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Biomedical subjects

N Brown

Publications and source records attributed to N Brown.

At least 91 records · Page 5Linked to original sources
PubMed1999

Health care costs associated with chronic hepatitis B.

The long-term health care costs of patients with chronic hepatitis B (CHB) were compared with those of patients without CHB. Patients with laboratory markers for CHB were identified from an HMO database and matched with up to four control patients (either not tested for hepatitis B infection or with negative test results). Cost data were collected retrospectively for both groups of patients for the period up to 30 days before identification of the first marker for hepatitis B (prediagnosis), 30 days before identification of the first marker through 180 days after the identification (peridiagnosis), and 181 days after identification through the end of the six-year study period. Costs were categorized as emergency room, inpatient, short-stay inpatient, laboratory, radiology, office visit, pharmacy, outside claim, or other and were analyzed as ratios of the costs of each patient with CHB to the median of the corresponding control patients. Eighty-eight patients were identified as having CHB; there were 342 control patients. In the seven months surrounding the appearance of their first diagnostic marker, the patients with CHB had costs 3.3 times those of the corresponding control patients and, after the first seven months, 2.9 times those of the control patients per month. Peridiagnosis costs in the categories of laboratory, radiology, office visits, and pharmacy were significantly higher for patients with CHB than for control patients. Except for emergency room costs, postdiagnosis costs per month of the patients with CHB were significantly higher than those of the corresponding control patients. Examination of an HMO database showed that, compared with patients without CHB, patients with CHB had significantly higher health care costs around and after the CHB diagnosis.

Adult↗
PubMed1999

Multicenter study of lamivudine therapy for hepatitis B after liver transplantation. Lamivudine Transplant Group.

Hepatitis B after liver transplantation is often fatal, and no proven medical therapy exists for this condition. We chose to study the potential efficacy of lamivudine therapy for patients with chronic hepatitis B after liver transplantation. Fifty-two patients with chronic hepatitis B after liver transplantation were treated in an open label, multicenter study. Each had detectable hepatitis B virus (HBV) DNA in serum and 45 (87%) had detectable serum hepatitis B e antigen before treatment. Patients were treated for 52 weeks with lamivudine (100 mg daily). The primary endpoint was undetectability of HBV DNA; secondary endpoints included normalization of serum alanine transaminase (ALT) levels, disappearance of hepatitis B e antigen, and improvement in liver histology. After treatment, 60% of patients had undetectable HBV DNA by solution hybridization assay, 14 (31%) of the initially positive patients lost hepatitis B e antigen; hepatitis B surface antigen was undetectable in 3 (6%); and serum ALT levels normalized in 71%. Blinded histological assessments showed improvement in the histological activity index (P =.007 for periportal necrosis,.001 for lobular necrosis, and.013 for portal inflammation). YMDD variants of HBV, potentially associated with drug resistance, were detected in 14 (27%) of the patients. Repeat liver biopsies in 7 patients with the mutated virus were unchanged in 2, improved in 2, and worse in 3. We conclude that lamivudine is a potentially effective therapy for hepatitis B after liver transplantation.

Adult↗
PubMed1999

Extended lamivudine retreatment for chronic hepatitis B: maintenance of viral suppression after discontinuation of therapy.

In patients with chronic hepatitis B, brief lamivudine therapy suppresses hepatitis B virus (HBV) DNA but results infrequently in sustained losses of virus replication posttreatment. We evaluated treatment response and its posttreatment durability during up to 18 months of lamivudine therapy (100 mg/d) in 24 patients who had hepatitis B e antigen (HBeAg) despite 1 to 3 months of prior therapy. Therapy was to be stopped after HBeAg loss or seroconversion (acquisition of antibody to HBeAg); posttreatment monitoring continued for 6 months. During therapy, which was well tolerated, HBV DNA became undetectable in all evaluable patients, accompanied by reduced alanine transaminase (ALT) activity. The cumulative 18-month confirmed loss of HBeAg during therapy was 9 of 24 (38%) and seroconversion was 5 of 24 (21%). Therapy was discontinued after HBeAg loss/seroconversion in 7 patients, and HBeAg status was maintained in all. Four of the patients with HBeAg responses lost HBsAg at least once. In 10 (43%) of 23 patients tested, we identified HBV polymerase YMDD mutations, 3 with detectable HBV DNA (2 with ALT elevations) and 7 without virological/biochemical breakthrough. In conclusion, up to 18 months of lamivudine therapy was well tolerated, suppressed HBV replication consistently, and tripled the frequency of HBeAg losses observed during brief-duration therapy; HBeAg loss/seroconversion remained durable posttreatment. The emergence of YMDD-variant HBV was relatively common but occurred typically without reappearance of detectable HBV DNA or ALT elevation. Our observations suggest that lamivudine can be stopped after confirmed HBeAg loss or seroconversion.

Adult↗
PubMed1999

Human eosinophils release matrix metalloproteinase-9 on stimulation with TNF-alpha.

BACKGROUND: The eosinophil is a prominent cell in allergic lung inflammation and is exposed to a range of cytokines, including TNF-alpha, at the site of allergen challenge. Matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) produced by inflammatory cells are thought to play a crucial role in interstitial matrix turnover and tissue remodeling in acute and chronic lung diseases. In addition, protein kinase C is known to be important in MMP-9 expression and secretion. OBJECTIVE: We investigated the regulation of eosinophil-derived MMP-9 and TIMP proteins by TNF-alpha. METHODS: Using RT-PCR and gelatin zymography, we investigated the ability of human eosinophils to produce and secrete active MMP-9 on stimulation with TNF-alpha. We also studied the production of TIMP-1 and TIMP-2 in eosinophils by using Western blotting. RESULTS: The gelatinolytic activity of MMP-9 in unstimulated eosinophils was low, but it increased by 95% after TNF-alpha stimulation. This increase was regulated at both the transcriptional and translational levels. The transcription inhibitor actinomycin D, the nuclear factor kappaB (NFkappaB) inhibitor N-CBZ-Leu-Leu-Leu-AL, the protein synthesis inhibitor cycloheximide, and the protein kinase C inhibitor H7 significantly decreased MMP-9 activity in TNF-alpha-treated cells. TIMP-1 and TIMP-2 gene expression and protein production varied significantly among different cell donors. CONCLUSION: Eosinophils, on stimulation with TNF-alpha, may play a major role in asthmatic airway remodeling through increased MMP-9 production at the inflammatory site.

Asthma↗
PubMed1999

Controlling MRSA.

Explore the source record for details and available documents.

Cross Infection↗
PubMed1999

Comparison of antiplatelet activity of microencapsulated aspirin 162.5 Mg (Caspac XL), with enteric coated aspirin 75 mg and 150 mg in patients with atherosclerosis.

AIMS: A new formulation, low dose microencapsulated aspirin, permits slow absorption of aspirin and presystemic acetylation of platelet cyclo-oxygenase within the portal circulation, potentially avoiding deleterious effects on gastric and systemic prostaglandin synthesis. The objective of this study was to determine whether the administration of microencapsulated aspirin was as effective as enteric coated (EC) aspirin as an inhibitor of platelet function in patients with atherosclerosis. METHODS: One hundred and four patients were enrolled and randomised after a run in period of at least 14 days on aspirin EC 75 mg (day 0), to receive either microencapsulated aspirin 162.5 mg (n=34), aspirin EC 150 mg (n=36) or continue on aspirin EC 75 mg (n=34) for 28 days. Serum thromboxane B2 and collagen-induced platelet aggregation and release of 5-hydroxytryptamine (EC50 values) were measured on days 0 and 28. Aggregation/release EC50s were then repeated in the presence of a large dose of aspirin added in vitro to determine the EC50 at the maximum level of platelet inhibition. RESULTS: Median thromboxane B2 levels were low after 14 days run-in therapy with aspirin EC 75 mg, but significant further reductions were seen on day 28 in patients randomised to microencapsulated aspirin 162.5 mg (P=0.0368) and aspirin EC 150 mg (P=0.0004) compared with those remaining on aspirin EC 75 mg. Median EC50 s on day 28 showed small but significant increases from baseline (day 0) in aggregation in patients randomised to microencapsulated aspirin 162.5 mg (0.62-0.85, P=0.0482) and in both aggregation and release in patients randomised to aspirin EC 150 mg (0.95-1.20, P=0.0002, 8.4-11.7, P<0. 0001, respectively) signifying enhanced antiplatelet activity. No changes were seen in patients continuing on aspirin EC 75 mg. Results following addition of high dose aspirin in vitro suggest that mechanisms other than thromboxane synthesis may be operative in the long term effects of microencapsulated aspirin 162.5 mg and aspirin EC 150 mg over aspirin EC 75 mg. CONCLUSIONS: The results show good inhibition of thromboxane B2 synthesis and subsequent platelet activity by all preparations of aspirin, although both microencapsulated aspirin 162.5 mg and aspirin EC 150 mg are slightly more effective than aspirin EC 75 mg. A randomised trial is now required to determine whether microencapsulated aspirin is associated with fewer gastric side-effects.

Arteriosclerosis↗
PubMed1999

An antibiotic policy associated with reduced risk of Clostridium difficile-associated diarrhoea.

BACKGROUND: antibiotic-associated diarrhoea caused by Clostridium difficile is increasing in hospitals, and older people are at particular risk. OBJECTIVE: to establish whether reducing patient exposure to injectable third-generation cephalosporins by substituting alternative antibiotics can produce a cost-effective reduction in the incidence of antibiotic-associated diarrhoea. DESIGN: we prospectively investigated 2157 patients admitted to the department of elderly medicine in the year before introduction of antibiotic restrictions and 2037 patients admitted in the following year. Patients admitted to other wards, where antibiotic prescribing was unchanged, acted as controls. SETTING: a 900-bed teaching hospital in Cambridge, UK. MEASUREMENTS: use and cost of injectable antibiotics prescribed in the department of elderly medicine and the other wards studied; occurrence of C. difficile-associated diarrhoea. RESULTS: in the wards for older people, consumption of injectable cephalosporins fell by 92% (compared with 8% on other wards) and cases of C. difficile-associated diarrhoea fell from 98 to 45 (cases in other wards rose from 213 to 253; P < 0.001). The Pound Sterling 8062 increase in injectable antibiotic costs on the elderly wards were offset by the release of 1087 wasted bed-days attributable to the 53 fewer cases, with potential savings of Pound Sterling 212,000. CONCLUSIONS: restricting the consumption of injectable third-generation cephalosporins is a cost-effective method of reducing the incidence of C. difficile-associated diarrhoea.

Aged↗
PubMed1999

Clinical experience over 48 years with pheochromocytoma.

OBJECTIVE: To analyze the presentation, localization, surgical management, pathology, and long-term outcome of a large series of patients with pheochromocytomas. SUMMARY BACKGROUND DATA: There are several areas of controversy pertaining to pheochromocytomas. Although many studies report a higher rate of malignancy for extraadrenal pheochromocytomas than for adrenal pheochromocytomas, the number of patients with the former tumor are small and statistical analysis is lacking. There has also been recent debate as to whether microscopic features of the tumor may be predictive of future behavior. METHODS: From 1950 to 1998, the authors observed 108 pheochromocytomas in 104 patients. The outcome of these patients has been followed prospectively. The medical records of these patients were reviewed for data on the presentation, localization, surgical management, pathology, and outcome. Patient survival was analyzed using Kaplan-Meier survival distributions. RESULTS: This study included 66 female patients and 38 male patients. The average age at surgery was 42.3 years. Sporadic cases accounted for 84% of the patients; the other 16% had multiple endocrine neoplasia type 2, von Recklinghausen's disease, von Hippel-Lindau disease, or Carney's syndrome. Of 64 adrenal tumors, 55 were initially considered benign, 6 had microscopic malignant features, and 3 had malignant disease. Mean patient follow-up was 12.6 years. To date, in five additional patients (none with microscopic disease) malignant disease developed (13% overall rate of malignancy). Recurrence occurred as late as 15 years after resection. Of 26 extraadrenal pheochromocytomas, 14 were initially considered benign, 8 had microscopic malignant features, and 4 had malignant disease. Thus, 46% of patients had either malignant disease or tumors with malignant features. Mean patient follow-up was 11.5 years. In one patient with benign disease and in one patient with malignant features, malignant disease developed (23% overall rate of malignancy). The difference in the rate of malignancy was not statistically significant between adrenal and extraadrenal pheochromocytomas. Patients with adrenal and extraadrenal pheochromocytomas also had similar rates of survival (p = NS). CONCLUSIONS: The data suggest that patients with extraadrenal pheochromocytomas have the same risk of malignancy and the same overall survival as patients with adrenal pheochromocytomas. Lifelong follow-up of these patients is mandatory.

Adolescent↗
PubMed1999

Reflective meniscometry: a non-invasive method to measure tear meniscus curvature.

AIMS: To devise a method to measure tear meniscus curvature by a non-invasive specular technique. METHODS: A photographic system was devised. The system consisted of a camera and an illuminated target with a series of black and white stripes oriented parallel to the axis of the lower tear meniscus. The target was mounted on a flash gun close to the objective of a Brown macrocamera and calibrated using a graduated series of glass capillaries of known diameter, ground down to expose the inner wall. It was then applied to normal human eyes (n = 45) to measure the tear meniscus curvature. A video system was also assessed which provided qualitative online information about the tear meniscus. RESULTS: Using the photographic system, measured values for capillary radii were in excellent agreement with theoretical calculations (r2 = 0.996, p < 0.0001). The radii of curvature of lower tear menisci in normal human subjects (mean 0.365 (SD 0.153) mm, range 0.128-0.736; n = 45) were similar to those reported in the literature. Both systems demonstrated variations in meniscus shape. The video system provided stable images of human menisci over prolonged periods of time and promises to be useful for the analysis of dynamic changes in meniscus volume. CONCLUSIONS: Reflective meniscometry is a non-invasive technique providing quantitative information about tear meniscus shape and volume and of potential value in the study of ocular surface disease.

Calibration↗
PubMed1999

Quality of life four years after acute myocardial infarction: short form 36 scores compared with a normal population.

OBJECTIVES: To assess the impact of myocardial infarction on quality of life in four year survivors compared to data from "community norms", and to determine factors associated with a poor quality of life. DESIGN: Cohort study based on the Nottingham heart attack register. SETTING: Two district general hospitals serving a defined urban/rural population. SUBJECTS: All patients admitted with acute myocardial infarction during 1992 and alive at a median of four years. MAIN OUTCOME MEASURES: Short form 36 (SF 36) domain and overall scores. RESULTS: Of 900 patients with an acute myocardial infarction in 1992, there were 476 patients alive and capable of responding to a questionnaire in 1997. The response rate was 424 (89. 1%). Compared to age and sex adjusted normative data, patients aged under 65 years exhibited impairment in all eight domains, the largest differences being in physical functioning (mean difference 20 points), role physical (mean difference 23 points), and general health (mean difference 19 points). In patients over 65 years mean domain scores were similar to community norms. Multiple regression analysis revealed that impaired quality of life was closely associated with inability to return to work through ill health, a need for coronary revascularisation, the use of anxiolytics, hypnotics or inhalers, the need for two or more angina drugs, a frequency of chest pain one or more times per week, and a Rose dyspnoea score of >/= 2. CONCLUSIONS: The SF 36 provides valuable additional information for the practising clinician. Compared to community norms the greatest impact on quality of life is seen in patients of working age. Impaired quality of life was reported by patients unfit for work, those with angina and dyspnoea, patients with coexistent lung disease, and those with anxiety and sleep disturbances. Improving quality of life after myocardial infarction remains a challenge for physicians.

Aged↗
PubMed1999

Relevance of clinical trial results in myocardial infarction to medical practice: comparison of four year outcome in participants of a thrombolytic trial, patients receiving routine thrombolysis, and those deemed ineligible for thrombolysis.

OBJECTIVE: To assess the medium to long term outcome of patients ineligible for thrombolysis compared to those enrolled in a clinical trial of thrombolysis and patients receiving non-trial thrombolysis. DESIGN: Cohort study based on the Nottingham heart attack register. SETTING: Two district general hospitals serving a defined urban/rural population. SUBJECTS: All patients admitted with a confirmed acute myocardial infarction during 1992 categorised as either participants of a thrombolytic trial (group A, n = 140), receiving non-trial thrombolysis (group B, n = 329), or deemed ineligible for lytic treatment (group C, n = 431). MAIN OUTCOME MEASURES: Background characteristics, inhospital treatment, patterns of follow up, referrals to cardiologists, revascularisation rates, and short and long term survival. RESULTS: Clinical trial recruits were younger by almost 10 years, were less likely to have a previous history of myocardial infarction, and more likely to be in Killip class 1 on admission than those ineligible for thrombolysis. Cardiology follow up was mandatory for all surviving trial participants but 22% of patients in group B and 31% of patients in group C received no follow up, and during four years less than 50% ever saw a cardiologist. Revascularisation was performed in 17.2% of patients in group A, 13.6% of patients in group B, and 7.5% of patients in group C. Cumulative mortality at a median of four years was 24.3% in group A, 36.8% in B, and 59.6% in group C. Adjusting for age, sex, previous myocardial infarction, type of infarction, and Killip class in a logistic regression model the odds ratios (OR) of death at four years for groups B and C were 1.60 (95% confidence intervals (CI) 0.97 to 2.63, p = 0.065) and 2.64 (95% CI 1.61 to 4. 32, p < 0.001), respectively, when compared to group A (OR 1). CONCLUSIONS: Patients enrolled into thrombolytic trials are at low risk. Patients deemed ineligible for thrombolysis are high risk, receive less surveillance, are less likely to be revascularised or receive trial proven treatments, have a poor long term outcome not entirely explained by increased age or severity of infarction, and deserve further evaluation.

Aftercare↗
PubMed1999

Cardiac rehabilitation: socially deprived patients are less likely to attend but patients ineligible for thrombolysis are less likely to be invited.

OBJECTIVE: To identify factors associated with the uptake of cardiac rehabilitation following acute myocardial infarction. DESIGN: Retrospective analysis using multivariate logistic regression modelling. SETTING: Two large teaching hospitals in Nottingham. PATIENTS: Cohorts of patients admitted with acute myocardial infarction in 1992 and 1996. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Factors in multivariate analysis found to be associated with attendance at cardiac rehabilitation. Use of secondary prevention in those who were and were not invited and those who did and did not attend cardiac rehabilitation. RESULTS: 58% of all patients were offered cardiac rehabilitation. Attendance rates were 60% in 1992 and 74% in 1996. Invitations were more likely to be offered to younger patients, those who had received thrombolysis, and to patients admitted to one of the two Nottingham hospitals. Use of secondary prevention was only 48% in 1992 but this increased to 80% in 1996. Patients not receiving secondary prevention were less likely to be invited to cardiac rehabilitation. Social deprivation was the only factor significantly associated with poor uptake of cardiac rehabilitation in both years. There was no difference in the use of secondary prevention between those who did and did not attend cardiac rehabilitation. CONCLUSION: Those invited to attend a cardiac rehabilitation programme are likely to be in a good prognosis group, comprising those who are young and have received thrombolysis. Those at greatest risk, particularly patients from socially deprived areas, seem to be missing out on the potential benefits of cardiac rehabilitation. High risk patients should be specifically targeted to ensure that they are invited to, and encouraged to, attend a programme of cardiac rehabilitation.

Adult↗
PubMed1999

Synergism between neuropeptide Y and norepinephrine highlights sympathetic cotransmission: studies in rat arterial mesenteric bed with neuropeptide Y, analogs, and BIBP 3226.

Although abundant literature supports the notion that neuropeptide Y (NPY) synergizes in vivo and in vitro, the vasomotor activity elicited by norepinephrine (NE), the converse interaction (i.e., the adrenergic modulation of the NPY vasomotor response) has been less characterized. To assess whether NE synergizes the vasomotor effect of NPY, the rat arterial mesenteric bed was chosen as a model experimental system. Mesenteries were precontracted with NE and few minutes later were perfused with exogenous NPY. Under these conditions, NPY contracted the arterial mesenteric bed with an EC50 value of 0.72 +/- 0.06 nM. NPY was unable to contract this vascular territory without an agonist-induced precontraction. Other agonists, such as endothelin-1, a synthetic analog of prostaglandin F2alpha, or 5-hydroxytryptamine, also were effective primers because in their presence, NPY was a potent vasoconstrictor. In contrast, mesenteries precontracted with KCl failed to evidence the NPY-induced rise in perfusion pressure. Two structural analogs of NPY, PYY and [Leu31, Pro34]NPY, mimicked the activity of NPY. The NPY fragment 13-36 did not elicit such a response. All NPY analogs exhibited less efficacy and potency relative to NPY. The NPY- and related structural analog-induced vasoconstriction was competitively and reversibly antagonized by BIBP 3226; the pA2 of the NPY interaction was 7.0. The application of 0.1 to 1 microM BIBP 3226 or 0.1 to 10 nM prazosin at the peak of the NPY vasomotor response elicited a gradual blockade of the vasoconstriction. Although BIBP 3226 blocked the increase in perfusion pressure elicited by NPY, leaving unaffected the NE-induced tone, 10 nM prazosin blocked the full response, including the NE-induced component. Tissue preincubation with 200 nM nifedipine abolished the NPY-induced vasoconstriction; likewise, the acute application of 10 to 100 nM nifedipine blocked gradually the maximal NPY-induced contraction. Removal of the mesenteric endothelial layer increased the potency of NPY by 2-fold; it also slightly potentiated the antagonist activity of BIBP 3226. The synergism between NPY and NE backs the principle of sympathetic cotransmission.

Animals↗
PubMed1999

5-Aminolevulinic acid photosensitization of dysplastic Barrett's esophagus: a pharmacokinetic study.

Photodynamic therapy (PDT) using 5-aminolevulinic acid (ALA)-induced protoporphyrin IX (PpIX) may have a role in the treatment of dysplastic Barrett's esophagus. Before ALA-induced PDT can be used clinically, optimum treatment parameters must be established. In this study of 35 patients, the issues of drug dosage, time interval between drug and light delivery and side effects of oral ALA administration are addressed. Spectrofluorometric analysis of tissue samples demonstrates that oral ALA administration induces porphyrin accumulation in esophageal tissues, with maximum levels at 4-6 h. High-performance liquid chromatography confirms the identity of this porphyrin as PpIX, and fluorescence microscopy analysis demonstrates that it preferentially accumulates in the esophageal mucosa, rather than in the underlying stroma. Side effects of ALA administration included malaise, headache, photosensitivity, alopecia, transient derangement of liver function, nausea and vomiting. Fewer side effects and less hepatic toxicity was seen with 30 mg/kg than 50 mg/kg ALA. In conclusion, oral ALA administration induces preferential PpIX accumulation in the esophageal mucosa, with peak PpIX fluorescence noted at 4 h and minimal systemic toxicity at a dose of 30 mg/kg.

Aminolevulinic Acid↗
PubMed1998

Identification and characterization of mutations in hepatitis B virus resistant to lamivudine. Lamivudine Clinical Investigation Group.

Cirrhosis and hepatocellular carcinoma occur as long-term complications of chronic hepatitis B virus (HBV) infection. Antiviral therapy is potentially a successful approach for the treatment of patients with HBV infection, which includes the nucleoside analog, lamivudine [(-)2'-deoxy-3'-thiacytidine, 3TC]. Although resistance to lamivudine therapy has been reported in several HBV-infected patients, the pattern of resistance-associated mutations in HBV has not been fully characterized. We report a DNA sequence database that includes a 500-base pair region of the HBV polymerase gene from 20 patients with clinical manifestations of lamivudine resistance. Analysis of the database reveals two patterns of amino acid substitutions in the tyrosine, methionine, aspartate, aspartate (YMDD) nucleotide-binding locus of the HBV polymerase. HBV DNA from the sera of patients in Group I exhibits a substitution of valine for methionine at residue 552, accompanied by a substitution of methionine for leucine at residue 528. Patients in Group II had only an isoleucine-for-methionine substitution at position 552. Reconstruction of these mutations in an HBV replication-competent plasmid was performed in a transient transfection cell assay to determine the function/relevance of these mutations to lamivudine resistance. Both Group I and Group II mutations resulted in a substantial decrease in sensitivity to lamivudine treatment (> 10,000-fold shift in IC50 over wild-type [wt] IC50), strongly indicating that these mutations were involved in resistance to lamivudine. A hypothetical model of the HBV reverse transcriptase has been generated for further study of the role of these mutations in lamivudine resistance.

Amino Acid Sequence↗
PubMed1998

An evaluation of linear model analysis techniques for processing images of microcirculation activity.

Sequences of images of the cortical surface can be processed to reveal information about the cortical microcirculation, regional cerebral blood flow (rCBF), and changes induced by neuronal activity. This study examined the use of different analysis methodologies on intrinsic optical images taken from rat sensory motor cortex and testes. Generalized linear model (GLM) analysis was used and compared with standard signal processing methods including principal component analysis. The GLM method has been used by Friston et al. (1994, Hum. Brain Map., 1: 214-220) in the analysis of functional magnetic resonance imagery to identify regions of focal activity. We investigated the use of this method to analyze video image data of the modulation of rCBF from rat cortex. The results revealed spatiotemporal variations in rCBF in response to stimulation within local regions of cortex. The advantage of the GLM method is that it augments ordinary signal processing methods with an estimate of statistical reliability. The use of different wavelengths of illumination reveals spatial structures with different temporal relationships. In image time series data collected under green and red illumination a phase difference was found in the low frequency approximately 0.1 Hz vasomotion oscillation. This phase difference occurred in data from both cortex and testes. A possible explanation of these differences is that the spectral absorption characteristics of the tissue reflect changes in the volume proportions of the different hemoglobin derivatives in interacting with the modulation of the volume of blood. It is suggested that the combination of these effects produces the phase differences we detect.

Animals↗