Biomedical subjects
M Jaakkola
Publications and source records attributed to M Jaakkola.
The relationship between audiogenic seizure (AGS) susceptibility and forebrain tone-responsiveness in genetically AGS-prone Wistar rats.
The present study characterized the intensity-response functions of extracellular field responsiveness of different cortical/subcortical structures of the forebrain following the free-field presentation of tone stimuli, within a population of genetically audiogenic seizure (AGS)-prone KM-Wistar rats. The neural response properties of each case were compared to its propensity to exhibit AGSs during the continuous tone stimulation (15 kHz, 90 s at max.). The amplitudes or slope components of the evoked responses and their peak latencies showed significant positive (amplitude and slope) and negative (peak latency) Bolzmann's sigmoid relationships with the onset-latency of AGS. These relationships, with areal differences in the slopes of saturation functions, applied for the three different data sets recorded simultaneously from the stratum radiatum dendritic layer of the hippocampal CA1 area, primary auditory cortex layers II-IV, and frontal cortex surface. In addition, the similar type of functions between the evoked response variables and AGS onset latency held when all the areas were considered together. These data suggest that the neural responsiveness to acoustic stimulation of the primary sensory, multimodal and association cortices of the forebrain may altogether contribute to the seizure initiation by that modality in the genetically AGS-prone rats. It has been previously shown that there exist abundant and dispersed auditory projections from these forebrain areas to the brain stem and spinal cord, structures that are generally considered to be the key predisposing factors in the generation of AGS. Hence, the types of correlation found reflect the subject-specific stage of forebrain responsiveness, being either related or unrelated to genetic AGS-specific changes, and possibly its triggering impact upon the lower brain AGS network. Accordingly, the mere comparison of forebrain response measures of these AGS-prone animals with those of the AGS-resistant ones could not reveal the result presented.
Changing strategies in the surgical management of acute necrotizing pancreatitis.
During 1982-90 we changed the surgical treatment of acute necrotizing pancreatitis twice. The operative strategy consisted of early formal resection (n = 13) during 1982-84, early lavational surgery (n = 15) during 1985-87 and late necrosectomy (n = 17) during 1988-90. The mortality rate decreased from 54% to 40% and to 24%, respectively. The pattern of complications changed from bleeding in resections to pseudocysts and fistulas in late necrosectomy. Sepsis and multiorgan failure were still main problems. These results led us to begin a prospective study of planned repeated debridement by open packing after delayed necrosectomy.
Vulvar squamous cell carcinoma cell lines are sensitive to paclitaxel in vitro.
In the current study, paclitaxel sensitivity of eight vulvar squamous cell carcinoma (SCC) cell lines was tested using a 96-well plate clonogenic assay. The chemosensitivity was expressed as IC50 corresponding to the drug concentration causing 50% inhibition in clonogenic survival. IC50 values were obtained from dose-response curves after fitting the data to the linear quadratic equation. The paclitaxel sensitivity of the eight vulvar SCC cell lines expressed as IC50 varied from 0.6 to 2.9 nM. The observed differences between the individual cell lines were surprisingly small, only 4.8-fold at the most. Paclitaxel sensitivity of vulvar SCC cell lines is of the same magnitude as the paclitaxel sensitivity of endometrial and ovarian carcinoma cell lines tested in our preliminary experiments with the same assay. We have previously studied the intrinsic radiosensitivity of these vulvar SCC cell lines. No correlation could be found between radiosensitivity and paclitaxel sensitivity. These results indicate that vulvar SCC is consistently sensitive to paclitaxel in vitro. The role of chemotherapy in the treatment of vulvar carcinoma has not been clarified yet. The efficacy of paclitaxel should be tested further in clinical trials.