bacteria in deficit schizophrenia indicating leaky gut and gut dysbiosis. |
| T5 |
513-716 |
Sentence |
denotes |
The current study was performed to examine the integrity of the paracellular (tight and adherens junctions) and transcellular (cytoskeletal proteins) pathways in deficit versus non-deficit schizophrenia. |
| T5 |
513-716 |
Sentence |
denotes |
The current study was performed to examine the integrity of the paracellular (tight and adherens junctions) and transcellular (cytoskeletal proteins) pathways in deficit versus non-deficit schizophrenia. |
| T6 |
717-1038 |
Sentence |
denotes |
We measured IgM responses to zonulin, occludin, E-cadherin, talin, actin, and vinculin in association with IgA responses to Gram-negative bacteria, CCL-11, IgA responses to tryptophan catabolites (TRYCATs), immune activation and IgM to malondialdehyde (MDA), and NO-cysteinyl in 78 schizophrenia patients and 40 controls. |
| T6 |
717-1038 |
Sentence |
denotes |
We measured IgM responses to zonulin, occludin, E-cadherin, talin, actin, and vinculin in association with IgA responses to Gram-negative bacteria, CCL-11, IgA responses to tryptophan catabolites (TRYCATs), immune activation and IgM to malondialdehyde (MDA), and NO-cysteinyl in 78 schizophrenia patients and 40 controls. |
| T7 |
1039-1345 |
Sentence |
denotes |
We found that the ratio of IgM to zonulin + occludin/talin + actin + viculin (PARA/TRANS) was significantly greater in deficit than those in non-deficit schizophrenia and higher in schizophrenia than those in controls and was significantly associated with increased IgA responses to Gram-negative bacteria. |
| T7 |
1039-1345 |
Sentence |
denotes |
We found that the ratio of IgM to zonulin + occludin/talin + actin + viculin (PARA/TRANS) was significantly greater in deficit than those in non-deficit schizophrenia and higher in schizophrenia than those in controls and was significantly associated with increased IgA responses to Gram-negative bacteria. |
| T8 |
1346-1562 |
Sentence |
denotes |
IgM responses to zonulin were positively associated with schizophrenia (versus controls), while IgM to occludin was significantly associated with deficit schizophrenia (versus non-deficit schizophrenia and controls). |
| T8 |
1346-1562 |
Sentence |
denotes |
IgM responses to zonulin were positively associated with schizophrenia (versus controls), while IgM to occludin was significantly associated with deficit schizophrenia (versus non-deficit schizophrenia and controls). |
| T9 |
1563-1945 |
Sentence |
denotes |
A large part of the variance (90.8%) in negative and PHEM (psychosis, hostility, excitation, and mannerism) symptoms was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, IgM to E-cadherin and MDA, and memory dysfunctions, while 53.3% of the variance in the latter was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, CCL-11, TRYCATs, and immune activation. |
| T9 |
1563-1945 |
Sentence |
denotes |
A large part of the variance (90.8%) in negative and PHEM (psychosis, hostility, excitation, and mannerism) symptoms was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, IgM to E-cadherin and MDA, and memory dysfunctions, while 53.3% of the variance in the latter was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, CCL-11, TRYCATs, and immune activation. |
| T10 |
1946-2113 |
Sentence |
denotes |
The results show an upregulated paracellular pathway with breakdown of the tight and adherens junctions and increased bacterial translocation in deficit schizophrenia. |
| T10 |
1946-2113 |
Sentence |
denotes |
The results show an upregulated paracellular pathway with breakdown of the tight and adherens junctions and increased bacterial translocation in deficit schizophrenia. |
| T11 |
2114-2318 |
Sentence |
denotes |
These dysfunctions in the intestinal paracellular route together with lowered natural IgM, immune activation, and production of CCL-11 and TRYCATs contribute to the phenomenology of deficit schizophrenia. |
| T11 |
2114-2318 |
Sentence |
denotes |
These dysfunctions in the intestinal paracellular route together with lowered natural IgM, immune activation, and production of CCL-11 and TRYCATs contribute to the phenomenology of deficit schizophrenia. |