Age and growth of Meretrix casta (Chemnitz) in Vellar estuary, Parangipettai

Age and growth of Meretrix casta (Chemnitz) in Vellar estuary was studied from April 1975 to March 1976, Employing length-frequency method growth of M. casta at the end of I year was found to be about 24.0 mm. Months mode curve showed that this clam attained growth of 23.2 mm, 38.4 mm and 49.2 mm at the end of 1,11 and III year respectively. Growth estimated by probability plot method was 23.0 mm in 1 year, 38 3 mm In II year and 50.6 mm in III year.. The life span of M. casta was found to be 3 years in Vellar estuary

Seasonal variations in the biochemical composition of Meretrix casta (Chemnitz) occurring in Vellar estuary

Seasonal variation in biochemical composition of Meretrix casta (Chemnitz) occurring in Vellar estuary (Lat. 11 °29' N; Long 79°46' E), S. India was carried out monthly for a period of one year from April '75 to March '76. Gonad recorded high percentage of carbohydrates (5.2%-9.4%) than the other body components (viz- mantle, adductor muscle, gills, foot, siphon and digestive gland). Gonad also recorded the highest protein value of 74.4% but mean monthly values showed that mantle had higher percentage of protein (60.5%) than other body components. Digestive gland had high percentage of lipid (mean 3.05%) than the other body components. Digestive gland appears to be storage organs for fat and protein. Of the seven body components studied, gill showed very low percentage of protein (47.07%), carbohydrate (1.45%) and fat (1.73%). Protein content of gonad registered an increase before spawning and decrease after spawning. Thus, protein content of gonad showed seasonal changes associated with the annual reproductive cycle

Torsion of in-utero fetal ovarian cyst

A 22 years old primi-gravida was diagnosed to have a 6.3×5×5.37 cm hemorrhagic gonadal cyst in fetus at 38 weeks of gestation by growth scan, on follow-up. At term gestation, she delivered a female baby by vacuum assisted vaginal delivery, weighed 2.86 kg, no other anomalies. X-ray done at 1st hour of life showed mass on the right side. USG abdomen done showed an intraperitoneal cystic lesion (5.7×3.9×6.3 cm) in right lumbar quadrant of abdomen and pediatric surgeon was consulted. Baby taken for diagnostic laparoscopy on second day of life. Findings were right large ovarian cyst with torsion with adhesions to small bowel. 75 ml of hemorrhagic fluid drained and ovarian cystectomy done, sample sent for histopathological examination, turned out to be a simple cyst. Baby discharged on day 7 of life (POD-5), hemodynamically stable and on direct breast feeding, tolerated well

Prospective Study to compare Intra-articular versus Intravenous Tranexemic Acid in reducing Post-operative Blood Loss in staged bilateral Total Knee Arthroplasty

The number of total knee arthroplasties (TKA) performed is around two million annually worldwide and this number is expected to increase fivefold by 2025. The most common indication is osteoarthritis of the knee. Blood loss is significant during the post-operative period and blood transfusion when necessary has its own drawbacks. The use of intravenous tranexamic acid has significantly reduced blood loss. We analysed 35 patients who underwent staged bilateral TKA between August 2013 and February 2016 and had administered intra-articular tranexamic acid for one knee and intravenous tranexamic acid for the other knee. The results were analysed based on post-operative blood loss, change in haemoglobin (Hb) level and haematocrit (PCV) and the need for blood transfusion. The average postoperative blood loss was 129.57 ml and 277.71 ml for intra articular group and intravenous group respectively. A control group (no drug or placebo group) with age matched patients (n= 21) was chosen from medical records. The average blood loss in the control group was 493.81 ml. The fall in Hb level and PCV was 0.72 gm/dl and 2.62 % (Intra-articular Group), 1.36 gm/dl and 4.34 % (Intravenous Group) and 2.62 gm/dl and 5.52 % (Control). The number of transfusions were two (Intra-articular Group), five (Intravenous Group) and nine (Control). We conclude that when compared with intravenous route, intra-articular administration has significantly reduced blood loss, Hb level and PCV fall and the rate of blood transfusion

Role of Oxygen Free Radicals, Nitric Oxide and Mitochondria in Mediating Cardiac Alterations During Liver Cirrhosis Induced by Thioacetamide

Thioacetamide (TAA) administration is widely used for induction of liver cirrhosis in rats, where reactive oxygen radicals (ROS) and nitric oxide (NO) participate in development of liver damage. Cardiac dysfunction is an important complication of liver cirrhosis, but the role of ROS or NO in cardiac abnormalities during liver cirrhosis is not well understood. This was investigated in animals after TAA-induced liver cirrhosis and temporal changes in oxidative stress, NO and mitochondrial function in the heart evaluated. TAA induced elevation in cardiac levels of nitrate before development of frank liver cirrhosis, without gross histological alterations. This was accompanied by an early induction of P38 MAP kinase, which is influenced by ROS and plays an important signaling role for induction of iNOS. Increased nitrotyrosine, protein oxidation and lipid peroxidation in the heart and cardiac mitochondria, suggestive of oxidative stress, also preceded frank liver cirrhosis. However, compromised cardiac mitochondrial function with a decrease in respiratory control ratio and increased mitochondrial swelling was seen later, when cirrhosis was evident. In conclusion, TAA induces elevations in ROS and NO in the heart in parallel to early liver damage. This leads to later development of functional deficits in cardiac mitochondria after development of liver cirrhosis

Acute fatty liver of pregnancy: an update on mechanisms

Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis

Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: changes in glycosylation and luminal bacteria

Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl4-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis

Renal Damage in Experimentally-Induced Cirrhosis in Rats: Role of Oxygen Free Radicals

Cirrhosis with ascites is associated with impaired renal function accompanied by sodium and water retention. Although it has been suggested that mediators such as nitric oxide play a role in the development of renal failure in this situation, other mechanisms underlying the process are not well understood. This study examined the role of oxidative stress in mediating renal damage during the development of cirrhosis in order to understand mechanisms involved in the process. It was shown that carbon tetrachloride– or thioacetamide-induced cirrhosis in rats results in oxidative stress in the kidney as seen by increased lipid peroxidation and protein oxidation, accompanied by altered antioxidant status. Cirrhosis was also found to affect renal mitochondrial function, as assessed by measurement of the respiratory control ratio, the swelling of mitochondria, and calcium flux across mitochondrial membranes. Increased lipid peroxidation and changes in lipid composition were evident in the renal brush border membranes, with compromised transport of 14C glucose across these membranes. In conclusion, renal alterations produced as a result of cirrhosis in the rat are possibly mediated by oxidative stress

Intestinal Mucosal Alterations in Rats With Carbon Tetrachloride-Induced Cirrhosis: Changes in Glycosylation and Luminal Bacteria

Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl4-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis