scholarly journals Pathological diagnosis of cirrhotic ascites in a Caucasian Dog

2021 ◽  
Vol 2 (2) ◽  
pp. 31-36
Author(s):  
Samson Eneojo Abalaka ◽  
Sylvester Sunday Obeta ◽  
Uchenna Stephen Asogwa ◽  
Nuhu Abdulazeez Sani ◽  
Idoko Sunday Idoko ◽  
...  
Keyword(s):  
Smooth Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Tissue Proliferation ◽  
Distended Abdomen ◽  
Appropriate Treatment ◽  
Mucous Membranes ◽  
End Stage ◽  
Eventual Death ◽  
Tentative Diagnosis ◽  
Prompt Diagnosis

Although ascites is widely reported in dogs, those of cirrhotic ascites are scanty, especially in Abuja, Nigeria, hence the need for this report on cirrhotic ascites in a 2-year-old Caucasian dog. The reported complaints of anorexia, weakness, and distended abdomen before the presentation for proper veterinary attention led to a tentative diagnosis of suspected liver-induced ascites. The dog later died while receiving treatment necessitating the performance of a post-mortem examination on the severely emaciated carcass, which had pale mucous membranes, distended abdomen, and slightly oedematous distal limbs. Grossly, the lungs had multiple areas of congestion with visible hydrothorax and hydroperitoneum while the liver was shrunken, firm, nodular, misshapen, and haemorrhagic. Pulmonary congestion and oedema characterized the lung microscopically. The liver showed hepatic haemorrhage, cytoplasmic vacuolation, and necrosis with mononuclear cellular infiltration, fibrous connective tissue proliferation, and nests of apparently normal hepatocytes. The positive alpha-smooth muscle actin and vimentin immunoreactivity confirmed the hepatic fibrosis. Microscopic renal lesions indicated nephropathy. Consequently, the definitive diagnosis became cirrhotic ascites. The observed liver pathology indicated end-stage liver damage responsible for the ascites and eventual death of the dog. Prompt diagnosis with appropriate treatment is very crucial in the prognosis of cirrhotic ascites in affected dogs.

Oncocytic Lipoadenoma: Report of 3 Rare Cases Involving the Parotid Gland, Including a Synchronous Presentation With Paraganglioma of the Right Carotid Bifurcation and Literature Review

2021 ◽  
pp. 106689692110219
Author(s):  
John L.S. Cunha ◽  
Marco A. Peñalonzo ◽  
Ciro D. Soares ◽  
Bruno A.B. de Andrade ◽  
Mário J. Romañach ◽  
...  
Keyword(s):  
English Language ◽  
Smooth Muscle Actin ◽  
Salivary Gland Tumor ◽  
Surgical Excision ◽  
Carotid Bifurcation ◽  
Alpha Smooth Muscle Actin ◽  
S 100 ◽  
The Right ◽  
Adequate Management ◽  
Adipose Cells

Oncocytic lipoadenoma (OL) is a rare salivary gland tumor characterized by the presence of oncocytic cells and mature adipose tissue. To date, only 30 cases of OL have been reported in the English-language literature. We present 3 additional OL cases involving the parotid, including a synchronous presentation with paraganglioma of the right carotid bifurcation. Microscopically, both the OLs were composed of a mixed population of oncocytes and adipocytes in varying proportions surrounded by a thin, connective tissue fibrous capsule. Oncocytes were positive for pan-cytokeratins (CKs) AE1/AE3, epithelial membrane antigen, CK5, CK7, CK14, CK18, and CK19. Calponin, p63, alpha-smooth muscle actin, and carcinoembryonic antigen were negative. Vimentin and S-100 protein were positive only in adipose cells. Despite distinctive morphologic features, OL is often misdiagnosed, given its rarity. We hope to contribute to surgeons’ and pathologists’ awareness and knowledge regarding the existence of this tumor and provide adequate management through conservative surgical excision.

scholarly journals The AP-1 Transcription Factor Fosl-2 Regulates Autophagy in Cardiac Fibroblasts during Myocardial Fibrogenesis

2021 ◽  
Vol 22 (4) ◽  
pp. 1861
Author(s):  
Jemima Seidenberg ◽  
Mara Stellato ◽  
Amela Hukara ◽  
Burkhard Ludewig ◽  
Karin Klingel ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Cardiac Fibrosis ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Smooth Muscle Actin ◽  
Beclin 1 ◽  
Type I ◽  
Alpha Smooth Muscle Actin

Background: Pathological activation of cardiac fibroblasts is a key step in development and progression of cardiac fibrosis and heart failure. This process has been associated with enhanced autophagocytosis, but molecular mechanisms remain largely unknown. Methods and Results: Immunohistochemical analysis of endomyocardial biopsies showed increased activation of autophagy in fibrotic hearts of patients with inflammatory cardiomyopathy. In vitro experiments using mouse and human cardiac fibroblasts confirmed that blockade of autophagy with Bafilomycin A1 inhibited fibroblast-to-myofibroblast transition induced by transforming growth factor (TGF)-β. Next, we observed that cardiac fibroblasts obtained from mice overexpressing transcription factor Fos-related antigen 2 (Fosl-2tg) expressed elevated protein levels of autophagy markers: the lipid modified form of microtubule-associated protein 1A/1B-light chain 3B (LC3BII), Beclin-1 and autophagy related 5 (Atg5). In complementary experiments, silencing of Fosl-2 with antisense GapmeR oligonucleotides suppressed production of type I collagen, myofibroblast marker alpha smooth muscle actin and autophagy marker Beclin-1 in cardiac fibroblasts. On the other hand, silencing of either LC3B or Beclin-1 reduced Fosl-2 levels in TGF-β-activated, but not in unstimulated cells. Using a cardiac hypertrophy model induced by continuous infusion of angiotensin II with osmotic minipumps, we confirmed that mice lacking either Fosl-2 (Ccl19CreFosl2flox/flox) or Atg5 (Ccl19CreAtg5flox/flox) in stromal cells were protected from cardiac fibrosis. Conclusion: Our findings demonstrate that Fosl-2 regulates autophagocytosis and the TGF-β-Fosl-2-autophagy axis controls differentiation of cardiac fibroblasts. These data provide a new insight for the development of pharmaceutical targets in cardiac fibrosis.

Cold Plasma Treatment Promotes Full-thickness Healing of Skin Wounds in Murine Models

2021 ◽  
pp. 153473462110021
Author(s):  
Joon M. Jung ◽  
Hae K. Yoon ◽  
Chang J. Jung ◽  
Soo Y. Jo ◽  
Sang G. Hwang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Plasma Treatment ◽  
Cold Plasma ◽  
Smooth Muscle Actin ◽  
Treated Group ◽  
Control Group ◽  
Alpha Smooth Muscle Actin ◽  
Skin Wound Healing

Cold plasma can be beneficial for promoting skin wound healing and has a high potential of being effectively used in treating various wounds. Our aim was to verify the effect of cold plasma in accelerating wound healing and investigate its underlying mechanism in vitro and in vivo. For the in vivo experiments, 2 full-thickness dermal wounds were created in each mouse (n = 30). While one wound was exposed to 2 daily plasma treatments for 3 min, the other wound served as a control. The wounds were evaluated by imaging and histological analyses at 4, 7, and 11 days post the wound infliction process. Immunohistochemical studies were also performed at the same time points. In vitro proliferation and scratch assay using HaCaT keratinocytes and fibroblasts were performed. The expression levels of wound healing–related genes were analyzed by real-time polymerase chain reaction and western blot analysis. On day 7, the wound healing rates were 53.94% and 63.58% for the control group and the plasma-treated group, respectively. On day 11, these rates were 76.05% and 93.44% for the control and plasma-treated groups, respectively, and the difference between them was significant ( P = .039). Histological analysis demonstrated that plasma treatment promotes the formation of epidermal keratin and granular layers. Immunohistochemical studies also revealed that collagen 1, collagen 3, and alpha-smooth muscle actin appeared more abundantly in the plasma-treated group than in the control group. In vitro, the proliferation of keratinocytes was promoted by plasma exposure. Scratch assay showed that fibroblast exposure to plasma increased their migration. The expression levels of collagen 1, collagen 3, and alpha-smooth muscle actin were elevated upon plasma treatment. In conclusion, cold plasma can accelerate skin wound healing and is well tolerated.

scholarly journals Regulation of Cellular Senescence Is Independent from Profibrotic Fibroblast-Deposited ECM

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1628
Author(s):  
Kaj E. C. Blokland ◽  
Habibie Habibie ◽  
Theo Borghuis ◽  
Greta J. Teitsma ◽  
Michael Schuliga ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cellular Senescence ◽  
Transforming Growth Factor ◽  
Cell Function ◽  
Smooth Muscle Actin ◽  
Transforming Growth Factor Β1 ◽  
Tissue Growth ◽  
Alveolar Epithelial Cells ◽  
Lung Fibroblasts ◽  
Alpha Smooth Muscle Actin

Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with poor survival. Age is a major risk factor, and both alveolar epithelial cells and lung fibroblasts in this disease exhibit features of cellular senescence, a hallmark of ageing. Accumulation of fibrotic extracellular matrix (ECM) is a core feature of IPF and is likely to affect cell function. We hypothesize that aberrant ECM deposition augments fibroblast senescence, creating a perpetuating cycle favouring disease progression. In this study, primary lung fibroblasts were cultured on control and IPF-derived ECM from fibroblasts pretreated with or without profibrotic and prosenescent stimuli, and markers of senescence, fibrosis-associated gene expression and secretion of cytokines were measured. Untreated ECM derived from control or IPF fibroblasts had no effect on the main marker of senescence p16Ink4a and p21Waf1/Cip1. However, the expression of alpha smooth muscle actin (ACTA2) and proteoglycan decorin (DCN) increased in response to IPF-derived ECM. Production of the proinflammatory cytokines C-X-C Motif Chemokine Ligand 8 (CXCL8) by lung fibroblasts was upregulated in response to senescent and profibrotic-derived ECM. Finally, the profibrotic cytokines transforming growth factor β1 (TGF-β1) and connective tissue growth factor (CTGF) were upregulated in response to both senescent- and profibrotic-derived ECM. In summary, ECM deposited by IPF fibroblasts does not induce cellular senescence, while there is upregulation of proinflammatory and profibrotic cytokines and differentiation into a myofibroblast phenotype in response to senescent- and profibrotic-derived ECM, which may contribute to progression of fibrosis in IPF.

Symptomatic kidney stones in an anuric patient on dialysis: A case report

2021 ◽  
pp. 039156032110359
Author(s):  
Hossein Dialameh ◽  
Farshad Namdari ◽  
Mehrdad Mahalleh ◽  
Mohammad Lotfi ◽  
Zoha Ali
Keyword(s):  
Renal Colic ◽  
Chest Ct ◽  
Chief Complaint ◽  
Flank Pain ◽  
The Past ◽  
Extracorporeal Shock Wave ◽  
Stage Renal Disease ◽  
End Stage ◽  
Prompt Diagnosis ◽  
Chest Ct Scan

Introduction: Renal colic is a colicky-type of flank pain that can commonly be presented in patients undergoing dialysis especially if they are anuric considering the fact that there are multiple controversies and little published experience on this topic, we found it very important to report this case. We also aimed to increase awareness and emphasize the importance of renal colic in anuric patients on dialysis. Case description: We herein report a case of a 42-year old man with a chief complaint of bilateral colic flank pain, He had developed end stage renal disease due to ADPKD and was on hemodialysis since the past 5 years. Previously, he went through a series of workup but was left undiagnosed. Abdomen-pelvic and chest CT scan without contrast was performed showing bilateral renal pelvic stones and some nephrocalcinosis in both kidneys. bilateral ureteroscopy was performed and bilateral DJ was installed for a total of 6 weeks and extracorporeal shock wave lithotripsy was done. With prompt diagnosis, the patient was pain free and stone free before discharge. The patient is also reported to be stone free 6 months after the procedure. Conclusion: Patients on dialysis are still capable of forming symptomatic renal tract stones even if they are anuric.

scholarly journals mTOR inhibitors potentially reduce TGF-β2-induced fibrogenic changes in trabecular meshwork cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nozomi Igarashi ◽  
Megumi Honjo ◽  
Makoto Aihara
Keyword(s):  
Trabecular Meshwork ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Mtor Inhibitors ◽  
In Vivo Model ◽  
Type I ◽  
Fibrotic Response ◽  
Alpha Smooth Muscle Actin

AbstractWe examined the effects of mTOR inhibitors on the fibrotic response induced by transforming growth factor-beta2 (TGF-β2) in cultured human trabecular meshwork (hTM) cells. TGF-β2-induced expression of fibronectin, collagen type I, alpha 1 chain (COL1A1), and alpha-smooth muscle actin (αSMA) in hTM cells was examined in the presence or absence of mTOR inhibitors using quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemistry. The migration rates of hTM cells were examined in the presence of TGF-β2 with or without mTOR inhibitors. An in vitro study showed that the expression of fibronectin, COL1A1, and αSMA was upregulated by TGF-β2 treatment of hTM cells; such upregulation was significantly suppressed by mTOR inhibitors. The inhibitors significantly reduced the migration rate of TGF-β2-stimulated hTM cells. mTOR inhibitors may usefully reduce the fibrotic response of hTM cells and we may have to explore if it is also effective in in vivo model.

scholarly journals P149 The intracellular chloride channel 4 (CLIC4) plays an important role in systemic sclerosis fibroblast activation

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Christopher Wasson ◽  
Rebecca Ross ◽  
Ruth Morton ◽  
Jamel Mankouri ◽  
Francesco Del Galdo
Keyword(s):  
Systemic Sclerosis ◽  
Ion Channel ◽  
Smooth Muscle Actin ◽  
Chloride Ion ◽  
Dermal Fibroblasts ◽  
Cancer Associated Fibroblasts ◽  
Alpha Smooth Muscle Actin ◽  
Direct Role ◽  
Fibroblast Activation ◽  
Intracellular Chloride

Abstract Background/Aims  The intracellular chloride ion channel CLIC4 mediates the activation of cancer associated fibroblasts. Interestingly, systemic sclerosis (SSc) fibroblasts display a number of similar properties to cancer associated fibroblasts. Tissue fibrosis in SSc is driven by active fibroblasts (myofibroblasts). Therefore in this study we investigated the role of CLIC4 in SSc fibroblast activation. Methods  Dermal fibroblasts were obtained from full thickness skin biopsies from SSc patients (early-diffuse). RNA and protein were collected from the fibroblasts and CLIC4 transcript and protein levels were assessed by qPCR and western blot. SSc patient fibroblasts were treated with the chloride ion channel inhibitors NPPB and IAA-94. Results  CLIC4 was found to be expressed at significantly higher levels in SSc patients fibroblasts compared to healthy controls, at both the transcript (3.7 fold) and protein (1.7 fold) levels. Inhibition of the TGF-β signalling pathway led to reduced CLIC4 expression in SSc fibroblasts, confirming this pathway as the main driver of CLIC4 expression. Finally, treatment of SSc fibroblasts with small molecule inhibitors that target the channel led to reduced expression of the myofibroblast markers collagen type 1 and alpha-smooth muscle actin, suggesting a direct role for CLIC4 in SSc associated skin fibrosis. Conclusion  We have identified a novel role for CLIC4 in SSc myofibroblast activation, which further strengthen the similarities between SSc fibroblasts and cancer associated fibroblasts. Furthermore this study highlights this channel as a novel target for therapeutic intervention. Disclosure  C. Wasson: None. R. Ross: None. R. Morton: None. J. Mankouri: None. F. Del Galdo: None.

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