Muscle Necrosis Research Articles

Histologic Observations of Dermal Wound Healing in a Free‐Ranging Blacktip Shark from the Southeastern U.S. Atlantic Coast: A Case Report

Despite indications that sharks have an exceptional capacity to heal from traumatic injuries, no detailed microscopic observations of integumental wounds have been reported for sharks. This study details the histopathological features of such wounds in a free-ranging shark. An adult male Blacktip Shark Carcharhinus limbatus was collected in 2017 during fisheries-independent sampling efforts in the coastal southeastern U.S. Atlantic. The shark had numerous lesions on his head, torso, and left pectoral fin that were compatible with shark bites. Representative samples from two wounds on the head were examined by light microscopy. The epidermal changes included hyperplasia and hypertrophy; intracellular edema; and the absence of goblet cells, denticles, and chromatophores. In the dermis, fibrinocellular exudation, granulation tissue, and marked skeletal muscle necrosis and regeneration were observed. The above features were comparable to wound healing in bony fish, albeit minor differences were found. Although this case documents exceptionally good regeneration of skeletal muscle in the shark, we found no evidence of unique morphological healing patterns. Further studies on wound healing are needed because recent molecular and genetic findings do suggest evolutionary adaptations enhancing healing in sharks.

Assessment of the potential impact of embedded radioactive fragments following the use of a crude radiological dispersal device (‘dirty bomb’)

This work was undertaken to understand what would happen if a high-activity radioactive fragment became embedded in an individual following the use of a crude radiological dispersal device (‘dirty bomb’). Two areas were addressed: how would a high-activity fragment be viewed on modern digital x-ray imaging systems; and, what would be the impact on medical management for the patient? A set of experimental trials were undertaken using an iridium-192 source and a DRagon mobile x-ray set equipped with a Canon CXDI-50G portable flat panel digital detector plate. In addition, the potential doses to a surgical team were calculated and potential doses to a patient were assessed using a Monte Carlo code, in which a radioactive point source of nil volume was located within a limb of an anthropomorphic voxel phantom. Three distinct effects on the digital imaging systems were observed, referred to in this paper as a localised ‘bloom’ effect, a ‘discontinuity’ effect towards the middle of the image and ‘fogging’ across the entire image. The first two of these effects were unexpected, and possible reasons for their appearance are discussed. The Monte Carlo modelling showed that the patient exposure can potentially lead to very high localised absorbed doses, which may result in symptoms associated with acute radiation syndrome. While the dose clearly depends upon the activity of the fragment and the length of time that the fragment is present inside the patient, it is clear that radiation necrosis of bone, muscle and other tissues may threaten the medium term viability of the limb. The dose rates associated with high-activity fragments may also restrict the time a surgeon has to operate, leading to challenging ethical and surgical decisions. Low-activity fragments allow for conventional surgical management to be considered with appropriate control measures.

Characterization of macrophages, giant cells and granulomas during muscle regeneration after irradiation

Macrophages play a fundamental role in the different stages of muscle regeneration although the precise mechanisms involved are not entirely understood. Here we investigated the types of macrophages and cytokines that appeared in muscles after local gamma irradiation of mini-pigs that underwent no subsequent treatment or received three successive adipose tissue-derived stem cell (ASC) injections. Although some variability was observed among the three animals included in each study group, a general picture emerged. No macrophages appeared in control muscles from regions that had not been irradiated nor in muscles from irradiated regions derived from two animals. A third irradiated, but untreated animal, with characteristic muscle fibrosis and necrosis due to irradiation, showed invasion of M2 macrophages within small muscle lesions. In contrast, among the three ASC-treated and irradiated animals, one of them had completely recovered normal muscle architecture at the time of sampling with no invading macrophages, muscle from a second one contained mostly M1 macrophages and some M2-like macrophages whereas muscle from a third one displayed granulomas and giant cells. ASC treatment was associated with the presence of similar levels of pro-inflammatory cytokines within the two animals in the process of muscle regeneration whereas the levels of IL-4 and IL-10 expression were distinct from one animal to another. Microspectrofluorimetry and in situ hybridization revealed strong expression of TGF-β1 and TNFα in regenerating muscle. Overall, the data confirm the critical role of macrophages in muscle regeneration and suggest the involvement of a complex network of cytokine expression for successful recovery.

Emicizumab Associated Rhabdomyolysis in Hemophilia A

Emicizumab is increasingly the front-line treatment for patients with Hemophilia A with or without inhibitors. Rhabdomyolysis is a syndrome of muscle necrosis and release of intracellular muscle constituents into the circulation. Creatine kinase (CK) levels are typically markedly elevated, and muscle pain and myoglobinuria may be present. The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening disease associated with extreme enzyme elevations, electrolyte imbalances, acute kidney injury and disseminated intravascular coagulation. We present a case of an African American male with severe hemophilia A and history of factor VIII inhibitor, maintained on emicizumab prophylaxis, who developed rhabdomyolysis with a symptomatic hyperCKemia. To date, there is no known link between rhabdomyolysis to emicizumab. This report brings to light the possibility of symptomatic rhabdomyolysis as a potential side effect of emicizumab after moderate exertional activity.

Getting it Right the First Time: Frozen Sections for Diagnosing Necrotizing Soft Tissue Infections

BackgroundThe aim of this study was to investigate which histopathologic findings are most indicative for necrotizing soft tissue infections (NSTIs) in ambivalent cases.MethodsPatients undergoing surgical exploration for suspected NSTIs with obtainment of incisional biopsies for histopathological assessment were included from January 2013 until August 2019. The frozen sections and formalin-fixed paraffin-embedded (FFPE) samples were retrospectively re-assessed. The primary outcome was the discharge diagnosis.ResultsTwenty-seven (69%) biopsies of the 39 included samples were from patients with NSTIs. Microscopic bullae (p = 0.043), severe fascial inflammation (p < 0.001) and fascial necrosis (p < 0.001) were significantly more often present in the NSTI group compared to the non-NSTI group. Muscle edema (n = 5), severe muscle inflammation (n = 5), muscle necrosis (n = 8), thrombosis (n = 10) and vasculitis (n = 5) were most frequently only seen in the NSTI group. In thirteen tissues samples, there were some discrepancies between the severity of findings in the frozen section and the FFPE samples. None of these discrepancies resulted in a different diagnosis or treatment strategy.ConclusionMicroscopic bullae, severe fascial or muscle inflammation, fascial or muscle necrosis, muscle edema, thrombosis and vasculitis upon histopathological evaluation all indicate a high probability of a NSTI. At our institution, diagnosing NSTIs is aided by using intra-operative frozen section as part of triple diagnostics in ambivalent cases. Based on the relation between histopathologic findings and final presence of NSTI, we recommend frozen section for diagnosing NSTIs in ambivalent cases.

Bioaccumulation of heavy metals and histopathological changes in muscles of common carp (Cyprinus carpio L.) in the Iraqi rivers

The aim of this study is to evaluate the contamination status of Iraqi rivers in the north of the Tigris river (Tikrit city) and the middle region of Euphrates (Babylon Governorate). In this study As, Zn, Fe, Pb, and Cu in the muscle tissue of carp fish were measured. The results show that the concentration of arsenic in the fish muscles in the middle region was 425.05 ppm higher than its concentration of about 192.25 ppm in fish muscle in the Tigris river with statistical significance (p < 0.05). Which it causes histopathological changes characterized by Zenker necrosis in skeletal muscle and infiltration of inflammatory cells with edema additional to edematous dermatitis. Other heavy metals in fish muscle were less than in fish muscles which agreement with the international legislation limits. Also, there were positive correlation ships between Zn and Pb and between Cu and Zn. While negative correlation has been detected between arsenic and both (Pb) and(Zn). This study is concluded that the accumulation of heavy metals causes histological changes in fish muscle provides an opportunity to assess fish health as well as information on possible health hazards coming from their environment.

DMD – BIOMARKERS & OUTCOME MEASURES: P.122 Translational implications of increased S100-beta and Tau5 proteins in dystrophic nerves of mdx mouse and rat models for Duchenne muscular dystrophy

In dystrophic mdx mouse and dog models of Duchenne muscular dystrophy (DMD) repeated intrinsic muscle necrosis also damages the neuromuscular junctions (NMJs) with progressively altered NMJ morphology. We propose that these altered NMJs result in premature changes in dystrophic nerves and this was tested by immunoblotting. These analyses were built upon our observations related to normal ageing and sarcopenia, where time course studies show denervation of NMJs and myofibres along with neurodegeneration of peripheral nerves by 18 to 22 months(m), and also changes in normal old spinal cords.

Acute compartment syndrome caused by hematoma after shoulder surgery: a case series

The development of acute compartment syndrome (ACS) of the upper extremity after an elective surgical shoulder procedure is rare but can have devastating results. We describe a series of patients who developed ACS of the upper extremity caused by hematoma formation and subsequent upper extremity swelling after undergoing elective surgical shoulder procedures. We retrospectively reviewed the database of our tertiary care institution between 2004 and 2019 to find patients who developed ACS after elective shoulder surgery. We found 4 such patients and reviewed their medical records and extracted data on their history, clinical examination, predisposing factors, treatment, and clinical and radiographic outcomes. Of the 4 patients treated, 2 had undergone reverse total shoulder arthroplasty, 1 had undergone open biceps tenodesis, and 1 had undergone closed manipulation for adhesive capsulitis. Two patients developed symptoms of ACS within 24 hours of the index procedure. Both were treated with immediate decompression of the hematoma, and both experienced complete pain relief and full recovery of function at 1-year follow-up. Two patients were on anticoagulation therapy. Of these, 1 patient developed ACS symptoms 14 days after a revision reverse total shoulder arthroplasty and was treated successfully with compartment release. Despite treatment, the other patient developed extensive necrosis of muscles and nerves in the upper extremity and severe neurologic deficits in hand and forearm function. ACS of the upper extremity caused by hematoma formation can lead to catastrophic outcomes if diagnosis and treatment are not immediate. Providers should be aware of ACS and the need for prompt diagnosis and treatment.

Dystrophic Dmdmdx rats show early neuronal changes (increased S100β and Tau5) at 8 months, supporting severe dystropathology in this rodent model of Duchenne muscular dystrophy

The intrinsic necrosis of skeletal muscles in animal models of Duchenne muscular dystrophy (DMD) damages neuromuscular junctions (NMJs) with progressively altered NMJs associated with denervation and premature changes in dystrophic nerves. In the mdx mouse model of DMD, the proteins S100β and Tau5 are significantly increased in sciatic nerves by 13 months (M) of age, far earlier (by 9 M) than in normal wildtype (WT) nerves. Since dystrophic Dmdmdx rats are reported to have a more severe dystropathology than mdx mice, we hypothesised that Dmdmdx rat nerves would show earlier neuronal changes compared with mdx nerves. We quantified levels of 8 proteins (by immunoblotting) in sciatic and radial nerves from young adult Dmdmdx rats (aged 8 M) and mdx mice (9 M), plus levels of 7 mRNAs (by qPCR) in rat nerves only. Sciatic nerves of 8 M Dmdmdx rats had more consistently increased levels of S100β and Tau5 proteins, compared with 9 M mdx mice, supporting pronounced dystropathology in the rat model. There were no differences for mRNA levels, apart from higher gelsolin mRNA in Dmdmdx sciatic nerves. The pronounced protein changes in Dmdmdx nerves indicate a severe ongoing myonecrosis, and likely consequent myofibre denervation, for the dystrophic rat model. These data support increased neuronal proteins in dystrophic nerves as a novel pre-clinical readout of ongoing myonecrosis for DMD research. In older DMD boys, such progressive neuronal changes over many years are likely to contribute to loss of muscle function, and may complicate evaluation of late-onset clinical therapies.

Post-mortem examination of the Caribbean spiny lobster (Panulirus argus, Latreille 1804) and pathology in a fishery of the Lesser Antilles

The Caribbean spiny lobster, Panulirus argus (Latreille, 1804) is a highly commercial species and comprises the largest spiny lobster fishery in the world. Although populations have declined throughout its range, there is little known regarding its diseases and pathogens. The objectives of this study were to provide illustrated and standardized methods for postmortem examination, and to describe baseline gross and microscopic pathology for P. argus. From July 2017–March 2019, a postmortem examination including comprehensive histological assessment was performed on 313 fishery-caught lobsters. Epibionts and lesions observed include branchial cirriped infestation (69%), branchial encysted nemertean worm larvae (23%), tail fan necrosis (11%), skeletal muscle necrosis (7%), antennal gland calculi (6%), branchial infarction (2%), and microsporidiosis (0.6%). This report confirms the rare prevalence of microsporidiosis in P. argus and describes nemertean worm larvae in the gill. This study also reports a condition resembling excretory calcinosis in spiny lobster. The methods and data produced by this study facilitate disease diagnosis and sustainable stock management of P. argus.

Simultaneous detection of scale drop disease virus and Flavobacterium columnare from diseased freshwater-reared barramundi Lates calcarifer.

Freshwater farming of barramundi Lates calcarifer in Thailand is a growing sector in aquaculture, but mortalities due to infectious diseases are still a major threat to this industry. In 2018, an episode of severe mortality in juvenile barramundi was noted in a freshwater earth pond site. Fish presented with severe gill necrosis, as well as severe cutaneous hemorrhages, scale loss, and discoloration at the base of dorsal fin (saddleback lesions). Histopathology revealed extensive necrosis of skeletal muscle and gill filaments, as well as basophilic inclusion bodies and megalocytosis in muscle, gill, liver, and kidney. Scale drop disease virus (SDDV) infection was subsequently confirmed by virus-specific semi-nested PCR. Further, DNA sequences of the viral major capsid protein (MCP) and ATPase genes had a respective homology of 99.85 and 99.92% with sequences of SDDV infecting barramundi in saltwater culture. Gill necrosis and saddleback lesions are not typical lesions associated with scale drop syndrome. Their presence was explained by Flavobacterium columnare isolation from the gill, followed by positive F. columnare-specific PCR. To our knowledge, this is the first report of SDDV-associated mortality in freshwater-farmed barramundi. Furthermore, this mortality presented as a concurrent infection with SDDV and F. columnare, with typical lesions of both infections.

Curcumin protects cardiomyopathy damage through inhibiting the production of reactive oxygen species in type 2 diabetic mice

Type 2 diabetes mellitus (DM)-induced cardiomyopathy is a multifactorial and complex disease involving oxidative stress, lipids, and fibrosis. It is based on metabolic disorders and microvascular disease and causes extensive focal necrosis of the heart muscle. Curcumin (CUR) is a natural polyphenol isolated from turmeric rhizomes and plays an important role in the antioxidant, anti-apoptotic and anti-inflammatory effects of diabetes. Therefore, we established a mouse model of diabetic cardiomyopathy (DCM) in type 2 diabetic db/db mice in our study. We divided the experiment into three groups: the control group, DM group and DM + CUR group.We performed cardiac dissection on mice treated in different conditions and conducted special pathological staining on isolated cardiac tissue. We were surprised to find that a high glucose environment can promote cardiomyocyte apoptosis by TUNEL assay. In addition, after detecting dihydroethiidine (DHE), hematoxylin-eosin (H&E) and Oil Red O staining, we unexpectedly found that CUR can inhibit the production of reactive oxygen species (ROS), reduce myocardial apoptosis, and myocardial lipid accumulation. CUR upregulated the expression of Bcl-2, and downstream the expression of Bax and Caspase-3 proteins by immunohistochemical determination and western blotting. Therefore, these results suggest that CUR has a certain protective effect on diabetic cardiomyopathy by inhibiting the production of ROS.

"The Social Network" and Muscular Dystrophies: The Lesson Learnt about the Niche Environment as a Target for Therapeutic Strategies.

The muscle stem cells niche is essential in neuromuscular disorders. Muscle injury and myofiber death are the main triggers of muscle regeneration via satellite cell activation. However, in degenerative diseases such as muscular dystrophy, regeneration still keep elusive. In these pathologies, stem cell loss occurs over time, and missing signals limiting damaged tissue from activating the regenerative process can be envisaged. It is unclear what comes first: the lack of regeneration due to satellite cell defects, their pool exhaustion for degeneration/regeneration cycles, or the inhibitory mechanisms caused by muscle damage and fibrosis mediators. Herein, Duchenne muscular dystrophy has been taken as a paradigm, as several drugs have been tested at the preclinical and clinical levels, targeting secondary events in the complex pathogenesis derived from lack of dystrophin. We focused on the crucial roles that pro-inflammatory and pro-fibrotic cytokines play in triggering muscle necrosis after damage and stimulating satellite cell activation and self-renewal, along with growth and mechanical factors. These processes contribute to regeneration and niche maintenance. We review the main effects of drugs on regeneration biomarkers to assess whether targeting pathogenic events can help to protect niche homeostasis and enhance regeneration efficiency other than protecting newly formed fibers from further damage.

Effects of alpha-lipoic acid on skeletal muscle ischemia-reperfusion injury in mice

Aim: The main problem in the treatment of cardiovascular diseases, which is the most common cause of death in the world today, is reperfusion injury. In our study, we investigated the effects of alpha-lipoic acid on lower limb ischemia-reperfusion injury. Methods: In this study, 30 male Swiss breed albino mice weighing 45-65 g were used. Mice were randomly divided into 5 groups (Control group (C), Dimethyl Sulfoxide (DMSO) group, ischemia-reperfusion (IR) group, alpha-lipoic acid control group (ALA), alpha-lipoic acid - IR group (ALA+IR)), 6 mice in each group. All groups were administered 100 IU/kg intravenous heparin bolus 30 minutes before the procedure. Lower limb ischemia (2 hours) and reperfusion (2 hours) protocols were applied to the IR and ALA+IR groups by clamping the main femoral artery. Alpha-lipoic acid was administered to ALA and ALA+IR groups 1 hour before the experimental procedure (100 mg/kg intraperitoneal). After the experiment protocol, the lower limb gastrocnemius muscles were collected from the sacrificed mice and total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), Myeloperoxidase (MPO) and Malondialdehyde (MDA) levels were determined in the tissue. In addition, edema, necrosis, and inflammatory cell infiltration levels in the skeletal muscle were determined by histologic grading, and apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Results: TAS measurements of ALA group subjects were higher than the control group (P=0.01). The TOS level of the ALA+IR group was lower than the IR group (P=0.01), but higher than the C, ALA, and DMSO groups. The OSI index of the IR group was significantly higher than the ALA+IR group (P=0.01). It was observed that the IR group was at higher levels than the ALA+IR group (P=0.01). MDA measurements of IR group subjects were higher than that of the C, ALA, DMSO, ALA+IR groups (P=0.01). Edema of the IR and ALA+IR group subjects were higher than the C, ALA, DMSO groups (P=0.01). Necrosis measurements of IR and ALA+IR group subjects were higher than C, ALA, DMSO groups (P=0.01). Inflammatory cell infiltration measurements of IR and ALA+IR group subjects were higher than C, ALA, DMSO groups (P=0.01). Apoptosis level was significantly lower in the ALA+IR group than in the IR group. (P=0.01). Conclusion: The results showed us that alpha-lipoic acid has a protective effect against oxidative damage, inflammation, and apoptosis in the tissue in lower limb ischemia-reperfusion.

Leatherback Sea Turtle (Dermochelys coriacea) Embryo and Hatchling Pathology in Grenada, with Comparison to St. Kitts

Globally, the hatch success of leatherback sea turtles (Dermochelys coriacea) is much lower than any other sea turtle species. Causes of embryonic mortality, a contributing factor to the low hatch success of the species, are poorly understood. Muscle necrosis, renal mineralization, and bacterial pneumonia are prevalent among embryos and hatchlings in St. Kitts, where hatch success is much lower (<∼ 20%) than the global average (∼ 50%), yet the significance of these conditions in the wider region is unknown. The objective of this study was to describe the pathology of hatchlings and embryos in Grenada as a comparison population for St. Kitts. In 2017, 20 hatchlings, 6 pipped hatchlings, 35 late stage embryos, and 5 early stage embryos were sampled for comprehensive postmortem examination from 12 leatherback nests on Levera Beach, Grenada and 2 nests on St. Kitts. Pathology affected 71% of nests and 44% of individuals from Grenada and 100% of nests and 56% of individuals from St. Kitts. Lesions observed in both populations included skeletal muscle degeneration and necrosis (19%), bronchopneumonia (8%), and renal tubular degeneration (5%) while chorioallantoitis (17%) and mycotic dermatitis (5%) were only observed in Grenada. Gonads were histologically classified as female in all instances (n = 60), suggestive of high incubation temperatures in nests at both locations. Further study is needed to find interventions that reduce the prevalence of perinatal pathology and to identify the basis for the large proportion of eggs that fail to develop as well as embryos that die without significant pathology.

Initial seronegative immune-mediated necrotising myopathy with subsequent anti-HMGCR antibody development and response to rituximab: case report

BackgroundImmune-mediated necrotising myopathy (IMNM) is characterised by severe muscle weakness and necrosis with a paucity of inflammation on muscle biopsy. Around 60% of cases are associated with antibodies to the signal recognition particle (SRP) or 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR); the remainder are seronegative. IMNM is more treatment resistant than inflammatory myopathies.Case presentationA 69-year-old woman with previous statin exposure presented aged 63 with muscle weakness and raised creatinine kinase (CK). Anti-SRP and anti-HMGCR antibodies were not detected, but muscle biopsy revealed changes consistent with necrotising myopathy. Statins were discontinued, and she was treated with prednisolone and methotrexate achieving disease remission. Clinical and biochemical parameters were largely stable until 6 years after diagnosis she experienced a rapid deterioration. This was found to be associated with new development of anti-HMGCR antibody. Rituximab was commenced, resulting rapidly in remission. She has remained in remission since, following 2 cycles of rituximab.ConclusionsTo our knowledge, this is the first reported case of serologically negative IMNM whose subsequent rapid deterioration was associated with development of anti-HMGCR antibody. The response to rituximab and subsequent sustained remission suggests a role for early use of rituximab in aggressive cases of anti-HMGCR myopathy.

Effects of ASC Application on Endplate Regeneration Upon Glycerol-Induced Muscle Damage.

Amongst other approaches, adipose-derived stromal cells (ASCs) have recently been tested with respect to their regenerative capacity for treatment of neuromuscular disorders. While beneficial effects of ASCs on muscle recovery were observed previously, their impact on regeneration of neuromuscular junctions (NMJs) is unclear. Here, we used a murine glycerol damage model to study disruption and regeneration of NMJs and to evaluate the effects of systemic application of ASCs on muscle and NMJ recovery. In mice that were not treated with ASCs, a differential response of NMJ pre- and post-synapses to glycerol-induced damage was observed. While post-synapses were still present in regions that were necrotic and lacking actin and dystrophin, pre-synapses disappeared soon in those affected areas. Partial regeneration of NMJs occurred within 11 days after damage. ASC treatment slightly enhanced NMJ recovery and reduced the loss of presynaptic sites, but also led to a late phase of muscle necrosis and fibrosis. In summary, the results suggest a differential sensitivity of NMJ pre- and post-synapses to glycerol-induced muscle damage and that the use of ASC for the treatment of neuromuscular disorders needs further careful evaluation.

Protective Role of Juniperus phoenicea L. Leaves Extract against Gamma-irradiation-induced Oxidative Stress.

Radiation exposure can cause several harmful effects in biological systems due to free radical production. Several antioxidants have been tested as potential hepatoprotective agents against ionizing radiation as they lower oxidative stress in normal cells induced by Reactive Oxygen Species (ROS). The present study was conducted to evaluate the possible ameliorative effects of Juniperus phoenicea L. Aqueous leaves extract on different biochemical and histopathological parameters against whole body gamma-irradiation-induced oxidative stress, organ dysfunction and metabolic disturbances in experimental Swiss Albino rats. After a single dose of gamma-radiation (6 Gy), there was a significant reduction in albumin, total protein and globulin levels and a significant increase in the liver enzymes (ALT, AST, ALP and GGT) and lipid profile parameters (cholesterol, triglyceride, HDL-cholesterol and LDL-cholesterol) in gamma-irradiated rats unlike in normal controls. The gamma-irradiated rats pre-treated with J. phoenicea leaf extracts, however, showed a significant increase in albumin, total protein and globulin levels and a significant reduction in liver enzymes and lipid profile parameters as opposed to the untreated ones. The gamma-irradiated rats showed toxic changes in the liver, whereas, the rats pre-treated with J. phoenicea leaves extract demonstrated a protective effect. Additionally, gamma- irradiation caused myocardial degenerative changes, interstitial edema between muscle fibers, necrosis and inflammatory cells infiltration and fibrotic and cellular damages to the heart, but J. phoenicea leaves extract were found to ameliorate the gamma-irradiation-induced changes in the heart. The results suggested that treatment with J. phoenicea leaves extract is possibly safe and can ameliorate gamma-irradiation-induced oxidative damage and tissue injury in rats. The leaves of J. phoenicea could serve as a potential source of therapeutic antioxidants.

A Case of Deep Femoral Artery Aneurysm with Necrosis of the Femoral Muscle

A Case of Deep Femoral Artery Aneurysm with Necrosis of the Femoral Muscle

Histological changes in skin and gill of fresh water EUS infected fish Channa punctatus

Histopathology is an important diseases diagnostic tool. Penetration into the host is the first step for a microbial agent to mutiply and invade the vital organs of its host. Like all animals fishes suffers from environmental, stress, which is followed by pathogenic attacks and parasitic afflictions causing Epizootic Ulcerative syndrome (EUS). Histological investigations of tissues of EUS infected fish Channa punctatus showed an eroded epidermis, necrosis of skeletal muscles and intense granulomatous inflammation, infiltration of mixed inflammatory cells in muscular as well as submuscular layers of the skin. Also a characteristic focal grannular granuloma in the gill lamellae was noticed. The electron microscopic observations, of the tissue cells of the fishe showed viruses like Parvovirus even at a red spot stage. Thus, it can be said that Viruses being crystalline in nature have cellular penetrating power &amp; the EUS infection follows the phyllogenetic evolution in life in true sense i.e. RNA virus followed by Bacterial cell and then Fungus. Thus, the presence of EUS in Channa punctatus is confirmed histologically.