Biomedical subjects

A Lin

Publications and source records attributed to A Lin.

At least 91 records · Page 5Linked to original sources

PubMed1999

Efficacy of proton magnetic resonance spectroscopy in clinical decision making for patients with suspected malignant brain tumors.

We wished to determine the utility of single voxel proton (1H) magnetic resonance spectroscopy (MRS) when used as an alternative or adjunct to brain biopsy in patients harboring lesions suggestive of brain tumors identified by MRI scan. Fifteen patients (age 7-58 years) with MRI scans and clinical histories suggestive of primary brain tumors underwent single voxel 1H-MRS. MRS (16 regions of interest in 15 patients) was used to aid in differentiation between tumor and other pathologies such as stroke or demyelinating plaque (n = 6), radiation necrosis (n = 5), or edema (n = 5). Spectra were quantified to determine absolute molar values of N-acetyl aspartate (NAA), choline (Cho), creatine (Cr), lactate (LAC), and myo-inositol (mI), metabolite ratios relative to Cr were calculated, and spectra were interpreted based on metabolite ratios. Subsequent clinical management was based on MRS interpretation, and patients were then followed to determine if MRS interpretation accurately predicted clinical outcome or surgical findings. Mean follow-up was 12.5 months (range 3-28 months). MRS suggested the presence of recurrent tumor in 7 cases, all of which were subsequently 'confirmed' by tumor resection (n = 4) or disease progression (n = 3). MRS suggested the presence of new tumor in 1 case, subsequently confirmed by surgical resection. MRS suggested the presence of necrosis in 3 patients; all 3 remained radiographically stable during the follow-up period, and one was confirmed by stereotactic biopsy. MRS suggested non-neoplastic lesions in 4 cases, 3 of whom were followed until radiographic resolution of lesions and one of which was confirmed as a pyogenic abscess via stereotactic aspiration. Overall, MRS accurately predicted the pathological nature and clinical outcome of lesions in 15/16 (96%) situations, influenced clinical decision making in 12 cases, and altered surgery planning in 7 patients. In appropriate circumstances MRS can reduce the need for biopsy, and provide an important guide for clinical decision-making in difficult cases.

Adult↗

PubMed1999

Activation of the JNK pathway is important for cardiomyocyte death in response to simulated ischemia.

Multiple signaling pathways, including the c-Jun N-terminal kinase (JNK) pathway, are activated in myocardial ischemia and reperfusion (MI/R) and correlate with cell death. However, the role of the JNK pathway in MI/R-induced cell death is poorly understood. In a rabbit model, we found that ischemia followed by reperfusion resulted in JNK activation which could be detected in cytosol as well as in mitochondria. To address the functional role of the JNK activation, we examined the consequences of blockade of JNK activation in isolated cardiomyocytes under conditions of simulated ischemia. The JNK activity was stimulated approximately sixfold by simulated ischemia and reperfusion (simulated MI). When a dominant negative mutant of JNK kinase-2 (dnJNKK2), an upstream regulator of JNK, and JNK-interacting protein-1 (JIP-1) were expressed in myocytes by recombinant adenovirus, the activation of JNK by simulated MI was reduced 53%. Furthermore, the TNFalpha-activated JNK activity in H9c2 cells was completely abolished by dnJNKK2 and JIP-1. In correlation, when dnJNKK2 and JIP-1 were expressed in cardiomyocytes, both constructs significantly reduced cell death after simulated MI compared to vector controls. We conclude that activation of the JNK cascade is important for cardiomyocyte death in response to simulated ischemia.

Adenoviridae↗

PubMed1999

A genomic screen of autism: evidence for a multilocus etiology.

We have conducted a genome screen of autism, by linkage analysis in an initial set of 90 multiplex sibships, with parents, containing 97 independent affected sib pairs (ASPs), with follow-up in 49 additional multiplex sibships, containing 50 ASPs. In total, 519 markers were genotyped, including 362 for the initial screen, and an additional 157 were genotyped in the follow-up. As a control, we also included in the analysis unaffected sibs, which provided 51 discordant sib pairs (DSPs) for the initial screen and 29 for the follow-up. In the initial phase of the work, we observed increased identity by descent (IBD) in the ASPs (sharing of 51.6%) compared with the DSPs (sharing of 50.8%). The excess sharing in the ASPs could not be attributed to the effect of a small number of loci but, rather, was due to the modest increase in the entire distribution of IBD. These results are most compatible with a model specifying a large number of loci (perhaps >/=15) and are less compatible with models specifying </=10 loci. The largest LOD score obtained in the initial scan was for a marker on chromosome 1p; this region also showed positive sharing in the replication family set, giving a maximum multipoint LOD score of 2.15 for both sets combined. Thus, there may exist a gene of moderate effect in this region. We had only modestly positive or negative linkage evidence in candidate regions identified in other studies. Our results suggest that positional cloning of susceptibility loci by linkage analysis may be a formidable task and that other approaches may be necessary.

Adolescent↗

PubMed1999

Biochemical analysis of a 5S rRNA-associated sub-particle from trypsinized eukaryotic ribosomes.

On limited trypsinization, eukaryotic ribosomes released sub-particles that comprised a 5S rRNA molecule and two peptides (a 32 kDa and a 14 kDa). By tryptic finger-printing and amino-terminal sequence analysis, these two peptides were determined to be derived from large subunit ribosomal protein L5 (rpL5). The 32 kDa peptide represents the rpL5 protein minus the amino terminal eight residues and the carboxyl terminal ends (approximately 21 residues), whereas the 14 kDa peptide comprised near the amino-terminal region. The time course of ribosome trypsinization revealed that the two peptides were released kinetically. The indicated that the amino and carboxyl terminal ends of rpL5 were the first to be hydrolyzed, suggesting that the two ends of the rpL5 protein were exposed on the surface of ribosomes. Exposure of the carboxyl-terminal end was confirmed by use of an anti-L5c antibody raised against the carboxyl terminal region of rpL5. The kinetic data also revealed that the nearby amino terminal region of rpL5 (represented by the 14 kDa peptide) was the last part of rpL5 to be hydrolyzed, which was considered to be the 5S rRNA binding site.

Animals↗

PubMed1999

Agonist gating and isoflurane potentiation in the human gamma-aminobutyric acid type A receptor determined by the volume of a second transmembrane domain residue.

Gamma-aminobutyric acid type A (GABA(A) )receptors are targets for allosteric modulation by general anesthetics. Mutation of Ser270 within the second transmembrane domain of the GABA(A) receptor alpha subunit can ablate the modulation of the receptor by the anesthetic ether isoflurane. To investigate further the function of this critical amino acid residue, we made multiple amino acid substitutions at Ser270 and analyzed the concentration-dependent gating by GABA and regulation by isoflurane in each mutant receptor. There is a strong negative correlation between the EC(50) for GABA and the molecular volume of the amino acid residue at position 270. Replacement of Ser by large residues such as His and Trp produced a shift of the GABA concentration-response curve to the left, whereas replacement of Ser with Gly had the opposite effect. There also was a strong negative association between the molecular volume of the amino acid residue at 270 and the degree of enhancement of submaximal GABA responses by isoflurane. These results indicate the significance of the amino acid at position alpha270 in gating of the GABA(A) receptor. In addition, the data on isoflurane are consistent with the existence of a cavity of finite size in the region of alpha270 that may be filled by the anesthetic molecule or by the side chain of a larger residue at alpha270. The introduction of isoflurane, or of a large residue, into this cavity may stabilize the open state of the GABA(A) receptor relative to the closed state.

Anesthetics, Inhalation↗

PubMed1999

Immunoendocrine findings in patients with eating disorders.

Immune changes may occur in patients with anorexia nervosa (AN) or bulimia nervosa (BN), and a role for proinflammatory cytokines has been proposed in the pathogenesis of both disorders. We measured plasma levels of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), soluble forms of the cytokine receptor proteins gp130 and leukemia inhibitory factor receptor (LIF-R), the anti-inflammatory Clara cell 16-kD protein (CC16), prolactin (PRL), cortisol and 17beta-estradiol in 21 anorexic women, 21 bulimic women and 21 healthy females. As compared to healthy subjects, anorexics exhibited significantly increased plasma levels of gp130 and LIF-R, whereas bulimics had significantly decreased blood concentrations of CC16. No significant differences emerged in the blood levels of the remaining immune parameters. Both patient groups manifested higher plasma levels of cortisol and reduced plasma concentrations of PRL and 17beta-estradiol. In anorexics, a significant negative correlation was found between plasma levels of gp130 or LIF-R and the body mass index. These findings do not support the hypothesis that proinflammatory cytokines may play a pathogenetic role in eating disorders.

Adult↗

PubMed1999

Changes in platelet alpha-2-adrenoceptors in fibromyalgia: effects of treatment with antidepressants.

The aim of this study was to determine platelet alpha(2)-adrenergic receptor (alpha(2)-AR) binding sites in fibromyalgia both before and after treatment with sertraline or placebo. The maximum number of binding sites (B(max)) and their affinity (K(d)) for [(3)H]rauwolscine, a selective alpha(2)-AR antagonist, were measured in 13 normal volunteers and 22 fibromyalgia patients. Severity of illness was evaluated by means of the Hamilton Depression Rating Scale (HDRS) and dolorimetric assessments of tenderness at tender points. Fibromyalgia patients had repeated measurements of [(3)H]rauwolscine binding characteristics both before and after subchronic treatment with sertraline or placebo for 12 weeks. [(3)H]rauwolscine binding K(d) values were significantly higher in fibromyalgia patients than in normal volunteers. There were significant inverse correlations between [(3)H]rauwolscine binding K(d) values and duration of illness, age and lower energy. Significantly higher [(3)H]rauwolscine binding K(d) values were found in fibromyalgia patients in an early phase of illness (<3 years) than in fibromyalgia patients with a protracted illness (>3 years). Repeated administration of sertraline had no significant effects on [(3)H]rauwolscine binding B(max) or K(d) values. The results suggest that fibromyalgia and, in particular, fibromyalgia in an early phase of illness, is accompanied by lowered affinity of platelet alpha(2)-ARs.

Adrenergic alpha-Antagonists↗

PubMed1999

Asialo GM1(+) CD8(+) T cells play a critical role in costimulation blockade-resistant allograft rejection.

Simultaneous blockade of the CD40 and CD28 costimulatory pathways is an effective treatment strategy to promote allograft acceptance but does not lead to indefinite allograft survival. The immune mechanisms responsible for costimulation-independent rejection are not defined. Here we have studied the rejection responses of murine C57BL/6 recipients, which we show to be relatively resistant to inhibition by combined CD40/CD28 blockade. We demonstrate that asialo GM1(+) CD8(+) cells play a critical role in this costimulation blockade-resistant rejection. These results provide new insights into the costimulatory requirements for T-cell subsets and demonstrate for the first time that combined blockade of the CD40 and CD28 pathways does not adequately inhibit CD8-mediated skin allograft rejection. Furthermore, we provide evidence that asialo GM1 is a potentially important therapeutic target for CD8-dependent immune responses.

Animals↗

PubMed1999

Insulin aspart (B28 asp-insulin): a fast-acting analog of human insulin: absorption kinetics and action profile compared with regular human insulin in healthy nondiabetic subjects.

OBJECTIVE: To study the pharmacokinetic and pharmacodynamic profile of insulin aspart (a new fast-acting human insulin analog) after subcutaneous administration in the deltoid, abdominal, and thigh sites and to compare this profile with regular human insulin (Novolin; Novo Nordisk A/S, Copenhagen). RESEARCH DESIGN AND METHODS: A total of 20 healthy subjects were studied in a single-center six-period double-blind randomized crossover trial with 6 study days and a washout period of 1 week between each single daily dose of the trial drug. Subjects were randomized to receive a single dose of 0.2 U/kg of insulin aspart or regular insulin on each of the 6 study days in three different sites (the deltoid, the abdomen, and the thigh) during a 10-h euglycemic clamp (two drugs and three injection sites). Pharmacokinetic and pharmacodynamic measurements were derived from blood sample measurements of glucose, insulin, and C-peptide during these clamps. RESULTS: The pharmacodynamic data from the euglycemic clamp study showed that, regardless of injection site, the maximal glucose infusion rate (GIR Cmax) was greater and occurred at an earlier time (GIR Tmax) after administration of insulin aspart than regular insulin (GIR Cmax: abdomen 813 vs. 708, deltoid 861 vs. 736, and thigh 857 vs. 720 g/min, P < 0.05 for all; GIR Tmax: abdomen 94 vs. 173, deltoid 111 vs. 192, and thigh 145 vs. 193 g/min, P < 0.05 for all). Pharmacokinetic parameters were also consistent with faster absorption and higher peak insulin concentrations after insulin aspart administration. From all sites, the peak insulin concentration (Cmax) was higher and occurred earlier (Tmax) after administration of insulin aspart than of regular insulin (Cmax: abdomen 501 vs. 260, deltoid 506 vs. 252, thigh 422 vs. 220 pmol/l, P < 0.001 for all sites; Tmax: abdomen 52 vs. 109, deltoid 54 vs. 98, and thigh 60 vs. 107 min, P < 0.01 for all sites). The absorption and glucose-lowering action of insulin aspart did not differ between sites (similar GIR Cmax, Tmax, and area under the curve parameters). However, the duration of the glucose-lowering effect was up to 34 min shorter (P < 0.01) for the abdomen injections than for the deltoid or thigh injections (lower time of 50% glucose disposal). In addition, the amount of glucose infused was significantly lower by 10-14% in the abdomen than in other sites. CONCLUSIONS: Subcutaneous administration of insulin aspart causes a more rapid and intense maximal effect compared with regular insulin during euglycemic clamp studies in nondiabetic subjects. Abdominal administration of insulin aspart has a shorter duration of glucose-lowering effect compared with administration in the deltoid or thigh.

Absorption↗

PubMed1999

Lack of elevated MAP kinase (Erk) activity in pancreatic carcinomas despite oncogenic K-ras expression.

Activating mutations within the K-ras gene have been found in up to 90% of pancreatic carcinomas. Although multiple Ras effector pathways have been identified, the Raf protein kinases which are upstream regulators of the mitogen-activated protein kinases (MAPK/Erk) are believed to be the primary mitogenic effectors. Constitutive upregulation of this pathway by oncogenic ras is thought to promote cellular transformation. To explore the biological effects of mutated K-ras, we analyzed the Ras signaling pathway in a panel of cell lines derived from human pancreatic carcinomas. We found that despite high levels of Ras-GTP in each cell line expressing mutant K-ras, elevated levels of active Erk1 and Erk2 were not detectable under conditions of exponential growth or serum-starvation. Depending upon the cell line, the block in Erk signaling was observed to occur at either the level of Raf or Erk. Increased levels of active Erk1 and Erk2 were detected in only 2 out of 10 normal tissue-matched primary pancreatic tumors with mutated K-ras. Our results suggest that Erk signaling is not aberrantly upregulated in pancreatic cancers containing oncogenic K-ras mutations. The lack of Erk activation observed in both cell lines and primary tumor tissue suggests that constitutive Erk activation may not be required for tumor maintenance or progression in K-ras transformed pancreatic cells. We hypothesize that other Ras-dependent signaling pathways or an unidentified Raf/Mek-dependent pathway may be important for carcinogenesis in the pancreas. These findings may have important implications for drug treatment strategies which currently target the MAP kinase branch of the Ras signaling pathway.

Calcium-Calmodulin-Dependent Protein Kinases↗

PubMed1999

Clustering and the design of preference-assessment surveys in healthcare.

OBJECTIVE: To show cluster analysis as a potentially useful tool in defining common outcomes empirically and in facilitating the assessment of preferences for health states. DATA SOURCES: A survey of 224 patients with ventricular arrhythmias treated at Kaiser Permanente of Northern California. STUDY DESIGN/METHODS: Physical functioning was measured using the Duke Activity Status Index (DASI), and mental status and vitality using the Medical Outcomes Study Short Form-36 items (SF-36). A "k-means" clustering algorithm was used to identify prototypical health states, in which patients in the same cluster shared similar responses to items in the survey. PRINCIPAL FINDINGS: The clustering algorithm yielded four prototypical health states. Cluster 1 (21 percent of patients) was characterized by high scores on physical functioning, vitality, and mental health. Cluster 2 (33 percent of patients) had low physical function but high scores on vitality and mental health. Cluster 3 (29 percent of patients) had low physical function and low vitality but preserved mental health. Cluster 4 (17 percent of patients) had low scores on all scales. These clusters served as the basis of written descriptions of the health states. CONCLUSIONS: Employing a clustering algorithm to analyze health status survey data enables researchers to gain a data-driven, concise summary of the experiences of patients.

Adult↗

PubMed1999

[Low level of residual renal function in the initial month and high transport characteristic as important causes of peritoneal dialysis failure].

OBJECTIVE: To evaluate what kind of patients was at high risk on peritoneal dialysis (PD) treatment. METHODS: 96 patients on PD for (23.1 +/- 10.0) months were studied. The patients were divided into two groups. Group A: patients (25) who died or switched to hemodialysis because of cardiovascular disease, malnutrition, ultrafiltration inefficiency, hydrothora, relapsing peritonitis, etc. Group B: stable PD patients (71) up to now. Age, body surface area (BSA) and dialysate fill volume (DV) were not different between the two groups. The nutritional status, dialysis adequacy, peritoneal membrane transport characteristics, and residual renal function (RRF) in the initial month of dialysis were compared. Patient survival rate was studied by Kaplan-Meier method. RESULTS: It was demonstrated that Kt/V and Ccr in group A were lower than those in group B (P < 0.05). Meanwhile, RRF was significantly different between the two groups; patients with better RRF (> or = 2 ml/min) had higher survival. The percentage of high transporters in group A was greater than in group B. CONCLUSION: Higher clearance in the initial month of dialysis seems to keep PD successful. PD failure maybe related to high transport characteristic and its treatment modality is DAPD. Hemodialysis will be a better choice when RRF is very low as water balance is poorly controlled by DAPD.

Adolescent↗

PubMed1999

[The protective effect against Toxoplasma infection in mice immunized with laser-irradiated Toxoplasma tachyzoites].

AIM: To observe the level of immune responses and protective immunity in mice induced by laser-irradiated Toxoplasma tachyzoites (LIT). METHODS: ICR mice were immunized with LIT. After one month, the mice were challenged with live Toxoplasma tachyzoites to observe the effect of LIT. Indirect immunofluorescence assay and ELISA were used to detect CD4+/CD8+ lymphocyte subpopulation and IgG antibody. RESULTS: Immunization with LIT could partially protect the mice from Toxoplasma infection, prolong the survival time, enhance the CD4+/CD8+ ratio and produce specific IgG antibody. CONCLUSION: Intraperitoneal injection with LIT can induce partial protective immunity and specifically elicit ICR mice to generate humoral and cell-mediated immune responses.

Animals↗

PubMed1998

Clinical and molecular aspects of the Simpson-Golabi-Behmel syndrome.

The Simpson-Golabi-Behmel syndrome (SGBS) is an overgrowth/multiple congenital anomalies/dysplasia syndrome caused by a mutant X-linked gene. The spectrum of its clinical manifestations is broad, varying from very mild forms in carrier females to infantile lethal forms in affected males. A typically affected male will show tall stature, "coarse" face, supernumerary nipples, congenital heart defect, and generalized muscular hypotonia. Mental development is normal in most cases. There is an increased risk of neoplasia in infancy, especially Wilms tumor. The SGBS gene spans 500 kilobases in the Xq26 region and contains eight exons. It encodes an extracellular proteoglycan, designated glypican 3 (GPC3), capable of interacting with the insulin-like growth factor IGF2. At present, only deletions of various sizes have been found in a number of affected families.

Abnormalities, Multiple↗

PubMed1998

Induction of apoptosis by SB202190 through inhibition of p38beta mitogen-activated protein kinase.

p38, a subfamily of the mitogen-activated protein kinase, regulates gene expression in response to various extracellular stimuli. The pyridinyl imidazoles like SB202190 are specific inhibitors of p38alpha and p38beta and have been widely used in investigation of the biological functions of p38. Here we show that SB202190 by itself was sufficient to induce cell death, with typical apoptotic features such as nucleus condensation and intranucleosomal DNA fragmentation. SB202190 stimulated the activity of CPP32-like caspases, and its apoptotic effect was completely blocked by the protease inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone and expression of bcl-2. In addition, SB202190 was able to potentiate apoptosis induced by Fas(APO-1) ligation or UV irradiation. Expression of p38beta attenuated the apoptotic effect of SB202190 and the cell death induced by Fas ligation and UV irradiation. In contrast, expression of p38alpha induced cell death mildly. These results indicate that SB202190 induces apoptosis through activation of CPP32-like caspases and suggest that distinct members of the p38 subfamily of mitogen-activated protein kinase have different functions in apoptosis.

Apoptosis↗

PubMed1998

The inflammatory response system in treatment-resistant schizophrenia: increased serum interleukin-6.

There is some evidence that the pathophysiology of schizophrenia is related to activation of the inflammatory response system (IRS), as indicated by increased serum concentrations of interleukin-6 (IL-6), IL-6 receptor (IL-6R), IL-1R antagonist (IL-1RA) and IL-2R and lower serum concentrations of CC16, an endogenous anti-inflammatory protein with immunosuppressive and anti-inflammatory effects. The aims of the present study were to examine serum CC16 in relation to IL-6, IL-6R and gp130, the IL-6 transducing signal protein, in schizophrenia and in treatment-resistant schizophrenia (TRS). Serum IL-6 and sIL-6R were significantly higher in medicated schizophrenic patients than in normal controls. Serum IL-6 was significantly higher in TRS than in normal volunteers, whereas schizophrenic patients without TRS showed intermediate values. Serum CC16 was significantly lower in schizophrenic patients with a positive family history for psychoses than in normal volunteers and patients without a positive family history. There was a significant inverse relationship between serum CC16 and serum IL-6 or sIL-6R in schizophrenic patients, but not in normal volunteers. The results suggest that the inflammatory response in schizophrenia, as indicated by increased serum IL-6 and sIL-6R, may be causally related to lower serum CC16 and that the latter might be a trait marker for schizophrenia.

Adult↗

PubMed1998

Caveolin-mediated regulation of signaling along the p42/44 MAP kinase cascade in vivo. A role for the caveolin-scaffolding domain.

The p42/44 mitogen-activated protein (MAP)-kinase cascade is a well-established signal transduction pathway that is initiated at the cell surface and terminates within the nucleus. More specifically, receptor tyrosine kinases can indirectly activate Raf, which in turn leads to activation of MEK and ERK and ultimately phosphorylation of Elk, a nuclear transcription factor. Recent reports have suggested that some members of p42/44 MAP kinase cascade can be sequestered within plasmalemmal caveolae in vivo. For example, morphological studies have directly shown that ERK-1/2 is concentrated in plasma membrane caveolae in vivo using immunoelectron microscopy. In addition, constitutive activation of the p42/44 MAP kinase cascade is sufficient to reversibly down-regulate caveolin-1 mRNA and protein expression. However, the functional relationship between the p42/44 MAP kinase cascade and caveolins remains unknown. Here, we examine the in vivo role of caveolins in regulating signaling along the MAP kinase cascade. We find that co-expression with caveolin 1 dramatically inhibits signaling from EGF-R, Raf, MEK-1 and ERK-2 to the nucleus. Using a variety of caveolin-1 deletion mutants, we mapped this in vivo inhibitory activity to caveolin-1 residues 32-95. Peptides derived from this region of caveolin 1 also inhibit the in vitro kinase activity of purified MEK-1 and ERK-2. Thus, we show here that caveolin-1 expression can inhibit signal transduction from the p42/44 MAP kinase cascade both in vitro and in vivo. Taken together with previous data, our results also suggest that a novel form of reciprocal negative regulation exists between p42/44 MAP kinase activation and caveolin-1 protein expression, i.e. up-regulation of caveolin-1 protein expression down-modulates p42/44 MAP kinase activity (this report) and up-regulation of p42/44 MAP kinase activity down-regulates caveolin-1 mRNA and protein expression.

Animals↗

PubMed1998

Serotonin-immune interactions in detoxified chronic alcoholic patients without apparent liver disease: activation of the inflammatory response system and lower plasma total tryptophan.

The aims of the present study were to examine (1) the inflammatory response system (IRS), through measurements of serum interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), sgp130 (the soluble form of the IL-6 transducer signal protein), CC16 (Clara Cell protein; an endogenous anti-cytokine), IL-1R antagonist (IL-1RA), IL-8 and sCD14; and (2) the availability of plasma total tryptophan to the brain in chronic alcoholic patients without apparent liver disease (AWLD). Detoxified AWLD patients had significantly lower plasma tryptophan and serum CC16 and significantly higher serum IL-1RA and IL-8 concentrations than normal volunteers. There were significant correlations between the availability of tryptophan to the brain and serum IL-6, IL-8 and IL-1RA (all negative) and CC16 (positive). The results suggest that (1) there is, in detoxified AWLD patients, an activation of the monocytic arm of cell-mediated immunity and a lowered anti-inflammatory capacity of the serum; and that (2) lower availability of plasma tryptophan to the brain in detoxified AWLD patients is related to activation of the IRS. Lower CC16 may be one factor predisposing chronic alcoholic patients toward infectious disorders.

Adult↗