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D S Jassal

Publications and source records attributed to D S Jassal.

10 recordsLinked to original sources
PubMed2001

Calcific myonecrosis: case report and review.

Although a rare diagnosis, with few reports in the literature, calcific myonecrosis is a diagnosis that must be entertained in individuals presenting with expanding masses in the muscle compartments occurring years after an initial injury. The authors report a previously healthy 66-year-old man with an expanding right lower extremity mass felt initially to be an abscess. Despite presumably appropriate antimicrobial therapy, the lesion continued to expand, causing pain and loss of function. The patient subsequently underwent extensive debridement and free muscle flap transfer with an excellent outcome. This patient serves to remind us that, although calcific myonecrosis is an uncommonly encountered condition, it must be maintained in the differential diagnosis of an expanding muscle compartment mass.

Aged↗
PubMed2001

A diagnostic dilemma of fever and back pain postpartum.

A 26-year-old woman presented with fever, chills, and back pain 6 weeks postpartum. An infused CT scan of the abdomen and pelvis with IV contrast confirmed septic pelvic vein thrombophlebitis as the diagnosis. To the best of our knowledge, this is the first case report describing such a massive thrombophlebitis extending from the superior vena cava to the femoral vein inferiorly responsive to conventional anticoagulation therapy. This exceptional case reminds us to entertain septic pelvic thrombophlebitis in the differential of any patient who presents with fever and back pain of unknown etiology.

Adult↗
PubMed2000

Interaction between angiotensin II and Smad proteins in fibroblasts in failing heart and in vitro.

Angiotensin II (angiotensin) and transforming growth factor (TGF)-beta(1) play an important role in cardiac fibrosis. We examined Smad proteins in 8-wk post-myocardial infarction (MI) rat hearts. AT(1) blockade (losartan) attenuated the activation of TGF-beta(1) in target tissues. Losartan administration (8 wk, 15 mg. kg(-1). day(-1)) normalized total Smad 2 overexpression in infarct scar and remnant heart tissue and normalized Smad 4 in infarct scar. Phosphorylated Smad 2 (P-Smad 2) staining decreased in cytosol from failing heart vs. the control, which was normalized by losartan, suggesting augmented P-Smad 2 movement into nuclei in untreated failing hearts. Using adult primary rat fibroblasts treated with angiotensin (10(-6) M), we noted rapid translocation (15 min) of P-Smad 2 into the nuclei from the cytosol. Nuclear P-Smad 2 protein level increased with angiotensin treatment, which was blocked by losartan. We conclude that angiotensin may influence total Smad 2 and 4 expression in post-MI heart failure and that angiotensin treatment is associated with rapid P-Smad 2 nuclear translocation in isolated fibroblasts. This study suggests that cross talk between angiotensin and Smad signaling is associated with fibrotic events in post-MI hearts.

Active Transport, Cell Nucleus↗
PubMed1997

Effect of AT1 receptor blockade on cardiac collagen remodeling after myocardial infarction.

OBJECTIVE: Previous work has shown that cardiac fibrosis occurs after myocardial infarction (MI) in non-infarcted ventricular tissue and that this event is associated with abnormal cardiac function. Our aim was to investigate the effect of AT1 receptor blockade on cardiac collagen remodeling in post-MI rat heart remote from the infarct site by addressing collagen mRNA abundance, posttranslational hydroxylation of collagen monomers, and mature collagen deposition. Prolyl 4-hydroxylase (PH) mediates hydroxylation of procollagen alpha-chains in the endoplasmic reticulum of cardiac fibroblasts and thus regulates the downstream formation and secretion of helical procollagen molecules. METHODS: The effects of losartan (15 mg/kg/day) on collagen deposition and mRNA abundance were monitored in viable left and right ventricles in sham-operated (control) and experimental groups in the presence or absence of losartan. Immunoreactive PH concentration in viable tissues as well as cardiac function in control and experimental groups was determined by ELISA. RESULTS: Immunohistochemical staining and 4-hydroxyproline assays confirmed that losartan treatment attenuates fibrosis in experimental hearts. Northern analysis revealed that losartan treatment of 1, 2, or 4 week experimental groups had no effect on collagen mRNA abundance compared to untreated post-MI rats. On the other hand, immunoreactive PH concentration was significantly decreased in the post-MI group treated with losartan. Determination of cardiac mass and cardiac function revealed that losartan treatment was associated with attenuated cardiac hypertrophy and improved left ventricular (LV) function in experimental animals. CONCLUSIONS: AT1 blockade is associated with a significant decrease in cardiac fibrosis in treated post-MI rats, and this trend is positively correlated to a significant decrease in immunoreactive PH compared to untreated experimental animals. The expression of cardiac PH may be regulated by angiotensin via AT1 receptor activation, and the suppression of PH with losartan treatment may be an important mechanism for modulation of collagen deposition in the post-MI rat heart.

Angiotensin II↗
PubMed1996

Effect of ramipril and losartan on collagen expression in right and left heart after myocardial infarction.

Although increased deposition of collagen proteins has been described after myocardial infarction (MI), little is known of time-dependent transcriptional alteration of specific cardiac collagen sub-types as well as the degradative mechanisms for cardiac collagens in right and left ventricular myocardium remote to large left ventricular infarction. We sought to study collagen mRNA abundance and the deposition of specific collagen subtypes in noninfarcted left and right rat heart muscle at different times after MI. We also assessed the activity of different myocardial matrix metalloproteinases (MMP) using zymography to gain some information about degradative pathways for collagen. Furthermore, we assessed passive compliance properties of the right ventricle in experimental hearts. Finally we investigated the role of the renin angiotensin system in the collagen gene expression by administration of an angiotensin converting enzyme (ACE) inhibitor (ramipril) and an angiotensin II receptor type I antagonist (losartan) in experimental animals. We observed that the mRNA abundance of types I and III collagen were increased 3 days after myocardial infarction in both viable left and uninfarcted right ventricular tissues, that they peaked at 7-14 days, and were maintained at relatively high levels in the 28 and 56 days experimental groups. Stiffness of the right ventricular myocardium was significantly increased in the 56 days experimental group when compared to that of control values. These findings correlated with increased immunohistochemical staining patterns of different collagen species in the surviving right (and left) cardiac interstitium of 14, 28, and 56 day experimental cardiac groups. The elevation of fibrillar collagen mRNA abundance in noninfarcted muscle from ventricular chambers was not significantly altered after treatment of experimental animals with ramipril and losartan for up to 14 days. MMP activity was increased in viable left ventricle at 14, 28 and 56 days and at 14 days in the right ventricle in experimental animals when compared to controls. These results indicated that (1) activation of transcription of collagen types I and III gene occurs in acute and chronic MI, and that fibrillar collagen proteins are deposited in the noninfarcted cardiac interstitium after a lag period relative to increased corresponding mRNA abundance; (2) an increase in MMP activity in chronic experimental hearts indicates that increased collagen deposition may be due to an increment in collagen synthesis rather by reduced degradation of collagen, and that MMP activation may be important in remodeling of the noninfarcted cardiac stroma; (3) an increase of right ventricular stiffness was associated with increased deposition of collagen; (4) as losartan treatment is not associated with any normalization of elevated collagen mRNA abundance, the upregulation of collagen gene expression in this model is not mediated by AT1 receptor; and (5) the reduction of cardiac fibrosis mediated by ACE inhibition and losartan treatment may reside at the post-translational level in cardiac collagen metabolism.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Morphology of pulmonary intravascular macrophages (PIMs) in ruminants: ultrastructural and cytochemical behavior of dense surface coat.

Recent studies have indicated that pulmonary intravascular macrophages (PIMs) are a resident cell population which in structure and function resemble mature macrophages of the mononuclear phagocyte system (MPS) in various domestic species, particularly the ruminants. The ultrastructural features of PIMs of the goat and calf lungs were studied by using vascular perfusion and direct airway instillation of fixatives. Staining with tannic acid as a component of paraformaldehyde-glutaraldehyde-based fixative revealed the presence of an electron-dense coat on the surface of the cell membrane of the PIMs. The surface coat disappeared after heparin infusion and after enzymatic digestion with lipolytic lipase, suggesting that the surface coat was predominantly lipoprotein in nature. The lipoprotein coat was organized in the form of a linear chain of spherical globules with a consistent periodicity created by the intervening translucent space between individual globules. The surface coat was separated from the outer-leaflet of the cell membrane by an empty space measuring 35-39 nm in width. PIMs possessed a significant number of coated pits and coated vesicles, the cell organelles of receptor-mediated endocytosis of lipoproteins. In concurrence with the coated pits and vesicles, microtubules, multivesicular bodies, and lipoprotein-positive vesicles were also observed. It is conceivable that PIMs are involved in lipid metabolism and are the major source of vasoactive substances, which significantly influence both the dynamics of pulmonary circulation and the surfactant turnover of the ruminant lung.

Animals↗