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Electron spin resonance studies of nitrosyl haemoglobin in human liver, colon and stomach tumour tissues.

Iron nitrosyl haemoglobin (HbFeNO) gives well defined ESR spectra, and can be detected at room temperature, in contrast with most transition metal complexes of biological importance. This is because the unpaired electron remains strongly localised on the NO ligand. It is of importance because it proves the formation of nitric oxide, which unfortunately cannot be detected directly by ESR spectroscopy. We have studied a range of tissues taken from human liver, colon and stomach tumours which have been directly frozen to 77K and studied at 77K. The results show that formation of HbFeNO is rare in tissue adjacent to tumour tissue ("peripheral tissue"), but is always found in necrotic central regions, if present. However, in several cases, HbFeNO was also detected in tumour tissue which was not necrotic. Two factors contribute to the formation of this complex. One is the presence of "free" NO molecules in the cellular regions, and the other is the presence of deoxyferrohaemoglobin, since neither ferrihaemoglobin nor oxyhaemoglobin react to give this complex. [For systems containing myoglobin these comments include the possibility of the formation of nitrosylmyoglobin, which gives very similar ESR spectra.

Adenocarcinoma↗

[Ionic channels and second messenger alterations in Alzheimer's disease. Relevance of studies in nonneuronal cells].

INTRODUCTION: Numerous observations indicate that, while the predominant clinical expression arises from brain pathology, Alzheimer s disease (AD) has systemic expression at the cellular and molecular levels. Although these alterations seem to be inconsequential outside the central nervous system, their parallel expression in the brain could be considered a plausible pathophysiological model and explain part of the clinical manifestations; in particular those related to memory loss. DEVELOPMENT: Recent research has provided experimental evidence of a direct or indirect linkage between alteration in ion channels, PKC, calcium homeostasis and amyloid processing in peripheral tissues. Some evidence also indicates similar phenomena in the brain, attesting to the relevance of the changes in non CNS cells. CONCLUSION: Considering the difficulties of using post mortem material to study dynamic and/or early event in mostly end stage, disease ridden tissues, peripheral cells such as fibroblasts offer a model to study cellular aspects of AD pathophysiology.

Alzheimer Disease↗

Intermingling of central and peripheral nervous tissues in rat dorsolateral vagal rootlet transitional zones.

The morphology of the CNS-PNS transitional zone of adult rat dorsolateral vagus nerve rootlets is uniquely complex. A typical rootlet contains a transitional zone over 300 microns long, consisting of a central tissue projection extending distally into each rootlet and a peripheral tissue insertion extending for a longer distance deep into the brainstem. The peripheral tissue insertion is continuous with the peripheral tissue of the free rootlet through channels traversing or running parallel to the central tissue projection. Accordingly, the vagal CNS-PNS interface is topologically much more complex than that found elsewhere. In some rootlets the peripheral tissue in the brainstem constitutes an isolated island deep within the neuraxis. In others, peripheral continuity is established only through a cross connection with the peripheral tissue insertion of a neighbouring rootlet. About one fifth of all vagal myelinated axons alternate between the CNS and PNS tissue compartments. This distinguishes the vagus from all other nerves studied to date. These axons are myelinated by Schwann cells distal to the transitional zone, by oligodendrocytes in the central tissue projection and by one or more short intercalated Schwann internodes further centrally, mostly in the peripheral tissue insertion, where their perikarya commonly form closely apposed aggregates. More than four fifths of all unmyelinated axon bundles alternate between central and peripheral tissue compartments, commonly more than once. In the peripheral tissue insertion axons are enveloped by series of non-myelinating Schwann cells. Schwann processes commonly extend for over 50 microns into the central compartment at each central-peripheral transition. Around one fifth of peripherally unmyelinated axons have an oligodendrocytic sheath in the central compartment. Of these axons possessing more than one intercalated Schwann internode, over one quarter display alternation of myelinated and unmyelinated segments in the peripheral tissue insertion. Astrocytes in the transitional zone segregate PNS tissue, a role played by sheath cells further peripherally in the vagal rootlets. Astrocytes form the surface limiting membranes of the central tissue projection and the barrier between the peripheral tissue insertion and the surrounding brainstem. The barrier consists only of an attenuated layer of processes. This is deficient in places, where oligodendrocytic myelin sheaths are directly exposed to the endoneurial space of the peripheral tissue insertion and in some instances are apposed to myelinating or non-myelinating Schwann cells. Such communication between the central and peripheral compartments is unique to the vagal transitional zone. The findings are consistent with a range of possible events during development.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Differential expression of basement membrane components in lymphatic tissues.

Peripheral lymphoid tissues act as important organs of immunological defense. Characteristic of their architecture is the rich reticular fiber meshwork composed of various extracellular matrix (ECM) molecules with which the stationary non-lymphatic cells stay in intimate contact and form channels through which the lymphatic cells travel. Here we studied the distribution of various laminin (Ln) chains and different types of collagens in human spleen, lymph node, and tonsil to clarify their chain-specific distribution. The most widely distributed proteins in all these organs were Ln chains alpha5, beta1, gamma1 and collagen types IV and XVIII, which were present in practically all compartments. Conversely, Ln alpha1, alpha2, alpha4, and type VII collagen showed a more restricted expression pattern. A unique feature was that Ln alpha3-, beta3-, and gamma2-chains, which normally are not localized to the vascular wall in non-lymphatic tissues, were present also in capillary basement membranes (BMs) of the follicular structures of lymph node and tonsil and in Ln alpha1-chain and type VII collagen also in the splenic white pulp. We also found that collagen XVII was exclusively present in the ring fibers of the spleen. The results indicate that BMs of lymphatic tissues contain a variety of macromolecules that probably contribute strongly to immunological events. In addition, capillaries of the lymphoid tissue exhibit a specified BM composition resembling that in epithelial BMs of non-lymphoid tissues.

Basement Membrane↗

The conversion of thyroxine to triiodothyronine in the lung: comparison of activity of type I iodothyronine 5' deiodinase in lung cancer with peripheral lung tissues.

UNLABELLED: Triiodothyronine (T3) is the main active hormone, which is derived 20% from the thyroid gland and 80% from peripheral tissues. Thyroxin--5' deiodinases play a leading role in maintaining appropriate T3 concentrations in the different cells and organs: including the lung. The deiodinases present in pneumocytes were found to be localised in endoplasmatic reticulum. Aims of this study were: 1. To estimate activities of Type I and Type II iodothyronine 5' deiodinases (DI, DII) in two histological types of lung cancer. 2. To investigate possible differences in DI and DII activities between tumour tissue and peripheral lung tissue. 3. To study whether DI and DII activities are related to the extent of the disease process and grade of differentiation of lung cancer. MATERIAL: We studied 44 patients undergoing thoracotomy due to lung cancer. Histologically: 23 pts--squamous cell cancer, 21 pts adenocarcinoma. In all patients both tumour and peripheral lung tissue were studied. DI activity was measured in pmol 1251- released from 125 IrT3/min/mg of proteins, DII activity--in fmol 125I- released from 125IT4/hour/mg of protein. RESULTS: In most specimens DI and DII activities were observed. DI activity in specimens from lung peripheral tissue was: 3.3-58.3 pmol/min/mg of protein (mean 22.20) and in lung cancer tissue was: 2.0-44.7 pmol/min/mg of proteins (mean 13.3). DII activity in lung peripheral tissue ranged from 19 to 242 fmol/h/mg protein (mean 94.4) and in lung cancer ranged from 21 to 253 fmol/h/mg protein (mean 107.9). CONCLUSIONS: 1. Conversion of T4 to T3 occurs also in the lung. 2. The activity of DI is statistically significantly lower, in lung cancer than in peripheral lung tissue (13.3 +/- 9.5 vs 22.20 +/- 13.4 pmol/min/mg protein) respectively, p < 0.001. 3. DII activity in lung is present and similar in peripheral lung and lung cancer tissue. 4. There is a non-significant trend for correlation of DI activity and grade of differentiation (G1-G3) of tumour tissue and stage of lung cancer. Abbreviations' list: T3--triiodothyronine, T4--thyroxine, FT4--free thyroxine, rT3--revers triiodothyronine TSII--Thyroid Stimulating Hormone Type I lodothyronine 5'deiodinase = type I 5'deiodinase = 5'DI = DI Type II Iodothyronine 5'deiodinase = typeII 5'deiodinase = 5'DII = DII E.S.S.--Euthyroid Sick Syndrome, hDII = human type II iodothyronine deiodinase HDII-b, hDII-c = two novel splice variants SCC--Squamous Cell Cancer, A--adenocarcinoma, BMI--Body Mass Index BSA--Bovine Standard Albumin, DTT-1,4 Dithio-L-treitol, PTU--Propylothiouracil TCA--Tricholoroacetic Acid, TNM--Tumour Nodule Metastases (class.) G1-G3-grade of differentiation, COPD--Chronic Obstructive Pulmonary Disease.

Adenocarcinoma↗

Functional recovery in chronic paraplegic rats after co-grafts of fetal brain and adult peripheral nerve tissue.

BACKGROUND: In recent years, experimental studies have sought some type of functional improvement in traumatic paraplegia by transplanting neural tissue into the injured spinal cord. The aim of this work is to study the possibility of functional recovery in chronic paraplegic rats after co-transplantation of fetal cerebral tissue and adult peripheral nerve tissue. METHODS: Seventy adult female Wistar rats were subjected to spinal cord injury at the T6-T8 level, causing complete paraplegia. Three months later, in 50 rats (grafted group) the injured spinal cord tissue received a graft of fetal brain cortex associated with crushed adult peripheral nerve. All the animals (grafted and control groups) were subjected to daily rehabilitation procedures from the first week after the injury, and evaluated weekly for motor and sensory recovery. Statistical analysis of different behavioral data between control and grafted animals was performed using the Kruskal-Wallis ANOVA and the nonparametric Wilcoxon test. RESULTS: Between 8 and 12 months after transplantation, progressive signs of functional recovery were observed in the grafted animals, associated with an increase in muscle mass in the lower extremities, findings that were significantly different from those in nongrafted animals (p < 0.05). At this time, donor cerebral tissue is integrated into previously injured spinal cord and results in formation of bundles of nerve fibers that emerge from the area of the transplant and surround the spinal cord beneath the lesion. CONCLUSIONS: Delayed co-transplantation of fetal cerebral tissue and peripheral nerve tissue can be used to achieve anatomical remodeling and long-term functional recovery in rats rendered paraplegic as result of severe spinal cord injury. These findings support the possibility of functional recovery after chronic traumatic paraplegia.

Analysis of Variance↗

Peripheral and liver tissue oxygen tensions in hemorrhagic shock.

BACKGROUND AND METHODS: Hepatic dysfunction after severe hemorrhagic shock is common and may be a consequence of visceral tissue hypoxia. Peripheral tissue PO2 has been suggested to correlate with the development of visceral hypoxia. To test the hypothesis that changes in peripheral tissue PO2 reflect changes in hepatic PO2, we measured subcutaneous PO2, transcutaneous PO2, transconjunctival PO2, and liver tissue PO2, and their relationship with changes in mean arterial blood pressure (MAP) and systemic oxygen transport (DO2), during progressive bleeding in pigs (n = 23). In addition to the tissue PO2, portal vein PO2 and circulating lactate concentrations were also measured in six of the animals. The animals were anesthetized and bled to an MAP of 50 mm Hg within 1 hr. RESULTS: After an induced 10% reduction of MAP, only the DO2 decreased significantly (p less than .05). After a 20% reduction of MAP, the DO2 decreased further and was associated with a significant (p less than .05) reduction of all peripheral tissue PO2 values. A significant (p less than .05) reduction of liver tissue PO2 was observed later during bleeding, after induction of a 30% reduction in MAP. In the subgroup with portal venous PO2 and lactate measurements, reductions of all peripheral tissue PO2 and portal venous PO2 values occurred after a 20% reduction (p less than .05) of MAP. An increase (p less than .05) in the portal venous lactate concentration was observed after a 50% reduction of MAP, and a decrease (p less than .05) in liver tissue PO2 was noted after a 60% reduction of MAP. CONCLUSIONS: Reductions of both peripheral and portal venous PO2 values occur early during hemorrhage. The liver tissue PO2, though initially low, appears to be better defended, suggesting either redistribution of splanchnic blood flow or adaptation in hepatic oxygen demand.

Animals↗

Adenoviral vector-mediated expression of a foreign gene in peripheral nerve tissue bridges implanted in the injured peripheral and central nervous system.

Axons of the CNS do normally not regenerate after injury, in contrast to axons of the PNS. This is due to a different microenvironment at the site of the lesion as well as a particular intrinsic program of axonal regrowth. Although transplantation of peripheral nerve tissue bridges is perhaps the most successful approach to promoting regeneration in the CNS, ingrowth of CNS nerve fibers with such transplants is limited. Genetic modification of peripheral nerve bridges to overexpress outgrowth-promoting proteins should, in principle, improve the permissive properties of peripheral nerve transplants. The present study shows that pieces of peripheral intercostal nerve, subjected to ex vivo adenoviral vector-mediated gene transfer and implanted as nerve bridges in transected sciatic nerve, avulsed ventral root, hemi-sected spinal cord and intact brain, are capable of expressing a foreign gene. In vitro studies showed expression of the reporter gene LacZ up to 30 days in Schwann cells. After implantation, LacZ expression could be detected at 7 days postimplantation, but had virtually disappeared at 14 days. Schwann cells of the transduced nerve bridges retained the capacity of guiding regenerative peripheral and central nerve fiber ingrowth. Transduction of intercostal nerve pieces prior to implantation should, in principle, enable enhanced local production of neurotrophic factors within the transplant and has the potential to improve the regeneration of injured axons into the graft.

Adenoviridae↗

An aromatase-associated cytoplasmic inclusion, the "stigmoid body," in the rat brain: II. Ultrastructure (with a review of its history and nomenclature).

The ultrastructure of aromatase-associated "stigmoid (dot-like) structures," which were detected in a previous study using light-microscopic immunohistochemistry (Shinoda et al.: J. Comp. Neurol. 322:360-376, '92), were examined in the rat medial preoptic region, bed nucleus of the stria terminalis, medial amygdaloid nucleus, and arcuate nucleus by pre- and post-embedding marking with a polyclonal antibody against human placental antigen X-P2 (hPAX-P2) for immuno-electron microscopic analysis. The immunoreactive stigmoid structure was identified as a distinct, non-membrane-bounded cytoplasmic inclusion (approximately 1-3 microns in diameter), which has a granulo-fuzzy texture with moderate-to-low electron density in non-immunostained preparations. It consists of at least four distinct granular and three distinct fibrillo-tubular elements forming a granulo-fibrillar conglomerate. This type of inclusions was formally termed the "stigmoid body" under the electron microscope. The stigmoid body is composed of the outer granulo-fibrillar and inner hyaloplasmic compartments. The immunoreactivity for hPAX-P2 is mainly localized to the former, especially to the low density granulo-fuzzy materials associated with the fibrillo-tubular elements. Identification of the ultrastructure of stigmoid body clarified their prevalence not only in the limbic and hypothalamic regions, but also in sex-steroid-sensitive peripheral tissues (e.g., peripheral sensory ganglia, ovary, testis) by consulting earlier electron-microscopic studies. Reviewing the history and nomenclature of this inclusion body, we reorganized the terminology of related neuronal cytoplasmic inclusions, the terms of which have often been confused, and discussed its functional significance on the basis of the present and previously accumulated data. In conclusion, we emphasized the importance of the stigmoid bodies in the sex-steroid-sensitive neural system because of their large size, high frequency, specific distribution in brains and peripheral tissues, effects of sex-steroids, and immunological and histochemical characteristics of the antibody marking the inclusion. The stigmoid bodies may provide a subcellular site for sex-steroid metabolism in their target tissues and play a critical role in cytosolic modulation of their actions (e.g., by aromatization) prior to their receptor binding.

Amygdala↗

Identification of the prolactin-releasing peptide-producing cell in the rat adrenal gland.

Prolactin-releasing peptide (PrRP) is a novel peptide found in bovine hypothalamus as an endogenous ligand of an orphan G-protein-coupled receptor (hGR3). It is known that PrRP is widely distributed and plays roles in the central nervous system (CNS). In particular, PrRP acts as a neurotransmitter that mediates stress and activates the hypothalamo-pituitary-adrenal axis. On the other hand, only a few studies have so far been performed on PrRP in peripheral tissues. Among peripheral tissues, appreciable levels of PrRP are found only in the adrenal gland; however, the PrRP-producing cells in the adrenal gland have not been identified. In this study, we detected PrRP mRNA in the rat adrenal medulla. So, we tried to identify the PrRP-producing cells in primary culture cells of the adrenal medulla. We found immunopositive PrRP cells among the cultured cells from the adrenal gland, but not in the adrenal gland tissue, by means of immunocytochemistry. The PrRP immunopositive cells were double positive for tyrosine hydroxylase (TH) and for phenylethanolamine N-methyltransferase (PNMT), which indicates that PrRP may be produced in a part of the adrenaline cells in the adrenal gland. This is the first report that PrRP is produced in the adrenaline-containing cells of the adrenal gland.

Adrenal Medulla↗

Heterogeneity of macrophage populations in human lymphoid tissue and peripheral blood.

Human lymphoid tissue and peripheral blood leukocytes were stained with six monoclonal antibodies directed against monocyte/macrophage populations. The staining pattern described by each of these monoclonal reagents was compared with the distribution of morphologically distinguishable tissue macrophages. The results show that there exists considerable heterogeneity of tissue macrophages based on the expression of surface and/or cytoplasmic antigens; furthermore, the distribution of cells bearing particular antigenic determinants is associated with distinct regions in normal lymphoid tissue. Double staining methods demonstrated that these antibodies bind to different, as well as to identical, macrophage populations. OKM-1 antibody binds predominantly to sinus histiocytes and tingible body macrophages. The Leu M-1 reagent stains interdigitating reticulum cells, while the KiM-4 antibody labels follicular dendritic cells. Leu M-3 antibody identifies cells predominantly in the germinal center, and histiocytes lining the sinuses. Both CM-1 and BRL-M.1 appear to stain tissue macrophages distributed throughout the lymphoid tissue.

Antibodies, Monoclonal↗

Rhythmic messenger ribonucleic acid expression of clock genes and adipocytokines in mouse visceral adipose tissue.

Various peripheral tissues show circadian rhythmicity, which is generated at the cellular level by their own core oscillators that are composed of transcriptional/translational feedback loops involving a set of clock genes. Although the circulating levels of some adipocytokines, i.e. bioactive substances secreted by adipocytes, are on a 24-h rhythmic cycle, it remains to be elucidated whether the clock gene system works in adipose tissue. To address this issue, we investigated the daily mRNA expression profiles of the clock genes and adipocytokines in mouse perigonadal adipose tissues. In C57BL/6J mice, all transcript levels of the clock genes (Bmal1, Per1, Per2, Cry1, Cry2, and Dbp) and adipocytokines (adiponectin, resistin, and visfatin) clearly showed 24-h rhythms. On the other hand, the rhythmic expression of these genes was mildly attenuated in obese KK mice and greatly attenuated in more obese, diabetic KK-A(y) mice. Obese diabetes also diminished the rhythmic expression of the clock genes in the liver. Interestingly, a 2-wk treatment of KK and KK-A(y) mice with pioglitazone impaired the 24-h rhythmicity of the mRNA expression of the clock genes and adipocytokines despite the antidiabetic effect of the drug. In contrast, pioglitazone improved the attenuated rhythmicity in the liver. These findings suggest that the intracellular clock gene system acts in visceral adipose tissues as well as liver and is influenced by the conditions of obesity/type 2 diabetes and pioglitazone treatment.

Adipocytes↗

Assessment of the effectiveness of peripheral administration of fentanyl with lidocaine in inflamed dentoalveolar tissues.

Peripheral action of opioids for pain control, for which local inflammation has been shown to be crucial, is being increasingly used in clinical practice. The aim of this study was to evaluate the hypothesis that addition of fentanyl to lidocaine, when injected into inflamed dentoalveolar tissues, can improve the quality of analgesia during surgery. Seventy-one patients reporting with pain and tenderness in the maxillary tooth were assigned into the experimental (LAF) or control (LA) group in a prospective, randomized double-blind trial. The LAF group (n = 36) was injected submucosally with a mixture of 40 microg of fentanyl (0.8 ml) and 2% lidocaine hydrochloride with 1:200000 adrenaline (2 ml). In the LA group (n = 35) 0.9% of saline (0.8 ml) was added instead of fentanyl. The pain scores were recorded before injecting, 5 min after injection, and immediately after surgery using a visual analogue scale. The mean pain scores were not significantly different at all time intervals. Twelve patients in the LAF group (2.75+/-0.72 ml) and ten patients in the LA (2.90+/-0.70 ml) group required additional local anaesthetic to achieve pain control. In conclusion, there was no improvement in quality of intraoperative analgesia on addition of fentanyl to lidocaine in inflamed dentoalveolar tissues.

Administration, Oral↗

Neuropathic pain in rats is associated with altered nitric oxide synthase activity in neural tissue.

Peripheral nerve injury may lead to a chronic neuropathic pain state that results from an increase in excitability of central neurons. This central sensitization is mediated via an N-methyl-D-aspartic acid (NMDA) receptor and may involve the production of nitric oxide (NO). As NO is suggested to play a role in nociceptive transmission following nerve injury, we examined for altered NO synthase activity at multiple levels of peripheral and spinal neural tissue in a rat model of neuropathic pain. Peripheral neuropathy was induced in rats (N = 12) by ligation of the left L5 and L6 nerve roots. Six other rats had sham surgery. An ipsilateral decrease in paw withdrawal threshold to mechanical stimuli confirmed the presence of a neuropathic pain state. Samples of the lumbar and thoracic spinal cords, L4, L5, and L6 dorsal root ganglia (DRGs), and the sciatic nerves were obtained from the lesioned and contralateral sides at 2 and 4 weeks after neuropathic surgery (N = 6 per group). In the lumbar spinal cord, a bilateral decrease in nitric oxide synthase (NOS) activity was observed 2 and 4 weeks after neuropathic surgery. NOS activity was increased in the ipsilateral L5 and 6 DRGs 2 weeks following neuropathic surgery. An increase in NOS activity in the DRG may be an early mechanism for inducing more central changes. The bilaterally decreased NOS activity in the lumbar spinal cord may be secondary to a negative feedback mechanism resulting from increased NO production in the spinal dorsal root ganglia. Multiple alterations in expression of NOS activity that occur in both peripheral and central processing may play a role in the pain behavior resulting from peripheral nerve injury. (Preliminary results of these studies have been presented in abstract form at the annual meetings of the Society for Neuroscience, 1994, and the American Society of Anesthesiologists, 1994).

Analysis of Variance↗

Relative V beta transcript levels in thymus and peripheral lymphoid tissues from various mouse strains. Inverse correlation of I-E and Mls expression with relative abundance of several V beta transcripts in peripheral lymphoid tissues.

We have measured the relative levels of transcripts for 15 of the 22 known V beta gene segments. The level of transcripts for the highest and lowest expressed V beta gene segment differed by greater than 20-fold in the thymus and an even larger difference was observed in the periphery. The levels of expressions were unrelated to the order of the V beta genes on the chromosome. For most of the V beta gene segments, the relative transcript levels were the same in the thymus and periphery, suggesting that thymic selection in general does not act solely upon the V beta gene segment. One V beta gene segment in the BALB and B10 mice strains was an exception to this rule. V beta 5.2 expression in the periphery of BALB and B10 mice inversely correlated with the expression of the MHC class II molecule I-E. Five V beta gene segments had reduced transcript levels in the periphery of Mls-1a mice compared with their thymic levels or to the levels found in Mls-1b mice. The peripheral level of V beta 3 transcripts vary with MHC and Mls-2 haplotypes. The observation that certain V beta transcript levels are reduced in the periphery when compared with the thymus favors the hypothesis that self tolerance at the T cell level results in the elimination of self-reactive T cells, rather than paralysis by a block at some post-transcriptional step. Finally, the wide variability of V beta gene segment expression in the thymus suggests mechanisms exist to import an early bias to the repertoire. Whether this bias results from differential V beta segment rearrangement rates, differential V beta expression rates, or events occurring after TCR-alpha/beta expression on immature/nonmature thymocyte cell surfaces is yet to be determined.

Animals↗

Complement receptors in human peripheral nerve tissue.

Cryostat sections of human peripheral nerve tissue adsorbed sheep erythrocytes sensitized with antibody and human complement (EAC). Activated complement was essential for the reaction to occur. The receptor had specificity for the C3b fragment. In order to obrain binding to nerve tissue, the indicator cells had to be coated with more complement than that required for binding to C3b receptors in spleen and renal tissue. The receptors are located within the nerve fascicles and are probably of glycoprotein nature. The receptors for C3b in peripheral nerve tissus may be of significance in the deposition of immune complexes, which may play a role in acute polyradiculoneuritis.

Complement Activation↗