Making physiology learning memorable: a mobile phone-assisted case-based instructional strategy.

The goal of the present study was to determine whether an active learning/teaching strategy facilitated with mobile technologies can improve students' levels of memory retention of key physiological concepts. We used a quasiexperimental pretest/posttest nonequivalent group design to compare the test performances of second-year medical students (n = 311) taught by conventional didactic methods (traditional group) with those involved in a case-based problem-solving learning approach facilitated with mobile phones as web-based "clickers" (experimental group). Using their cell phones, students answered the same questions about the key physiological concepts three times. A pretest to determine their baseline knowledge was followed by two followup tests after 1 wk and 2 mo, respectively. The experimental group scored a mean of 93.2% correct items after 1 wk and 84.8% correct items after 2 mo [95% confidence intervals: (89.4, 97.0) and (79.4, 90.3), respectively]. Compared with their colleagues in the traditional group who scored 33.3% [95% confidence interval: (18.9, 47.8)] and 38.5% [95% confidence interval: (23.6, 53.4)] correct items, respectively, this was a significant increase of ∼50% (P < 0.0001). Furthermore, for the experimental group, Cohen's effect size (d) values of d = 1.67 (1-wk posttest) and d = 1.38 (2-mo posttest) suggested a very high practical significance. In contrast, in the traditional group, Cohen's d values of d = 0.04 (1-wk posttest) and d = 0.15 (2-mo posttest) assumed a very low practical significance.

[Experimental allergic encephalomyelitis as an animal model for multiple sclerosis]. / Eksperimentalni alergijski encefalomijelitis kao zivotinjski model multiple skleroze.

Experimental allergic encephalomyelitis is an animal model for demyelinating autoimmune disease of central nervous system, whose clinical and pathological characteristics resemble those in human disease multiple sclerosis. Multiple sclerosis is a chronic inflammatory disease followed by central nervous system demyelination, which is the result of an autoimmune process followed by central nervous system infiltration with autoreactive lymphocytes, activated macrophages and by local production of proinflammatory cytokines. Finally, the destruction of oligodendrocytes and myelin sheath occurs, caused by immunologic effector mechanisms. In this paper we reviewed fundamental and new facts about the most used models, induction, clinical and immunological characteristics of the experimental allergic encephalomyelitis in comparison with multiple sclerosis. Aethology and pathogenesis of multiple sclerosis are still unknown, but experiments on its animal models have improved our knowledge, not only about multiple sclerosis, but autoimmune diseases in general.

[Immunologic aspects of disorders of neuromuscular transmission. 1. Myasthenia gravis]. / Imunoloski aspekti poremecaja neuromuskularnog prijenosa. 1. Miastenija gravis.

Myasthenia gravis (MG) is an autoimmune disease, characterized by disturbances of neuromuscular transmission. In this paper immunological aspects of the disease are discussed. Antigenic characteristics of acetylcholine receptors (AchR), ethiology, pathogenesis and immunodiagnostics of MG are described.

[Immunologic aspects of disorders of neuromuscular transmission. 2. Experimental autoimmune myasthenia gravis and the Lambert-Eaton myasthenic syndrome]. / Imunoloski aspekti poremecaja neuromuskularnog prijenosa. 2. Eksperimentalna autoimuna miastenja gravis i Lambert-Eatonov miastenicni sindrom.

This paper describes two condition caused by disfunction of neuromuscular transport: experimental autoimmune myasthenia gravis (EAMG) and Lambert-Eaton myasthenic syndrome (LEMS). EAMG can be caused by immunization with acetylcholine receptors (AChR). As in myasthenia gravis, anti-AChR antibodies reduce the number of these receptors, which impedes normal neuromuscular transmission. LEMS patients have normal AChR function: however there is a disfunction of acetylcholine release from the presynaptic terminals. This is due to the formation of antibodies against the voltage gated calcium channels on the presynaptic nerve terminals.

[Thermotherapy of tumors]. / Termoterapija tumorske bolesti.

In this paper a review as well as some of our results concerning the use of hyperthermia in the treatment of tumors are presented. Basically there are two broad categories of hyperthermia: systemic and localized. Local hyperthermia used as an adjunct to standard treatments (surgical therapy, radiation therapy, chemotherapy) as well as immunotherapy has gained more application in the experimental studies of thermotherapy in the clinic. Heat kills cells in a predictable and repeatable way, however, many of basic mechanisms relating to cell killing are still poorly understood. Despite that the intrinsic thermal sensitivity of tumor cells are identical to that of normal cells the difference in thermal sensitivity arises between tumor and normal tissue due to environmental and pathophysiological differences. The application of hyperthermia in multimodal tumor therapy has a strong biological rationale because using hyperthermia as an adjuvant to other therapies complementary and synergistic cytotoxic effects can be achieved leading to a significant improvement of the efficacy of tumor therapy. So did the combined treatment of local hyperthermia and immunotherapy show a synergistic effect due to enhancement of NK activity. However, the administration of some chemotherapeutics can abolish the observed synergism indicating that the use of a combined therapy in clinics should be attempted cautiously.

Effect of thermoimmunotherapy with OK-432 on the development of spontaneous lung metastases in mice.

The effect of combined hyperthermia and intratumoral administration of OK-432 (Picibanil) on the development of spontaneous lung metastases was studied. The spontaneous non-immunogenic fibrosarcoma, FSa-II, transplanted into the right foot of C3Hf/Sed mice, was used throughout. Hyperthermia was given locally by immersing the animal foot in a water bath set at 44.0 degrees C for 30 min. OK-432 in the dose of 2.5 KE was injected into the tumour 3 h before hyperthermia. This treatment has been shown to strongly inhibit local tumour growth. Sham hyperthermia, i.e. restraining the mice in holders, as well as local injection of saline solution, increased metastases incidence. The high incidence of metastases following combined sham hyperthermia and saline injection was substantially reduced by intratumoral administration of OK-432 given alone or combined with hyperthermia.

Augmentation of mouse natural killer cell activity by combined hyperthermia and streptococcal preparation, OK-432 (Picibanil) treatment.

It has previously been demonstrated that the local administration of OK-432 (Picibanil) enhances the response of a murine tumour and normal tissue to elevated temperatures. The experimental animals were C3Hf/Sed mice and the tumours were the fourth generation isotransplants of a spontaneous non-immunogenic fibrosarcoma, FSa-II. The thermal enhancement ratio was greater for the tumour than for normal tissue, resulting in a favourable differential effect between normal and malignant tissues. Further studies were conducted to disclose the mechanism of OK-432 induced thermal enhancement. Although OK-432 showed a slight direct cytotoxic activity against tumour cells in vitro, the in vivo antitumour effect of combined OK-432 and hyperthermia treatments was greater than the effect expected from in vitro cytotoxicity, indicating the involvement of the host-mediated mechanisms. Whole body irradiation (WBI), which suppressed the host's immune reaction, did not affect the thermal enhancement mediated by OK-432, suggesting that radiosensitive cells (sensitive to WBI) were not involved in this process. As expected, the i.v. injections of the anti-mouse T-cell serum did not have any effect on the thermal enhancement of OK-432. The administration of blockers of the reticuloendothelium system, i.e. silica or trypan blue, did not inhibit the OK-432 induced thermal enhancement. Moreover, local intratumoural injections of normal or OK-432 induced macrophages showed no effect on tumour growth. The thermal enhancement by OK-432 was eliminated following treatments with anti-(asialo GM1) globulin. Despite the fact that the cytotoxic effect of anti-(asialo GM1) globulin was not selective to natural killer (NK) cells, all the experimental results indicated that NK cells were probably attributable to thermal enhancement by OK-432 in vivo. The NK cell activity was stimulated when the OK-432 was locally administered with hyperthermia.

Enhancement of the thermal response of murine tumour and normal tissues by a streptococcal preparation, OK-432 (Picibanil).

We have studied the effect of a streptococcal preparation, OK-432, given alone or in combination with hyperthermia on murine tumour and normal tissues. The experimental tumour was a spontaneous non-immunogenic fibrosarcoma FSa-II transplanted in the foot of C3Hf/Sed mice. Local hyperthermia was achieved by immersing the mouse foot into a constant temperature water bath (42-45 degrees C) for various lengths of time. Tumour response was studied by analysing the tumour growth (TG) time. Various doses of OK-432 (1-5 KE/mouse) were injected locally into the tumour. Local administration of OK-432 alone (without hyperthermia) had no effect on the TG time. Thermal enhancement ratio (TER) for combined treatment was independent of drug dose greater than or equal to 2 KE, and the mean TER was 1.48 +/- 0.27 (95% CL). The TER was greater for 6 mm tumours than for 4 mm tumours, and it was greatest if the time interval between hyperthermia and drug administration was 3 h or less. There was no effect if the drug was administrated 4 days before hyperthermia, but its application 9 days prior to hyperthermia caused a slight prolongation of the TG time of non-heated tumours, and a reduction in the TG time of heated tumours. Normal-tissue response was studied by scoring the peak foot reaction and RD50 (the treatment time to induce a specified response in one-half of the treated animals). The effect of OK-432 on the thermal response of the foot was also studied at various temperatures. The mean TER was 1.11 +/- 0.07. Local administration of OK-432 failed to modify significantly the kinetics of thermotolerance. Present experiments demonstrated that OK-432 after local administration enhanced the thermal response of murine tumour and normal tissues. This enhancement was greater for the tumour than for the normal tissue, resulting in a favourable differential effect between normal and malignant tissues (the average therapeutic gain was 1.33 +/- 0.19).