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I Janssen

Publications and source records attributed to I Janssen.

At least 55 records · Page 3Linked to original sources
PubMed1998

Complement C1-inhibitor expression in Alzheimer's disease.

In situ and in vitro studies suggest that activation of locally produced complement factors may act as a mediator between amyloid deposits and neurodegenerative changes seen in Alzheimer's disease (AD). C1-esterase inhibitor (C1-Inh), which regulates activation of C1 of the complement classical pathway, can be detected immunohistochemically in its inactivated form in activated astrocytes and dystrophic neurites in AD plaque areas. In this study, designed to investigate the cellular source of C1-Inh, C1-Inh was found to be secreted in a functionally active form by astrocytes cultured from postmortem human brain specimens as well as by neuroblastoma cell lines. Recombinant human interferon-gamma (IFN-gamma), which stimulates C1-Inh synthesis in various cell types, several-fold stimulated C1-Inh protein secretion by cultured human astrocytes derived from different regions of the central nervous system and by one (SK-N-SH) of two neuroblastoma cell lines (SK-N-SH and IMR-32) included in this study. In contrast to IFN-gamma, other cytokines [interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha] that can be found in brain areas affected by AD, did not stimulate C1-Inh secretion by astrocytes or neuroblastomas in vitro. This inability to secrete C1-Inh is probably due to unresponsiveness at the transcriptional level, since C1-Inh secretion paralleled the expression of the 2.1-kb C1-Inh mRNA. In situ hybridization with a C1-Inh RNA antisense probe labeled neurons rather than astrocytes, suggesting a role for neurons as producers of complement regulatory proteins in vivo. Since IFN-gamma is apparently lacking in the brain parenchyma, and amyloid plaque-associated cytokines (IL-1beta, IL-6, TNF-alpha) do not stimulate C1-Inh expression in vitro, the nature of the stimulus responsible for neuronal C1-Inh expression in AD brains remains to be investigated.

Aged↗
PubMed1998

Biological activity of structural analogs and effect of oil as a carrier of trypsin modulating oostatic factor of the gray fleshfly Neobellieria bullata.

The trypsin modulating oostatic factor from the gray fleshfly Neobellieria bullata (Neb-TMOF) is released from the ovary at the end of vitellogenesis and inhibits trypsin biosynthesis in the midgut. This inhibition indirectly results in an arrest of oocyte growth. Additional experiments with N. bullata were performed to characterize its trypsin modulating and oostatic properties in more detail. After suspending the peptide in wheat germ oil, the threshold dose for oostatic activity was lowered one thousand times (2.10(-5) in oil versus 2.10(-2) pmoles per fly in Ringer). By use of the Neobellieria trypsin biosynthesis assay, 17 analogs of the hexapeptide were tested for inhibitory activity. The following structural elements were demonstrated to be critical for biological activity: the alcohol function at position 3 (Thr residue); a positively charged basic group at the C terminus (His residue); and the Asn side chain at positions 1 and 4.

Amino Acid Sequence↗
PubMed1998

Cloning of the cDNA encoding Scg-SPRP, an unusual Ser-protease-related protein from vitellogenic female desert locusts (Schistocerca gregaria).

The cDNA coding for a Ser-protease-related protein (Scg-SPRP) was cloned from desert locust (Schistocerca gregaria) midgut. The derived amino acid sequence consists of 260 residues and shows strong sequence similarity to insect trypsin-like molecules. It is, however, likely that Scg-SPRP is not a proteolytically active enzyme and that it plays another physiologically relevant role, since two out of three residues which are indispensable for catalytic activity of Ser-proteases are replaced. Northern analysis revealed that the Scg-SPRP gene is expressed in midgut tissue and that this expression is strongly induced in adult female locusts. Moreover, the occurrence of the transcript (1.2 kb) fluctuates during the molting cycle and during the female reproductive cycle. Juvenile hormone (JH III) dependence of transcription was investigated by chemical allatectomy (precocene I) of adult females. This resulted in inhibition of vitellogenesis and in disappearance of the Scg-SPRP transcript. Expression of Scg-SPRP in precocene-treated locusts could be reinduced by additional treatment with JH III or with 20-OH-ecdysone.

Amino Acid Sequence↗
PubMed1997

Activin A and follistatin are dynamically regulated during human pregnancy.

Activin A (beta A-beta A) and activin B (beta B-beta B) are related dimeric proteins that regulate numerous cellular activities. Activin activity is bioneutralized by follistatin, a specific and high-affinity binding protein. Recently, our group developed specific and sensitive enzyme-linked immunosorbent activin assays that do not detect either activin isoform when bound to follistatin, therefore, the assays are specific for biologically relevant ligands. Activin A is measurable in the serum of pregnant women (cross-sectional sample collection), while activin B is not detected in maternal serum. However, activin B is measurable in amniotic fluid and cord blood sera. The purpose of this study was to measure serum activin A, activin B, and follistatin prospectively in longitudinally collected samples during pregnancy. This study design offered observations of relative changes in serum hormone concentration with each person serving as an internal reference. Serum samples were collected bimonthly from seven pregnant women beginning within the second month of gestation, and up to, but not including, the onset of labor. Six of the seven women had normal labor and delivery. One patient required pitocin (an oxytocin agonist) for induction of labor which led to delivery. Activin A, activin B, total follistatin, free follistatin, human chorionic gonadotropin, estradiol, progesterone, FSH, and LH were measured in maternal serum samples using specific assays. Serum activin A levels increased in the final month of pregnancy in the six patients who delivered following normal labor (< 0.78 ng/ml (first trimester) to 1-6 ng/ml (term)). Activin B was not detected in any serum sample (< 0.78 pg/ml). Total serum follistatin (free follistatin, follistatin-activin, and follistatin-inhibin) increased 10- to 45-fold in the final month of pregnancy in four of the women undergoing normal labor (10 ng/ml (first trimester) to 100-450 ng/ml (final month)). Total follistatin was high and variable in two women throughout pregnancy. Total follistatin returned to basal serum concentration in three of the patients during the last 2 weeks of pregnancy. Free follistatin was detected throughout pregnancy (range < 2-35 ng/ml). Free follistatin represented a small percentage of the total follistatin throughout the time of pregnancy and did not rise coincident with the rise in total follistatin. Serum activin A and activin B were not detected during the entire course of pregnancy in the one patient who did not have normal labor and total follistatin did not rise in the last trimester of pregnancy. Gonadotropin and steroid hormones were measured in all patients and were within normative ranges for human pregnancy (inclusive of the non-laboring patient). The results suggest that immunodetectable activin A is present in the third trimester of pregnant women who have normal onset labor. The total follistatin assay results suggest that follistatin-activin (or -inhibin) complexes are upregulated during the third trimester of pregnancy. Importantly, activin A production exceeds the binding capacity of circulating follistatin. Because binding protein free activin A is biologically active we conclude that the activin A detected in late pregnancy is biologically relevant. The findings are consistent with our hypothesis that activin A is an endocrine factor during the last trimester of human pregnancy and may be involved in normal labor.

Activins↗
PubMed1996

Molecular sequencing and modeling of Neobellieria bullata trypsin. Evidence for translational control by Neobellieria trypsin-modulating oostatic factor.

Trypsin mRNA from the grey fleshfly (Neobellieria bullata) was reversed transcribed and amplified by means of PCR. Two cDNA species of 600 bp and 800 bp were cloned and sequenced. The 3' end of the gene (300 bp) was amplified by means of the rapid-amplification-of-cDNA-ends method, cloned and sequenced. The deduced protein sequence of 254 amino acids exhibited 46% identity to Drosophila trypsin and 32% identity to Anophiline trypsin and Aedes trypsin. Three-dimensional models of Neobellieria trypsin and Drosophilia trypsin were built and compared. Both models contain two domains of beta-barrel sheets as was shown by means of X-ray crystallography of mammalian trypsin. The catalytic active site is composed of the canonical triad of His42, Asp87 and Ser182 whereas Asp176 sits as the bottom of the specificity pocket. Southern blot analysis suggested that Neobellieria trypsin is encoded by one gene. Northern blot analysis showed that an early trypsin transcript is found in the midgut of sugar-fed females. This message disappeared after a liver meal, and was replaced by a late transcript. Injection of trypsin-modulating oostatic factor (TMOF) at 10(-9) M prevented the disappearance and the translation of the early transcript. TMOF did not prevent the appearance of the late transcript. However, in the presence of the hormone the late transcript was not translated. Thus, TMOF is the biological signal that terminates the translation of trypsin mRNA in the fleshfly gut and probably in the mosquito gut.

Amino Acid Sequence↗
PubMed1996

Isolation of NEB-LFamide, a novel myotropic neuropeptide from the grey fleshfly.

A methanolic extract of 350,000 adult grey fleshflies Neobellieria bullata, was prepared and screened for myotropic activity. After fractionation on the first column, all fractions were screened in two heterologous (Locusta oviduct and Leucophaea hindgut) and one homologous (Neobellieria hindgut) myotropic bioassay. We here report the purification of one fraction, which stimulates the contractions of the Locusta oviduct. Electrospray Mass Spectrometry of the peptide revealed a molecular mass of 1395.82. The primary structure has been determined as AYRKPPFNGSLF-amide. This novel peptide was designated Neb-LF-amide. This sequence is different from the other known myotropic peptides in insects. The threshold concentration of the synthetic peptide is 1 x 10(-7) M on the Locusta oviduct. On the hindgut of Neobellieria or Leucophaea, the synthetic peptide is not active. By use of a polyclonal antiserum raised against the synthetic peptide, immunoreactivity was localized in median neurosecretory cells in the pars intercerebralis of the fly brain, indicating that Neb-LF-amide is a neuropeptide.

Amino Acid Sequence↗
PubMed1996

Isolation and identification of a cAMP generating peptide from the flesh fly, Neobellieria bullata (Diptera: Sarcophagidae).

The Manduca sexta Malpighian tubule assay system, developed to monitor adenylate cyclase activity, was used in combination with HPLC to isolate a novel cAMP generating peptide from 350,000 whole flesh flies, Neobellieria bullata. Mass spectrometry revealed a molecular mass of 5,047 daltons, and Edman degradation the following sequence: AGAEAEKLSGLSKYFNGTTMAGRANVAKATYAVIGLIIAYNVMKPKKK. This 48-mer peptide, called Neb-cGP, does not belong to the corticotropin releasing factor family of insect diuretic peptides. Electrophoresis and subsequent immunoblotting of peptides immunoprecipitated from a homogenate of entire flies showed that one fly contained approximately 0.003 to 0.03 micrograms Neb-cGP and that 10 micrograms represents the lowest immunostainable amount on a Western blot.

Amino Acid Sequence↗
PubMed1996

Immunolocalization of the oostatic and prothoracicostatic peptide, Neb-TMOF, in adults of the fleshfly, Neobellieria bullata.

The hexapeptide Neb-TMOF (H-NPTNLH-OH, trypsin modulating oostatic factor of the gray fleshfly, Neobellieria bullata)2 occurs in vitellogenic ovaries and is involved in negative feedback regulation of trypsin biosynthesis in the gut of late vitellogenic females. Polyclonal antisera were raised against the synthetic peptide and were used to identify and immunolocalize Neb-TMOF epitopes in different fleshfly tissues. Neb-TMOF-immunoreactive material first appears in the cortical layer of young vitellogenic oocytes and later spreads over the yolk granules. This suggests a pinocytosis with the three yolk polypeptides (vitellogenins). Controls treated with the preimmune sera or with anti-Neb-TMOF antiserum preadsorbed to Neb-TMOF peptide coupled to a solid phase support did not stain. There was no immunostaining in the central nervous system (brain and ventral nerve cord), the retrocerebral complex, the fat body, or the testes. Western blot analysis showed that the anti-Neb-TMOF antisera specifically recognize a putative hormone precursor polypeptide (Mr 75 kDa) from vitellogenic ovaries. This protein is virtually absent from the hemolymph. It is not immunologically related to the three yolk polypeptides, since it is not recognized by yolk polypeptides antisera. In adult females the ovary appears to be the only site of synthesis of Neb-TMOF and of its precursor. Immunopositive staining is found in the apical areas of ovarian follicle cells, suggesting these cells as a site of hormone precursor biosynthesis. This is the first demonstration that a protein colocalized with yolk proteins might act as a precursor for a folliculostatic hormone.

Animals↗
PubMed1996

Early complement components in Alzheimer's disease brains.

Activation products of the early complement components C1, C4 and C3 can be found colocalized with diffuse and fibrillar beta-amyloid (beta/A4) deposits in Alzheimer's disease (AD) brains. Immunohistochemically, C1-esterase inhibitor (C1-Inh) and the C1 subcomponents C1s and C1r can not, or only occasionally, be detected in plaques or in astrocytes. The present finding that C1q, C1s and C1-Inh mRNA are present in both AD and control brains suggests that the variable immunohistochemical staining results for C1r, C1s and C1-Inh are due to a rapid consumption, and that the inability to detect C1s, C1r or C1-Inh is probably due to the dissociation of C1s-C1-Inh and C1r-C1-Inh complexes from the activator-bound C1q into the fluid phase. Employing monoclonal antibodies specific for different forms of C1-Inh, no complexed C1-Inh could be found, whereas inactivated C1-Inh seems to be present in astrocytes surrounding beta/A4 plaques in AD brains. These findings, together with our finding (using reverse transcriptase-polymerase chain reaction) that C1-Inh is locally produced in the brain, suggest that in the brain complement activation at the C1 level is regulated by C1-Inh. Immunohistochemically, no evidence for the presence of the late complement components C5, C7 and C9, or of the membrane attack complex (MAC), was found in beta/A4 plaques. In contrast to the mRNA encoding the early components, that of the late complement components appears to be hardly detectable (C7) or absent (C9). Thus, without blood-brain-barrier impairment, the late complement components are probably present at too low a concentration to allow the formation of the MAC, which is generally believed to be responsible for at least some of the neurodegenerative effects observed in AD. Therefore, the present findings support the idea that in AD, complement does not function as an inflammatory mediator through MAC formation, but through the action of early component activation products.

Aged↗
PubMed1996

Stimulus parameters and inertial load: effects on the incidence of protective stepping responses in healthy human subjects.

OBJECTIVE: To test the hypotheses that the incidence of protective stepping in response to sudden translations of the support would (1) increase as a function of both the magnitude of surface displacement and velocity of platform movement, and (2) decrease in association with an increase in external loading applied to the body. DESIGN: A log-linear approach was used to analyze the incidence of stepping by testing several models incorporating different platform stimulus parameters (direction, displacement, velocity) and external loading (0% and 20% body weight). SETTING: Institutional-based research laboratory. PARTICIPANTS: Eight healthy younger adult (21 to 28 years) volunteers. MAIN OUTCOME MEASURES: The incidence and number of protective steps served as the primary planned outcome variables. RESULTS: Steps occurred more frequently for anterior (83 steps) versus posterior (45 steps) translations. Step occurrence was generally proportional to platform velocity, and increased with displacements up to 15cm, but then plateaued. External loading was associated with a reduction in the number of steps for lower magnitudes of platform motion but had little effect at higher magnitudes. CONCLUSION: The tendency to step in response to externally applied disturbances to stance appears to be a complex function of direction, velocity, displacement, and inertial load.

Adult↗
PubMed1996

Hormones and the cytoskeleton of animals and plants.

It is often overlooked that a cell can exert its specific functions only after it has acquired a specific morphology: function follows form. The cytoskeleton plays an important role in establishing this form, and a variety of hormones can influence it. The cytoskeletal framework has also been shown to function in a variety of cellular processes, such as cell motility (important for behavior), migration (important for the interrelationship between the endocrine and immune systems, e.g., chemotaxis), intracellular transport of particles, mitosis and meiosis, maintenance of cellular morphology, spatial distribution of cell organelles (e.g., nucleus and Golgi system), cellular responses to membrane events (e.g., endocytosis and exocytosis), intracellular communication including conductance of electrical signals, localization of mRNA, protein synthesis, and--more specifically in plants--ordered cell wall deposition, cytoplasmic streaming, and spindle function followed by phragmoplast function. All classes of hormones seem to make use of the cytoskeleton, either during their synthesis, transport, secretion, degradation, or when influencing their target cells. In this review special attention is paid to cytoskeleton-mediated effects of selected hormones related to growth, transepithelial transport, steroidogenesis, thyroid and parathyroid functioning, motility, oocyte maturation, and cell elongation in plants.

Animals↗
PubMed1996

Molecular cloning of the papillary renal cell carcinoma-associated translocation (X;1)(p11;q21) breakpoint.

A combination of Southern blot analysis on a panel of tumor-derived somatic cell hybrids and fluorescence in situ hybridization techniques was used to map YACs, cosmids and DNA markers from the Xp11.2 region relative to the X chromosome breakpoint of the renal cell carcinoma-associated t(X;1)(p11;q21). The position of the breakpoint could be determined as follows: Xcen-OATL2-DXS146-DXS255-SYP-t(X;1)-TFE 3-OATL1-Xpter. Fluorescence in situ hybridization experiments using TFE3-containing YACs and cosmids revealed split signals indicating that the corresponding DNA inserts span the breakpoint region. Subsequent Southern blot analysis showed that a 2.3-kb EcoRI fragment which is present in all TFE3 cosmids identified, hybridizes to aberrant restriction fragments in three independent t(X;1)-positive renal cell carcinoma DNAs. The breakpoints in these tumors are not the same, but map within a region of approximately 6.5 kb. Through preparative gel electrophoresis an (X;1) chimaeric 4.4-kb EcoRI fragment could be isolated which encompasses the breakpoint region present on der(X). Preliminary characterization of this fragment revealed the presence of a 150-bp region with a strong homology to the 5' end of the mouse TFE3 cDNA in the X-chromosome part, and a 48-bp segment in the chromosome 1-derived part identical to the 5' end of a known EST (accession number R93849). These observations suggest that a fusion gene is formed between the two corresponding genes in t(X;1)(p11;q21)-positive papillary renal cell carcinomas.

Animals↗
PubMed1995

Effects of temperature on motor unit action potentials during isometric contraction.

The effect of temperature on motor unit action potential (MUAP) configuration and recruitment was studied using automatic decomposition electromyography (ADEMG) recordings from a concentric needle electrode placed in the first dorsal interosseous (FDI) muscle of 10 normal adult subjects during isometric contraction. Focally cooling the FDI resulted in prolonged MUAP duration (P < 0.001, ANOVA), a finding congruent with those of Buchthal. Focal ulnar cooling at the elbow resulted in the increased MUAP frequency. In contrast to previous studies, there were no significant differences in amplitude or turns. Greater understanding of normal motor unit electrophysiology is necessary to improve diagnostic accuracy of EMG testing.

Adult↗
PubMed1995

Complement activation in amyloid plaques in Alzheimer's disease brains does not proceed further than C3.

In Alzheimer's disease (AD) patients, the complement components Clq, C4 and C3 can be detected in different types of beta/A4 plaques, one of the hallmarks of AD. Contradictory findings on the presence of late complement components in AD brains have been reported. Nevertheless, it was suggested in recent studies that in AD brain complement activation results in complement membrane attack complex (MAC) formation and that complement activation may act as an intermediate between beta/A4 deposits and the neurotoxicity observed in AD. In the present study the presence of a number of complement components and regulatory proteins in AD temporal cortex and, for comparison, in glomerulonephritis (GN) was analysed. In GN kidneys, besides Clq, Clr, Cls and C3, the late components and the C5b-9 complex are also associated with capillary basement membrane and mesangial immune complex deposits. In AD temporal cortex Clq, C4 and C3 are co-localized with beta/A4 deposits. However, in contrast to the GN kidney, the late complement components C5, C7 and C9, as well as the C5b-9 membrane attack complex cannot be detected in beta/A4 positive plaques. The absence of the cytolytic C5b-9 complex in AD brain suggests that in AD, the complement MAC does not function as the proposed inflammatory mediator between beta/A4 deposits and the neurofibrillary changes.

Aged↗
PubMed1995

Folliculostatins, gonadotropins and a model for control of growth in the grey fleshfly, Neobellieria (sarcophaga) bullata.

The sequences of two folliculostatic peptides of the fleshfly Neobellieria bullata have been determined recently. The first peptide (Neb-TMOF: H-NPTNLH-OH), originates from a 75 kDa precursor protein found in vitellogenic oocytes. The hexapeptide directly inhibits the synthesis of trypsin-like enzymes in the gut, and thus lowers the concentration of yolk polypeptides in the hemolymph. It also inhibits the biosynthesis of ecdysone in the larval ring gland. Therefore, it could also be named prothoracicostatic hormone (Neb-PTSH). The second peptide (Neb-colloostatin: H-SIV-PLGLPVPIGPIVVGPR-OH) acts on previtellogenic follicles and is a cleaved product of a collagen-like precursor molecule. Our results indicate that peptides that are cleaved from matrix proteins could act as growth-inhibiting factors. Gonadotropin releasing hormone (GnRH)-immunolike peptides were not identified, but progress is being made in the isolation and characterization of factors which stimulate cAMP production by the ovary. Using these results, a novel model of growth control in which matrix proteins play an important role as a potential source of growth regulators has been developed.

Amino Acid Sequence↗
PubMed1994

Hepatotoxicity related to total parenteral nutrition: comparison of low-lipid and lipid-supplemented solutions.

PURPOSE: Because it is unclear whether or not the lipid or carbohydrate component of total parenteral nutrition solutions determines the development of cholestasis during total parenteral nutrition, a prospective randomized clinical trial of a predominantly carbohydrate solution (group I) versus one with isocaloric substitution of 30% nonprotein calories with lipid (group II) was performed. METHODS: Twelve patients in group I, 4 female and 8 male, and 14 patients in group II, 8 female and 6 male, were studied. Each subject received 100% to 150% of the basal energy needs, determined by the Harris-Benedict equation. Amino acids were supplied to provide a protein:kilocalorie ratio of 1:150 to 200. There were no differences between the groups in terms of mortality, nitrogen balance, and maintenance of weight. Weekly serum aspartate aminotrasferase (AST) and alkaline phosphatase (AP) levels were obtained. The change from baseline values was calculated. RESULTS: The observed difference between the two groups for AST was 5.7 (higher for group II), P = .55, and for AP, 39.1 (higher for group I), P = .23. A power calculation was performed to determine the number of patients required for a statistically significant difference in AP between the two groups with an alpha of 0.05 and a power of 0.85:67 patients. CONCLUSIONS: With these statistical considerations, we conclude that there was probably no statistically significant difference between the groups for an increase in AST or AP levels during total parenteral nutrition.

Adult↗
PubMed1994

Effect of carotid endarterectomy on patterns of cerebrovascular reactivity in patients with unilateral carotid artery stenosis.

BACKGROUND AND PURPOSE: Patients with unilateral significant carotid artery stenosis present with a variable intracranial hemodynamic status. In the majority of patients, hemodynamics are normal because of sufficient collateral flow. One subgroup shows poor ipsilateral hemodynamics because of a severely reduced blood supply, whereas in another subgroup of patients a steal phenomenon from the contralateral to the ipsilateral hemisphere can be observed during pharmacological provocation. The present study examined the effect of carotid endarterectomy (CEA) on these patterns of cerebrovascular hemodynamics in patients with carotid artery stenosis. METHODS: The CO2 reactivity of the cerebral resistance index (CRi) was determined with transcranial Doppler sonography in 63 patients with unilateral high-grade to threadlike carotid artery stenosis before and 3 months after CEA and in 37 control subjects. The interhemispheric asymmetry of CRi reactivity of the control group was used to differentiate between normal and abnormal findings. RESULTS: In patients with normal CRi asymmetry (comparable CRi reactivities at both hemispheres, n = 41), CEA did not change hemispheric CRi reactivity. In patients in whom CRi reactivity was absent at the contralateral hemisphere (intracerebral steal during hypercapnia, n = 12), CEA abolished the steal phenomenon by significantly increasing CRi reactivity at the contralateral hemisphere (preoperative, -1.0 +/- 2.1 %CRi/vol%CO2; postoperative, 5.2 +/- 0.7 %CRi/vol%CO2; P < .01). Patients who showed severely diminished ipsilateral CRi reactivity, compatible with a significantly reduced perfusion pressure at the poststenotic hemisphere (n = 10), demonstrated an improvement of ipsilateral CRi reactivity after surgery (preoperative, 0.6 +/- 0.8 %CRi/vol%CO2; postoperative, 3.7 +/- 1.1 %CRi/vol%CO2; P < .01). CONCLUSIONS: Most patients do not respond significantly to CEA. One small subgroup of patients who presented with severely disturbed ipsilateral hemodynamics demonstrated postoperative improvement at the poststenotic hemisphere, whereas in another small subgroup, who showed a steal phenomenon at the contralateral hemisphere, CEA improved contralateral hemodynamics. Determination of preoperative CRi reactivity allowed precise prediction of the effect of CEA on intracerebral hemodynamics.

Aged↗