Search PubMed⌕ Search

Biomedical subjects

A Martinez

Publications and source records attributed to A Martinez.

At least 55 records · Page 3Linked to original sources

Adrenomedullin expression is up-regulated by ischemia-reperfusion in the cerebral cortex of the adult rat.

Changes in the pattern of adrenomedullin expression in the rat cerebral cortex after ischemia-reperfusion were studied by light and electron microscopic immunohistochemistry using a specific antibody against human adrenomedullin (22-52). Animals were subjected to 30 min of oxygen and glucose deprivation in a perfusion model simulating global cerebral ischemia, and the cerebral cortex was studied after 0, 2, 4, 6, 8, 10 or 12 h of reperfusion. Adrenomedullin immunoreactivity was elevated in certain neuronal structures after 6-12 h of reperfusion as compared with controls. Under these conditions, numerous large pyramidal neurons and some small neurons were intensely stained in all cortical layers. The number of immunoreactive pre- and post-synaptic structures increased with the reperfusion time. Neurons immunoreactive for adrenomedullin presented a normal morphology whereas non-immunoreactive neurons were clearly damaged, suggesting a potential cell-specific protective role for adrenomedullin. The number and intensity of immunoreactive endothelial cells were also progressively elevated as the reperfusion time increased. In addition, the perivascular processes of glial cells and/or pericytes followed a similar pattern, suggesting that adrenomedullin may act as a vasodilator in the cerebrocortical circulation. In summary, adrenomedullin expression is elevated after the ischemic insult and seems to be part of CNS response mechanism to hypoxic injury.

Adrenomedullin↗

Frequent 3p allele loss and epigenetic inactivation of the RASSF1A tumour suppressor gene from region 3p21.3 in head and neck squamous cell carcinoma.

Studies of allelic imbalance and suppression of tumourigenicity have consistently suggested that the short arm of chromosome three (3p) harbours tumour suppressor genes (TSGs) whose inactivation leads to the development of various types of neoplasia including head and neck squamous cell carcinoma (HNSCC). Previously, we defined a critical minimal region of 120kb at 3p21.3 that contains overlapping homozygous deletions in lung and breast tumour lines and isolated eight genes from the minimal region. Mutation analysis in a large panel of lung and breast cancers revealed only rare mutations, but the majority of lung tumour lines showed loss of expression for one of the eight genes (RASSF1A) due to hypermethylation of a CpG island in the promoter region of RASSF1A. We found RASSF1A to be methylated in the majority of lung tumours, but to a lesser extent in breast and ovarian tumours. In order to define the role of 3p TSGs, in particular RASSF1A in HNSCC, we (a) analysed 43 primary HNSCC for allelic loss in regions proposed to contain 3p TSGs (3p25-26, 3p24, 3p21-22, 3p14 and 3p12), (b) analysed 24 HNSCC for evidence of RASSF1A methylation and (c) undertook mutation analysis of RASSF1A in HNSCC. We found that 81% of HNSCC showed allele loss at one or more 3p markers, 66% demonstrated loss for 3p21.3 markers and 56% showed allelic losses at 3p12 loci. Thus, 3p loss is common in HNSCC and extensive 3p loss occurs even in early stage tumours. RASSF1A promoter region hypermethylation was found in 17% (4/24) of the sporadic HNSCC, but RASSF1A mutations were not identified. Furthermore, we found RASSF1A methylation to be significantly higher in poorly differentiated then in moderate to well differentiated HNSCC (P=0.0048). Three of the four tumours showing RASSF1A methylation also underwent 3p21.3 allelic loss, hence RASSF1A behaves as a classical TSG (two hits, methylation and loss). One tumour with RASSF1A methylation had retention of markers at 3p providing further evidence of specific inactivation of RASSF1A as a critical step in some HNSCC. Although the frequency of 3p21.3 allele loss was substantially higher than that of RASSF1A methylation this does not necessarily suggest that other genes from 3p21.3 are also implicated in HNSCC, as 3p21.3 LOH was invariably found with LOH at other 3p loci. Thus, the presence of 3p21.3 allele loss without RASSF1A methylation might reflect a propensity for 3p21.3 loss to occur as a secondary consequence of large 3p deletions targeted at other 3p TSG regions. Furthermore, in the presence of homozygous inactivation of other 3p TSGs, RASSF1A haploinsufficiency might be sufficient to promote tumourigenesis in many HNSCC.

Carcinoma, Squamous Cell↗

Immune mediated chorea encephalopathy syndrome in childhood.

We report four previously healthy female children, aged between 3 and 8 years, who presented with encephalopathy and an extrapyramidal movement disorder (chorea n=4, rigidity n=2, oculogyric crisis n=2). In addition, an acute behavioural disturbance occurred in two patients and mutism in two others. Seizures heralded the onset of the illness in three patients. Acute MRI was either normal or initially normal with later generalized cerebral atrophy. All infective (including streptococcus), biochemical, and metabolic investigations were normal, although all four patients had oligoclonal bands in the (CSF) but not the serum, indicating intrathecal immunoglobulin synthesis. All four children made an apparently full recovery within four months of the onset. We suggest that these patients represent an immune-mediated movement disorder and encephalopathy syndrome.

Atrophy↗

Matched-pair analysis comparing allogeneic PBPCT and BMT from HLA-identical relatives in childhood acute lymphoblastic leukemia.

This multicenter study was designed to evaluate whether allo-PBPCT provides some advantages, if any, over BMT in terms of engraftment kinetics, acute and chronic GVHD incidence, TRM, relapse incidence and survival in acute lymphoblastic leukemia patients (ALL). From January 1995 to December 1999, 67 ALL patients (34 in the PBPCT group and 33 in the BMT group) were included in this study. Median age for both groups was 8 years (range, 1-18). There were 24 patients in first or second CR in the PBPCT group and 28 such patients in the BMT group. Preparatory regimens were TBI-based in 26/34 in the PBPC group and 25/33 in the BMT group. GVHD prophylaxis was CsA alone in 38 patients (18 PBPCT vs 20 BMT) and CsA plus short Mtx in 29 (16 PBPCT vs 13 BMT). Engraftment was achieved in all cases. Median days to neutrophil recovery was 10 (range, 7-18) after PBPCT vs 14 (range, 9-21) after BMT (P < 0.0001). Platelet engraftment (>50 x 10(9)/l) was also faster for PBPCT patients (median 13 days, range, 9-40 vs 23 days, range, 15-165) (P < 0.0001). Acute GVHD grade II-IV incidence was similar in both groups (46.4 +/- 8.8% vs 42.7 +/- 8.6%) (P = 0.45). Probability of chronic GVHD was 50.6 +/- 12.2% after PBPCT vs 27.8 +/- 9.2% after BMT (P = 0.1). Probability of relapse was similar (28.7 +/- 9.2% for PBPCT vs 27.1 +/- 8.2% for BMT) (P = 0.89). There were eight patients who died from transplant-related complications after PBPCT vs 5 after BMT (P, NS). With a median follow-up of 25 months the event-free survival probability was 53 +/- 8.9% for PBPCT vs 54.9 +/- 9.7% for BMT (P = 0.54). Using PBPC for allogeneic transplantation in childhood ALL results in faster hematopoietic recovery compared to BM, with a similar incidence of aGVHD, TRM, relapse and disease-free survival. However, the issue of cGVHD remains unresolved.

Adolescent↗

Variation in mortality and intraventricular haemorrhage in occupants of Pacific Rim nurseries.

OBJECTIVE: A network of neonatal intensive care units in Pacific Rim countries was formed to compare infant risk factors, clinical practices, and outcomes for very low birthweight infants. METHODOLOGY: A multicentre, prospective study compared outcomes for infants born smaller than 1501 g or at less than 31 weeks gestation. RESULTS: Gestational age-specific survival and incidence of intracranial haemorrhage varied for infants born in these nurseries. We found differences in infant risk factors among the nurseries. There were also significant differences in the use of antenatal steroids, but similar rates for Caesarean section and surfactant treatment. The factor most predictive of neonatal death and severe intracranial abnormality was an elevated Clinical Risk Index for Babies (CRIB) score. Antenatal steroid treatment (>24 h prior to delivery) was associated with improved survival and decreased incidence of severe intracranial abnormalities. Antenatal steroid treatment for less than 24 h prior to delivery was not associated with improved survival. Caesarean delivery was associated with improved survival, but showed no benefit regarding the incidence of severe intracranial abnormality. CONCLUSIONS: Our Pacific Rim nursery network found differences in neonatal outcomes that correlated best with measures of neonatal risk at birth, antenatal steroid treatment, and Caesarean delivery. These data emphasize the importance of obstetric care to improve postnatal outcomes in premature infants, and highlight the usefulness of CRIB scores in these patients.

Analysis of Variance↗

Arthroscopic technique for the knee in morbidly obese patients.

Patients with morbid obesity present an additional surgical difficulty for routine knee arthroscopy. Accurate portal placement in these patients is of utmost importance in order to achieve adequate access to the surgical pathology. To facilitate portal placement, we changed our standard surgical technique, establishing operative portals under direct arthroscopic visualization. We present our technique in this article as an option in the approach to treating these patients.

Arthroscopy↗

Role of three SF-1 binding sites in the expression of the mvdp/akr1-b7 isocaproaldehyde reductase in Y1 cells.

Mvdp/akr1-b7 encodes an aldose-reductase-like enzyme expressed in the zona fasciculata of the adrenal cortex, the function of which is essential for the detoxification of the cholesterol side chain cleavage product, isocaproaldehyde. The -510/+41 akr1-b7 promoter fragment is able to reproduce the endogenous gene zona fasciculata restricted, ACTH-controlled expression, in transgenic mice adrenals. Here, we report that three response elements contained within this promoter (positions -102, -458, -503) are able to bind SF-1, the essential regulator of steroidogenesis, although the low affinity site at -503 retains some other specific proteins present in Y1 nuclear extracts. Mutation of the -102 site results in a lowering of the activity of the -510/+41 promoter in Y1 cells, whereas mutation of the -458 site induces a reduction both in the global activity and forskolin sensitivity of the promoter. Interestingly, differential mutations of the -503 site nucleotides either induce an increase or a decrease in the basal and forskolin-induced activity.

Adrenal Cortex↗

Cerebrovascular carbon dioxide reactivity in sheep: effect of propofol or isoflurane anaesthesia.

Propofol and isoflurane are commonly used in neuroanaesthesia. Some published data suggest that the use of these agents is associated with impaired cerebral blood flow/carbon dioxide (CO2) reactivity. Cerebrovascular CO2 reactivity was therefore measured in three cohorts of adult merino sheep: awake (n=6), anaesthetized with steady-state propofol (15 mg/min; n=6) and anaesthetized with 2% isoflurane (n=6). Changes in cerebral blood flow were measured continuously from changes in velocities of blood in the sagittal sinus via a Doppler probe. Alterations in the partial pressure of carbon dioxide in arterial blood (PaCO2) over the range 18-63 mmHg were achieved by altering either the inspired CO2 concentration or the rate of mechanical ventilation. Cerebral blood flow/CO2 relationships were determined by linear regression analysis, with changes in cerebral blood flow expressed as a percentage of the value for a PaCO2 of 35 mmHg. Propofol decreased cerebral blood flow by 55% relative to pre-anaesthesia values (P=0.0001), while isoflurane did not significantly alter cerebral blood flow (88.45% of baseline, P=0.39). Significant linear relationships between cerebral blood flow and CO2 tension were determined in all individual studies (r2 ranged from 0.72 to 0.99). The slopes of the lines were highly variable between individuals for the awake cohort (mean 4.73, 1.42-7.12, 95% CI). The slopes for the propofol (mean 2.67, 2.06-3.28, 95% CI) and isoflurane (mean 2.82, 219-3.45, 95% CI) cohorts were more predictable. However, there was no significant difference between these anaesthetic agents with respect to the CO2 reactivity of cerebral blood flow.

Anesthetics, Inhalation↗

The cerebrovascular effects of adrenaline, noradrenaline and dopamine infusions under propofol and isoflurane anaesthesia in sheep.

Infusions of catecholamines are frequently administered to patients receiving propofol or isoflurane anaesthesia. Interactions between these drugs may affect regional circulations, such as the brain. The aim of this animal (sheep) study was to determine the effects of ramped infusions of adrenaline, noradrenaline (10, 20, 40 micrograms/min) and dopamine (10, 20, 40 micrograms/kg/min) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR) and cerebral metabolic rate for oxygen (CMRO2). These measurements were made under awake physiological conditions, and during continuous propofol (15 mg/min) or 2% isoflurane anaesthesia. All three catecholamines significantly and equivalently increased mean arterial pressure from baseline in a dose-dependent manner in the three cohorts (P < 0.001). In the awake cohort (n = 8), dopamine (P < 0.01) significantly increased CBF from baseline whilst adrenaline and noradrenaline did not (P > 0.05). Under propofol (n = 6) and isoflurane (n = 6), all three catecholamines significantly increased CBF (P < 0.001). Dopamine caused the greatest increase in CBF, and was associated with significant increases in ICP (awake: P < 0.001; propofol P < 0.05; isoflurane P < 0.001) and CVR (isoflurane P < 0.05). No significant changes in CMRO2 were demonstrated. Under propofol and isoflurane anaesthesia, the cerebrovascular effects of catecholamines were significantly different from the awake, physiological state, with dopamine demonstrating the most pronounced effects, particularly under propofol. Dopamine-induced hyperaemia was associated with other cerebrovascular changes. In the presence of an equivalent effect on mean arterial pressure, the exaggerated cerebrovascular effects under anaesthesia appear to be centrally mediated, possibly induced by propofol- or isoflurane-dependent changes in blood-brain barrier permeability, thereby causing a direct influence on the cerebral vasculature.

Anesthesia↗

The position and volume of the small bowel during adjuvant radiation therapy for rectal cancer.

PURPOSE: The rate of small bowel toxicity from adjuvant pelvic radiation therapy (RT) for rectal cancer has been reported to be lower for patients treated preoperatively (Preop). This was probably due to a lesser volume of irradiated small bowel; however, studies of postoperative treatment reported that patients with an abdominoperineal resection (APR), who likely have the largest volume of small bowel in the pelvis, had less acute and chronic toxicity than those with a low anterior resection (LAR). In this study, three-dimensional treatment planning techniques were used to characterize the position and volume of small bowel in the pelvis and compare these to repeat studies obtained during the typical 5-week course of treatment to attempt to explain the above observations. METHODS AND MATERIALS: Treatment planning CT scans were obtained in 30 patients with rectal cancer (10 Preop, 10 LAR, 10 APR), including 12 patients with weekly CT scans during RT (65 scans). The position of the small bowel was measured by the distance to the nearest small bowel from the bones of the posterior pelvis and by the volume of small bowel within four anatomically defined regions of the pelvis. The motion of the small bowel was expressed as the standard deviation of the small bowel position measured with both the distance and the volume in the 12 patients with repeat studies. RESULTS: Contrast-containing small bowel was found an average 2.9 cm more anterior than small bowel without contrast below the sacral promontory. The position of the small bowel in Preop patients was significantly more anterior (p < or = 0.01) with less volume (p < or = 0.04) in the pelvis than postoperatively treated patients. The small bowel was also more anterior for patients with an LAR vs. APR (p < or = 0.03) but with similar volume in all pelvic regions. Small bowel motion, expressed as the standard deviation of the distance from the bones of the posterior pelvis to the closest small bowel, was 2.9 cm, 1.4 cm, and 0.2 cm for the Preop, LAR, and APR group, respectively. The LAR group had a considerable degree of motion in the posterior pelvis. Increased bladder volume was associated with reduced small bowel volumes, although this benefit decreased during treatment. CONCLUSION: Because treatment planning CT scans can detect small bowel that does not contain contrast, they may be more accurate than the traditional small bowel series. The Preop patients had significantly less pelvic small bowel supporting the clinical observation of better tolerance to therapy. The higher small bowel toxicity reported for LAR vs. APR patients may be explained by the greater variability of both the position and volume of the small bowel in the posterior pelvis for LAR patients. This finding suggests that a single planning study may not be accurate for the block design used for boost treatment of LAR patients. Bladder-filling techniques were useful for Preop and LAR but not APR patients, and decreased in benefit over time. This study suggested that treatment planning CT scans were more useful than a small bowel series and that more than one treatment planning CT may be obtained in any patient receiving > 45 Gy for rectal cancer. However, further research will be necessary to determine the optimal timing and total number of repeat studies.

Diarrhea↗

Mapping of contralateral space in retinotopic coordinates by a parietal cortical area in humans.

The internal organization of a higher level visual area in the human parietal cortex was mapped. Functional magnetic resonance images were acquired while the polar angle of a peripheral target for a delayed saccade was gradually changed. A region in the superior parietal cortex showed robust retinotopic mapping of the remembered target angle. The map reversed when the direction of rotation of the remembered targets was reversed and persisted unchanged when study participants detected rare target reappearances while maintaining fixation, or when the eccentricity of successive remembered targets was unpredictable. This region may correspond to the lateral intraparietal area in macaque monkeys.

Brain Mapping↗

29Si NMR and hidden order in URu2Si2.

Below T(N) approximately 17 K the 29Si NMR line in URu2Si2 exhibits a previously unobserved field-independent nearly isotropic contribution to the linewidth, which increases to approximately 12 G as T-->0. We argue that this feature does not arise from static freezing of the U-spin magnetization, but is due to coupling between 29Si spins and a hidden order parameter. We discuss time-reversal symmetry-breaking orbital antiferromagnetism and indirect nuclear spin-spin interactions as possible coupling mechanisms. Further NMR experiments and theoretical calculations are suggested.

Journal Article↗

Epigenetic inactivation of the RASSF1A 3p21.3 tumor suppressor gene in both clear cell and papillary renal cell carcinoma.

Renal cell carcinoma (RCC), the most common adult kidney neoplasm, is histopathologically heterogeneous, with most sporadic RCCs ( approximately 80%) classified as clear cell (CC) tumors. Chromosome 3p allele loss is the most frequent genetic alteration in RCC but is associated specifically with sporadic and hereditary forms of clear cell RCC (CC-RCC) and is not a feature of non-CC-RCC, such as papillary (chromophilic) RCC. The VHL tumor suppressor gene (TSG) maps to chromosome 3p25, and somatic inactivation of the VHL gene occurs in up to 70% of CC-RCC tumors and cell lines. However, VHL inactivation is not sufficient for CC-RCC tumorigenesis, and inactivation of 3p12-p21 TSG(s) appears to be necessary in CC-RCC irrespective of VHL gene inactivation status. Recently, we demonstrated that the candidate 3p21 TSG, RASSF1A, is hypermethylated in most small cell lung cancers. We have now investigated the role of RASSF1A inactivation in primary RCC tumors. RASSF1A promoter methylation was detected in 23% (32 of 138) of primary CC-RCC tumors. In CC-RCC cell lines, RASSF1A methylation was associated with silencing of RASSF1A expression and restoration of expression after treatment with 5'-azacytidine. The frequency of RASSF1A methylation was similar in CC-RCC with and without VHL gene inactivation (24% versus 21%), and there was no association between epigenetic silencing of the RASSF1A and VHL TSGs, because 0 of 6 tumors with VHL hypermethylation had RASSF1A methylation, and VHL was not methylated in 26 CC-RCCs with RASSF1A methylation. Although 3p allele loss has been reported rarely in papillary RCC, we identified RASSF1A methylation in 44% (12 of 27) of papillary RCCs analyzed. Thus: (a) inactivation of RASSF1A is a frequent event in both CC-RCC and papillary RCC tumors; (b) there is no relationship between epigenetic silencing of RASSF1A and VHL inactivation status in CC-RCC. Fifty-four CC-RCCs analyzed for RASSF1A methylation were informative for 3p21 allele loss, and 20% (7 of 35) with 3p21 allele loss demonstrated RASSF1A methylation. All informative CC-RCCs with 3p21 allele loss and no RASSF1A methylation also demonstrated allele losses at other regions of 3p so that tumorigenesis in these cases may result from: (a) haploinsufficiency of RASSF1A; (b) inactivation of other 3p21 TSGs; or (c) inactivation of 3p TSGs from outside of 3p21. RASSF1A is the first TSG to be inactivated frequently in both papillary and CC-RCCs. The finding of frequent epigenetic inactivation of RASSF1A in papillary RCCs despite previous studies reporting infrequent 3p21 allele loss in this tumor type illustrates how the systematic identification of all major human cancer genes will require detailed analysis of the cancer genome and epigenome.

Adenocarcinoma, Clear Cell↗

Spectroscopic properties of Er3+, Yb3 + and Er3 + /Yb3+ doped metaphosphate glasses.

The absorption and emission spectroscopies of Er3+ doped and Er3+/Yb3+ codoped Ca(PO3)2, Sr(PO3)2 and Ba(PO3)2 glasses have been studied. From the Judd-Ofelt intensity parameters, the spontaneous emission probabilities of some relevant transitions and the radiative lifetimes of several excited states of Er3+ have been calculated. The decay curves of the Er3+ emission at 1.5 microm have been measured at different temperatures. The data have been fitted using a stretched exponential function and the obtained experimental lifetimes have been compared with the calculated radiative lifetimes. The difference between the experimental and calculated lifetimes is attributed to the presence of traces of OH groups in the host glasses. The absolute OH content in some glasses has been determined from the infrared spectra. The emission spectra at 1.5 microm of the Er3+ ion in the codoped glasses have been measured at different temperatures. The integrated emission intensities decrease significantly on passing from room temperature to 13 K, suggesting a temperature dependence of the rate of the energy transfer process between Yb3+ and Er3+.

Biophysical Phenomena↗

Five-lipoxygenase inhibitors can mediate apoptosis in human breast cancer cell lines through complex eicosanoid interactions.

Many arachidonic acid metabolites function in growth signaling for epithelial cells, and we previously reported the expression of the major arachidonic acid enzymes in human breast cancer cell lines. To evaluate the role of the 5-lipoxygenase (5-LO) pathway on breast cancer growth regulation, we exposed cells to insulinlike growth factor-1 or transferrin, which increased the levels of the 5-LO metabolite, 5(S)-hydrooxyeicosa-6E,8C,11Z,14Z-tetraenoic acid (5-HETE), by radioimmunoassay and high-performance liquid chromatography. Addition of 5-HETE to breast cancer cells resulted in growth stimulation, whereas selective biochemical inhibitors of 5-LO reduced the levels of 5-HETE and related metabolites. Application of 5-LO or 5-LO activating protein-directed inhibitors, but not a cyclooxygenase inhibitor, reduced growth, increased apoptosis, down-regulated bcl-2, up-regulated bax, and increased G1 arrest. Exposure of breast cancer cells to a 5-LO inhibitor up-regulated peroxisome proliferator-activated receptor (PPAR)a and PPARg expression, and these same cells were growth inhibited when exposed to relevant PPAR agonists. These results suggest that disruption of the 5-LO signaling pathway mediates growth arrest and apoptosis in breast cancer cells. Additional experiments suggest that this involves the interplay of several factors, including the loss of growth stimulation by 5-LO products, the induction of PPARg, and the potential activation of PPARg by interactions with shunted endoperoxides.

Apoptosis↗

Unequal VH gene rearrangement frequency within the large VH7183 gene family is not due to recombination signal sequence variation, and mapping of the genes shows a bias of rearrangement based on chromosomal location.

Much of the nonrandom usage of V, D, and J genes in the Ab repertoire is due to different frequencies with which gene segments undergo V(D)J rearrangement. The recombination signal sequences flanking each segment are seldom identical with consensus sequences, and this natural variation in recombination signal sequence (RSS) accounts for some differences in rearrangement frequencies in vivo. Here, we have sequenced the RSS of 19 individual V(H)7183 genes, revealing that the majority have one of two closely related RSS. One group has a consensus heptamer, and the other has a nonconsensus heptamer. In vitro recombination substrate studies show that the RSS with the nonconsensus heptamer, which include the frequently rearranging 81X, rearrange less well than the RSS with the consensus heptamer. Although 81X differs from the other 7183-I genes at three positions in the spacer, this does not significantly increase its recombination potency in vitro. The rearrangement frequency of all members of the family was determined in microMT mice, and there was no correlation between the in vitro recombination potential and V(H) gene rearrangement frequency in vivo. Furthermore, genes with identical RSS rearrange at different frequencies in vivo. This demonstrates that other factors can override differences in RSS potency in vivo. We have also determined the gene order of all V(H)7183 genes in a bacterial artificial chromosome contig and show that most of the frequently rearranging genes are in the 3' half of the region. This suggests that chromosomal location plays an important role in nonrandom rearrangement of the V(H)7183 genes.

Animals↗

Direct comparison of visual cortex activation in human and non-human primates using functional magnetic resonance imaging.

We report a technique for functional magnetic resonance imaging (fMRI) in an awake, co-operative, rhesus macaque (Macaca mulatta) in a conventional 1.5T clinical MR scanner, thus accomplishing the first direct comparison of activation in visual cortex between humans and non-human primates with fMRI. Activation was seen in multiple areas of striate and extra-striate visual cortex and in areas for motion, object and face recognition in the monkey and in homologous visual areas in a human volunteer. This article describes T1, T2 and T2* values for macaque cortex, suitable MR imaging sequences, a training schedule, stimulus delivery apparatus and restraining hardware for monkey fMRI using a conventional 19 cm knee coil. Much of our understanding of the functional organization of the primate brain comes from physiological studies in monkeys. Direct comparison between species using fMRI such as those described here will help us to relate the wealth of existing knowledge on the functional organization of the non-human primate brain to human fMRI.

Adolescent↗