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Biomedical subjects

R Mir

Publications and source records attributed to R Mir.

At least 19 recordsLinked to original sources
PubMed2000

Early angiotensin converting enzyme inhibitor therapy enhances the benefits of late coronary artery reperfusion on infarct expansion.

BACKGROUND: Individually, both late reperfusion and early angiotensin converting enzyme (ACE) inhibitor treatment prevent infarct expansion after acute myocardial infarction. OBJECTIVE: To examine the effect and mechanism of early post-myocardial infarction ACE inhibitor treatment, when used in combination with late coronary artery reperfusion, on infarct expansion. METHODS: Sprague-Dawley rats underwent 8 h of coronary occlusion followed by permanent reperfusion. The treatment group received enalapril, started 1 h after coronary occlusion and continued for 13 days. A control group received placebo. Two weeks after acute myocardial infarction, hemodynamic, morphometric and histologic analyses were performed. RESULTS: Hemodynamic parameters were similar in both groups (P = NS). Infarct size was similar in the ACE inhibitor and placebo treatment groups (44 +/- 4% compared with 39 +/- 4%, P = NS). Septal thickness was also similar in the two groups (2.8 +/- 0.3 mm compared with 2.7 +/- 0.3 mm, P = NS). The ACE inhibitor-treated group had thicker infarcts than those in the placebo-treated group (0.93 +/- 0.07 mm compared with 0.76 +/- 0.04 mm, P < 0.05) and these infarcts were less expanded (expansion index 1.17 +/- 0.12 compared with 1.57 +/- 0.12, P < 0.05). ACE inhibitor treatment was associated with hypertrophy of viable myocytes within the scar compared with placebo treatment (cell diameter 11.1 +/- 0.5 microns compared with 8.9 +/- 0.4 microns, P < 0.01). CONCLUSIONS: Early post-myocardial infarction ACE inhibitor treatment enhances the benefits of late coronary reperfusion on infarct expansion. The benefits may be related to hypertrophy of still-viable myocytes within the infarcted zone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Diagnostic significance of papillary structures and intranuclear inclusions in Hurthle-cell neoplasms of the thyroid.

Papillary structures and intranuclear inclusions, features which are not ordinarily associated with Hurthle-cell lesions, are occasionally noted within Hurthle-cell-rich aspirates. The diagnostic significance of these features in this setting, if any, is unknown. The purpose of this study was to determine whether these features are diagnostically useful. Specifically, since fine-needle aspiration cytology cannot distinguish between Hurthle-cell adenoma and carcinoma, we wanted to know whether the presence of either feature might aid in preoperatively assessing the likelihood of carcinoma vs. adenoma. We identified 12 cases in which a diagnosis of Hurthle-cell lesion was made by thyroid fine-needle aspiration biopsy. All cases had subsequent surgery. For every case, all cytology slides were reviewed for the presence or absence of papillary structures and intranuclear inclusions, after which the findings were correlated with the final surgical pathological diagnosis. Seven of the 12 cases had identifiable papillary structures, ranging from cases where papillary structures comprised the predominant architectural pattern to cases where rare papillary structures were found amidst a predominance of sheets and single Hurthle cells. Four of the 12 cases had intranuclear inclusions. In all cases, intranuclear inclusions were uncommon. Of 6 cases that proved to be Hurthle-cell carcinoma, 5 had papillary structures on the antecedent fine-needle aspirate cytology, and 2 had intranuclear inclusions. Of 6 cases that proved to be Hurthle-cell adenoma, 2 had papillary structures, and 2 had intranuclear inclusions. Papillary structures had a sensitivity of 83% for the presence of carcinoma, a specificity of 66%, a positive predictive value of 71%, and a negative predictive value of 80% (P = 0.2). Intranuclear inclusions had a sensitivity of 33%, a specificity of 66%, and positive and negative predictive values of 50%. Papillary structures are more common in Hurthle-cell aspirates than previously recognized. Their presence is not diagnostic of carcinoma, but neither does their absence rule out carcinoma. However, when found, the likelihood of an ultimate diagnosis of Hurthle-cell carcinoma is increased. On the other hand, intranuclear inclusions, when rare, appear to have no diagnostic value.

Adenocarcinoma↗
PubMed1999

Changes in venous histology in chronic hemodialysis patients.

Because most hemodialysis access fails at the venous side, we studied samples of brachial vein obtained during access creation in 15 patients with end-stage renal disease who gave consent. Veins were examined by computer-assisted histomorphometry, and the results correlated with the patients' clinical data. The mean venous medial width was 239 +/- 31 microm, and mean intimal width was 6.0 +/- 0.9 microm. Mean venous medial width was 358 +/- 74 microm and mean venous intimal width was 9.2 +/- 1.2 microm in the 4 patients who had been undergoing dialysis more than 6 months, compared with 196 +/- 23 microm and 4.9 +/- 0.8 microm, respectively, in the 11 patients undergoing dialysis less than 6 months (P < 0.01). The number of months undergoing hemodialysis correlated well with venous medial width (r = 0.79; P < 0.001). Correlation between number of months undergoing dialysis and intimal width did not reach statistical significance. Medial and intimal widths of the 4 patients with diabetes were not significantly different from those of the patients without diabetes. Serum parathyroid hormone level did not correlate with either medial or intimal venous width. We conclude there may be changes in the veins of hemodialysis patients with time that cause thickening of layers, even in veins not directly used for access. This may affect the creation or survival of subsequent vascular accesses.

Adult↗
PubMed1999

Tubulointerstitial nephritis associated with minimal self reexposure to rifampin.

We report the case of a 27-year-old Asian man who self-medicated with two capsules of rifampin 1 year after completing a continuous course of chemotherapy for tuberculosis that included that drug. He developed flank pain and edema and presented with uremia requiring dialysis; despite this, he had a serum potassium of only 3.5 mEq/L. Renal biopsy showed interstitial infiltrate with inflammation of the tubules. Renal function began to improve after a 3-week course of prednisone. This case is remarkable for the severity of the renal failure despite such a minimal self-exposure.

Acute Disease↗
PubMed1995

Aspirin enhances the benefits of late reperfusion on infarct shape. A possible mechanism of the beneficial effects of aspirin on survival after acute myocardial infarction.

BACKGROUND: The time window of the benefits of late reperfusion on infarct shape is limited. In rats, these benefits diminish in a wave front over time, with minimal benefits when reperfusion follows 16 hours of coronary occlusion. The mechanism of the benefits of aspirin on survival after acute myocardial infarction is unknown. The purpose of this study was to test the ability of aspirin to enhance the benefits of late coronary artery reperfusion on infarct shape and to examine the mechanism of the benefits of aspirin on infarct shape. METHODS AND RESULTS: Rats were entered into two different protocols, the morphometric and the histological protocols. In the morphometric protocol, rats were randomized into two groups: the aspirin group, in which rats underwent left coronary artery occlusion followed by treatment with aspirin (12 mg/kg i.v.), and the control group, in which rats underwent left coronary artery occlusion followed by treatment with placebo. Rats in both groups were reperfused 8 hours after coronary occlusion. Rats in the aspirin group received aspirin in the drinking water (12 +/- 2 mg/kg daily). Morphometric analysis was performed 2 weeks after acute myocardial infarction. In the histological protocol, rats underwent the same randomization, coronary occlusion, and reperfusion protocols. Hearts were removed 24 hours after coronary occlusion, and microvessels were assessed for patency. Infarct size expressed as a percent of circumference was similar in the aspirin and placebo treatment groups (28 +/- 2% versus 33 +/- 3%, P = NS). Septal thickness was also similar in both groups (1.8 +/- 0.1 versus 2.1 +/- 0.1 mm, P = NS for aspirin versus placebo). The aspirin-treated group had thicker infarcts compared with the placebo-treated group (0.8 +/- 0.1 versus 0.5 +/- 0.1 mm, P < .05) and less expanded infarcts (expansion index, 1.2 +/- 0.1 versus 2.0 +/- 0.2, P < .05). Aspirin was associated with increased patency of the microvessels in the infarcted area compared with the placebo group (96% versus 64% of microvessels patent, P < .001). CONCLUSIONS: Aspirin enhances the benefit of late coronary artery reperfusion on infarct shape after 8 hours of coronary occlusion. The benefits of aspirin on infarct shape after late reperfusion are related to increased patency of the microvessels in the infarcted area.

Animals↗
PubMed1995

Ki-67 reactivity in breast carcinoma analyzed by a computer-assisted image system: preliminary results.

The proliferative index of 63 breast carcinomas was measured on Ki-67 immunostained frozen tissue sections with a computer-assisted image analysis system. The mean proliferative index in estrogen-positive breast carcinomas was lower than in estrogen-negative carcinomas. An inverse relationship between proliferative index and short-term disease-free survival was noted.

Breast Neoplasms↗
PubMed1993

Hodgkin disease in patients 60 years of age or older. Histologic and clinical features of advanced-stage disease. The Cancer and Leukemia Group B.

BACKGROUND: This article reviews the salient pathologic and clinical features of 171 patients with Stage III-IV disease who were 60 years of age or older who were treated on four Hodgkin disease (HD) protocols from 1969 to 1988. METHODS: Pretherapy sections were reviewed centrally for correlation of the histologic classification with anatomic sites of involvement and survival. RESULTS: The diagnosis of HD was confirmed in 114 (66.7%) patients. Non-Hodgkin lymphomas (NHL) and a miscellaneous non-HD group accounted for 52 (30.4%) and 5 (2.9%) of the cases. The overall median survival times of patients with Stage III-IV HD and NHL who were 60 years of age or older in the four protocols were not significantly different (1.5 versus 1.3 years, respectively; P = 0.28). There also was no significant correlation between the survival of these patients with HD and either the Rye classification, 19 specific histologic parameters, or the British National Lymphoma Investigation grading system for HDNS. In the last protocol, the 5-year survival rate of patients with HD who were 60 years of age or older was lower than that of patients 40-59 years of age or that of those younger than 40 years of age (31% versus 63% versus 79%, respectively, P < 0.0001). Patients with HD entered into the two most recent protocols showed lower incidences of involvement of cervical and iliac-inguinal-femoral lymph nodes and skin-subcutaneous tissues than the patients with NHL who were misdiagnosed as HD. Moreover, patients with Stage III-IV HD in the most recent protocol who were 60 years of age or older had lower rates of involvement of the cervical and mediastinal-hilar lymph nodes and a higher rate of involvement of the gastrointestinal tract than younger patients. CONCLUSIONS: Patients with Stage III-IV HD and NHL who are 60 years of age or older differ with respect to the rates of involvement of specific anatomic sites but not in survival when treated with HD protocols. In contrast, patients of different age groups with Stage III-IV HD disease differ with regard to the rates of involvement of anatomic sites and survival.

Age Factors↗
PubMed1992

Prognostic significance of DNA measurement determined by image analysis in human breast carcinoma.

The nuclear DNA of human breast carcinoma cells was studied by image analysis using archival paraffin-blocked tissues from two groups of patients with breast cancers. One group had survived greater than 10 years (N = 20) and the other less than 3 years (N = 26) after the initial diagnosis. Cellular preparations were made from pepsin-digested deparaffinated sections. The nuclear DNA was stained with Feulgen stain and measured by a computerized image analysis system. The data show that in addition to nodal status the pattern of DNA histograms obtained from image analysis can provide powerful prognostic information in breast carcinoma. The prognostic value of DNA histogram patterns may be independent of nodal status.

Breast↗
PubMed1992

Correlation of proliferative index (PCNA reactivity and Ki-67 reactivity) in primary breast carcinoma with hormone status, lymph node status, and disease-free survival.

The proliferative activity in 42 cases of breast cancer were assessed immunohistochemically using antibodies to proliferating cell nuclear antigen (PCNA) and Ki-67. These indices were correlated with the steroid receptor status, pathologic stage, and disease-free survival. There was a strong direct correlation between the two proliferation indices (r = .902, P < 0.001, Kendall's rank correlation). There was a weak correlation between the hormone receptor status and proliferation indices that was not significant when statistically tested. The cases were stratified into PCNA low proliferative index (PI) group (< 4.5% positive cells) and PCNA high PI group (> 4.5% positive cells). In the low PI group, five of 18 (28%) patients were node-positive in contrast to eight of 14 (58%) patients in the high PI group. After a follow-up period of 42-60 months, 14 of 19 (74%) patients in the low PI group were disease-free compared to 10 of 17 (53%) patients in the high PI group. The PCNA and Ki-67 proliferative indices appear to be of great prognostic value and may help identify a subset of breast cancer patients who should be given adjuvant therapy.

Antigens, Neoplasm↗
PubMed1992

Association of solubilized angiotensin II receptors with phospholipase C-alpha in murine neuroblastoma NIE-115 cells.

The peptide angiotensin II (AngII) has been reported to stimulate phosphoinositide-specific phospholipase C (PLC) activity in the murine neuroblastoma cell line N1E-115. In the present study, polyclonal antibodies raised against a PLC isoenzyme, PLC-alpha, reacted with a 60-kDa protein present in both membrane and cytosolic fractions of differentiated N1E-115 cells. In order to examine the possible association of PLC-alpha with cell surface AngII receptors (AngII-Rs), membranes from differentiated N1E-115 cells were solubilized, using the zwitterionic detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS). CHAPS (1%) solubilized AngII-Rs, from N1E-115 cells, that maintained their high affinity for agonists. Gel filtration analysis of the solubilized membranes revealed that the majority of the specific binding of 125I-AngII eluted as a large protein complex with a molecular mass of 380 kDa and that agonist binding was partially reduced by guanosine-5'-O-(3-thio)triphosphate (GTP gamma S), within this complex. CHAPS also effectively solubilized immunoreactive PLC-alpha, from N1E-115 cell membranes, that was similarly present within the 380-kDa AngII-binding complex. Anti-PLC-alpha antisera immunoprecipitated approximately 16% of the total phosphatidylinositol-4,5-bisphosphate-specific PLC activity in the 1% CHAPS extract and 40% of cytosolic PLC activity. Moreover, a 60-kDa 35S-Trans S-labeled protein, comigrating with immunoreactive PLC-alpha, was immunoprecipitated from the 1% CHAPS extract by the antisera. In addition, anti-PLC-alpha antisera immunoprecipitated approximately 20% of solubilized AngII-Rs prebound with 125I-AngII but failed to precipitate receptors prebound with the antagonist 125I-Sarc1,Ile8-AngII. The anti-PLC-alpha antisera also immunoprecipitated AngII-Rs when intact membranes were labeled with 125I-AngII before solubilization in 1% CHAPS, suggesting that the AngII-R interaction with PLC-alpha was not the result of detergent-promoted protein-protein interaction. On the other hand, monoclonal antibodies against another PLC isozyme, PLC-gamma, did not precipitate AngII-Rs in solubilized N1E-115 membranes. Finally, the formation of the immunoprecipitated AngII-R-PLC-alpha complex was disrupted by the nonhydrolyzable guanine nucleotide analog GTP gamma S, suggesting that the interaction between AngII-Rs and PLC-alpha is likely to involve a heterotrimeric guanine nucleotide-binding protein in neuron-like cells.

Angiotensin II↗