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The emerging of drug resistant against Leishmania parasites prompts scientists to seek for novel therapeutic strategies against theses infectious protozoan parasites. Among different strategies, the use of larvae secretions could be suggested as a possible therapy with low side effects. Accordingly, the current study evaluated the in vitro and in vivo effects of Lucilia sericata larval secretions on Leishmania major, the causative agent of cutaneous leishmaniasis (CL). After preparation of L. sericata larval stages (L2 and L3) secretions, the potential effects of secretions were evaluated against L. major promastigotes and amastigotes (in vitro) using MTT assay. The cytotoxicity effects of secretions were also checked on uninfected macrophages. In addition, in vivo experiments were also conducted to investigate the effects of larvae's secretions on the CL lesions induced in the BALB/c mice. Although the increased concentration of larvae secretions exhibited a direct effect on the promastigotes proliferation (viability), contrarily, L2 secretions at a concentration of 96 µg/ml represented the highest inhibitory effect on parasite (amastigotes) burden in infected macrophages. Interestingly, L3 secretions > 60 µg/ml induced inhibitory effects on amastigotes. The results relevant to the cytotoxicity effects of L2 and L3 secretions on uninfected-macrophages showed a dose dependent correlation. In vivo results were also significant, compared to the positive control group. This study suggested the plausible inhibitory effects of L. sericata larvae's secretions on the L. major amastigotes and CL lesions progression. It seems that the characterization of all effective components/proteins in the larvae secretions and their specific targets in parasite structure or in cell (macrophage) responses could further reveal more details regarding the anti-leishmanial properties of these compounds.
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Background: Semaphorins play prominent roles in physiological and pathological processes such as vascular development, tumor growth and immune responses. Semaphorins have different roles in various kinds of cancers, but there is no study concerning their expression in the chronic lymphocytic leukemia (CLL). This study aimed to assess the SEMA3A, SEMA4A and SEMA4D expression in patients with CLL. Materials and Methods: Peripheral blood specimens were collected from 30 newly-diagnosed untreated patients with CLL and 30 healthy subjects as a control group. The SEMA3A, SEMA4A and SEMA4D expression was determined by real-time PCR method. Results: The fold change expression of SEMA3A and SEMA4D was 7.58 ± 2.66 and 3.20 ± 0.99 in patients with CLL, and was 1.01 ± 0.31 and 1.00 ± 0.27 in healthy subjects, respectively. The CLL patients expressed higher amounts of SEMA3A and SEMA4D in comparison with healthy subjects (P<0.02 and P<0.03, respectively). The fold change expression of SEMA3A in patients with stage II (11.12 ± 5.35) was also higher than patients with stage I (4.49 ± 1.61, P<0.05). No significant difference was also observed in the expression of SEMA4A and SEMA4D between patients with stage I and stage II CLL. In both CLL and control groups, the fold change expression of SEMA3A was higher in men than in women (P<0.03 and P<0.02, respectively). Conclusion: The results of the study indicated elevated expression of the SEMA3A and SEMA4D in patients with CLL. The SEMA3A expression was influenced by tumor stage and gender of participants.
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INTRODUCTION: Muscle atrophy, spasticity, and deformity are among long term complication of spinal cord injury (SCI) veterans. There are numerous studies evaluating effect of functional electrical stimulation on muscle properties of SCI people, but less research has focused on the benefits of passive cycling in the management of spasticity and improving ROM of lower limbs in individuals with SCI. AIMS: To evaluate the effect of electrical passive cycling on passive range of movement spasticity and electrodiagnostic parameters in SCI veterans. METHODS: Sixty-four SCI veterans referred to two clinical and research center in Tehran were recruited in this prospective clinical trial. The subjects were divided into two groups according to electrical passive cycling usage: (1) patients who did not use pedal exercise (control group), (2) patients used Electrical passive cycling up to optimal level (intervention group). Main outcome measures included hip, knee, and ankle range of motion, spasticity scale, and electrodiagnostic parameters including F-Wave Consistency, F-Wave Amplitude, H/M Ratio, F/M Ratio, H-Reflex Onset Latency, and H-Reflex Amplitude. Data were recorded at the time of receiving and 1 year after pedal exercise usage. RESULTS: Sixty-four SCI patients including 95.3% male, 4.7% female with mean age 43 years old were included in this study. All patients except one suffered from complete SCI. The involved spinal levels were cervical (17.2%), upper thoracic (34.4%), lower thoracic (45.3%), and lumbar (3.1%). Spasticity scale decreased significantly after passive cycling in group 2. Also hip, knee, and ankle ROM in group 2 were significantly improved after pedal exercise. There was a significant difference in H max/M max (RT<) and F/M ratio after versus before electric passive cycling system in group 2. CONCLUSION: These findings suggest that passive rhythmic leg exercise can lead to decrease in spasticity, increase in passive ROM of lower limbs and improvement in electrodiagnostic parameters of spasticity in patients with SCI.
