Vascular, cardiac, and renal lesions attributed to primary systemic hypertension in western pygmy marmosets (Cebuella pygmaea).

In a retrospective study of a western pygmy marmoset (Cebuella pygmaea) colony, postmortem examination of 1/8 juvenile and 29/47 adult animals identified vascular, cardiac, and renal lesions consistent with systemic hypertension. This included frequent renal arteriolar hypertrophy, hyaline and proliferative arteriolosclerosis, fibrinoid necrosis of arterioles, glomerulosclerosis, and nephrosclerosis. Affected animals ranged from 0.6 to 12 years of age (mean 6 years) and had an observed male predominance. Genealogical relatedness was evident in several breeding pairs and spanned multiple generations. Concurrent cardiac and renal disease was commonly identified, although frequently subclinical, and both were important causes of morbidity and mortality in affected animals. Cardiomegaly and hypertrophy were typical features and were accompanied by left atrial thrombosis in 10 animals. Signs of heart failure included chronic pulmonary edema in 20 cases and body cavity effusions in 17. In the kidneys, 19 cases had glomerular disease and hypertensive vasculopathy, and 26 cases had nephrosclerosis or glomerulosclerosis. Common extrarenal secondary causes of hypertension were excluded by necropsy examination. The pathogenesis is suggested to involve primary hypertension leading to renal and cardiac disease. Elevated sympathetic activity might be an underlying factor in the frequent development of primary systemic hypertension in the pygmy marmoset, as for the owl monkey.

Two branchial pathological conditions, nuclear hypertrophy and abnormal epithelial proliferation, in Mya arenaria from northwest Russian coasts.

Histopathological analysis of soft-shell clams Mya arenaria collected from 2 northwest Russian locations disclosed high prevalence of 2 pathological gill conditions. One involved the occurrence of more or less extended gill areas in which the branchial filaments showed hyperchromatic (basophilic) epithelium with some hypertrophied nuclei, which were considered presumptive signs of viral infection. Another pathological condition involved abnormal proliferation of the branchial epithelium, which lost the main differential features of the normal branchial epithelium (ciliated and simple cell layer structure), becoming non-ciliated, pseudostratified or stratified hyperchromatic epithelium with abundant mitotic figures and frequent apoptotic cells. The most complex cases involved loss of the normal branchial filament architecture, which was replaced with tumour-like growths consisting of branching, convoluted epithelial projections with a connective stroma. Images suggesting migration (invasion) of cells from the abnormally proliferating epithelium to the subjacent connective tissue, which would involve malignancy, were observed in one individual. The occurrence of both pathological conditions in clams from both locations and their co-occurrence in one clam suggest the possibility of a common, possibly viral, aetiology. Furthermore, the high prevalence of the abnormal proliferative disorder in non-polluted areas suggests an infectious aetiology. Additional studies are needed to assess a viral aetiology for the nuclear hypertrophy and/or the abnormal epithelial proliferation as well as the malignancy of the latter condition.

Dorsal Atlantoaxial Ligament Hypertrophy as a Cause for Clinical Signs in Dogs with Dens Abnormalities.

The objective of this study is to suggest clinical and subclinical atlantoaxial (AA) instability as a cause for dorsal AA ligament hypertrophy responsible for clinical signs in dogs with dens abnormalities. Clinical information from five dogs with malformed dens and dorsal spinal cord compression at the AA junction was collected. All dogs had neck pain, associated with tetraparesis in three cases. Radiological examination revealed hypoplastic dens in two dogs and a defect in its ossification in the other three. Stress views were able to demonstrate obvious AA instability only in two cases, but it was suspected in the other owing to response to surgical fixation of the joint and the presence of a dorsal compressive band, which was considered an enlarged dorsal AA ligament. Surgical and histopathological examination of compressive tissue confirmed hypertrophy of the ligament. Long-term prognosis in the four operated cases, either by dorsal decompression and ventral fixation or by ventral fixation alone, was excellent. A malformed dens can cause subclinical instability, unnoted in dynamic studies. As instability may lead to hypertrophy of joint ligaments, soft tissue changes (specifically dorsal AA ligament hypertrophy) points out this instability and the need for joint fixation if surgical management is required.

CT findings in a dog with subacute myopathy and later fibrotic contracture of the infraspinatus muscle.

A 5-year-old Norwegian elkhound was referred due to an acute onset of lameness and persistent shoulder pain over a period of 3 weeks. Computed tomography demonstrated an enlarged, hypoattenuating right infraspinatus muscle with peripheral contrast enhancement and a nonenhancing center, without concurrent lesions in superficial structures or bones. The right infraspinatus muscle showed progressive atrophy on consecutive CT studies. The dog developed clinical symptoms compatible with fibrotic infraspinatus contracture 2 months after the initial presentation, and was treated with infraspinatus tenotomy. Histopathological diagnoses based on intraoperative biopsy samples were fibrotic muscle atrophy and muscle hypertrophy with regeneration.

Myocardial Changes in Diabetic and Nondiabetic Nonhuman Primates.

Diabetic human patients have increased risk of heart failure compared to healthy subjects. The underlying mechanisms for this are not fully understood, and to help develop improved treatment strategies, well-characterized animal models are essential. To investigate cardiac dysfunction in diabetes, this study evaluated myocardial changes in 10 aging rhesus monkeys with and without diabetes. Based on evaluation of plasma glycosylated hemoglobin and glucose, 7 of 10 rhesus macaques had diabetes for a minimum of 11 months, while 3 of 10 were categorized as nondiabetic. A detailed histological examination of formalin-fixed left ventricular myocardial samples was followed by a semiquantitative evaluation of myocardial fibrosis and fat infiltration; digital quantifications of myocardial collagen, lipofuscin, and nuclear area fractions; and measurements of cardiomyocyte diameter. Histological myocardial evaluation revealed the presence of lipofuscin; large nuclei; interstitial, replacement, and vascular fibrosis; adipocyte infiltration; and vacuolar degeneration with atrophy of cardiomyocytes and fibrosis. However, there were no differences between groups for semiquantitative fat infiltration, fibrosis, cardiomyocyte size, collagen, or nuclear and lipofuscin area fraction. Lipofuscin area fraction correlated with plasma insulin, triglyceride, total cholesterol, and high-density lipoprotein cholesterol concentrations. In conclusion, myocardial pathological changes were found in left ventricular myocardium in aged rhesus macaques, independent of the stage of diabetes. The duration of diabetes might have been too short to cause differences between groups.

Pseudodiverticula of the Small Intestine Associated With Idiopathic Smooth Muscle Hypertrophy in Domestic Rabbits ( Oryctolagus cuniculus).

Acquired outpouches of the intestinal tract are referred to as pseudodiverticula or false pulsion diverticula. In contrast to true diverticula, in which the wall contains all layers of the intestinal tract, the wall of pseudodiverticula lacks the tunica muscularis. Smooth muscle hypertrophy of the small intestine is commonly considered a cause of pseudodiverticulosis in animals due to increased intraluminal pressure. This study reports pseudodiverticula associated with idiopathic smooth muscle hypertrophy of the small intestine in lagomorphs. Four domestic rabbits had single or multiple (up to 200) pseudodiverticula of various size in the small intestine. In all cases the tunica muscularis was diffusely thickened, significantly exceeding reference thickness of 14 rabbits (mean, 112.3 µm; range, 26.3-389.0 µm). Clinical signs were considered to be caused by severe necrosis and inflammation of the wall of large pseudodiverticula, leading to perforation with subsequent peritonitis and mesenteric and omental abscess formation in 2 cases.

γ-Secretase Inhibition Induces Muscle Hypertrophy in a Notch-Independent Mechanism.

A wide variety of cellular processes and signaling events are regulated by the proteolytic enzyme γ-secretase. Notch-1 is one of the substrates of γ-secretase and its role in the regulation of muscle differentiation has been well described. Importantly, besides Notch-1, a number of proteins have been identified to undergo proteolysis by γ-secretase. To date, the specific role of γ-secretase during embryonic skeletal muscle differentiation has not been studied. Therefore, we address this question through the analysis of in vitro grown chick myogenic cells during the formation of multinucleated myotubes. The γ-secretase inhibitor DAPT (N-N[-(3,5-Difluorophenacetyl-l-alanyl)]-S-328 phenylglycine-t-butyl-ester) induces muscle hypertrophy. Knockdown of Notch-1 using siRNA specific to chick shows no significant effect in myotube size, suggesting that γ-secretase-dependent effects on muscle hypertrophy in chick myogenic cells are Notch-1-independent. We also investigate the effects of γ-secretase inhibition in the whole proteomic profile of chick myogenic cells. We identified 276 differentially expressed proteins from Label-free proteomic approach. Data overview of interaction network obtained from STRING show that after γ-secretase inhibition cells exhibited imbalance in protein metabolism, cytoskeleton/adhesion, and Sonic Hedgehog signaling. The collection of these results provides new insights into the role of γ-secretase in skeletal muscle hypertrophy.

Esophageal Dysfunction in Friesian Horses: Morphological Features.

Megaesophagus appears to be more common in Friesian horses than in other breeds. A prevalence of approximately 2% was observed among Friesian horses presented to the Wolvega Equine Clinic and the Utrecht University Equine Clinic. In this study, morphologic changes in the esophagi of Friesian horses with megaesophagus were compared with those of 6 control horses. Of 18 horses with clinically observed megaesophagus, only 12 animals had esophageal dilation at necropsy, usually involving the thoracic portion. Muscular hypertrophy of the distal esophagus was present in only one-third of the affected horses, indicating that this change is not the most relevant cause of megaesophagus in Friesians. Increased deposition of clumped and disorganized collagen was present in these clinically affected horses mainly in the non-dilated portion of the esophagus. At necropsy, a decrease in neural elements and elastin was present principally in horses with megaesophagus. Mild degeneration and necrosis of the tunica muscularis along the entire length of the esophagus were present in clinically affected horses and encountered only rarely in control animals. There were no significant differences among affected and control horses with respect to inflammation, mineralization, or the number of cells of Cajal. The increased occurrence of megaesophagus in the Friesian breed compared with other horse breeds, together with the presence of abnormal collagen in very young foals, supports the hypothesis that megaesophagus is hereditary in Friesians.

Imaging diagnosis--muscular hypertrophy of the small intestine and pseudodiverticula in a horse.

A 14-year-old Thoroughbred gelding was presented for chronic colic and weight loss. Transcutaneous and transrectal abdominal ultrasonography revealed distended, thickened small intestine with primary thickening of the muscularis and a focally more thickened loop with an echoic structure crossing the wall from the mucosa to the serosa. Visualization of diffuse thickening of the muscularis (muscular hypertrophy of the small intestine) and a focal lesion (pseudodiverticulum) helped clinicians make informed decisions. This case illustrates the importance of transabdominal and transrectal ultrasonography in horses with chronic colic and the relevance of considering the abnormalities in layering pattern of the intestinal wall.

Megaesophagus in Friesian horses associated with muscular hypertrophy of the caudal esophagus.

Friesian horses have a perceived high rate of congenital or hereditary diseases, including megaesophagus, that may lead to choke and death. A retrospective study was performed to determine the prevalence and pathologic characteristics of esophageal disease in 852 horses, including 17 Friesians, that had been necropsied over a 6-year period at the Diagnostic Center for Population and Animal Health. Forty-two horses had grossly described esophageal lesions (25 muscular hypertrophy, 7 hemorrhage, 6 megaesophagus, 4 erosion/ulceration, 3 obstruction, 2 tears, 2 secondary neoplasms, 2 lymphoid patches, 1 thin wall, 1 esophagitis). Some of these lesions occurred concurrently in the same horse. Ten of these horses died or were euthanatized because of severe esophageal disease (6 megaesophagus causing tears in 2 horses, 3 esophageal obstruction with food bolus, and 1 esophagitis). All 6 horses with megaesophagus were Friesians. No cause for megaesophagus was noted in the necropsy reports; however, 5 of these 6 Friesians had marked caudal esophageal muscular hypertrophy (wall thickness: 1.9 ± 0.3 cm). Microscopic review of the esophagus of these Friesians confirmed smooth muscle hypertrophy, with no obvious fibrosis, degeneration, or loss of myenteric plexi. Unlike the Friesians, the 4 non-Friesian horses with severe esophageal disease had esophageal obstruction with an intraluminal food bolus or severe esophagitis. None had caudal esophageal muscular hypertrophy. It is concluded that in comparison to other horse breeds, Friesians have a higher prevalence of severe esophageal disease, specifically megaesophagus, that is commonly associated with marked caudal muscular hypertrophy.

Treatment of clitoral hypertrophy containing an os clitoris and urethra in a young greyhound dog: a detailed surgical description.

This report provides a detailed description and images of a clitorectomy with a urethral transposition. As described, the clitorectomy is a straight-forward procedure, creating more normal female-like anatomy, and it resolves the clinical signs resulting from the exposed clitoris.

Traitement d'une hypertrophie du clitoris contenant un orifice de clitoris et l'urètre chez un jeune chienne Greyhound: description chirurgicale détaillée. Ce rapport fournit une description détaillée et des images d'une clitorectomie avec une transposition urétérale. Tel que décrite, la clitorectomie est une intervention simple, qui crée une anatomie femelle plus normale et règle les signes cliniques découlant d'un clitoris exposé.(Traduit par Isabelle Vallières).

Research Note: Muscle hypertrophy is associated with reversed sexual dimorphism in body size of quail.

Sexual dimorphism is phenotypic differences between males and females in the same species. In general, males in most animals are larger than females at the same age, however, in quail, females have a larger body size with greater muscle mass than males. To understand what characteristics in muscle growth play roles in reversed sexual dimorphism in quail, the weights and the characteristics of the pectoralis major and gastrocnemius muscles (PM and GM, respectively) of male and female quail were compared in the current study. The data showed that 15-wk-old female quail have significantly heavier bodies, and PM and GM weights compared to male quail (1.27-folds, 1.29-folds, and 1.16-folds, respectively). To compare muscle characteristics such as hypertrophy (increased size) and hyperplasia (increased cell number), the PM and GM were stained using hematoxylin and eosin, and then histological characteristics such as total cross-sectional area (CSA), number and size of myofibers, and muscle bundle of the muscles were measured and analyzed. In both PM and GM, there were no differences in total numbers of myofibers and muscle bundles as well as the average numbers of myofibers per bundle between sexes. However, the sizes of myofiber and the bundle were significantly increased in female compared to male (1.33-folds and 1.28-folds in PM, and both 1.23-folds in GM, respectively). The findings of the current study suggest that muscle hypertrophy in female quail, not hyperplasia, can be attributed to the sexual dimorphism in quail size.

In ovo probiotic supplementation promotes muscle growth and development in broiler embryos.

In chickens, muscle development during embryonic growth is predominantly by myofiber hyperplasia. Following hatch, muscle growth primarily occurs via hypertrophy of the existing myofibers. Since myofiber number is set at hatch, production of more muscle fibers during embryonic growth would provide a greater myofiber number at hatch and potential for posthatch muscle growth by hypertrophy. Therefore, to improve performance in broilers, this study investigated the effect of in ovo spray application of probiotics on overall morphometry and muscle development in broiler embryos. For the study, fertile Ross 308 eggs were sprayed with different probiotics; Lactobacillus paracasei DUP 13076 (LP) and L. rhamnosus NRRL B 442 (LR) prior to and during incubation. The embryos were sacrificed on d 7, 10, 14, and 18 for embryo morphometry and pectoralis major muscle (PMM) sampling. Muscle sections were stained and imaged to quantify muscle fiber density (MFD), myofiber cross-sectional area (CSA), and nuclei density. Additionally, gene expression assays were performed to elucidate the effect of probiotics on myogenic genes. In ovo probiotic supplementation was found to significantly improve embryo weight, breast weight, and leg weight (P < 0.05). Further, histological analysis of PMM revealed a significant increase in MFD and nuclei number in the probiotic-treated embryos when compared to the control (P < 0.05). In 18-day-old broiler embryos, myofibers in the treatment group had a significantly smaller CSA (LP: 95.27 ± 3.28 µm2, LR: 178.84 ± 15.1 µm2) when compared to the control (211.41 ± 15.67 µm2). This decrease in CSA was found to be associated with a concomitant increase in MFD (fibers/mm2) in the LP (13,647 ± 482.15) and LR (13,957 ± 463.13) group when compared to the control (7,680 ± 406.78). Additionally, this increase in myofibrillar hyperplasia in the treatment groups was associated with upregulation in the expression of key genes regulating muscle growth including MYF5, MYOD, MYOG, and IGF-1. In summary, in ovo spray application of probiotics promoted overall embryo growth and muscle development in broilers.

Short communication: In ovo injection of all-trans retinoic acid causes adipocyte hypertrophy in embryos but lost its effect in posthatch chickens.

The regulation of adipose deposition in broiler chickens is an important factor for production efficiency to poultry producers and health concerns to customers. Although vitamin A and its metabolite [all-trans retinoic acid (atRA)] have been used for studies on adipogenesis in mammals and avian, effects of embryonic atRA on adipose development in embryonic (E) and posthatch (D) ages in broiler chickens have not been studied yet. Different concentrations of atRA (0 M-2 µM) were injected in broiler eggs at E10, and adipose tissues were sampled at E16. Percentages of adipose tissues in chicken embryos were significantly increased in the group injected with 500 nM of atRA compared to the 0 M group (P < 0.05). In addition, the adipocyte cross-sectional area (CSA) was significantly greater by in ovo injection of 500 nM atRA compared to the injection of 0 M (P < 0.01). Moreover, in ovo atRA-injected embryos were hatched and BWs were measured at D0, D7, and D14. BWs were not different from those of the 0 M group. Percentages of adipose tissues and CSA of the in ovo atRA-injected group (500 nM) were not different from those of the 0 M group at D14. Taken together, the current study clearly showed that in ovo injection of atRA promoted adipose deposition with hypertrophy during embryonic development, but its effects were not maintained in early posthatch age in broiler chickens, implying that embryonic atRA has an important role in the regulation of adipose development in chicken embryos.

Aorto-septal angle, isolated basal septal hypertrophy, and systolic murmur in 122 cats.

INTRODUCTION/OBJECTIVES: Systolic murmurs in the absence of cardiac structural abnormalities are common in cats. Narrow aorto-septal angle (AoSA) and septal remodeling can be a cause of a systolic murmur in elderly human beings. The aim of this study was to measure the AoSA in cats and to investigate the association between the AoSA and the presence of a murmur and isolated basal septal hypertrophy (IBSH). ANIMALS: The study population comprised 122 cats. MATERIALS AND METHODS: A physical exam, blood pressure measurement, chest radiographs, and echocardiography were performed. RESULTS: A systolic murmur was audible in 39/122 cats. A difference between cats with and without a murmur was found for age (P=0.0001), interventricular basal septal thickness (BIVSd) (P=0.004), AoSA (P=0.003), aortic (P<0.0001), and pulmonic (P=0.021) flow velocity, the presence of IBSH (P<0.0001), and systolic anterior motion of the mitral valve (P=0.0002). More than 50% of cats with a murmur had an AoSA ≤122°. Less than 25% of the cats with an AoSA ≥137° had a murmur. The AoSA narrowed 0.55°/year of age (P<0.001), whereas the BIVSd increased 0.11 mm/year of age (P<0.0001); the BIVSd increased as the AoSA narrowed. In all cats with AoSA < 120°, IBSH was present. CONCLUSIONS: This study demonstrates that the probability of having a systolic murmur in cats is increased by the presence of a narrow AoSA. Aging was associated with a narrower AoSA and a thicker basal septum; these findings might represent an age-related heart remodeling.

Melatonin supplementation promotes muscle fiber hypertrophy and regulates lipid metabolism of skeletal muscle in weaned piglets.

Melatonin has been reported to play crucial roles in regulating meat quality, improving reproductive properties, and maintaining intestinal health in animal production, but whether it regulates skeletal muscle development in weaned piglet is rarely studied. This study was conducted to investigate the effects of melatonin on growth performance, skeletal muscle development, and lipid metabolism in animals by intragastric administration of melatonin solution. Twelve 28-d-old DLY (Duroc × Landrace × Yorkshire) weaned piglets with similar body weight were randomly divided into two groups: control group and melatonin group. The results showed that melatonin supplementation for 23 d had no effect on growth performance, but significantly reduced serum glucose content (P < 0.05). Remarkably, melatonin increased longissimus dorsi muscle (LDM) weight, eye muscle area and decreased the liver weight in weaned piglets (P < 0.05). In addition, the cross-sectional area of muscle fibers was increased (P < 0.05), while triglyceride levels were decreased in LDM and psoas major muscle by melatonin treatment (P < 0.05). Transcriptome sequencing showed melatonin induced the expression of genes related to skeletal muscle hypertrophy and fatty acid oxidation. Enrichment analysis indicated that melatonin regulated cholesterol metabolism, protein digestion and absorption, and mitophagy signaling pathways in muscle. Gene set enrichment analysis also confirmed the effects of melatonin on skeletal muscle development and mitochondrial structure and function. Moreover, quantitative real-time polymerase chain reaction analysis revealed that melatonin supplementation elevated the gene expression of cell differentiation and muscle fiber development, including paired box 7 (PAX7), myogenin (MYOG), myosin heavy chain (MYHC) IIA and MYHC IIB (P < 0.05), which was accompanied by increased insulin-like growth factor 1 (IGF-1) and insulin-like growth factor binding protein 5 (IGFBP5) expression in LDM (P < 0.05). Additionally, melatonin regulated lipid metabolism and activated mitochondrial function in muscle by increasing the mRNA abundance of cytochrome c oxidase subunit 6A (COX6A), COX5B, and carnitine palmitoyltransferase 2 (CPT2) and decreasing the mRNA expression of peroxisome proliferator-activated receptor gamma (PPARG), acetyl-CoA carboxylase (ACC) and fatty acid-binding protein 4 (FABP4) (P < 0.05). Together, our results suggest that melatonin could promote skeletal muscle growth and muscle fiber hypertrophy, improve mitochondrial function and decrease fat deposition in muscle.

Due to its extensive biological functions, melatonin has been widely used in animal production in recent years. The purpose of this study was to investigate the effects of melatonin on growth performance, muscle development, and lipid metabolism of weaned piglets. Twelve 28-d-old DLY (Duroc × Landrace × Yorkshire) weaned piglets were randomly divided into two groups: control group and melatonin group. The results showed that melatonin supplementation daily had no effect on growth performance, but increased muscle weight, eye muscle area, and decreased the liver weight in weaned piglets. Consistently, the cross-sectional area of myofiber increased, while triglyceride levels decreased in muscle. Melatonin induced the expression of genes related to skeletal muscle hypertrophy and fatty acid oxidation in muscle through transcriptome sequencing. Additionally, melatonin regulated cholesterol metabolism, protein digestion and absorption, and mitophagy signaling pathways in muscle. Gene set enrichment analysis also confirmed the effects of melatonin on skeletal muscle development and mitochondrial function. Moreover, melatonin supplementation elevated the gene expression of cell differentiation and muscle fiber development. Additionally, melatonin inhibited the mRNA expression related to fat synthesis while improved mitochondrial function in muscle. Together, our results suggest melatonin could promote skeletal muscle growth and muscle fiber hypertrophy, enhance mitochondrial function and decrease fat deposition in muscle.

Clinical findings using echocardiography and plasma cardiac troponin I and pathological findings in dogs with hypertrophic cardiomyopathy: A retrospective study.

Background: Hypertrophic cardiomyopathy (HCM) is considered rare in dogs, and there is a lack of clinical data. Cardiac troponin I (cTnI) is a biomarker of cardiomyocyte damage and necrosis and can be used to diagnose cat and human HCM. Aim: We investigated whether the presence of cTnI in clinical data can be used in conjunction with echocardiography to diagnose canine HCM. Methods: This study comprised client-owned dogs with clinical evidence of concentric hypertrophy on echocardiographic images, serum total thyroxine levels of ≤5 µg/dl, systolic blood pressure of ≤180 mmHg, and absence of aortic stenosis. All cases were necropsied. Results: Cardiomyocyte hypertrophy (mean diameter, 18.3 ± 1.8 µm), myocardial fiber disarray (70%), interstitial fibrosis (80%), and small vessel disease (100%) were assessed. In dogs with HCM, the left ventricles were concentric, almost symmetrical, and hypertrophied above the aortic diameter. The end-diastolic interventricular septum normalized to body weight [intraventricular septal thickness in diastole (IVSDN)] was 0.788 [interquartile range (IQR), 0.7-0.92], which exceeded the normal range (5%-95%, IQR: 0.33-0.52). In total, 70% of the dogs with HCM had syncope and dyspnea, and all dogs had high cTnI levels (median, 3.94 ng/ml), exceeding the upper limit of normal (0.11 ng/ml) and indicating cardiomyocyte damage. IVSDN and serum cTnI levels were correlated (ρ = 0.839, p = 0.01). Conclusion: Ventricular wall thickening and high serum cTnI levels can provide a presumptive diagnosis of HCM and prompt the initiation of treatment or additional diagnostic investigations.

Unilateral orchidectomy in mature cats is not followed by compensatory hypertrophy.

The aim of this study was to describe the effect of unilateral orchidectomy on testicular characteristics of mature domestic cats. Five, 1- to 2-year-old, cross-bred male cats were unilaterally orchidectomized on day 0 (right) and day 60 (left). The testes were processed for histological and immunohistochemical evaluation and groups compared by Student's t-test. No significant differences (p > 0.05) were found between testes groups for any of the gross (volume and gonadosomatic index) and microscopic (tubular diameters, axis, area, length and perimeter, germinal epithelium height, spermatogonias, spermatocytes, spermatids, spermatozoa, Sertoli and Leydig cells, intertubular compartment, lumen, cellular debris, tubular- intertubular proportion and basement membrane) parameters assessed. According to these biometric and morphometric results, mature cats do not develop compensatory hypertrophy within 60 days of unilateral orchidectomy.

Neural Hypertrophy and Hyperplasia in a Case of Chronic Ovine Pancreatitis.

Nerves can be severely reshaped in human pancreatic diseases such as chronic pancreatitis (CP) and pancreatic cancer, in which pancreatic nerves can undergo hypertrophy or hyperplasia. This neural plasticity is associated with neuropathic pain. Although there are several animal models of CP, pancreatic neuropathy is not well-characterized. Thus, the translational value of these in-vivo models cannot be entirely ascertained for the study of neural plasticity. We now describe spontaneous alterations characteristic of pancreatic neural plasticity in a lamb. Microscopic lesions of chronic sclerosing pancreatitis were associated with neuronal hypertrophy and hyperplasia. Although CP and pancreatic tumours are common in many animal species, to the authors' knowledge, spontaneous occurrence of associated pancreatic neural plasticity has not been reported in any non-human species. Sheep might be a suitable animal model for the study of this condition.

Pathogenesis of venous hypertrophy associated with schistosomiasis in whooper swans (Cygnus cygnus) in Japan.

Thirteen whooper swans (Cygnus cygnus) affected with schistosomiasis were examined pathologically. Venous hypertrophy, characterized by marked nodular proliferation of medial smooth muscle fibers with frequent obliteration of the vascular lumen, was observed in eight of the 13 whooper swans. Venous hypertrophy was located in the medium-sized veins of the mesentery, the serosa, and the muscular layer of the duodenum, jejunum, ileum, and cecum. In addition, vascular lesions were seen in the capsule and parenchymal interstitia of the liver, spleen, kidney, heart, aorta, air sac, and pleura. In mild lesions, segmental proliferation of medial smooth muscles was observed in the venous medium of the mesentery and serosa. Moderate lesions had a proliferation of smooth muscles in the veins with obliteration of venous lumens. In marked lesions, more severe proliferation of veins extended into the intestinal muscular layers and depressed them. Schistosome parasites were found in the venous lumens of each of the eight whooper swans with vascular lesions. Bile pigments and hemosiderin were observed in the livers of whooper swans. In addition, adult nematodes (Sarconema sp.) were localized in the myocardium of four of the eight whooper swans. The venous hypertrophy may be caused by the proliferation of medial smooth muscle fibers induced by schistosomiasis.