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Biomedical subjects

M Henry

Publications and source records attributed to M Henry.

At least 73 records · Page 4Linked to original sources
PubMed2000

Angioplasty and stenting of the extracranial carotid arteries.

We performed percutaneous transluminal angioplasty and stenting in patients with carotid artery stenosis to determine the efficacy of these techniques as an alternative to surgical endarterectomy. From April 1995 through July 1999, 315 carotid angioplasty procedures were performed (right, 151; left, 164) in 290 patients ranging in age from 40 to 93 years. Of these patients, 42% were symptomatic and 58% were asymptomatic. Twenty-five patients underwent bilateral procedures. The mean percentage of stenosis was 82.3%+/-8.7% SD. Angioplasty and stenting were performed without cerebral protection in 165 arteries and with protection in 150. Two methods of protection were used: the Theron technique and the PercuSurge Guardwire temporary occlusion and aspiration system. Balloon dilation and stent placement were successful in 289 patients; in the last patient, severe arterial tortuosity prevented catheterization and stenting. We observed 13 periprocedural neurologic complications due to ischemia (4.2%): 4 transient ischemic attacks (1.3%), 4 minor strokes (1.3%), and 5 major strokes (1.6%), including 1 death. At 6 months, 210 patients had a follow-up angiogram (155) or duplex ultrasound (55). There were 10 restenoses (4.7%), 1 of which was symptomatic and 2 of which showed mild compression of a Palmaz stent without marked stenosis. Primary and secondary 4-year patency rates were 96% and 99%, respectively. These results demonstrate acceptable mortality and morbidity rates related to carotid angioplasty and stenting. However, we found the risk of embolic stroke to be substantial. Cerebral protection may improve the results of carotid angioplasty and expand the indications for this procedure.

Aged↗
PubMed2000

Percutaneous endovascular treatment of peripheral aneurysms.

BACKGROUND: To evaluate the feasibility and efficacy of percutaneous endovascular treatment of peripheral aneurysms. METHODS: Forty-eight patients, M: 41, F: 7, mean age: 65.7 +/- 10.1 years (47-85 years), with 50 aneurysms were treated: 45 with covered stents (Cragg/Passager 22, Corvita 21, Wallgraft 1, Endotex 1) 4 with non-covered stents and 1 with stent graft. Twenty-six aneurysms located at the iliac artery, 12 at the femoral and 12 at the popliteal artery. Mean lesion length: 61.1 +/- 21.3 mm. Percutaneous approach used in all cases, femoral antegrade (n=24), retrograde (n=23), contralateral (n=2), popliteal (n=1). Stents used were 6-12 mm in diameter and 30-120 mm in length. Multiple stents used to cover all lesions in 20 cases. RESULTS: Immediate technical success was 96% (48/50). In 1 case of long, tortuous femoropopliteal aneurysm, it was impossible to cover the low part, due to rigidity of the device used, in 1 case of large iliac aneurysm there was incomplete immediate exclusion. No complication during the procedure. Four patients developed non-infectious fever/local pain. Eight thromboses occurred: 2 at iliac, 1 at femoral and 5 at the popliteal level. All other stents remained patent, the aneurysms completely excluded over a mean follow-up of 20.6 +/- 13.2 m, maximum 61 m. Primary patency: all lesions 82%, iliac 92%, femoropopliteal 78%. Secondary patency: all lesions 88%, iliac 96%, femoropopliteal 86%. CONCLUSION: Percutaneous endoluminal treatment of peripheral aneurysms seems safe and effective with high technical success and good long-term results, except for popliteal localization. It could be an alternative to surgery.

Aged↗
PubMed1999

Apoptotic fraction in childhood ALL assessed by DNA in situ labelling is ploidy independent.

BACKGROUND: Apoptotic cell fraction and presence or degree of aneuploidy may both affect treatment outcome in childhood acute lymphoblastic leukaemia (ALL), which is largely defined by drug resistance. Independence of the variables is at present not established. Until the development of in situ labelling of cells committed to the apoptotic pathway, the fraction of cells in apoptosis could not be determined objectively. AIM: To determine the relationship between apoptotic cell fraction and karyotype in childhood ALL using in situ labelling. METHODS: 1.3.1. Study Groups and Samples. Diagnostic, pretreatment bone marrow trephine and aspirate samples of 24 consecutive, unselected cases of childhood ALL were included in the study: Normal karyotype (n = 11, 5M,6F), high hyperdiploid aneuploidy (DNA index > 1.5, n = 7, 1M,6F), complex karyotypic anomalies (n = 6, 5M,1F). 1.3.2. Apoptotic Cell Labelling. In situ labelling of the 3'-OH ends of the apoptosis specific DNA (Klenow) fragment (Frag-EL, CalBiochem, USA). 1.3.3. Quantitation. Apoptotic cell fraction was established using 10 systematically random fields of > 20 nuclei. Results were tabled per group. After calculations of means, differences between groups were assessed using t-test. RESULTS: Apoptotic cell fraction, ranging from < 1 to 95%, did not differ statistically significant between the three study groups. CONCLUSION: Apoptotic cell fraction in childhood leukaemia is independent of ploidy status and euploid karyotypic anomalies.

Apoptosis↗
PubMed1999

PCNA bearing structures are retained in apoptotic phase of childhood ALL cell cycle.

BACKGROUND: Drug resistance to DNA directed therapy may depend on proliferative as well as apoptotic cell fraction. PCNA/Ki67 ratio excess, possibly reflecting DNA excision repair, is of additional interest to drug resistance in MTT testing. The cell cycle phase/antigen expression pattern in childhood acute lymphoblastic leukemia (ALL) is not known. AIMS: To study the relationship between nuclear expression of PCNA, Ki-67 and Frag-EL positivity in childhood ALL. METHODS: 1.3.1. Study Groups. Diagnostic bone marrow trephine biopsies of 32 consecutive unselected cases of childhood ALL were included in the study. 1.3.2. Immunohistochemistry. Commercially available Moab PCNA (PC10, DAKO, USA), Ki-67 (MM1, NovaCastra, UK) were used to label cycling cells in routinely processed 5 microns paraffin sections. 1.3.3. In-Situ Labelling of Apoptotic Cells. The 3'-OH ends of apoptosis specific DNA fragments were labelled in-situ on subsequent 10 microns sections (Frag-EL, CalBiochem, USA). 1.3.4. Quantitation. After blinding and randomisation, 10 systematic random fields of > 20 nuclei and nuclear size bias correction was used to determine positive nuclei fraction. RESULTS: While the sum of apoptotic and proliferative cell fraction (Ki-67 + Frag-EL%) equalled 100% in 5/32 cases, PCNA expression into at least the early phases of apoptosis ([%PCNA-%K-67] > [100-%Frag-EL] was found in 17/32 cases. CONCLUSIONS: PCNA/Ki67 ratio excess may not reflect DNA excision repair activity but rather slow degradation of antigen bearing structures limiting relevance to drug resistance study.

Apoptosis↗
PubMed1999

Apoptosis corrected proliferation fraction in childhood ALL is related to karyotype.

BACKGROUND: Tumour doubling time, a parameter in drug sensitivity testing, reflects both cell proliferation and apoptosis. Variable apoptosis fractions may explain the poor correlation of S-fraction and drug response. DNA aneuploidy (reflecting intrinsic DNA instability) may, by increasing apoptosis, affect drug response. AIM: To assess the relationship between apoptosis corrected proliferation fraction and DNA ploidy in childhood acute lymphoblastic leukemia (ALL). METHODS: 1.3.1. Study Groups. Thirty two consecutive, unselected diagnostic cases of childhood ALL were included in the study. 1.3.2. Karyotype. A normal karyotype was found in 15 cases (7M, 8F, age 8 m-12 yrs); high hyperdiploid aneuploidy (DNA index > 1.5) was found in 7 patients (1M, 7F, age 3-12 yrs) whereas complex karyotypic anomalies, but with 2n or near 2n DNA were present in 10 patients (7M, 3F, age 1 y 7 m -16 yrs). 1.3.3. Proliferation Fraction Assessment. Immunocytochemical demonstration of S-phase associated nuclear expression of the Ki-67 antigen (MM1, NovaCastra, UK). 1.3.4. Apoptosis Fraction Assessment. Binding of a horse radish peroxidase labelled DNA probe for the 3'-OH ends of apoptosis derived Klenow fragments (Frag-EL, CalBiochem, USA). 1.3.5. Quantitation. Computer assisted image analysis (Quantimet 570C), of 10 systematically random fields of a minimum of 20 nuclei each. A nuclear size bias correcting counting frame and rule were used to correct for cell proliferation associated nuclear volume increase and for the expected nuclear volume reduction resulting from apoptosis. RESULTS: Corrected for apoptosis, proliferation fraction was highest (mean 57.5%, range 1-100) in poor prognosis, complex karyotype anomalies. Good prognosis, high hyper diploidy showed significantly lower proliferation rates (mean 24.7%, range 12-40) (p < 0.01, t-test). CONCLUSION: Apoptosis corrected cell proliferation rate in childhood ALL is not independent of karyotype abnormality which may partly explain a relation to therapy response and prognosis.

Adolescent↗
PubMed1999

Proliferation and apoptosis does not affect presenting white cell count in childhood ALL.

BACKGROUND: Treatment response/drug resistance in childhood acute lymphoblastic leukaemia (ALL) is related to presenting white cell count. This relationship might be explained by high proliferation fraction or by absence of significant apoptosis, but is presently unknown. AIMS: To study the relationship between proliferation and apoptosis in childhood ALL. METHODS: 1.3.1. Study Groups. Thirty consecutive, unselected cases of childhood ALL (15M,15F). White cell count varied from 1-200 at presentation. 1.3.2. Proliferation/Apoptosis Fraction. Immunocytochemical detection of Ki-67 (MM1, NovaCastra, UK) on 5 microns paraffin slides, Immunocytochemical detection of apoptosis specific DNA (Klenow) fragments by labelling of 3'-OH ends in 10 microns paraffin sections (Frag-EL, CalBiochem, USA). 1.3.3. Quantitation. Image analysis (Quantimet 570C) using nuclear size bias correcting counting frame and rule. Calculation of proliferation (%Ki-67) fraction and of apoptosis corrected proliferation fraction (%Ki-67/100-%apoptosis). RESULTS: Using both linear, logarithmic regression as well as power analysis, no relationship between variables was detected. CONCLUSION: Presenting white cell count is not related to apoptotic or cell proliferative activity or to net tumour growth defined by the balance between these two processes. The relationship to treatment resistance still requires explanation.

Adolescent↗
PubMed1999

Prolactin exerts hematopoietic growth-promoting effects in vivo and partially counteracts myelosuppression by azidothymidine.

Prolactin (PRL) is a neuroendocrine hormone that influences immune and hematopoietic development. The mechanism of action of this hormone in vivo remains unclear; therefore, we assessed the effects of PRL on hematopoiesis in vivo and in vitro. Normal resting mice were treated with 0, 1, 10, or 100 microg of recombinant human prolactin (rhPRL) for 4 consecutive days and euthanized on the fifth day for analysis of myeloid and erythroid progenitors in the bone marrow and spleen. Both frequencies and absolute numbers of splenic colony-forming unit granulocyte-macrophage (CFU-GM) and burst-forming unit-erythroid (BFU-e) were significantly increased in mice receiving rhPRL compared to the controls that had received saline only. Bone marrow cellularities were not significantly affected by any dose of rhPRL, but the absolute numbers and frequencies of bone marrow CFU-GM and BFU-e were augmented by rhPRL. These results suggest that rhPRL can promote hematopoiesis in vivo. Because rhPRL augments myeloid development in vivo, we examined the potential of the hormone to reverse the anemia and myelosuppression induced by azidothymidine (AZT). Mice were given rhPRL injections concurrent with 2.5 mg/mL AZT in drinking water. rhPRL partially restored hematocrits in the animals after 2 weeks of treatment and increased CFU-GM and BFU-e in both spleens and bone marrow. The experiments with AZT and rhPRL support the conclusion that the hormone increases myeloid and erythroid progenitor numbers in vivo, and they suggest that the hormone is clinically useful in reversing myelosuppression induced by AZT or other myeloablative therapies.

Animals↗
PubMed1999

Laser angioplasty of restenosed coronary stents: results of a multicenter surveillance trial. The Laser Angioplasty of Restenosed Stents (LARS) Investigators.

OBJECTIVES: This study evaluated safety and efficacy of excimer laser angioplasty for treatment of restenosed or occluded coronary stents. BACKGROUND: Balloon angioplasty of in-stent restenosis is limited by a high recurrence rate. Debulking by laser angioplasty is a novel concept to treat in-stent restenosis. METHODS: A total of 440 patients with restenoses or occlusions in 527 stents were enrolled for treatment with concentric or eccentric laser catheters and adjunctive balloon angioplasty. RESULTS: Laser angioplasty success (< or =50% diameter stenosis after laser treatment or successful passage with a 2.0-mm or 1.7-mm eccentric laser catheter) was achieved in 92% of patients. Adjunctive balloon angioplasty was performed in 99%. Procedural success (laser angioplasty success followed by < or =30% stenosis with or without balloon angioplasty) was 91%. There was neither a significant difference in success with respect to lesion length, nor were there differences between small and large vessels or native vessels and vein grafts. Success was higher and residual stenosis lower using large or eccentric catheters. Serious adverse events included death (1.6%, not directly laser catheter related), Q-wave myocardial infarction (0.5%), non-Q-wave infarction (2.7%), cardiac tamponade (0.5%) and stent damage (0.5%). Perforations after laser treatment occurred in 0.9% of patients and after balloon angioplasty in 0.2%. Dissections were visible in 4.8% of patients after laser treatment and in 9.3% after balloon angioplasty. Reinterventions during hospitalization were necessary in 0.9% of patients; bypass surgery was performed in 0.2%. CONCLUSIONS: Excimer laser angioplasty with adjunctive balloon angioplasty is a safe and efficient technology to treat in-stent restenoses. These data justify a randomized comparison with balloon angioplasty.

Adult↗
PubMed1999

Systemic and pulmonary oxidative stress in idiopathic pulmonary fibrosis.

An oxidant/antioxidant imbalance has been proposed in patients with idiopathic pulmonary fibrosis (IPF). We tested this hypothesis by measuring various parameters of the oxidant/antioxidant balance in the plasma of 12 patients with IPF (7 nonsmokers and 5 smokers); in the bronchoalveolar lavage fluid (BALF) of 24 patients with IPF (17 nonsmokers and 7 smokers) and 31 healthy subjects (23 nonsmokers and 8 smokers). The trolox equivalent antioxidant capacity (TEAC) in plasma and BALF was lower in nonsmoking patients with IPF (plasma 0.55+/-0.1 mM, p<.001; BALF 4.8+/-1.2 microM, mean +/-SEM, p<.01), compared with healthy nonsmokers (plasma 1.33+/-0.03 mM; BALF 10+/-2 microM). Similar trends in plasma and BALF TEAC were observed in smoking patients with IPF in comparison with healthy smokers. The decrease in BALF TEAC was concomitant with a decrease in BALF protein thiol levels, but the decrease TEAC levels in plasma in IPF patients was not accompanied by a decrease in protein thiol levels. Reduced glutathione (GSH) was lower in BALF in nonsmoking patients with IPF (1.0+/-0.1 microM) compared with healthy nonsmokers (2.3+/-0.2 microM, p<.001). In contrast, GSH levels were higher in smoking patients with IPF (5.2+/-1.1 microM, p<.001) than in nonsmoking patients. GSSG levels were not different in any of the groups. The levels of products of lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS) in plasma and BALF were significantly increased in both smoking (plasma 2.2+/-0.5 microM, p<.01; BALF 0.18+/-0.04 microM, p<.001), and nonsmoking (plasma 2.1+/-0.3 microM, p<.01; BALF 0.22+/-0.05 microM, p<.001) IPF patients, compared with healthy nonsmokers (plasma 1.4+/-0.3 microM; BALF 0.05+/-0.004 microM). These data show evidence of oxidant/antioxidant imbalance in the lungs of patients with IPF, which is also reflected as systemic oxidant stress.

Bronchoalveolar Lavage Fluid↗
PubMed1999

Infection of circulating CD34+ cells by HHV-8 in patients with Kaposi's sarcoma.

Human herpesvirus type 8 (HHV-8) has been identified as the most likely candidate to be involved in the development of Kaposi's Sarcoma (KS). HHV-8 has been associated with all forms of KS, primary effusion lymphoma, and multicentric Castleman's disease and detected in various non-neoplastic cells. Its presence in cells of the different hemopoietic lineages has not yet been investigated in a comprehensive and systematic manner. In this study we searched for the presence of HHV-8 in different subpopulations of peripheral blood mononuclear cells (PBMC) from patients with classic and AIDS-associated KS, as well as from HIV-1 sero-positive and sero-negative persons without KS. Thirty-four samples of PBMC were isolated from 30 patients. Subpopulations were isolated with immunomagnetic beads. Polymerase chain reaction for HHV-8 DNA was performed on PBMC and subpopulations with a primer pair selected from ORF26 of the viral genome. Polymerase chain reaction products were subsequently Southern blotted and hybridized. In patients with KS, HHV-8 DNA was detected in nine of 11 (81%) CD19+ cells, four of 11 (36%) CD2+ cells, three of 11 (27%) CD14+ cells, and nine of 11 (81%) of the remaining depleted cell populations (DP) that contain CD34 positive cells. In a subsequent set of experiments HHV-8 DNA was detected in 10 of 12 (83%) CD34 positive cell fractions. All cell subpopulations from the non-KS group were HHV-8 negative, with the exception of one positive B cell sample obtained from an HIV-infected patient. Our data demonstrate that in peripheral blood HHV-8 is detectable not only in CD19+ cells, as previously reported, but also in other cells, including T cells, monocytes, and cells devoid of specific lineage markers. We also show for the first time that CD34+ cells in peripheral blood of KS patients are a predominant HHV-8-harboring population, suggesting that they represent an additional important reservoir for this virus in vivo.

Antigens, CD19↗
PubMed1999

5-aminolevulinic acid-mediated photodynamic therapy of intraepithelial neoplasia and human papillomavirus of the uterine cervix--a new experimental approach.

The aim of this study was to treat patients for ectocervical dysplasia [cervical intraepithelial neoplasia (CIN) grades 1 and 2] and associated human papilloma virus (HPV) infections with photodynamic therapy (PDT). In 20 patients, 5-aminolevulinic acid (5-ALA, 12% w/v) was applied topically with a cervical cap 8 h prior to illumination. A thermal light source (150 W halogen lamp) emitting a broadband red light (total energy: 100 J/cm2, fluence rate: 90 mW/cm2) was used for superficial illumination of the portio. In addition, an Nd:YAG pumped dye laser (652 nm) was used to illuminate the cervical canal (total energy: 50 J/cm2, fluence rate: 300 mW/cm2). Preliminary results of follow-ups at 1, 3, 6, and 9 months posttherapy showed a cytological improvement in the grading of the PAP smears in 19 patients and the eradication of cervical HPV in 80%. These results demonstrate that ectocervical dysplasia and associated HPV infections can be treated by PDT.

Administration, Intravaginal↗
PubMed1999

Time- and surgery-dependent effects of lipopolysaccharide on gut, cardiovascular and nitric oxide functions.

Lipopolysaccharide (LPS) is considered a major effector of hypotension in septic shock, partly through increasing nitric oxide (NO) formation. LPS-activation of leukocytes that express cytokines which induce NO synthase (iNOS) has also been considered an important contributor to shock. However, LPS, cytokines, and NO are not necessarily associated with hypotensive shock. We investigated whether the timing of LPS injection after initial surgery could influence responses to LPS. E. coli LPS (17 mg/kg 0111:B4 and 026:B6 serotypes) was injected 15 or 120 min after tracheal and femoral cannulation in the anesthetized rat. LPS caused hypotension for 2 h when injected 15 min (early injection) after initial surgery. LPS decreased blood pressure for only 15 min when injected 2 h (late injection) after initial surgery. Plasma NO was increased and leukocytes were decreased after both the early and late LPS injection. Blood pressure responded the same when a second surgery (ileal cannulation and luminal perfusion) followed the early or preceded the late LPS injection. Ileal NO secretion increased and effective mucosal blood flow decreased when LPS followed gut surgery, but these did not change when gut surgery followed LPS. Plasma NO was increased and leukocytes were decreased when LPS followed gut surgery, but these did not change when gut surgery followed LPS. Ileal water absorption was not affected by LPS. These observations suggest that a desensitization to the hypotensive effect of LPS develops with time after an initial trauma. An additional gut trauma does not change the blood pressure response, but does have effects on leukocyte sequestration and NO synthesis. NO synthesis alone could not explain the effects on blood pressure.

Analysis of Variance↗
PubMed1999

Alterations in hepatic gluconeogenesis, prostanoid, and intracellular calcium during sepsis.

OBJECTIVE: The metabolic alterations observed during sepsis may be associated with changes in local concentrations of intracellular calcium (Ca2+) and prostanoid synthesis in the liver. The authors studied hepatocyte intracellular Ca2+ and the release of glucose and prostanoid in an in-vivo murine liver perfusion model. METHODS: Sepsis was induced in anesthetized, fasted rats by cecal ligation and puncture (CLP, n = 42). Hepatic glucose release was studied in control (n = 10) and CLP (n = 10) groups using a non-recirculating liver perfusion model with and without lactate as gluconeogenic substrate. Hepatocyte intracellular Ca2+ (n = 11) was measured using the selective indicator Fura-2 under basal and epinephrine (10(-5) M) stimulated conditions. 6-Keto-prostaglandin F1alpha (6-Keto) and thromboxane B2 (TxB2) were determined from liver perfusate by radioimmunassay (n = 11). Data were analyzed using t-tests and repeated-measures ANOVA. RESULTS: Plasma glucose was significantly lower in CLP groups compared with controls (74.9+/-6.6 vs 115.7+/-4.6 mg/dL, p < 0.05). Plasma lactate was significantly higher in CLP vs controls (3.7+/-0.4 vs 1.4+/-0.1 mM, p < 0.05). Glucose release in isolated perfused livers was significantly lower in CLP vs controls (8.5 vs 16+/-1.2 microM/g/hr, p < 0.001). With the addition of lactate + pyruvate to the perfusate, glucose output in CLP livers was significantly lower following 5 (9.9+/-0.7 vs 17.7+/-1.1 microM/g/hr, p < 0.05) and 10 (11.9+/-1.2 vs 20.6+/-1.3 microM/g/hr, p < 0.001) minutes of perfusion. The basal level of intracellular calcium ([Ca2+]i) in CLP rats (460.1+/-91.6 nM) was significantly higher than in control rats (196.3+/-35.5 nM) (p < 0.05). A significant increase (p < 0.05) in [Ca2+]i occurred after the addition of epinephrine in hepatocytes in control (196.3+/-35.5 vs 331.8+/-41.4 nM) but not CLP (460.1+/-91.6 vs 489.4+/-105 nM) rats. 6-Keto was significantly lower in CLP compared with controls at 30 minutes (25.7+/-3.9 vs 33.4+/-5.5 pg/mL, p < 0.05), whereas TxB2 was not significantly altered (52.1+/-34.7 vs 87.5+/-43.2 pg/mL). CONCLUSION: These results demonstrate that CLP sepsis is associated with an increase in hepatocyte intracellular free Ca2+ concentration along with attenuation of hormone-mediated Ca2+ mobilization and hepatic gluconeogenesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Severe pulmonary hemorrhage in the premature newborn infant: analysis of presurfactant and surfactant eras.

We undertook a case-control study of premature infants who developed clinically significant, severe pulmonary hemorrhage (PH) in the presurfactant and surfactant eras to learn more about the cause of severe PH and whether the pathogenesis of severe PH has changed with the advent of surfactant therapy. Severe PH was defined as an acute onset of severe endotracheal bleeding with an acute drop in hematocrit and the development of multilobar infiltrates on chest radiograph. Eleven premature infants from the presurfactant era population and 17 premature infants from the surfactant era population met the criteria for severe PH, all with gestational ages <32 weeks and birth weights <1,500 g (very low birth weight infants). These were each matched by gestational age, date of birth, birth order (for twins), and birth weight to 2 controls. The incidence of severe PH in infants of gestational age <32 weeks was similar in the two eras (1.8% in the presurfactant era and 3.0% in the surfactant era). Severe PH was not associated with maternal characteristics such as drug use or prenatal care, pregnancy complications, evidence of intrauterine anoxia, hyaline membrane disease, frequency of endotracheal suctioning, or patent ductus arteriosus. Premature infants suffering from severe PH in the presurfactant era required more delivery room resuscitation and had more severe early respiratory disease during the first 12 h of life as compared with their controls. However, these differences were not present in the group from the surfactant era. Infants with severe PH were more likely to have birth weights below the third percentile for gestation (severe intrauterine growth restriction). The proportion of infants receiving surfactant, and the number of surfactant doses used, did not differ between severe-PH infants and their controls in the surfactant era group. We conclude that severe intrauterine growth restriction represents a risk factor for severe PH in very low birth weight infants. The introduction of surfactant therapy has not altered the incidence of severe PH, even though it has apparently helped remove the severity of early lung disease as a risk factor. The physiological basis of severe PH requires further investigation.

Case-Control Studies↗
PubMed1999

Immunohistochemical detection of alpha1E voltage-gated Ca(2+) channel isoforms in cerebellum, INS-1 cells, and neuroendocrine cells of the digestive system.

Polyclonal antibodies were raised against a common and a specific epitope present only in longer alpha1E isoforms of voltage-gated Ca(2+) channels, yielding an "anti-E-com" and an "anti-E-spec" serum, respectively. The specificity of both sera was established by immunocytochemistry and immunoblotting using stably transfected HEK-293 cells or membrane proteins derived from them. Cells from the insulinoma cell line INS-1, tissue sections from cerebellum, and representative regions of gastrointestinal tract were stained immunocytochemically. INS-1 cells expressed an alpha1E splice variant with a longer carboxy terminus, the so-called alpha1Ee isoform. Similarily, in rat cerebellum, which was used as a reference system, the anti-E-spec serum stained somata and dendrites of Purkinje cells. Only faint staining was seen throughout the cerebellar granule cell layer. After prolonged incubation times, neurons of the molecular layer were stained by anti-E-com, suggesting that a shorter alpha1E isoform is expressed at a lower protein density. In human gastrointestinal tract, endocrine cells of the antral mucosa (stomach), small and large intestine, and islets of Langerhans were stained by the anti-E-spec serum. In addition, staining by the anti-E-spec serum was observed in Paneth cells and in the smooth muscle cell layer of the lamina muscularis mucosae. We conclude that the longer alpha1Ee isoform is expressed in neuroendocrine cells of the digestive system and that, in pancreas, alpha1Ee expression is restricted to the neuroendocrine part, the islets of Langerhans. alpha1E therefore appears to be a common voltage-gated Ca(2+) channel linked to neuroendocrine and related systems of the body.

Animals↗
PubMed1999

Carotid stenting with cerebral protection: first clinical experience using the PercuSurge GuardWire system.

PURPOSE: To study the feasibility and safety of carotid angioplasty and stenting using a new cerebral protection device that temporarily occludes the distal internal carotid artery (ICA). METHODS: Forty-eight high-risk patients (39 men, mean age 69.1 +/- 8 years, range 54 to 86) with 53 ICA stenoses underwent percutaneous angioplasty and stenting via the femoral approach under cerebral protection afforded by a 0.014-inch GuardWire balloon occlusion device. Mean stenosis was 82.1% +/- 9.65% (range 70 to 96) and mean lesion length was 16.0 +/- 7.5 mm (range 6 to 50). Thirty-three (62%) lesions were calcified, and 38 (72%) were ulcerated. Thirty-two (60%) of the lesions were asymptomatic. With the occlusion balloon inflated in the distal ICA, the lesion was dilated and stented. The area was cleaned by aspiration and flushed via an aspiration catheter advanced over the wire. Blood samples were collected from the external carotid artery (ECA) and analyzed to measure the size and number of particles collected. Computed tomography and neurological examinations were performed the day after the procedure. RESULTS: Immediate technical success was achieved in all patients with the implantation of 38 Palmaz stents, 8 Expander stents, and 11 Wallstents. Carotid occlusion was well tolerated in all patients but 1 who had multiple, severe carotid lesions and poor collateralization. Mean cerebral flow occlusion time was 346 +/- 153 seconds during predilation and 303 +/- 143 seconds during stent placement. Total mean flow occlusion time was 542 +/- 243 seconds. One immediate neurological complication (transient amaurosis) occurred in a patient who had an anastomosis between the external carotid (EC) and ICA territories. Debris was removed in all patients with a mean 0.8-mm diameter catheter. CONCLUSION: Cerebral protection with the GuardWire device is easy, safe, and effective in protecting the brain from cerebral embolism. Larger studies are warranted.

Aged↗