[A 52-year-old woman with acute shock and purpura fulminans. Pneumococcal sepsis]. / 52-jährige Patientin mit akuter Schocksymptomatik und Purpura fulminans. Pneumokokkensepsis.

We report a 52-year-old female patient admitted with fever, chills, and myalgias since the previous day. On the day of admission she had a generalized seizure. The patient had no previous illnesses. Laboratory investigations showed consumptive coagulopathy with clinical manifestations of shock and development of multiple organ failure. Pneumococci were detected in blood cultures. Furthermore the skin showed purpura fulminans all over. The patient died within 24 h after admission in the intensive care unit. On autopsy, in addition to adrenal and myocardial hemorrhages, hypoplasia of the spleen was found. Fulminant pneumococcal sepsis is a life-threatening disease that occurs in patients with risk factors like splenic hypoplasia or asplenia. Sometimes a fulminant pneumococcal sepsis may be the first clinical manifestation of a hitherto unknown splenic hypoplasia. In this context the general recommendation of vaccination against pneumococci in patients with risk factors like splenic hypoplasia or asplenia, in patients older than 60, and in children from 2 months onward has to be emphasized.

Low-grade T-cell lymphoma of the kidney and Waldenström's macroglobulinemia in a patient presenting with renal failure.

Renal failure is rarely the presenting manifestation of non-Hodgkin's lymphoma. We describe the unusual case of a patient who presented with uremia due to lymphomatous infiltration of the kidney by a low-grade T-cell lymphoma. The diagnosis of lymphoma was made by renal biopsy. Extrarenal nodular or extra-nodular involvement could not be detected. However, simultaneously, a lymphoplasmacytic lymphoma was found on bone marrow biopsy associated with IgM paraproteinemia. To our knowledge, this is the first report of a renal T-cell lymphoma associated with Waldenström's macroglobulinemia.

IgA nephropathy in a young man with primary hyperparathyroidism.

We report the first documented case of IgA nephropathy occurring after treatment of primary hyperparathyroidism. A 29-year-old man with a history of kidney stones and primary hyperparathyroidism underwent kidney biopsy for persistent proteinuria and microhematuria 18 months after resection of an ectopic parathyroid adenoma with subsequent normalization of serum calcium and parathyroid hormone levels. On ultrasound, renal intraparenchymal calcifications were noted. Renal biopsy revealed IgA nephropathy in addition to tubulointerstitial microcalcifications. The development of IgA nephropathy may have been influenced by hyperparathyroidism and/or its treatment. The case highlights the role of renal biopsy in patients with a history of kidney stones and abnormal urinary findings.

Sonographic cervical volumetry in higher order multiple gestation.

OBJECTIVE: The aim of this study of multifetal pregnancies was the comparison of three-dimensional (3D) volumetry of the cervix, conventional sonographic cervical length measurement and clinical assessment. METHODS: 10 mothers were investigated in an observational study between 5/1999 and 9/2000. A total of 34 consecutive 2D- and 3D-transabdominal ultrasound measurements were performed. RESULTS: Volumetry of the cervix was possible in all 34 exams. 2D-cervical length assessment could not be obtained in 6% because the presenting fetal part obstructed the sonographic plane. Both methods allowed equal judgement of the configuration of the cervix. A significant correlation was found between mean 2D-cervical length (28.7 mm, 7.7 SD) and mean cervical volume (30.0 cm3, 16.0 SD). Parity, subjective preterm labor or need of tocolytics showed no correlation with any biometrical parameter studied. CONCLUSION: Volumetry was superior for the assessment of cervical biometry and conformation in women when the transabdominal 2D-plane was obstructed. When cervical length was obtainable by a conventional scan, the technically more complex 3D-imaging did not provide further information.

Expression of inter-alpha-trypsin inhibitor and tumor necrosis factor-stimulated gene 6 in renal proximal tubular epithelial cells.

BACKGROUND: Our previous studies have demonstrated that renal proximal tubular epithelial cells (PTCs) may contribute to renal interstitial fibrosis by the generation of transforming growth factor-beta1 (TGF-beta1). In these in vitro experiments, TGF-beta1 was, however, secreted in its latent form. Plasmin has been implicated as a potential physiological activator of TGF-beta1. The inter-alpha-trypsin inhibitor (IalphaI) family of serum protease inhibitors together with tumor necrosis factor-stimulated gene 6 (TSG-6) recently have been implicated in the regulation of this protease pathway. The aim of the current study was to examine PTC synthesis of these proteins and to relate it to alterations of plasmin-protease activity. METHODS: PTCs were grown to confluence and stimulated under serum-free conditions with either interleukin-1beta (IL-1beta) or 25 mmol/L D-glucose. Alterations in IalphaI and TSG-6 generation were detected by Western analysis of both membrane extracts and supernatant samples. Alterations in gene expression were examined by reverse transcription-polymerase chain reaction. The effect of alteration in synthesis of TSG-6 on plasmin activity was determined by quantitating plasmin inhibitory activity of supernatant samples by in vitro calorimetric assay prior to and following TSG-6 immunoprecipitation. RESULTS: The data demonstrate that human PTCs constitutively express mRNA for bikunin and heavy chain 3 (H3) of IalphaI. Neither IL-1beta (1 ng/mL) nor 25 mmol/L D-glucose influenced their mRNA expression nor protein synthesis. In contrast, the addition of either IL-1beta or 25 mmol/L D-glucose increased TSG-6 mRNA expression. This was accompanied by an early up-regulation of TSG-6 protein expression following IL-1beta stimulation (24 h) and a late up-regulation after the addition of 25 mmol/L D-glucose (96 h) in the cell culture supernatant and associated with the cell membranes. Early induction of TSG-6 mRNA by IL-1beta was unaffected by the addition of the protein synthesis inhibitor cycloheximide. In contrast, the later glucose-stimulated induction of TSG-6 mRNA was abrogated by the addition of cycloheximide. Stimulation of TSG-6 by either IL-1beta or 25 mmol/L D-glucose was associated with an inhibition of total percentage plasmin activity. Immunoprecipitation of TSG-6 in these samples returned plasmin activity to control levels. CONCLUSIONS: : The data demonstrate that human PTCs constitutively express the bikunin and H3 components of the IalphaI family of serum protease inhibitors. Moreover, the addition of IL-1beta or 25 mmol/L D-glucose up-regulates the expression of TSG-6 in these cells, resulting in an inhibition of plasmin activity.

Association of prolonged hyperglycemia with glomerular hypertrophy and renal basement membrane thickening in the Goto Kakizaki model of non-insulin-dependent diabetes mellitus.

The aim of the current study was to characterize the effects of prolonged hyperglycemia on renal structure and function using a model of non-insulin-dependent diabetes mellitus: the Goto Kakizaki (GK) rat, which does not have confounding variables, such as hyperlipidemia, obesity, or elevated blood pressure. The data show that hyperglycemia in this model was not associated with the development of significant proteinuria, but it was associated with the development of definitive age-dependent renal structural changes. These changes consisted of thickening of glomerular basement membrane at 35 weeks and tubular basement membrane. This thickening was accompanied by marked glomerular hypertrophy resulting from a parallel increase in total capillary luminal volume and mesangial volume, but fractional capillary and mesangial volumes remained unchanged. There was evidence of podocyte injury, as assessed by de novo expression of desmin. In contrast, there was no evidence of mesangial cell activation, as assessed by their de novo expression of alpha-SMA. Interstitial monocyte/macrophage influx increased significantly in GK rats at 12 weeks compared with Wistar controls. Glomerular macrophage infiltration was elevated significantly in 35-week GK rats. The structural changes described in the GK rat are similar to those described in prolonged non-insulin-dependent diabetes mellitus patients who have not developed overt renal disease. This model allows us to investigate further the mechanisms involved in the pathogenesis of the consequences of prolonged hyperglycemia.

[Functional MRI of the pelvic floor. The methods and reference values]. / Funktionelle MRT des Beckenbodens. Methodik und Referenzwerte.

PURPOSE: Functional cine MRI of the pelvic floor is a yet another modality in addition to various radiological fluoroscopic techniques. This article describes our own method in view of the recent literature and provides morphometric reference values. MATERIAL AND METHOD: We examined 20 nulliparous women (range of age: 25-51 years) with normal findings in the gynecological and urodynamic examination. Functional cine MRI was performed on a 1.5 Tesla equipment after opacification of the vagina and rectum. We used a T2-weighted gradient-echo sequence (Ture-FISP) to determine the position of the reference organs at rest and during straining/defecation. Two different reference lines were used. In addition 29 morphometric and functional parameters were measured, all of them being observer independent. RESULTS: Functional cine MRI was able to show the extent and interaction of the pelvic floor organs in all cases with the reference organs always remaining above the pubococcygeal reference line. The depth of the rectocele was 2 cm. With the exception of the diameter of urogenital hiatus the different parts of the levator ani muscle could not be determined. DISCUSSION: Functional cine MRI using an appropriate organ opacification and slice positioning is an objective, unifying diagnostic approach of the pelvic floor. The reference data given can be of help to distinguish normal from abnormal findings.

Early events leading to renal injury in obese Zucker (fatty) rats with type II diabetes.

UNLABELLED: Early events leading to renal injury in obese Zucker (fatty) rats with type II diabetes. BACKGROUND: More than half of the new patients admitted to dialysis therapy in some centers are diagnosed with type IIb diabetes, that is, diabetes associated with obesity. This study searched for a common final pathway of renal damage in this progressive renal disease. METHODS: The evolution of biochemical and morphological renal changes was examined in 6- to 60-week-old Zucker rats (fa/fa-rats), a model of obesity associated with type II diabetes. RESULTS: fa/fa-rats exhibited pronounced hyperinsulinemia and hyperlipidemia at 6 weeks and became diabetic after 14 weeks of age. Significant focal segmental glomerulosclerosis was first noted in 18-week-old fa/fa-rats and tubulointerstitial damage and proteinuria in 40-week-old fa/fa-rats. A comparison of kidneys of six-week-old fa/fa-and lean control (Fa/?) rats by immunohistology revealed a 1.8-fold increase in glomerular monocyte/macrophage counts in fa/fa-rats and a significant increase in de novo desmin expression in podocytes. Electron microscopy demonstrated an increase in the number of podocyte mitochondria and intracytoplasmic protein and fat droplets. Podocyte desmin scores markedly increased until week 18 in fa/fa-rats, whereas glomerular monocyte/macrophage counts peaked at 3.2-fold at week 14. Podocyte desmin expression, but not glomerular macrophage infiltration, correlated with damage in adjacent tubular cells, as evidenced by their de novo expression of vimentin. Progressive glomerular hypertrophy was detected in fa/fa-rats after 10 weeks. GBM width was significantly increased in 14-week-old fa/fa-rats as compared with lean controls. Mesangial cell activation (de novo expression of alpha-smooth muscle actin) and proliferation was low to absent throughout the observation period in fa/fa-rats. Renal cell death counts (TUNEL) remained unchanged in 6- to 40-week-old fa/fa-rats. Tubulointerstitial myofibroblast formation and matrix accumulation occurred late during the study duration in fa/fa-rats. CONCLUSION: These data suggest that early progressive podocyte damage and macrophage infiltration is associated with hyperlipidemia and type IIb diabetes mellitus, and antedates both the development of glomerulosclerosis and tubulointerstitial damage.

Activation of the acute phase response and complement C3 in patients with IgA nephropathy.

UNLABELLED: Recently we showed systemic complement activation in patients with immunoglobulin A (IgA) nephropathy (measured by "activated C3" [actC3], in other words, neoantigens developing on breakdown products after C3 activation) and reported that plasma levels of actC3 can indicate disease activity and renal outcome. In this study we investigated whether plasma C3a and C-reactive protein (CRP), which require tests that are more readily available, have a similar diagnostic and predictive value. CRP was measured using a highly sensitive enzyme-linked immunosorbent assay and C3a using a specific immunoassay. CRP and C3a levels were significantly higher in 56 patients with IgA nephropathy as compared with 55 healthy controls. C3a levels in IgA nephropathy patients were also significantly increased in comparison with 42 patients with hypertension or nonimmune renal diseases. Neither C3a nor CRP levels correlated with those of actC3 in IgA nephropathy patients. We also compared 10 IgA nephropathy patients with stable, normal renal function with eight IgA nephropathy patients progressing from normal to impaired renal function during mean follow-ups of 7.1 and 5.1 years, respectively. Mean CRP but not C3a levels during the observation period were significantly higher in IgA nephropathy patients with disease progression than in those with stable renal function. CONCLUSION: Systemic complement activation can be detected by measurement of plasma C3a in IgA nephropathy, but C3a levels cannot substitute for actC3 in predicting renal prognosis. Subclinical induction of the acute phase response is also present in patients with progressive IgA nephropathy, but again its prognostic value is limited. Repeated determinations performed over prolonged time courses may possibly improve the prognostic value of CRP levels.

Rodent models of nephropathy associated with type II diabetes.

End-stage renal disease from diabetic nephropathy, mainly due to type II diabetes, is an increasing problem in Western countries. The pathogenesis of diabetic nephropathy is still incompletely understood and much of the experimental insight has been obtained from insulinopenic animal models, resembling type I diabetes. This review therefore aims to describe available rodent models of nephropathy associated with type II diabetes. The review focusses on the metabolic as well as renal functional and structural changes. The usefulness of these rodent models to study renal involvement in type II diabetes is discussed with particular emphasis on confounding factors such as hyperlipidemia, hypertension, immunologic abnormalities, urogenital structural abnormalities and other associated pathological conditions. In addition recent observations on two rat strains, the obese Zucker (fatty) and Goto Kakizaki (GK) rat, are discussed in detail.

The representation of inflectional morphology: evidence from Broca's aphasia.

Dualistic models of inflection assume a qualitative distinction between affix-based regular forms and stored irregular forms, predicting that the two distinct mechanisms can be selectively affected in language disorders. We present data on German participle formation from 11 agrammatic Broca's aphasics which show that irregular participles can be selectively affected in agrammatism. Moreover, the distribution of errors reveals a frequency effect for irregular but not for regular participles. Both findings argue for a dualistic representation of inflection. Moreover, we want to propose a modification of dualistic models by suggesting that both regularity and irregularity are better conceived of as scalar.

Progression of diabetic nephropathy. Insights from cell culture studies and animal models.

Nephropathy in patients with type I and II diabetes mellitus is a rapidly increasing problem worldwide. Studies using both glomerular and tubular cells have delineated some of the consequences induced by acute hyperglycemia. In vitro studies have clearly demonstrated that exposure of cultured renal cells, such as glomerular mesangial cells and proximal tubular epithelial cells, to elevated glucose concentrations, may alter cell proliferation and/or extracellular matrix turnover. The latter is effected both directly and indirectly by the alteration of cytokine generation. Furthermore, these in vitro studies have allowed detailed examination of the mechanisms by which exposure of these cells to high ambient glucose concentrations may alter cell function. Extension of these studies to the experimental in vivo situation has confirmed most of the in vitro findings. Important insights gained from models of type I diabetes (i.e. streptocotocin-induced diabetes) as well as type II diabetes (i.e. Goto-Kakizaki (GK) rats and obese Zucker rats) include: (1) The demonstration that increased glomerular cell proliferation and renal matrix accumulation, driven by TGF-beta and/or PDGF, occur in streptocotocin-induced diabetes, yet that nephropathy in these rats does not progress to renal failure. (2) The demonstration that prolonged mild type II diabetes does induce morphological changes characteristic of pre-clinical diabetic nephropathy in GK-rats but does not result in albuminuria or progressive renal disease. (3) The demonstration that the association of type II diabetes with hyperlipidemia in obese Zucker rats results in early podocyte damage and subsequent progression to glomerulosclerosis, tubulointerstitial damage, and renal insufficiency. Identification of the mediators involved in the above processes and in particular of the conditions that will determine progression of subclinical morphological changes to overt nephropathy and renal failure will likely result in future novel therapeutic approaches to diabetic nephropathy.

Novel approach to specific growth factor inhibition in vivo: antagonism of platelet-derived growth factor in glomerulonephritis by aptamers.

Mesangial cell proliferation and matrix accumulation, driven by platelet-derived growth factor (PDGF), contribute to many progressive renal diseases. In a novel approach to antagonize PDGF, we investigated the effects of a nuclease-resistant high-affinity oligonucleotide aptamer in vitro and in vivo. In cultured mesangial cells, the aptamer markedly suppressed PDGF-BB but not epidermal- or fibroblast-growth-factor-2-induced proliferation. In vivo effects of the aptamer were evaluated in a rat mesangioproliferative glomerulonephritis model. Twice-daily intravenous (i.v.) injections from days 3 to 8 after disease induction of 2.2 mg/kg PDGF-B aptamer, coupled to 40-kd polyethylene glycol (PEG), led to 1) a reduction of glomerular mitoses by 64% on day 6 and by 78% on day 9, 2) a reduction of proliferating mesangial cells by 95% on day 9, 3) markedly reduced glomerular expression of endogenous PDGF B-chain, 4) reduced glomerular monocyte/macrophage influx on day 6 after disease induction, and 5) a marked reduction of glomerular extracellular matrix overproduction (as assessed by analysis of fibronectin and type IV collagen) both on the protein and mRNA level. The administration of equivalent amounts of a PEG-coupled aptamer with a scrambled sequence or PEG alone had no beneficial effect on the natural course of the disease. These data show that specific inhibition of growth factors using custom-designed, high-affinity aptamers is feasible and effective.

Improved survival and amelioration of nephrotoxic nephritis in intercellular adhesion molecule-1 knockout mice.

Intercellular adhesion molecule-1 (ICAM-1) expression is upregulated in nephrotoxic nephritis, a model of human rapidly progressive glomerulonephritis. To evaluate the pathogenetic relevance of ICAM-1 in this model, nephrotoxic nephritis was induced in ICAM-1 knockout mice and genetic controls. Mice were preimmunized with rabbit IgG in complete Freund's adjuvant. Seven days later they received rabbit anti-mouse glomerular basement membrane IgG. The early humoral immune responses (levels of circulating mouse anti-rabbit IgG, glomerular deposition of rabbit and mouse IgG and mouse C3c) were not altered in ICAM-1 knockout mice. During 28 d of follow-up, 3 of 19 control nephritic mice and 0 of 16 ICAM-1 knockout mice died. Proteinuria was high in nephritic control mice (means 10 to 12 mg/24 h at all time points investigated) and significantly reduced in nephritic ICAM-1 knockout mice (means <4.4 mg). Mean serum creatinine rose from 29 micromol/L at day -7 to 48 micromol/L (day 28) in nephritic control mice. This increase in serum creatinine was significantly lower in ICAM-1 knockout mice: 27 (day -7) and 36 micromol/L (day 28). Histologic analysis at day 28 revealed that ICAM-1 deficiency in nephrotoxic nephritis mice led to significantly reduced glomerular crescent formation (2+/-3% in ICAM-1 knockout mice versus 13+/-8% in nephritic controls) and tubulointerstitial injury (score 0.4+/-0.4 versus 2.0+/-1.1). By immunohistochemistry, ICAM-1 deficiency in nephritic mice led to significantly reduced (peri-)glomerular and/or interstitial macrophage influx, alpha-smooth muscle actin expression, and type IV collagen accumulation. These data indicate that ICAM-1 is a central mediator of glomerular and tubulointerstitial injury in murine nephrotoxic nephritis.

Human mitochondrial enoyl-CoA hydratase gene (ECHS1): structural organization and assignment to chromosome 10q26.2-q26.3.

The second step in mitochondrial fatty acid beta-oxidation is catalyzed by short chain enoyl-CoA hydratase (ECHS1; EC 4.2.1.17). Inherited disorders of this pathway of energy metabolism present clinical and laboratory features resembling sudden infant death syndrome and Reye-like syndrome. To investigate the role of ECHS1 further, the gene structure was analyzed and its chromosomal locus determined. A fragment of rat liver ECHS1 cDNA was employed for isolation and characterization of two overlapping genomic clones encompassing the entire human ECHS1 gene. The gene, approximately 11 kb, is composed of eight exons, with exons I and VIII containing the 5'- and 3'-untranslated regions, respectively. Two major transcription start sites, located 62 and 63 bp upstream of the translation initiation codon, were mapped by primer extension analysis. The immediate 5'-flanking region of the ECHS1 gene is GC-rich and contains several copies of the SP1 binding motive but no typical TATA or CAAT boxes are apparent. Alu repeat elements have been identified within the region -1052/-770 relative to the cap site and in intron 7. The human ECHS1 gene locus was assigned to chromosome 10q26.2-q26.3 by fluorescence in situ hybridization.

Enoyl-CoA hydratase and isomerase form a superfamily with a common active-site glutamate residue.

Mitochondrial 2-enoyl-CoA hydratase (mECH) and 3,2-trans-enoyl-CoA isomerase (mECI), two enzymes which catalyze totally different reactions in fatty acid beta-oxidation, belong to the low-similarity hydratase/isomerase enzyme superfamily. Their substrates and reaction mechanisms are similar [Müller-Newen, G. & Stoffel, W. (1993) Biochemistry 32, 11,405-11,412]. Glu164 of mECH is the only amino acid with a protic side chain that is conserved in these monofunctional and polyfunctional enzymes with 2-enoyl-CoA hydratase and 3,2-trans-enoyl-CoA isomerase activities. We tested our hypothesis that Glu164 of mECH is the putative active-site amino acid responsible for the base-catalyzed alpha-deprotonation in the hydratase/dehydrase and isomerase reaction. We functionally expressed rat liver mECH wild-type and [E164Q] mutant enzymes in Escherichia coli. Characterization of the purified wild-type and mutant enzymes revealed that the replacement of Glu164 by Gln lowers the kcat value more than 100,000-fold, whereas the Km value is only moderately affected. We have demonstrated in a previous study that Glu165 is indispensable for the 3,2-trans-enoyl-CoA isomerase activity. Taking these results together, we conclude that the conserved glutamic acid is the essential basic group in the active sites of 2-enoyl-CoA hydratase (Glu164) and 3,2-trans-enoyl-CoA isomerase (Glu165), and that these enzymes are not only evolutionarily but also functionally and mechanistically related.

[Manometric and clinical long-term outcome after grade III perineal rupture]. / Manometrische und klinische Langzeitresultate nach Dammriss III. Grades.

OBJECTIVE: To investigate the manometrical and clinical long-term results following a tear III. PATIENTS: 27 Primiparae with a tear III following a spontaneous vaginal delivery were retrospectively compared with 22 Primiparae without sphincter injury (follow-up: 27 months). METHODS: Water-Perfusion-Manometry and clinical assessment (modified Kelly-Score). Manometric parameter (at rest and during contraction): sphinctertone and - length, vectorvolume, radial asymmetry. Wilcoxon-Text (p < 0.05). RESULTS: Tear III patients showed a significant decrease in sphincter length and vector volume both at rest and during contraction. On clinical assessment there was no difference. CONCLUSION: A tear III weakens the anal sphincter by decreasing sphincter length and vector volume. This weakness can be demonstrated only manometrically but not clinically.

Human mitochondrial 3,2-trans-enoyl-CoA isomerase (DCI): gene structure and localization to chromosome 16p13.3.

A key enzyme in the mitochondrial beta-oxidation of unsaturated fatty acids is the 3,2-trans-enoyl-CoA isomerase (DCI; EC 5.3.3.8). It catalyzes the transformation of 3-cis and 3-trans intermediates arising during the stepwise degradation of all cis-, mono-, and polyunsaturated fatty acids to the 2-trans-enoyl-CoA intermediates. A genomic clone encoding the human DCI was isolated and characterized by use of the previously cloned human DCI cDNA. The entire gene encompasses approximately 12.5 kb, and the coding sequence is distributed over seven exons. One major and three minor transcription start sites were determined by primer extension analysis. In common with promoters of other housekeeping genes encoding mitochondrial proteins, the GC-rich, immediate 5'-flanking region of the DCI transcription initiation site lacks typical TATA and CAAT boxes; instead, two GC box consensus sequences are present. Introns 2 and 6 contain several Alu repetetive sequences. The human DCI gene locus was assigned to chromosome 16 by use of human-rodent somatic cell hybrids and to chromosome 16p13.3 by chromosomal in situ suppression hybridization studies.

Identification of a B-50-like protein in frog brain synaptosomes.

Vestibular compensation in the frog following unilateral labyrinthectomy is accompanied by distinct changes in the endogenous phosphoprotein patterns in total frog brain homogenate and isolated synaptosomes. The purpose of this study was to characterize one of these proteins, an acidic 45-kDa synaptosomal protein, resembling in some of its features the growth-associated protein GAP-43/B-50. Our results demonstrate by comparative analysis with purified rat B-50/GAP-43 that the 45-kDa protein (IP 4.8) in synaptosomal membranes of frog brain is phosphorylated by added purified PKC, cross-reacts with affinity-purified rabbit antibodies to rat B-50 and exhibits a Staphylococcus aureus V8 protease peptide digestion pattern corresponding to rat B-50. Therefore, we conclude that the acidic 45-kDa synaptosomal protein is a growth-associated B-50-like protein, probably involved in processes responsible for compensatory reorganization of the vestibular structures after hemilabyrinthectomy in the frog.