Assessing the adequacy of endoscopically tied knots: a functional approach

BACKGROUND AND STUDY AIMS: Endoscopic intracorporeal knots have potentially enormous applications in endoscopic surgery. We describe a method for testing the security of various types of endoscopically tied knots using a vessel perfusion manometer system. METHODS: A 4-cm segment of porcine splenic artery was placed on the mucosal surface of a pig stomach. The two ends of the vessel were brought out through the gastric wall and connected to a two-way manometer. One end was also joined to a pressure infusion bag. The stomach was mounted in an Erlangen training model. A long 3/0 nylon thread, previously introduced into the submucosal layer of the stomach and encircling the vessel, was brought out from the mouth. Three-throw square knots, Mayo knots, "surgeon's" knots and five-throw square knots were tied and pushed into place using a cap attached to a gastroscope. The pressure at the two ends of the artery was compared. If the pressure could be increased to over 200 mm Hg at one end without a change in the other, the knot was considered secure. RESULTS: Each type of knot was tested 12 times under endoscopic vision. The range for mean knotting time was 3.4 - 4.5 minutes. Five-throw knots took significantly longer to tie than three-throw knots (P < 0.005). There was one loose knot in each of the three-throw and Mayo groups, and three each in the "surgeon's" and five-throw groups (P > 0.05). CONCLUSIONS: This system is a reliable model for testing intracorporeal knots tied endoscopically. A three-half-hitches square knot with 3/0 nylon, tied using a flexible endoscope and knot-tightening cap, can withstand pressure up to 200 mm Hg.     

The pharmacology of a new pasteurized antihemophilic factor concentrate derived from human blood plasma

The pharmacology of a new pasteurized factor VIII (FVIII) concentrate derived from human blood plasma was studied in 23 adults with hemophilia A. In Part 1 of the study involving six nonbleeding subjects, the mean increase in FVIII activity was 1.43 +/- 0.34 U per ml 10 minutes after an intravenous dose of 50 U per kg. The intravascular survival kinetics in these six patients showed a biphasic decay curve with an initial mean half-life of 5.1 +/- 1.2 hours probably representing early redistribution, and a late half-life of 13.3 +/- 4.9 hours. In Part 2 of the study, the activity at 10 minutes was measured in another 17 patients, as well as in one patient already studied in Part 1. The mean increase in activity with the 24 observations was 1.13 +/- 0.37 U per ml with a mean FVIII dosage of 51.0 +/- 2.6 U per kg of body weight. Only one patient had an allergic reaction, which did not recur when the patient was given a second lot.     

Leishmania donovani glycosphingolipid facilitates antigen presentation by inducing relocation of CD1d into lipid rafts in infected macrophages

NKT cells respond to presentation of specific glycolipids with release of both Th1‐ and Th2‐type cytokines. Leishmania donovani (LD)‐infected splenic macrophages (sM?(I)) and bone marrow‐derived dendritic cells (BMDC(I)) failed to activate NKT cells in response to α‐galactosyl ceramide (α‐GalCer). The defective antigen presentation could be corrected by treating the cells with the immunostimulating glycosphingophospholipid (GSPL) of LD parasites. In vitro pulsing of BMDC(I) or sM?(I) with GSPL, caused the activation of the Vα14⁺ CD1d1‐specific NKT cell hybridoma DN32.D3. Localization of MHC II and CD1d molecules to membrane lipid rafts has been suggested to play an important role in antigen presentation. Confocal analysis clearly demonstrated that LD infection changed the pattern of CD1d distribution to the non‐lipid raft regions and this change could be reversed by GSPL treatment. Isoelectric focusing gel shift assay indicated that GSPL binds to CD1d. GSPL‐treated but not untreated BMDC(I) formed immune synapses with NKT cells and this was associated with calcium mobilization. In conclusion, GSPL treatment was associated with modification of BMDC(I)/sM?(I) lipid raft structure, which is a site for immune regulation.     

Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by dietary phosphate

The present study was aimed to test the hypothesis that inorganic phosphate may reduce arsenic toxicity by decreasing its intestinal transference. Co-administration of inorganic phosphate (6.56 M) and arsenic (6.07 mM) in the intestinal loops of rats, in situ, caused significant reduction of arsenic transference. Short-term arsenic exposure (3mg/kg body weight/day for 30 days) caused liver damage evidenced by activities of liver enzymes and necroinflammatory changes. These effects of arsenic were coupled with enhanced mitochondrial swelling, inhibition of cytochrome c oxidase, Ca(2+)-ATPase, a decrease in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress and iNOS expression. Arsenic also increased hepatic caspase 3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by arsenic could be alleviated by supplementation with inorganic phosphate, which likely suggests a protective role of phosphate against arsenic-induced hepatotoxic changes.     

Left atrial extension of lung malignancy with ECG changes resembling STEMI

Lung malignancy extending into left atrium is seen very infrequently. We had a patient with a fast growing symptomatic lung mass and electrocardiogram showing persistent coving ST elevation without any biomarker change. Transthoracic echocardiography showed a large left atrial mass which was fixed to the free walls and extended into the appendage. There was also a large lung mass that was compressing the heart from its lateral aspect. CT-scan of chest corroborated the lung mass & CT-guided FNAC showed small cell carcinoma.