Biomedical subjects
Publications and source records attributed to A Adam.
Frog sciatic nerves show a continuing addition of new myelinated and nonmyelinated fibers with body growth. Along with increases in fiber number there are also marked changes in axon calibers and in the relative thickness of the myelin sheaths. Our data show that frog nerves, as opposed to mammalian nerves, are composed of fibers of different ages, stages of growth and stages of myelination.
A surgically introduced biliary endoprosthesis in a patient with a cholangiocarcinoma prevented extraction of a calculus in the lower common bile duct through a T-tube track. The problem was solved by the introduction of a second endoprosthesis across the ampulla of Vater through the T-tube track in order to prevent obstruction of the common bile duct by the calculus.
The synthetic immunomodulator muramyl dipeptide (MDP) has previously been shown to be able to synergize with lymphokines in enhancing the specific immune response of purified splenic B cells. Here, we have examined the effect of MDP in the process of B cell activation. We found that MDP alone was ineffective on the proliferation of either murine resting or in vivo activated B cells, whereas it enhanced the DNA synthesis of B cells once stimulated with anti-IgM antibodies. In agreement with these findings, cell cycle analysis by flow cytometry after acridine orange staining indicated that MDP by itself could not trigger the entry into the G1 phase of the cell cycle of nonactivated B lymphocytes. In contrast, in the presence of anti-IgM antibodies plus BSF-1, MDP promoted further cell cycle progression preferentially into the G1B compartment and also through the G2/M phase. A kinetic study showed that MDP was the most effective when added after the activation of B cells by anti-IgM antibodies plus BSF-1. Our present results suggest that functional receptors for MDP may be expressed on already cycling B cells.
In patients with unresectable hilar cholangiocarcinoma, percutaneous transhepatic endoprosthesis insertion is one of the available methods of palliation. We reviewed our experience with it in 35 consecutive patients with hilar cholangiocarcinoma who were judged on clinical or radiologic evidence to be unsuitable for resective or palliative surgery. The 30-day mortality rate was 14 percent (5 of 35 patients). Of the remaining 30 patients, endoprosthesis placement was successful in 28, with 2 patients discharged with a permanent external drainage catheter. Twenty-four patients survived a median of 3 months (range 1 to 17 months), and 2 were lost to follow-up. Good or fair palliation of symptoms was achieved in 50 percent of the discharged patients and in 66 percent of those living longer than 3 months. We believe that percutaneous transhepatic endoprostheses can provide useful palliation in patients with hilar cholangiocarcinoma, even in the presence of advanced disease.
A new flexible, spiral-shaped biliary endoprosthesis is described. This spiral endoprosthesis can negotiate acute angles, can be cut to any length, and has been specifically designed to deal with the problem of stent migration. The authors report their initial experience with this endoprosthesis in 14 patients.
Eight patients with liver disease and seriously abnormal blood coagulation underwent biopsy of the liver performed through a percutaneously introduced sheath, followed by embolization of the biopsy track with steel coils. In all cases the biopsy procedure produced profuse bleeding through the sheath. However, the bleeding ceased within a few minutes after coil insertion.
The contact system of plasma includes 4 zymogens, Hageman factor, pre-kallikrein, factor XI and plasminogen, and a cofactor, the high molecular weight kininogen (HMWK). The activation of the contact system leads to the production of bradykinin, blood coagulation, fibrinolysis, complement activation and neutrophil stimulation. Consequently these phenomena generate a lot of pro-inflammatory factors which contribute to the local and systemic inflammatory processes.
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Presented is a patient with primary sclerosing cholangitis, extrahepatic bile duct obstruction, and associated occlusion of the main portal vein, who was treated by peripheral biliary drainage. Radiological follow-up showed considerable improvement of the ductal strictures and bile excretion through the normal anatomical route. The patient remains well and anicteric 60 months after surgery.
A novel analog of MDP, the 3'-iodo-4'-azido-L-phenylalanine methyl ester derivative of N-acetyl-L-alanyl-D-isoglutamine, has been prepared. This compound is capable of activating macrophages to the tumoricidal state and increasing the specific immune response of B cells. It thus appears to exhibit similar biological activities to MDP. Moreover, this compound is of potential interest for receptor photolabelling studies.
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Intravenous injection of ellagic acid (EA, 30 mg/Kg), an activator of the Hageman factor, induced congestion of lymph nodes and dilatation of the spleen in rats. The dilatation of the spleen was inhibited by heparin, thrombin, defibrase, clocoumarol, lambda carrageenan, SBTI, PCR 4099 and CCI 17810. The congestion of lymph nodes was inhibited by heparin, thrombin, defibrase, clocoumarol, SBTI, lambda carrageenan, aspirin, indomethacin and ketoprofen, phentolamine and hexamethonium. Thrombin, defibrase, lambda carrageenan did not induce any congestion of the lymphoid tissues. These results suggest the the dilatation of the spleen induced by ellagic acid would result from blood coagulation, platelet stimulation and kinin formation. The congestion of lymph nodes would depend on kinins, blood coagulation and prostaglandin;s. The activation of Hageman factor in acute inflammatory reactions could mediate the early congestion of lymph nodes.
We compared the major changes induced by ellagic acid (EA), a Hageman factor activator, in normal rats and in kininogen-deficient Brown Norway rats. In normal rats, large doses of EA induced a congestion of lymph nodes, spleen and liver, a prolongation of activated partial thromboplastin time, the consumption of prekallikrein, high molecular weight kininogen and fibrinogen, as well as the stimulation of platelets with their accumulation in lungs, liver and spleen. A systemic hypotension of long duration was also observed. The fibrinogen consumption, the thrombocytopenia and the lengthening of activated partial thromboplastin time were dose-dependent. In kininogen-deficient rats, EA induced only a minimal congestion of lymphoid tissues, the accumulation of platelets in lungs, a decrease of plasma fibrinogen and a short-lasting hypotension. It is concluded that the vascular changes induced by blood coagulation with ellagic acid resulted mainly from kinin formation.
A new method of replacing an occluded biliary endoprosthesis by using the modified version of the Cope catheter introduction set is described.
Focal changes involving the liver capsule, subjacent tumour and contiguous structures are described on computed tomography (CT) in patients with metastatic tumours in the liver. These changes were correlated with the relevant resected liver tissue which had been perfused and sliced in planes comparable to the CT slices. The capsular changes represented 'umbilication', overlying necrotic and fibrosed tumour with contiguous structures, usually the diaphragm, perihepatic fat or omentum, fixed to the liver capsule by inflammatory or organising processes, but not invaded by tumour. Localised hypodense areas on CT in the region of the capsule do not represent extracapsular spread of tumour and therapy ought to be planned accordingly.
It is not often appreciated that the Mirizzi syndrome represents a spectrum of pathological lesions of the proximal extrahepatic biliary tree consequent on chronic gallbladder disease. A patient with this syndrome and associated liver atrophy is presented, emphasising the view that the syndrome has neither uniform appearance nor typical features and that a high index of suspicion and comprehensive investigations are required for diagnosis and optimal therapy.
An enzyme-linked immunoassay has been recently set up for direct measurement of the binding capacity of plasma fibronectin to gelatin. This binding capacity could be completely inhibited in vitro by an eight-fold excess of gelatin, of Haemaccel, but not of Geloplasma. On the contrary, the levels of immunoreactive fibronectin measured by laser nephelometry did not change, in presence of 10 to 1000 micrograms ml-1 of gelatin, of Haemaccel or of Geloplasma. When infused into normal volunteers, Haemaccel provoked a strong and immediate inhibition of the plasma fibronectin binding capacity to gelatin. This inhibition was dose-dependent and maximal after infusion of 500 ml of Haemaccel. Twenty-four hours after this infusion, there was a progressive recovery of the gelatin-binding capacity, which was almost completely achieved 96 h later. The formation of complexes between Haemaccel and fibronectin was demonstrated by gel filtration chromatography and by affinity chromatography. Immunoreactive plasma fibronectin levels remained unchanged up to 24 h after infusion of 500 ml of Haemaccel. A transient decline to 50% of its initial value then occurred the second day after the infusion. Therefore, a delay existed between the formation of fibronectin-Haemaccel complexes and their elimination from the bloodstream. This delay decreased when smaller volumes of Haemaccel were infused, which strongly suggests that plasma fibronectin is cleared by means of Haemaccel and does not seem to play a role of opsonin in these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
A combined surgical and radiological approach to the management of complex biliary strictures is described. Radiological access for stricture dilatation or stone extraction is created at the time of surgery either by insertion of a transhepatic U-tube or superficial fixation of the afferent limb of the Roux-en-Y loop. Each of seven patients treated in this way had multiple complicating factors known to adversely affect the outcome of operative repair. Five of the seven have had an excellent outcome at a median follow-up of 15 months (mean 21 months, range 2-39 months).