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Biomedical subjects

M Camacho

Publications and source records attributed to M Camacho.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effect of an imidazolineoxyl nitric oxide on prostaglandin synthesis in experimental shock: possible role of nitrogen dioxide in prostacyclin synthase inactivation.

The effect of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a nitric oxide (NO) scavenger that yields nitrogen dioxide (NO(2)) in a rat endotoxemia model was investigated. Endotoxin (lipopolysaccharide [LPS]) increased NO synthase (NOS) activity and inducible NOS expression measured in lung and plasma levels of nitrite/nitrate, 6-oxo-prostaglandin (PG) F(1alpha), thromboxane B(2), and PGF(2alpha). Infusion of cPTIO significantly reduced LPS-induced mean arterial blood pressure decline and mortality and selectively reduced LPS-induced 6-oxo-PGF(1alpha) plasma levels and prostacyclin synthase (PGIS) activity measured in the lung and aorta. In vitro, PGIS activity in aorta rings was not modified by SNAP (NO donor), cPTIO slightly inhibited the enzyme but not in the presence of L-N(G)-monomethyl arginine, and SNAP in combination with cPTIO significantly inhibited PGIS. Thus, cPTIO may be beneficial in endotoxic shock because of NO scavenging and PGIS inactivation, which could be mediated by NO(2).

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Human vascular smooth muscle cells but not endothelial cells express prostaglandin E synthase.

In a previous work, we postulated that endothelial cells possess only the following 2 enzymes involved in prostanoid synthesis: cyclooxygenase and prostacyclin synthase. The present work focused on investigating the expression of prostaglandin (PG) E synthase (PGES) in vascular cells. After incubation of vascular smooth muscle cells (SMCs) and human umbilical vein endothelial cells (HUVECs) with [(14)C]arachidonic acid, the profile of prostanoid synthesis was assessed by HPLC. Untransformed PGH(2) released by the cells was evaluated as the difference in the formation of PGF(2alpha) in the incubations performed in the presence and in the absence of SnCl(2). Resting SMCs and SMCs stimulated with phorbol 12-myristate 13-acetate (PMA), lipopolysaccharide (LPS), interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha formed PGE(2) and PGI(2) (evaluated as 6-oxo-PGF(1alpha)), and in the presence of SnCl(2) only a small amount of PGE(2) was deviated toward PGF(2alpha). In contrast, resting and stimulated HUVECs produced PGI(2), PGE(2), PGF(2alpha), and PGD(2), and SnCl(2) completely diverted PGE(2) and PGD(2) toward PGF(2alpha). Reverse transcriptase-polymerase chain reaction analysis shows that mRNA encoding for PGES was not present in HUVECs and in endothelial cells from saphenous vein. Nevertheless, PGES was expressed in SMCs and induced by IL-1beta and TNF-alpha, and by PMA and LPS, although to a lesser extent. Whereas SMC stimulation led to an increase in the synthesis of PGE(2) and PGI(2) but not of untransformed PGH(2), stimulation of endothelial cells resulted in an enhanced release of the vasoconstricting prostanoid PGH(2).

Arachidonic Acid↗
PubMed2000

Transcellular formation of thromboxane A(2) in mixed incubations of endothelial cells and aspirin-treated platelets strongly depends on the prostaglandin I-synthase activity.

Despite an almost total suppression of platelet cyclooxygenase (COX) by aspirin, as monitored ex vivo, incomplete suppression of thromboxane (Tx)A(2) metabolite excretion has been detected in some patients with unstable angina treated with low doses of aspirin. A plausible explanation for this finding is the transcellular formation of TxA(2) by platelets from prostaglandin H(2) released by endothelial cells. We recently reported that probably only COX and PGI-synthase (PGIS) are involved in the biosynthesis of prostanoids in endothelial cells. The present work was thus focused to ascertain the dependence of the transcellular biosynthesis of TxA(2), by endothelial cells and aspirin-treated platelets, on the relative activity of these enzymes. Synthesis of eicosanoids from exogenous and endogenous arachidonic acid (AA) by mixed incubations of human umbilical vein endothelial cells (HUVEC) in culture and aspirin-treated platelets were determined by HPLC and enzyme immune assay. The ratio of COX to PGIS activities was modified in HUVEC by treatment with interleukin-1beta (IL-1beta). Transcellular formation of TxA(2) was only relevant when HUVEC overexpressed COX-2 (monitored by RT-PCR and Western blotting), and in these conditions TxA(2) formation started 2 minutes after substrate addition. Progression curves showed that half-times (t(1/2)) of the COX and PGIS activity were 2.73 and 0.47 minutes, respectively, in resting HUVEC, whereas these values for IL-1beta-treated cells were 1.33 and 0.07 minutes, respectively, indicating that expression of COX-2 increased the rate of PGIS "suicide" inactivation. Collectively, these results indicated that not only enhanced COX activity but also substantial PGIS inactivation was required for significant transcellular biosynthesis of TxA(2).

Aspirin↗
PubMed1999

Characteristic distribution of HTLV type I and HTLV type II carriers among native ethnic groups in South America.

To confirm the geographic and ethnic segregation of HTLV-I and HTLV-II carriers in native populations in South America, we have conducted a seroepidemiological study of native populations in South America, including HTLV-I carriers distributed among seven ethnic groups in the Andes highlands of Colombia, Peru, Bolivia, Argentina, and Chile, and two ethnic groups on Chiloe Island and Easter Island; and HTLV-II carriers distributed among seven ethnic groups of the lowlands along the Atlantic coast of Colombia, Orinoco, Amazon, and Patagonia, and one ethnic group on Chiloe Island. The incidence rate of HTLV-I and HTLV-II carriers varied among the ethnic groups, ranging from 0.8 to 6.8% for HTLV-I seropositivity and from 1.4 to 57.9% for HTLV-II seropositivity. A new HTLV-I focus was found among the Peruvian Aymara (1.6%), the Bolivian Aymara (5.3%) and Quechua (4.5%), the Argentine Puna (2.3%), and the Chilean Atacama (4.1%), while on HTLV-II focus was found among the Brazilian Kayapo (57.9%), the Paraguayan Chaco (16.4%), and the Chilean Alacalf (34.8%) and Yahgan (9.1%). The distribution of HTLV-I/II foci showed a geographic clustering of HTLV-I foci in the Andes highlands and of HTLV-II foci in the lowlands of South America. It was thus suggested that South American natives might be divided into two major ethnic groups by HTLV-I and HTLV-II carrier state.

Adolescent↗
PubMed1999

Leishmania amazonensis infection induces changes in the electrophysiological properties of macrophage-like cells.

Whole cell patch-clamp recordings were used to study the electrical properties of the macrophage-like cell line J774.1, after infection with Leishmania amazonensis. Infection induced a significant increase in cell size and membrane capacitance, suggesting that parasite invasion leads to the addition of plasma membrane to the host cell. By 24 hr after infection, the host cell membrane potential was significantly more hyperpolarized than control cells, and this difference remained for the subsequent 72 hr post-infection. The hyperpolarization was paralleled by an increase in the density of inward rectifying K(+) currents. The shape of the conductance vs. voltage curve, the kinetic properties and the pharmacological profile of these currents were not significantly altered by infection. These results suggest that infection by L. amazonensis causes an increase in the number of functional inward rectifying K(+) channels, leading to hyperpolarization of the host cell membrane.

Animals↗
PubMed1999

Amino acid residues involved in the catalytic mechanism of NAD-dependent glutamate dehydrogenase from Halobacterium salinarum.

The pH dependence of kinetic parameters for a competitive inhibitor (glutarate) was determined in order to obtain information on the chemical mechanism for NAD-dependent glutamate dehydrogenase from Halobacterium salinarum. The maximum velocity is pH dependent, decreasing at low pHs giving a pK value of 7.19+/-0.13, while the V/K for l-glutamate at 30 degrees C decreases at low and high pHs, yielding pK values of 7.9+/-0.2 and 9.8+/-0.2, respectively. The glutarate pKis profile decreases at high pHs, yielding a pK of 9. 59+/-0.09 at 30 degrees C. The values of ionization heat calculated from the change in pK with temperature are: 1.19 x 10(4), 5.7 x 10(3), 7 x 10(3), 6.6 x 10(3) cal mol-1, for the residues involved. All these data suggest that the groups required for catalysis and/or binding are lysine, histidine and tyrosine. The enzyme shows a time-dependent loss in glutamate oxidation activity when incubated with diethyl pyrocarbonate (DEPC). Inactivation follows pseudo-first-order kinetics with a second-order rate constant of 53 M-1min-1. The pKa of the titratable group was pK1=6.6+/-0.6. Inactivation with ethyl acetimidate also shows pseudo-first-order kinetics as well as inactivation with TNM yielding second-order constants of 1.2 M-1min-1 and 2.8 M-1min-1, and pKas of 8.36 and 9.0, respectively. The proposed mechanism involves hydrogen binding of each of the two carboxylic groups to tyrosyl residues; histidine interacts with one of the N-hydrogens of the l-glutamate amino group. We also corroborate the presence of a conservative lysine that has a remarkable ability to coordinate a water molecule that would act as general base.

Amino Acids↗
PubMed1999

Phase I-II study of 5-fluorouracil, recombinant interferon alpha2a, and cisplatin in combination with external beam radiation therapy followed by surgery in patients with locally advanced carcinoma of the esophagus.

Multimodality therapy has been demonstrated to be superior to external beam radiation therapy and possibly surgery alone for the treatment of carcinoma of the esophagus. The combination of 5-fluorouracil (5-FU), cisplatin, and recombinant interferon alpha2a (IFN) has yielded 65% response rates in metastatic and regionally advanced carcinoma of the esophagus. A phase I-II study was performed to assess the feasibility of combining 5-FU, IFN, and cisplatin with external beam radiation therapy followed by surgery in potentially resectable patients. Eligibility included biopsy-proven stage II-III squamous cell or adenocarcinoma of the esophagus with no prior therapy. External beam radiation therapy was administered concurrently with chemotherapy beginning on day 1, 5 days per week, twice a day with 1.5 Gy/fraction to a total dose of 45 Gy. 5-FU was administered at 750 mg/m2 on days 1, 8, 15, 22, and 29 after the administration of IFN and cisplatin. IFN was given at a dose of 6 million units subcutaneously three times per week beginning on day 1. Dose levels I, II, and III of cisplatin were 25, 30, and 35 mg/m2 administered on days 1, 8, 15, 22, and 29. The sequence of administration was IFN followed by cisplatin followed immediately by 5-FU. Dose escalation between patient cohorts occurred if 0/3 or < or = 1/6 patients had dose-limiting toxicity, i.e., grade II-III toxicity attributable to cisplatin. A phase II trial was planned using the maximum tolerated dose of cisplatin determined from the phase I trial. Patients who successfully completed therapy underwent thoracic exploration to resect residual disease. Twelve patients were enrolled; all were eligible. The demographics of the population were median age, 60 years (range, 44-77); nine male and three female patients; nine squamous cell carcinoma, one adenocarcinoma, and two adenosquamous histology; stage II:III, 2:10. Grade 3-4 toxicities included granulocytopenia (12 patients), thrombocytopenia (six), anemia (three), infection (six), diarrhea (two), mucositis (two), and renal and hepatic toxicities (one). Five patients had a clinical complete response, among whom four underwent surgery. At surgery, one patient had no evidence of residual disease and three patients had microscopic disease only. Two patients had progressive disease and five could not complete the therapy because of toxicities. Two patients are alive and disease free at 25 and 23 months, respectively. This regimen, though active, demonstrated an unfavorable toxicity profile and cannot be recommended for further study.

Adenocarcinoma↗
PubMed1998

Operation of glyoxylate cycle in halophilic archaea: presence of malate synthase and isocitrate lyase in Haloferax volcanii.

The occurrence of the glyoxylate cycle has not previously been demonstrated in any of the Archaea. In halophilic archaea, only isocitrate lyase activity has been detected. The halophilic archaeon Haloferax volcanii was tested for the presence of the other key enzyme of this pathway, malate synthase. High activities of this enzyme were detected when the carbon source was acetate. Both glyoxylate cycle key enzymes, isocitrate lyase and malate synthase, from Hf. volcanii were purified and characterized.

Glyoxylates↗
PubMed1998

Rate of vasoconstrictor prostanoids released by endothelial cells depends on cyclooxygenase-2 expression and prostaglandin I synthase activity.

This study was undertaken to investigate the enzymatic regulation of the biosynthesis of vasoconstrictor prostanoids by resting and interleukin (IL)-1(beta)stimulated human umbilical vein endothelial cells (HUVECs). Biosynthesis of eicosanoids in response to IL-1beta, exogenous labeled arachidonic acid (AA), or histamine, as well as their spontaneous release, was evaluated by means of HPLC and RIA. HUVECs exposed to IL-1beta produced prostaglandin (PG) I2 for no longer than 30 seconds after the substrate was added irrespective of the cyclooxygenase (COX) activity, whereas the time course of PGE2 and PGD2 formation was parallel to the COX activity. The ratio of PGE2 to PGD2 produced by HUVECs was similar to that obtained by purified COX-1 and COX-2. Production of PGF2alpha from exogenous AA was limited and similar in both resting and IL-1beta-treated cells. PGF2alpha was the main prostanoid released into the medium during exposure to IL-1beta, whereas when HUVECs treated with IL-1beta were stimulated with histamine or exogenous AA, PGE2 was released in a higher quantity than PGF2alpha. PGF2alpha released into the medium during treatment with IL-1beta and the biosynthesis of PGE2 and PGD2 in response to exogenous AA or histamine increased with COX-2 expression, whereas this did not occur in the case of PGI2. We observed that PGI synthase (PGIS) mRNA levels were not modified by the exposure to IL-1beta, but the enzyme was partially inactivated. When SnCl2 was added to the incubation medium, the transformation of exogenous AA-derived PGH2 into PGE2 and PGD2 was totally diverted toward PGF2alpha. Overall, these results support the conclusions that PGE2 and PGD2 (and also probably PGF2alpha) were nonenzymatically derived from PGH2 in HUVECs. The concept that a high ratio of PGH2 was released by the IL-1beta-treated HUVECs and isomerized outside the cell into PGE2 and PGD2 was supported by the biosynthesis of thromboxane B2 by COX-inactivated platelets, indicating the uptake by platelets of HUVEC-derived PGH2. The IL-1beta-induced increase in the release of PGH2 by HUVECs was suppressed by the COX-2-selective inhibitor SC-58125 and correlated with both COX-2 expression and PGIS inactivation. An approach to the mechanism of inactivation of PGIS by the exposure to IL-1beta was performed by using labeled endoperoxides as substrate. The involvement of HO. in the PGIS inactivation was supported by the fact that deferoxamine, pyrrolidinedithiocarbamate, DMSO, mannitol, and captopril antagonized the effect of IL-1beta on PGIS to different degrees. The NO synthase inhibitor NG-monomethyl-L-arginine also antagonized the PGIS inhibitory effect of IL-1beta, indicating that NO. was also involved. NO. reacts with O2-. to form peroxynitrite, which has been reported to inactivate PGIS. Homolytic fission of the O-O bond of peroxynitrite yields NO2. and HO.. The fact that 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), which reacts with NO. to form NO2., dramatically potentiated the IL-1beta effect suggests that NO2. could be a species implicated in the inactivation of PGIS. Cooperation of HO. was supported by the fact that DMSO partially antagonized the effect of carboxy-PTIO. Although our results on the exact mechanism of the inactivation of PGIS caused by IL-1beta were not conclusive, they strongly suggest that both NO. and HO. were involved.

Arachidonic Acid↗
PubMed1998

Biophysical linkage between MRI and EEG amplitude in closed head injury.

Nuclear magnetic resonance of brain water proton (1H) T2 relaxation times and measures of absolute amplitude of EEG were obtained from 19 closed head injured patients. The relationship between EEG and T2 relaxation time differed as a function of both EEG frequency and gray matter versus white matter. White matter T2 relaxation time was positively correlated with increased EEG amplitude in the delta frequency band (0.5-3.5 Hz). In contrast, lengthened gray matter T2 relaxation time was inversely correlated with EEG amplitude in the alpha and beta frequency bands (7-22 Hz). These findings are consistent with clinical EEG studies in which white matter lesions are related to increased EEG delta amplitude and gray matter lesions are related to decreased EEG alpha and beta frequency amplitude. Estimates of the severity of injury were obtained by neuropsychological measurements, in which lengthened T2 relaxation times in both the neocortical gray and white matter were correlated with diminished cognitive function. Decreased EEG beta and alpha amplitude and increased EEG delta amplitude were also correlated with diminished cognitive function. The findings imply a biophysical linkage between the state of protein-lipid structures of the brain as measured by the MRI and the scalp-recorded EEG.

Adult↗
PubMed1998

[Adjuvant therapy with a glycoprotein IIb-IIa inhibitor (abciximab) in coronary angioplasties with a high thrombotic risk].

INTRODUCTION: We retrospectively studied our experience with adjunctive therapy with glycoprotein IIb-IIIa inhibitor (abciximab) on patients with a high risk of thrombotic complications during coronary angioplasty (PTCA). PATIENTS AND METHODS: From September 1996 to November 1997, we performed PTCA in 210 patients, and abciximab was given to 38 (18%) of them. The interventions were urgent (primary PTCA in acute myocardial infarction) in 55% of the cases. The mean age of patients was 68.6 +/- 12 years and 71% were male. The reasons for coronary intervention were: acute myocardial infarction in 21 patients (55.3%), unstable angina in 9 (23.7%) and stable angina in 8 (21%). Coronary stents were implanted in 13 patients (34%) and an intra aortic balloon pump was used in 4 (11%). The reasons for using abciximab were: thrombus containing lesion: 22 (57.9%); other type B2/C lesion characteristics: 6 (15.9%); acute closure post balloon PTCA: 9 (23.7%), sub-acute stent thrombosis: 1 (2.6%). Oral acetilsalicilic acid and intravenous heparin were given to all patients at the beginning of the intervention. The mean APTT was 124 +/- 32 seconds at the end of the procedure. RESULTS: The arterial sheaths (8 French) were removed six hours after procedure, according to the normalisation of APTT values. Angiographic success in this group of patients was 100%. One patient died during hospitalisation due to left ventricular failure. There was no need for repeated angioplasty or coronary bypass grafting during hospital stay. The main complications related to the use of abciximab were: bleeding (requiring transfusion) in four patients 10.5%); severe thrombocytopenia (< 50,000 platelets/mm3): 1 (2.6%): cardiac tamponade (requiring pericardiocentesis): 1 (2.6%) and pseudo-aneurysm of femoral artery (requiring vascular surgery): 1 (2.6%). CONCLUSIONS: The use of abciximab as adjunctive therapy in this small group of patients undergoing coronary interventions with high risk of thrombotic complications is associated with high procedural success, but at the expense of high rates of bleeding complications. Therefore, special care must be applied during and after the procedure to enhance the safety of the patients treated with this drug.

Abciximab↗
PubMed1997

Selective induction of cyclo-oxygenase-2 activity in the permanent human endothelial cell line HUV-EC-C: biochemical and pharmacological characterization.

1. Cyclo-oxygenase (COX), the enzyme responsible for the conversion of arachidonic acid (AA) to prostaglandin H2 (PGH2), exists in two forms, termed COX-1 and COX-2 which are encoded by different genes. COX-1 is expressed constitutively and is known to be the site of action of aspirin and other nonsteroidal anti-inflammatory drugs. COX-2 may be induced by a series of pro-inflammatory stimuli and its role in the development of inflammation has been claimed. 2. Endothelial cells are an important physiological source of prostanoids and the selective induction of COX-2 activity has been described for finite cultures of endothelial cells, but not for permanent endothelial cell lines. 3. The HUV-EC-C line is a permanent endothelial cell line of human origin. We have determined the COX activity of these cells under basal conditions and after its exposure to two different stimuli, phorbol 12-myristate 13-acetate (PMA) and interleukin-1 beta (IL-1 beta). 4. Both PMA and IL-1 beta produced dose- and time-dependent increases of the synthesis of the COX-derived eicosanoids. These increases were maximal after the treatment with 10 nM PMA for 6 to 9 h. Under these conditions, the main eicosanoid produced by the cells was PGE2. 5. The increase of COX activity by PMA or IL-1 beta correlated with an increase of the enzyme's apparent Vmax, whilst the affinity for the substrate, measured as apparent Km, remained unaffected. 6. Treatment of the cells with PMA induced a time-dependent increase in the expression of both COX-1 and COX-2 mRNAs. Nevertheless, this increase was reflected only as an increase of the COX-2 isoenzyme at the protein level. 7. The enzymatic activity of the PMA-induced COX was measured in the presence of a panel of enzyme inhibitors, and the IC50 values obtained were compared with those obtained for the inhibition of human platelet COX activity, a COX-1 selective assay. Classical non-steroidal anti-inflammatory drugs (NSAIDs) inhibited both enzymes with varying potencies but only the three compounds previously shown to be selective COX-2 inhibitors (SC-58125, NS-398 and nimesulide) showed higher potency towards the COX of PMA-treated HUV-EC-C. 8. Overall, it appears that the stimulation of the HUV-EC-C line with PMA selectively induces the COX-2 isoenzyme. This appears to be a suitable model for the study of the physiology and pharmacology of this important isoenzyme, with a permanent endothelial cell line of human origin.

Cell Line↗
PubMed1997

Gene therapy of diabetes: glucose-stimulated insulin secretion in a human hepatoma cell line (HEP G2ins/g).

In order to design a feasible somatic cell gene delivery system for the treatment of type I diabetes, a suitable cell type needs to be determined. We have previously shown that the stable transfection of the full-length insulin cDNA into the human liver cell line, (HEP G2ins) resulted in synthesis, storage and acute regulated release of insulin to analogues of cAMP, but not to the physiological stimulus glucose. In attempting to explain the lack of glucose responsiveness of the HEP G2ins cells we have stably transfected these cells with the human islet glucose transporter GLUT 2 (HEP, G2ins/g cells). The HEP G2ins/g cell clones exhibit glucose-stimulated insulin secretion and glucose potentiation of the secretory response to nonglucose secretagogues. While glucose responsiveness commenced at a lower concentration than normal islets, a secretion curve approaching normal physiological conditions was generated. Immunoelectron microscopy revealed the presence of insulin-containing granules, similar in size and appearance to those of the normal beta cell. These results demonstrate that while it is most likely that the HEP G2ins/g cell line predominantly secretes insulin via the constitutive pathway, significant acute regulated release was seen in response to glucose, and thus represents significant progress in the creation of a genetically engineered 'artificial beta cell' from a human hepatocyte cell line.

Blotting, Northern↗
PubMed1997

An association between activity of the Na/K-pump and resistance of Schistosoma mansoni towards complement-mediated killing.

The Na/K-pump or Na+/K(+)-ATPase (EC 3.6.1.37), couples the hydrolysis of ATP to the active transport of Na+ and K+ ions across the plasma membrane of virtually all animal cells. The relationship between activity of the Na+/K(+)-ATPase and the sensitivity of Schistosoma mansoni to immunological attack has been investigated. It has been observed that ouabain, the specific inhibitor of the pump, via a synergistic effect with specific antibody and complement, affects the average membrane potential causing depolarization and death of complement resistant parasites. Thus, apparently, there is association between the inhibition of the Na/K-pump and the lysis and death of the complement-resistant parasite.

Animals↗
PubMed1997

Quantitative MRI of the gray-white matter distribution in traumatic brain injury.

Quantitative analyses were performed on magnetic resonance images (MRIs) obtained from the brains of 31 traumatic brain-injured (TBI) patients and 25 normal control subjects. The quantitative analyses involved comparisons of the shapes of proton density gray scale pixel histograms obtained from both 3-mm and 5-mm slice thickness. Image segmentation was accomplished by a multispectral fuzzy C-means and/or k-nearest-neighbor (kNN) algorithms and manual classification was used to label segmented classes into CSF, white matter, and other. Shape descriptors were derived from the pixel intensity histograms of the combined gray matter and white matter classes for each MRI slice. Statistical analyses revealed significant differences in pixel intensity distributions between TBI and control subjects. Normal control subjects tended to exhibit bimodal gray matter-white matter histograms, whereas, TBI patients tended to exhibit unimodal gray matter-white matter histograms. In the control subjects the pixels intermediate in intensity between gray and white matter were located primarily at the border between the gray and white matter, whereas TBI patients exhibited a thickening of the number of intermediate pixels at the border as well as an increase in intermediate pixels in the middle of the gray and white matter. The greater the severity of TBI, then the larger the number of intermediate intensity pixels within and between gray and white matter. Further analyses demonstrated shifts in magnetic resonance relaxation times in gray and white matter in TBI patients, which suggested that the tendency toward unimodality in TBI patients represents a pathological reduction in brain differentiation due to measurable biophysical change.

Adult↗