Biomedical subjects

S Yagihashi

Publications and source records attributed to S Yagihashi.

At least 19 recordsLinked to original sources

PubMed2006

Spindle cell metaplasia arising in thyroid adenoma: characterization of its pathology and differential diagnosis.

Spindle cell metaplasia in thyroid adenoma or carcinoma is rare and its pathological features are not well characterized. Distinction of this entity from medullary or anaplastic carcinoma has an important clinical implication. We encountered a case of thyroid follicular adenoma associated with spindle cell metaplasia. It showed "tumor in tumor appearance" and neoplastic spindle cells were positive for thyroglobulin, thyroid transcription factor-1, vimentin and focally chromogranin A and somatostatin (SS). MIB-1 index was <1%. Ultrastructure of the spindle cells was reminiscent of follicular cell origin. From the findings from our case, spindle cell metaplasia appears to be a benign clinical entity, suggestive of multidirectional differentiation of follicular cells.

Adenoma↗

PubMed2004

Ossifying gastric carcinoid tumor containing bone morphogenetic protein, osteopontin and osteonectin.

We report a case of gastric carcinoid tumor with ossification. A 47-yr-old man complaining of abdominal discomfort underwent gastrointestinal endoscopic examination, which revealed a submucosal tumor in his stomach. The tumor was extirpated by endoscopic enucleation. Histologically, the tumor was widely occupied by mature bone tissues, where scattered carcinoid tumor cell nests surrounded bone tissues or located in stromal areas. Immunohistochemically, the tumor cells were strongly positive for cytokeratin, chromogranin A, synaptophysin, neurofilaments and neuron-specific enolase, underscoring the diagnosis of carcinoid tumor. They also stained positive with markers of bone formation and differentiation, such as bone morphogenetic protein, osteopontin and osteonectin. There are only four cases in the world literature, including a current case of ossifying gastric carcinoid tumor, in which the excessive production of peptides promoting ossification was considered to be implicated in the unusual appearance of the bone.

Bone Morphogenetic Proteins↗

PubMed2003

Chronic granulomatous pleuritis caused by nocardia: PCR based diagnosis by nocardial 16S rDNA in pathological specimens.

Nocardiosis is an uncommon infection caused by the aerobic actinomycete nocardia. Identification of the pathogen is essential for the definitive diagnosis and for an effective treatment. This report describes a case of chronic granulomatous pleuritis caused by nocardia. A 59 year old Japanese man had a history of repeated pyothorax. Right pleural decortication and thoracic drainage were performed. Microbiological examinations of the drained fluid failed to identify a pathogen. Pathological examinations revealed Gram positive filamentous and branching bacilli in the granulomatous lesion of the pleura. Sequencing of the 971 bp 16S ribosomal DNA extracted and amplified from paraffin wax embedded sections identified the microorganism as Nocardia sp. IFM 0860. The patient received sulfamethoxazol/trimethoprim and minocycline. Although the presence of a brain abscess was disclosed by systemic examination, the clinical course has been favourable. In this patient, polymerase chain reaction analysis of 16S ribosomal DNA in pathological specimens was useful in making an accurate diagnosis of nocardiosis and in determining the appropriate treatment.

DNA, Bacterial↗

PubMed2002

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients.

AIMS/HYPOTHESIS: We examined the pancreatic islet lesions in Japanese patients with Type II diabetes mellitus to determine if the damage was related to oxidative stress. METHODS: Morphometric analyses were performed on immunostained sections of the tail portion of the pancreas from 14 diabetic and 15 non-diabetic patients. Amyloid deposition and oxidative stress-induced tissue damage were evaluated by Congo-red staining and immunostaining. Resistance to oxidative stress was assessed from immunostaining results for Cu, Zn-superoxide dismutase (SOD). Expression of (pro)insulin mRNA was assessed by in situ hybridisation. RESULTS: The pancreas from diabetic patients had amyloid deposition in about 15 % of the islets, intensified reactions of 8-OHdG and HNE, as well as reduced expression of SOD. Islet volume density of beta cells and total beta-cell mass in the pancreas from diabetic patients were reduced by 22 % (p < 0.001) and 30 % (p < 0.05). Islet volume density and total mass of (pro)insulin mRNA-positive cells were similarly reduced in diabetic patients by 22 % (p < 0.001) and 39 % (p < 0.05), respectively. Islet volume density of A cells was increased by 20 % (p < 0.001) but total mass did not change. There were no changes in volume densities of islet, D and PP cells. Reduced beta-cell volume density correlated with increased positive staining of 8-OHdG. CONCLUSION/INTERPRETATION: Japanese Type II diabetic patients show a reduction of beta-cell mass and evidence of increased oxidative stress-related tissue damage that is correlated with the extent of the beta-cell lesions.

Aged↗

PubMed2002

Diabetic microangiopathy: pathology and current understanding of its pathogenesis.

Recent drastic increase in diabetic population poses serious problems in both health sciences and socioeconomic conditions. The most important issue in the clinical practice of diabetic patients is the treatment and care of chronic complications. It is not fully clear, however, as to the pathophysiology of diabetic microangiopathy and its pathogenesis. Recent studies on microvessel pathology in diabetic patients and molecular analyses on the diabetic animal models disclosed novel features of the dynamic changes of specific organ pathology affected by diabetes and factors involved in its pathogenesis. Under long-term hyperglycemia, early stimuli elicit adaptive reactions of tissues showing acute inflammatory processes of vessel walls and then late irreversible and regressive changes of microangiopathy. Consequently, remodeling of vascular cells and excessive matrix production are cardinal feature. The precise mechanisms of how these tissue changes occur remain speculative; increased polyol pathway, excessive non-enzymatic glycation, increased protein kinase C activity, as well as oxidative stress are all interrelated for the cause and development of the microangiopathy.

Blood Vessels↗

PubMed2001

Enhanced in situ expression of aldose reductase in peripheral nerve and renal glomeruli in diabetic patients.

To explore the relationships between polyol pathway-related enzymes and pathologic features, we examined the immunohistochemical expression of aldose reductase (AR) and sorbitol dehydrogenase (SDH) in the peripheral nerve and kidney tissues collected postmortem from diabetic patients and compared it with those from non-diabetic patients. Tissue AR protein concentrations were also quantified. In non-diabetic patients, AR distributed in pericytes, smooth muscle cells of endo- and epi-neurial microvessels, Schwann cells in the sciatic nerve, and tubular cells of the renal medulla. By contrast, positive SDH reactions were observed in tubular cells of the renal cortex but were faint in the sciatic nerve. Diabetic patients frequently showed dense AR expressions in the sciatic nerve. In nephropathic diabetic patients, the glomerular mesangial area showed diffuse positive reactions for AR. The severity of structural changes in glomeruli correlated with the intensity of immunoreactive AR (r2=0.626, P<0.01). AR contents in the renal cortex and sciatic nerve from diabetic patients were 1.5- and 1.8-fold greater than those from non-diabetic patients, respectively (P<0.05 for both). These findings are the first to demonstrate enhanced AR expressions in peripheral nerve and renal glomeruli in diabetic patients and its relevance to the characteristic pathology.

Adult↗

PubMed2001

Effects of OPB-9195, anti-glycation agent, on experimental diabetic neuropathy.

BACKGROUND: Nonenzymatic glycation of neural proteins and their end-products (advanced glycation end-products, AGE) have been implicated in the pathogenesis of diabetic neuropathy. We need a development of effective ant-glycation agents for future clinical use. MATERIALS AND METHODS: We examined the effects of OPB-9195 (OPB), a new inhibitor of glycation, on the peripheral nerve structure and function in diabetic rats. Eight-week-old Wistar rats were made diabetic by streptozotocin (40 mg kg(-1), i.v.) and OPB (60 mg kg(-1) day(-1)) was given by gavage for 24 weeks. Age- and sex-matched normal Wistar rats were used for comparison. RESULTS: During the experimental period, OPB treatment did not affect the reduced body weight, elevated levels of blood glucose and glycated haemoglobin in diabetic rats. At the end of the experiment, delayed tibial motor nerve conduction velocity was significantly improved (by 60%) in treated diabetic rats, with reduction of serum AGE levels. Expression of immunoreactive AGE in the sciatic nerve was reduced in treated diabetic rats compared with those in untreated rats. Sciatic nerve (Na+, K+)-ATPase activity was also restored in treated diabetic rats. On the cross-sectioned sciatic nerves, positive cells with oxidative stress-related DNA damage, as expressed by 8-hydroxy-2'-deoxyguanosine, were less in the peripheral nerve of treated diabetic rats compared with those of untreated rats. CONCLUSION: The current study suggested that OPB is beneficial for the reduction of serum AGE and the prevention of diabetic neuropathy.

Animals↗

PubMed2001

Malignant glomus tumor in the branchial muscle of a 16-year-old girl.

Malignant glomus tumor is an extremely rare neoplasm and its histological features are not well characterized. We report a 16-year-old female patient with a malignant glomus tumor. The patient was admitted to our hospital presenting with a mass in the right upper arm that she had noticed for the previous 6 months. Computed tomography and magnetic resonance imaging revealed an expanded mass involving the surrounding tissues. At surgery, an ill-defined and expanded mass was found, 5 x 4 x 3 cm in size, in the right branchial muscle. The tumor was extirpated, along with neighboring muscle tissues. Histologically, tumor cells were round to short-spindle shaped, forming solid sheets admixed with vessels of varying size. Their nuclei were uniformly oval to round, and their cytoplasms were slightly eosinophilic. The growth pattern of the tumor cells resembled that of glomus tumor, but mitotic figures were frequent (as high as 10 per 10 high-power fields). Immunohistochemically, the tumor cells were positive for vimentin and muscle actin, but negative for desmin. There were no areas typical of benign glomus tumor or sarcomatous change. These findings led us to a diagnosis of primary malignant glomus tumor arising de novo. There has been no recurrence or metastasis for 21 months after wide excision.

Actins↗

PubMed2001

Neuropathy in diabetic mice overexpressing human aldose reductase and effects of aldose reductase inhibitor.

The present study was designed to examine the effect of aldose reductase (AR) overexpression on the development of diabetic neuropathy by using mice transgenic for human AR. At 8 weeks of age, transgenic mice (Tg) and non-transgenic littermates (Lm) were made diabetic with streptozotocin. After 8 weeks of untreated diabetes, plasma glucose levels and the reduction in body weight were similar between the groups of diabetic animals. Despite the comparable levels of hyperglycaemia, levels of sorbitol and fructose were significantly greater in the peripheral nerve of diabetic Tg than in diabetic Lm (both P < 0.01). Ouabain sensitive Na(+),K(+)-ATPase activity was similarly decreased in both diabetic Tg and Lm. Protein kinase C activity in the sciatic nerve membrane fraction was unaffected by diabetes in Lm, but was reduced by nearly 40% in the diabetic Tg. Although both groups of diabetic animals exhibited a significant decrease in tibial nerve motor nerve conduction velocity (MNCV), this decrease was significantly more severe (P < 0.01) in diabetic Tg than in diabetic Lm. Consistent with these findings, nerve fibre atrophy was significantly more severe in diabetic Tg than in diabetic Lm (P < 0.01). These findings implicate increased polyol pathway activity in the pathogenesis of diabetic neuropathy. In support of this hypothesis, treating diabetic Tg with an aldose reductase inhibitor (WAY121-509, 4 mg/kg/day) for 8 weeks significantly prevented the accumulation of sorbitol, the decrease in MNCV and the increased myelinated fibre atrophy in diabetic Tg.

Aldehyde Reductase↗

PubMed2001

Intramyocardial delivery of basic fibroblast growth factor-impregnated gelatin hydrogel microspheres enhances collateral circulation to infarcted canine myocardium.

The present study examined whether basic fibroblast growth factor (bFGF)-impregnated acidic gelatin hydrogel microspheres (AGHM) would enhance collateral development to the infarct area in dogs with coronary occlusion. Studies were conducted in 28 dogs with a 2-week occlusion of the proximal left anterior descending coronary artery (LAD). The dogs were divided into 3 groups according to treatment: Group A treated with bFGF-impregnated AGHM in the infarct area; Group B with free-form bFGF; Group C with AGHM alone. Coronary angiography (n=15; Group A, 7 dogs; Group B, 5 dogs; Group C, 3 dogs) and a regional myocardial blood flow study (n=13; Group A, 6 dogs; Group B, 4 dogs; Group C, 3 dogs) were repeated at a 2-week interval. Coronary angiography revealed that in Group A, antegrade flow in the LAD distal to the occlusion, which was assessed by Thrombolysis in Myocardial Infarction (TIMI) grade, was significantly increased after treatment. In contrast, in Groups B and C, the treatment did not change the flow grade in the LAD. In Group A, the regional myocardial blood flow in the collateral dependent area was significantly increased after treatment, and the regional myocardial blood flow reserve after adenosine injection was also significantly increased. These measurements remained after treatment in Groups B and C. The immunohistochemical study with factor VIII-related antigen revealed an increase of vascular density in the ischemic region in Group A. Intramyocardial delivery of bFGF-impregnated AGHM, but not free-form bFGF, improves the collateral circulation to the infarct area of a coronary occlusion in dogs.

Animals↗

PubMed2001

Granulomatous colitis associated with botryomycosis of Propionibacterium acnes.

Propionibacterium acnes, an anaerobic, non-spore-forming, gram-positive bacillus, is a common inhabitant of the skin, and its virulence is considered to be low in humans. This report describes an unusual case of granulomatous colitis associated with P acnes infection in a 46-year-old woman. The affected cecum exhibited a tumor histologically characterized by massive transmural infiltrates of small lymphocytes and noncaseating epithelioid granulomas with multinucleated giant cells. Botryomycotic granules were also found in the muscular layer and paracolic connective tissues and consisted of gram-positive bacilli with filamentous growth. Polymerase chain reaction confirmed the presence of P acnes 16S ribosomal DNA in the surgical specimen of the colon. The patient developed a postoperative P acnes-induced peritonitis, which subsided with treatment with antibiotics and surgical drainage. The present case indicates that P acnes is one of the possible pathogens for granulomatous colitis.

Cecum↗

PubMed2001

[Epidemiologic study of diabetic retinopathy in nine hospitals in the Aomori area].

PURPOSE: To examine the prevalence of diabetic retinopathy and the relationship between diabetic retinopathy and systemic risk factors. METHODS: A cross sectional study of diabetic retinopathy was conducted on 1,826 eyes of 913 randomly selected patients with type 2 diabetes in 9 central hospitals in Aomori Prefecture and the surrounding district. Retinopathy levels and maculopathy were assessed by binocular funduscopy, fundus photography and, if necessary, by fluorescein angiography. Multiple logistic regression analysis was performed to determine independent effects of systemic risk factors on diabetic retinopathy. RESULTS: The prevalence of background retinopathy was 31%, of preproliferative retinopathy 5%, and of proliferative retinopathy 5% in all patients. However, in 3 hospitals in which the patients were routinely examined by fluorescein angiography, background retinopathy was found to be present in 60%, preproliferative retinopathy in 5%, and prolifertive retinopathy in 7%. Maculopathy was found in 8% of diabetic patients and the prevalence was 11% in the eyes with background retinopathy, 40% with preproliferative retinopathy, and 50% with proliferative retinopathy. Multiple logistic regression analysis showed that retinopathy was significantly associated with duration of diabetes, methods of diabetic control, hypertension, nephropathy, and neuropathy. CONCLUSION: The detection rate of background diabetic retinopathy by fluorescein angiography was twice as sensitive as that by binocular funduscopy and fundus photography. The prevalence of maculopathy increases with the progression of retinopathy. Several systemic risk factors have significant association with diabetic retinopathy and maculopathy.

Aged↗

PubMed2000

Increased in situ expression of nitric oxide synthase in human colorectal cancer.

There is growing evidence that nitric oxide (NO) has an important role in tumor growth. However, information on the expression of NO synthase (NOS) in colorectal cancers is scanty. We therefore investigated the distribution and expression of NOS in human colorectal cancers. The expression of three types of NOS, inducible (iNOS), endothelial (eNOS) and neuronal (nNOS), was examined by immunohistochemistry in 25 cases of colorectal cancer. The expression of iNOS was also investigated at the mRNA level using the reverse transcriptase polymerase chain reaction (RT-PCR) in 6 cases. Correlations were made between iNOS expression and the histopathological findings. Immunoreactive iNOS was detected in the tumor cells in 22 cases (88%) with diffuse cytoplasmic reactions. Expression of iNOS-mRNA detected by RT-PCR in three tumor tissues was over five-fold that in normal mucosa. Intensified immunoreactivity of iNOS was associated with vascular invasion. iNOS expression did not correlate with pathological staging, tumor size, lymph node metastasis, p53 expression or tumor vessel density. Immunoreactive eNOS stained more strongly in the endothelial cells of microvessels within and around the tumor than in the areas remote from the tumor. There is enhanced expression of iNOS and eNOS in human colorectal cancers, which may correlate with tumor growth and vascular invasion.

Adult↗

PubMed2000

Inhibition of progressive reduction of islet beta-cell mass in spontaneously diabetic Goto-Kakizaki rats by alpha-glucosidase inhibitor.

The Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, exhibits mild hyperglycemia with a reduction of beta-cell mass. The mechanism for islet structural changes in this model and whether the changes are affected by metabolic control are not known. In the present study, we examined the process of islet changes in male GK rats aged 6, 8, 12, 24, and 36 weeks. Treatment effects with an alpha-glucosidase inhibitor (Voglibose; Takeda, Osaka, Japan) for 24 weeks (12 to 36 weeks of age) were also evaluated. The beta-cell mass increased until 8 weeks of age in both GK and control rats, but the increase was significantly (P < .01) smaller in GK rats versus at 8 weeks of age. Thereafter, the beta-cell mass decreased in GK rats, whereas it remained constant in controls. Voglibose treatment significantly (P < .01) inhibited the reduction of beta-cell mass in GK rats. Proliferative activity of beta cells as measured by bromodeoxyuridine (BrdU) uptake was significantly (P < .05) lower in GK rats versus control rats at 6 and 8 weeks, but the difference disappeared after 12 weeks of age, regardless of Voglibose treatment. The present study thus demonstrates a progressive loss of beta cells in GK rats that was mitigated by Voglibose treatment. We consider that the beta-cell loss in GK rats was due to an early impairment in proliferative activity and reduced survival. Voglibose did not appear to stimulate beta-cell proliferation, but exerted its effect via a reduction of hyperglycemia.

Aging↗

PubMed2000

Effects of 15-month aldose reductase inhibition with fidarestat on the experimental diabetic neuropathy in rats.

We examined the effects of long-term treatment with an aldose reductase inhibitor (ARI) fidarestat on functional, morphological and metabolic changes in the peripheral nerve of 15-month diabetic rats induced by streptozotocin (STZ). Slowed F-wave, motor nerve and sensory nerve conduction velocities were corrected dose-dependently in fidarestat-treated diabetic rats. Morphometric analysis of myelinated fibers demonstrated that frequencies of abnormal fibers such as paranodal demyelination and axonal degeneration were reduced to the extent of normal levels by fidarestat-treatment. Axonal atrophy, distorted axon circularity and reduction of myelin sheath thickness were also inhibited. These effects were associated with normalization of increased levels of sorbitol and fructose and decreased level of myo-inositol in the peripheral nerve by fidarestat. Thus, the results demonstrated that long-term treatment with fidarestat substantially inhibited the functional and structural progression of diabetic neuropathy with inhibition of increased polyol pathway flux in diabetic rats.

Aldehyde Reductase↗

PubMed2000

Apoptosis, bcl-2 expression and p53 accumulation in myelodysplastic syndrome, myelodysplastic-syndrome-derived acute myelogenous leukemia and de novo acute myelogenous leukemia.

Apoptosis and its dysregulation have been implicated in dysplastic and ineffective hematopoiesis and the neoplastic transformation of bone marrow in myelodysplastic syndrome (MDS). To explore the role of apoptosis in hematological disorders, we examined the frequency of apoptotic cells by the in situ end labeling method in bone marrow specimens from 37 patients with MDS [refractory anemia (RA) 10 cases, RA with excess of blasts (RAEB) 27 cases including 12 cases with leukemic transformation], 12 patients with MDS-derived acute myelogenous leukemia (AML) and 13 patients with de novo AML. In addition, we investigated the relationship of apoptosis to the immunohistochemical expression of bcl-2 and p53 in these cases, and the association of apoptosis, bcl-2, and p53 with the leukemic evolution of MDS by examining sequential bone marrow samples of the same patient from the time of initial diagnosis to the time of overt leukemia. The percentage frequency of apoptotic cells was significantly greater in MDS (RA: 9.46 +/- 2.99%, m +/- SD; RAEB: 5. 60 +/- 3.09) as compared with those in MDS-derived AML (0.62 +/- 0. 37), de novo AML (0.28 +/- 0.11) and controls (1.00 +/- 0.59). On the other hand, the cases of RAEB with leukemic transformation exhibited a lower frequency of apoptotic cells and a higher frequency of bcl-2- and p53-positive cells than those without transformation. When the RAEB cases transformed to AML, the frequency of apoptotic cells was significantly reduced (2.96 +/- 1. 54 --> 0.62 +/- 0.37), while the frequencies of bcl-2-positive cells and p53-positive cells were greater (10.88 +/- 3.66 --> 30.54 +/- 7. 14, and 20.21 +/- 6.21 --> 32.34 +/- 14.71, respectively). In contrast to MDS-derived AML, over a half of de novo AML cases showed few p53-positive cells. These findings corroborate the earlier notion that apoptosis may play a substantial role in dysplastic and ineffective hematopoiesis in MDS. It is also suggested that the suppression of apoptosis associated with enhanced bcl-2 expression and p53 accumulation increases the probability of developing leukemia in MDS, and that oncogenetic development might be different between MDS-derived AML and de novo AML.

Adolescent↗

PubMed1999

Only limited effects of aminoguanidine treatment on peripheral nerve function, (Na+,K+)-ATPase activity and thrombomodulin expression in streptozotocin-induced diabetic rats.

AIMS/HYPOTHESIS: Aminoguanidine, a potent anti-glycation reagent, is known to be beneficial in experimental diabetic neuropathy. In this study, we explored the mechanisms of how aminoguanidine inhibits neuropathic changes in diabetes and compared its effects with those of insulin treatment. METHODS: Wistar rats, aged 8 weeks, were made diabetic by streptozotocin and given aminoguanidine dissolved in drinking water (1 g/l) for 8 weeks. Effects of daily insulin (protamine-zinc) treatment were also examined for comparison. At the end of the 8 weeks, we examined the peripheral nerve function and (Na+,K+)-ATPase activity and their relation to serum thrombomodulin concentrations that are considered as a marker of endothelial injury. RESULTS: Aminoguanidine treatment reduced the diabetes-induced decrease in tibial nerve conduction velocity by 47% (p < 0.05 vs untreated diabetic rats) and inhibited the loss of sciatic nerve (Na+,K+)-ATPase activity by 54% (p < 0.05 vs untreated diabetic rats). Insulin-treatment of diabetic rats restored these variables by 83% and 75%, respectively (both, p < 0.01 vs untreated diabetic rats). Thrombomodulin concentrations were increased (p < 0.01) in diabetic rats compared with those in non-diabetic controls and unaffected by aminoguanidine treatment. In contrast, the concentrations remained within the normal range in the insulin-treated group. CONCLUSION/INTERPRETATION: Although aminoguanidine treatment improved nerve conduction velocity and (Na+,K+)-ATPase activity, its effects were considerably less than those of insulin and were not apparent in some measures of endothelial cell injury.

Animals↗

PubMed1999

Peripheral nerve structure and function in long-term galactosemic dogs: morphometric and electron microscopic analyses.

Experimental galactosemia for activating the polyol pathway is used extensively to explore the pathogenesis of diabetic complications. However, despite the presence of severe neuropathy in galactosemic rats, changes in the peripheral nerve have not been well established in galactosemic dogs. We therefore conducted biochemical, electrophysiological, and morphometric studies on peripheral nervous systems (PNS) in dogs given a 30% galactose diet for 44 months. Age- and sex-matched dogs given a 30% cellulose diet were used as control. Chronic galactosemia resulted in accumulation of galactitol and decrease in myo-inositol in the sciatic nerve. Electrophysiological and teased fiber analyses demonstrated no significant abnormalities in the ulnar and peroneal nerves in galactosemic dogs. Morphometric analyses revealed a tendency of myelinated fiber atrophy (24% reduction of average fiber size) associated with 20% decrease (P < 0.05 vs control) in mean myelinated fiber occupancy rate in the peroneal nerve in galactosemic dogs. In the anterior mesenteric ganglion, there was a slight but significant increase (8%) in mean neuronal cell size in galactosemic dogs (P < 0.05 vs control). Electron microscopy revealed that galactosemia did not produce dystrophic and degenerative changes in the autonomic ganglion in dogs. We conclude that structural and functional changes in the PNS of galactosemic dogs are mild and different from those of the rat model. These findings suggest that the severity of peripheral neuropathy induced by chronic galactosemia may be species dependent.

Animals↗