Biomedical subjects
Publications and source records attributed to J Janiszewski.
We are describing a case of undesired side effect of the cure (toxic hepatocellular damage) by Augmentin. The main symptoms were jaundice and pruritus. This is the next documented case of the hepatocellular damage by Augmentin in Poland. In the conclusion, we draw the attention to the role of interview in the diagnosis of the illness described and therapeutic management.
The development and application of membrane solid phase extraction (SPE) in 96-well microtiter plate format is described for the automated analysis of drugs in biological fluids. The small bed volume of the membrane allows elution of the analyte in a very small solvent volume, permitting direct HPLC injection and negating the need for the time consuming solvent evaporation step. A programmable liquid handling station (Quadra 96) was modified to automate all SPE steps. To avoid drying of the SPE bed and to enhance the analytical precision a novel protocol for performing the condition, load and wash steps in rapid succession was utilized. A block of 96 samples can now be extracted in 10 min., about 30 times faster than manual solvent extraction or single cartridge SPE methods. This processing speed complements the high-throughput speed of contemporary high performance liquid chromatography mass spectrometry (HPLC/MS) analysis. The quantitative analysis of a test analyte (Ziprasidone) in plasma demonstrates the utility and throughput of membrane SPE in combination with HPLC/MS. The results obtained with the current automated procedure compare favorably with those obtained using solvent and traditional solid phase extraction methods. The method has been used for the analysis of numerous drug prototypes in biological fluids to support drug discovery efforts.
Course of disease and treatment of 27-years old female patient suffering from celiac disease, who took Dapsone on suicidal purpose in a dose 23 times over maximal daily dose. Methemoglobinemia and hemolysis with anemia typical for this poisoning have been observed. In the first period after intoxication hypokalemia of unknown reason and shedding of hair 7 weeks after intoxication have been noticed. It is remarkable that methemoglobinemia maintained until 8 day after intoxication, in spite of intensive treatment with reducers and blood transfusions. That indicates tissular accumulation of Dapsone. Patient treated with Dapsone shouldn't possess the quantity of this drug that-taken as a single dose-can put him at risk.
Acute, accidental, oral poisoning with carbofuran in a chronic alcoholic was presented. In clinical picture muscarinic and nicotinic symptoms dominated. Toxicological examination revealed non acetylcholinesterase activity. A role of an interview and physical symptoms in diagnosing the poisoning with cholinesterase inhibitors, a specific treatment conduct and its side effects were discussed. So far six cases of poisoning with cholinesterase inhibitors have been treated at II Department of Internal Diseases and Acute Poisoning in Tarnów. The case presented below was characteristic for a considerable intensification of side effects during the treatment conduct. It was the reason for presenting this case.
The nervous and immune systems may communicate through the action of neurotransmitters on mast cells. We used patchclamp electrophysiology to assess the responses of rat peritoneal mast cells (PMC) to low levels of substance P (SP), which are likely to occur in situ. SP at 50 nM, or even 10,000 times reduced to 5 pM, triggered an outwardly rectified Cl- current (50 nM: 10 of 10 cells; 5 pM: 10 of 11 cells), although degranulation never occurred. Electrical responses were delayed (mean 102.6 s for 5 pM SP), appearing as brief current pulses. Reapplication of SP resulted in peak current augmentation (mean 15.3 pA before exposure to SP, 47.3 pA after 1st exposure, and 116.0 pA after 2nd exposure to 5 pM SP). Cells repetitively exposed to SP degranulated 5-15 min and > 25 min after the second exposure to 50 nM SP (10 of 10 cells) or 5 pM SP (5 of 9 cells), respectively. This effect was reduced by 10 microM 5-nitro-2-(3-phenylpropylamino)benzoic acid or when extracellular Ca2+ was removed, indicating a dependence on Cl- conductance and extracellular Ca2+. We propose that whole cell current oscillations in the absence of degranulation are the functional correlate of priming, a process that increases cellular responsiveness for the subsequent stimulation.
The activation of mast cells (MC) due to immunological stimulation causes an immediate and dramatic inflammatory response. We review current evidence indicating that the membrane permeabilities for calcium, chloride, sodium, and potassium have a significant role in the activation of these cells, and in some cases, specific ionic channels have been identified. Moreover, a number of intracellular mechanisms controlling these channels are pointed out, including different classes of G proteins, intracellular calcium, cAMP, and products of phosphoinositol breakdown. However, the interplay between factors controlling membrane conductances for different ions is not currently understood. The diversity of ionic effects on MC activation is depicted, illustrating that the ionic mechanisms of MC activation are specific for different MC types. Since nerve/mast cell interaction is a key element in the burgeoning field of neuroimmunology, we discuss the role of ionic channels as targets of neurotransmitter action in MC activation.
To investigate the basis of interactions between nerves and mast cells, we tested the actions of the neuropeptide substance P (SP) on whole cell current characteristics of RBL-2H3 cells (homologous to mucosal mast cells). Control RBL cells showed a K(+)-dependent inwardly rectified current. SP (10(-6) M) caused transient, frequently repetitive increases in current amplitude, which at a membrane potential (Vm) of -80 mV rose by -1,020.0 +/- 223.4 pA after SP application compared with -6.8 +/- 1.7 pA for control. This response was characterized by a lag phase of 102 +/- 16 s. Seventeen percent of cells showed spontaneous transients in the current amplitude from the beginning of the recording. After SP administration, the amplitude of these transients increased by 6.3 +/- 2.0-fold. Responses to SP were mimicked by the application of ionomycin. For both SP and ionomycin, there was a dose dependency of the lag phase. Removal of extracellular calcium abolished the response for 10(-6) M SP but not for 6.6 x 10(-6) M ionomycin. During current transients, the whole cell current had both inward and outward rectified components with the zero current Vm shifted from -87.3 +/- 3.2 mV at control to -10.8 +/- 1.7 mV. We compare the SP-evoked current responses in mucosal-type mast cells with those described in connective tissue type.
Indirect evidence links sensory nerves with mast cells (MC) in inflammatory reactions of airway, skin, and intestine. Isolated MC secrete histamine, serotonin, and other inflammatory mediators in response to neuropeptides such as substance P (SP) in vitro. To obtain direct evidence of nerve/MC interactions, we used a tissue culture model involving the co-culture of murine sympathetic neurons and rat basophilic leukemia (RBL) cells (homologous to mucosal MC). An electrophysiologic analysis of the consequences of neuron/RBL cell contacts showed that neurite contact with RBL cells reduced the control input resistance (Ro) of 61.8 +/- 3.2 (n = 110) M omega to 22.4 +/- 4.8 (n = 13) M omega (P less than 0.01) without change in the membrane potential. Time course studies showed that Ro of RBL cells with neurite contact was always lower by 30 to 54% than adjacent RBL cells lacking such contact. This effect was not seen in RBL cells cultured on rat fibroblasts. Direct application of SP, bradykinin, and somatostatin, but not acetylcholine, noradrenaline, or the putative neurotransmitter ATP, could partly mimic the effect of neurite contact. Therefore, neurotransmitter release from sympathetic neurons in contact with RBL cells may decrease RBL cell membrane resistance, possibly leading to activation.
Rat peritoneal mast cells (PMC) were activated with anti-IgE or 48/80 while in coculture with neurons dissociated from mouse superior cervical ganglia. At 18-24 h of coculture, microelectrode recordings from neurons were made 15 min after activation of PMC with anti-IgE antibody or the secretagogue compound 48/80. These recordings showed that PMC activation caused depolarization of the neurons and decreased their membrane resistance. Both methods of activation resulted in similar changes in these neuronal characteristics. The resting potential decreased by an average of 15% from the control value of -36.0 +/- 0.6 mV (SEM) (n = 121). The membrane resistance decreased by an average of 60% from the control value of 34.2 +/- 2.0 M omega (n = 75). Application of PMC secretion products directly onto neuronal somata caused reversible changes similar to those caused by activation of cocultured PMC. A decrease in membrane resistance that was observed in neurons cocultured with PMC for 18-24 h without stimulation was due to a proportion of PMC undergoing spontaneous activation. These changes in neuronal physiology are attributed to the action of substances released from the mast cells. This coculture model offers the means to study the cellular interactions involved in neuroimmune communication.
To investigate the metabolic and organ changes accompanying growth of a malignant tumor, ten male Fisher 344 rats weighing 150 to 200 g were inoculated subcutaneously with 10(6) viable MCA sarcoma cells (tumor-bearing). Ten other rats (controls) were similarly inoculated with saline. Both groups were allowed food and water ad libitum. An additional ten rats (pair-fed) were inoculated with saline and fed the same mean daily food intake as the tumor-bearing rats. Thirty-five days after inoculation the rats were killed by exsanguination. Livers, spleens, and tumors were weighed, and amino acid profiles and biochemical parameters were measured. Liver and spleen weights in tumor-bearing rats were significantly greater than control rats (P less than 0.05 and P less than 0.01, respectively). Liver weight in pair-fed rats was significantly less than control rats (P less than 0.01), but spleen weight was greater (P less than 0.01). Amino acid profiles of tumor-bearing rats and pair-fed rats were different from each other and from those of control rats. Branched-chain amino acids were lowest in tumor-bearing rats and significantly different from control and pair-fed rats. Lysine was significantly higher (P less than 0.01) and arginine significantly lower (P less than 0.05) in tumor-bearing rats compared with control rats. These different plasma amino acid profiles and changes in serum biochemistry of cachectic tumor-bearing rats compared with malnourished pair-fed rats suggest specific tumor effects on host metabolism not mediated solely by anorexia.
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A set for analysis of temperature effects on the CNS activity in insects is described. Thermostimulation can be applied to the whole body or to only some regions of CNS. An amplitude and rate interval analyzer (in cooperation with a microcomputer) makes it possible to do an analysis of the correlation between temperature and the neuronal firing rate. As an example of the use of this set an experiment on American cockroach Periplaneta americana was described. Thermosensitivity of the prothoracic ganglion was presented.
Application of thermocouples for measuring body temperature of insects is described in experiments on American cockroach (Periplaneta americana). The temperature of the head, mesothorax and abdomen was measured at rest and during flight. The overall accuracy of the measuring system was +/- 0.1 degrees C.