Monkeypox Detection Using CNN with Transfer Learning.

Monkeypox disease is caused by a virus that causes lesions on the skin and has been observed on the African continent in the past years. The fatal consequences caused by virus infections after the COVID pandemic have caused fear and panic among the public. As a result of COVID reaching the pandemic dimension, the development and implementation of rapid detection methods have become important. In this context, our study aims to detect monkeypox disease in case of a possible pandemic through skin lesions with deep-learning methods in a fast and safe way. Deep-learning methods were supported with transfer learning tools and hyperparameter optimization was provided. In the CNN structure, a hybrid function learning model was developed by customizing the transfer learning model together with hyperparameters. Implemented on the custom model MobileNetV3-s, EfficientNetV2, ResNET50, Vgg19, DenseNet121, and Xception models. In our study, AUC, accuracy, recall, loss, and F1-score metrics were used for evaluation and comparison. The optimized hybrid MobileNetV3-s model achieved the best score, with an average F1-score of 0.98, AUC of 0.99, accuracy of 0.96, and recall of 0.97. In this study, convolutional neural networks were used in conjunction with optimization of hyperparameters and a customized hybrid function transfer learning model to achieve striking results when a custom CNN model was developed. The custom CNN model design we have proposed is proof of how successfully and quickly the deep learning methods can achieve results in classification and discrimination.

Thiamethoxam-mediated alteration in multi-biomarkers of a model organism, Galleria mellonella L. (Lepidoptera: Pyralidae).

Thiamethoxam (TMX), a second-generation neonicotinoid, is extensively used to control numerous pests that infest crops. We investigated the effects of TMX (10, 20, 30, 40, and 50 µg/mL for 24, 48, 72, and 96 h) on biomarkers such as antioxidant enzymes (superoxide dismutase (SOD) and catalase (CAT)); malondialdehyde (MDA), protein, lipid, and carbohydrate levels; micronucleus formation; and total hemocyte count in a model organism, Galleria mellonella L. SOD and CAT activities significantly decreased after 72 and 96 h of treatment at all TMX concentrations compared with control. MDA level increased following treatment with all TMX doses, with the exception of that following treatment with the lowest dose (10 µg/mL) at all tested treatment durations. Lipid and carbohydrate levels significantly decreased following treatment with high doses of TMX (40 and 50 µg/mL) after 48, 72, and 96 h. Micronucleated cell number significantly increased following treatment with all TMX doses at all tested treatment durations, except with 10 µg/mL of TMX for 24 h, when compared with control. During the first 72 h, total hemocyte count significantly decreased following treatment with 20-, 30-, 40-, and 50-µg/mL TMX; however, it was significantly reduced at all doses of TMX after 96 h. These results suggest that TMX can induce immunotoxicity, oxidative stress, and genotoxicity in a potential target and also in the model organism, G. mellonella. In addition, our study provides additional information regarding the prospective toxic effects of TMX.

Comparison of the effects of local and systemic dexamethasone on the rat traumatic sciatic nerve model.

AIM: The aim of the study was to evaluate the effect of peroperatively locally administered dexamethasone on nerve recovery after induced nerve crush injury. MATERIAL AND METHODS: 4 groups of 8 animals were formed. The sciatic nerves of 32 rats were exposed at midthigh level and those of 24 rats were crushed for 30 seconds with a pair of jeweler's forceps. RESULTS: Sciatic functional index (SFI) measurements of all the animals included at days 7, 14, 21 and 28 was statistically significant (p < 0.05). Pinch tests that were done on the first 13 days gave negative results in all the groups. There was a difference between the test results of Group II and those of Group III and IV at days 14, 21 and 28. When the duration of the experiment was taken as a whole, no difference was observed between the test results of Group III and IV. CONCLUSION: Recovery in the group treated with local dexamethasone was more remarkable than that in the group treated with systemic dexamethasone in our study. As the difference was statistically significant, we recommend the perioperative use of local dexamethasone in procedures that might induce nerve injury.

Anti-nociceptive, analgesic and pathohistological effects of intrathecal dexmedetomidine and bupivacaine in rats.

BACKGROUND AND OBJECTIVES: This study investigates analgesic and nociceptive effects of adding dexmedetomidine to bupivacaine neuraxial anesthesia through Tail-flick (TF) and Hot-plate (HP) tests and the pathohistological changes on spinal nerves and nerve roots through light microscopy. METHODS: Forty anesthetized, male Sprague-Dawley rats were intrathecally catheterized. Basal values of TF and HP tests were measured before and after catheterization. Thirty-six successfully catheterized rats were assigned to four groups. Group B received 10 µg bupivacaine, Group BD3 received 10 µg bupivacaine + 3 µg dexmedetomidine, Group BD10 received 10 µg bupivacaine + 10 µg dexmedetomidine and Control group received 10 µL volume of artificial cerebrospinal fluid. TF and HP tests were performed between the 5(th) and 300(th) minutes of drug administration. Twenty-four hours after administration of drugs, rats were sacrificed and spinal cord and nerve roots were removed for pathological investigation. RESULTS: Baseline values of the TF and HP tests were not statistically different among the groups (6.8±0.15s). TF and HP latencies in the Control group did not change significantly during the study. TF and HP test results showed that adding 3 and 10 µg dexmedetomidine caused a dose-dependent increase in duration and amplitude of analgesic and nociceptive effect of bupivacaine (TF: 37.52±1.08%, 57.86±1.16% respectively, HP: 44.24±1.15%, 68.43±1.24% respectively). CONCLUSIONS: There were no apparent pathohistological changes at least 24 hours after the intrathecal administration of a single dose of dexmedetomidine 3 µg and 10 µg. Dexmedetomidine added to bupivacaine for spinal block improves analgesia and prolongs block duration.

Efeitos antinociceptivos, analgésicos e histopatológicos de dexmedetomidina e bupivacaína intratecal em rato / Anti-nociceptive, analgesic and pathohistological effects of intrathecal dexmedetomidine and bupivacaine in rats / Efectos antinociceptivos, analgésicos e histopatológicos de dexmedetomidina y bupivacaína intratecal en ratones

JUSTIFICATIVA E OBJETIVOS: Este estudo investigou os efeitos analgésicos e nociceptivos da adição de dexmedetomidina à bupivacaína em anestesia do neuroeixo usando os testes de retirada da cauda (tail-flick [TF]) e da placa quente (hot-plate [HP]) e microscopia de luz para as alterações histopatológicas de nervos espinhais e raízes nervosas. MÉTODOS: Quarenta ratos Sprague-Dawley anestesiados, machos, foram cateterizados intratecalmente. Os valores basais dos testes TF e HP foram medidos antes e depois do cateterismo. Trinta e seis ratos cateterizados com sucesso foram distribuídos em quatro grupos. O Grupo B recebeu 10 µg de bupivacaína, o Grupo BD3 recebeu 10 µg de bupivacaína + 3 µg de dexmedetomidina, o Grupo BD10 recebeu 10 µg de bupivacaína + 10 µg de dexmedetomidina e o Grupo Controle recebeu 10 µL de líquido cefalorraquidiano artificial. Os testes TF e HP foram feitos entre cinco e 300 minutos a partir da administração das drogas. Vinte e quatro horas após a administração, os ratos foram sacrificados e retiradas as medulas espinhais e raízes nervosas para investigação patológica. RESULTADOS: Os valores basais dos testes TF e HP não foram estatisticamente diferentes entre os grupos (6,8 ± 0,15 s). As latências de TF e HP no Grupo Controle não apresentaram alteração significativa durante o estudo. Os resultados dos testes TF e HP mostraram que a adição de 3 e 10 µg de dexmedetomidina causou um aumento dose-dependente na duração e amplitude do efeito analgésico e nociceptivo de bupivacaína (TF: 37,52 ± 1,08%, 57,86 ± 1,16%, respectivamente; HP: 44,24 ± 1,15%, 68,43 ± 1,24%, respectivamente). CONCLUSÕES: Não houve alterações histopatológicas aparentes em pelo menos 24 horas após a administração intratecal da dose única de dexmedetomidina (3 µg e 10 µg). Dexmedetomidina adicionado à bupivacaína para raquianestesia melhora a analgesia e prolonga a duração do bloqueio.

BACKGROUND AND OBJECTIVES: This study investigates analgesic and nociceptive effects of adding dexmedetomidine to bupivacaine neuraxial anesthesia through Tail-flick (TF) and Hot-plate (HP) tests and the pathohistological changes on spinal nerves and nerve roots through light microscopy. METHODS: Forty anesthetized, male Sprague-Dawley rats were intrathecally catheterized. Basal values of TF and HP tests were measured before and after catheterization. Thirty-six successfully catheterized rats were assigned to four groups. Group B received 10 µg bupivacaine, Group BD3 received 10 µg bupivacaine + 3 µg dexmedetomidine, Group BD10 received 10 µg bupivacaine + 10 µg dexmedetomidine and Control group received 10 µL volume of artificial cerebrospinal fluid. TF and HP tests were performed between the 5th and 300th minutes of drug administration. Twenty-four hours after administration of drugs, rats were sacrificed and spinal cord and nerve roots were removed for pathological investigation. RESULTS: Baseline values of the TF and HP tests were not statistically different among the groups (6.8 ± 0.15 s). TF and HP latencies in the Control group did not change significantly during the study. TF and HP test results showed that adding 3 and 10 µg dexmedetomidine caused a dosedependent increase in duration and amplitude of analgesic and nociceptive effect of bupivacaine (TF: 37.52 ± 1.08%, 57.86 ± 1.16% respectively, HP: 44.24 ± 1.15%, 68.43 ± 1.24% respectively). CONCLUSIONS: There were no apparent pathohistological changes at least 24 hours after the intrathecal administration of a single dose of dexmedetomidine 3 µg and 10 µg. Dexmedetomidine added to bupivacaine for spinal block improves analgesia and prolongs block duration.

JUSTIFICATIVAS Y OBJETIVOS: Este estudio investigó los efectos analgésicos y nociceptivos de la adición de dexmedetomidina a la bupivacaína en anestesia del neuro eje, usando los test de retirada de la cola (tail-flick [TF]) y de la placa caliente (hot-plate [HP]) y microscopía de luz para las alteraciones histopatológicas de nervios espinales y raíces nerviosas. MÉTODOS: Cuarenta ratones anestesiados, Sprague-Dawley machos, fueron cateterizados intratecalmente. Los valores basales de los testes TF y HP fueron medidos antes y después del cateterismo. Treinta y seis ratones cateterizados con éxito fueron distribuidos en cuatro grupos. El Grupo B recibió 10 µg de bupivacaína, el Grupo BD3 recibió 10 µg de bupivacaína + 3 µg de dexmedetomidina, el Grupo BD10 recibió 10 µg de bupivacaína + 10 µg de dexmedetomidina y el Grupo Control recibió 10 µL de líquido cefalorraquídeo artificial. Los test TF y HP se hicieron entre cinco y 300 minutos a partir de la administración de los fármacos. Veinte y cuatro horas después de la administración, los ratones fueron sacrificados y se les retiraron las médulas espinales y las raíces nerviosas para investigación patológica. RESULTADOS: Los valores basales de los test TF y HP no fueron estadísticamente diferentes entre los grupos (6,8 ± 0,15 s). Las latencias de TF y HP en el Grupo Control no tenían ninguna alteración significativa durante el estudio. Los resultados de los test TF y HP mostraron que la adición de 3 y 10 µg de dexmedetomidina causó un aumento dosis dependiente en la duración y en la amplitud del efecto analgésico y nociceptivo de bupivacaína (TF: 37,52 ± 1,08%, 57,86 ± 1,16%, respectivamente; HP: 44,24 ± 1,15%, 68,43 ± 1,24%, respectivamente). CONCLUSIONES: No hubo alteraciones histopatológicas aparentes en por lo menos 24 horas después de la administración intratecal de la dosis única de dexmedetomidina (3 µg y 10 µg). Dexmedetomidina añadido a la bupivacaína para raquianestesia mejora y prolonga la duración del bloqueo.

Anti-nociceptive, analgesic and pathohistological effects of intrathecal dexmedetomidine and bupivacaine in rats.

BACKGROUND AND OBJECTIVES: This study investigates analgesic and nociceptive effects of adding dexmedetomidine to bupivacaine neuraxial anesthesia through Tail-flick (TF) and Hot-plate (HP) tests and the pathohistological changes on spinal nerves and nerve roots through light microscopy. METHODS: Forty anesthetized, male Sprague-Dawley rats were intrathecally catheterized. Basal values of TF and HP tests were measured before and after catheterization. Thirty-six successfully catheterized rats were assigned to four groups. Group B received 10 µg bupivacaine, Group BD3 received 10 µg bupivacaine + 3 µg dexmedetomidine, Group BD10 received 10 µg bupivacaine + 10 µg dexmedetomidine and Control group received 10 µL volume of artificial cerebrospinal fluid. TF and HP tests were performed between the 5(th) and 300(th) minutes of drug administration. Twenty-four hours after administration of drugs, rats were sacrificed and spinal cord and nerve roots were removed for pathological investigation. RESULTS: Baseline values of the TF and HP tests were not statistically different among the groups (6.8 ± 0.15 s). TF and HP latencies in the Control group did not change significantly during the study. TF and HP test results showed that adding 3 and 10 µg dexmedetomidine caused a dose- dependent increase in duration and amplitude of analgesic and nociceptive effect of bupivacaine (TF: 37.52 ± 1.08%, 57.86 ± 1.16% respectively, HP: 44.24 ± 1.15%, 68.43 ± 1.24% respectively). CONCLUSIONS: There were no apparent pathohistological changes at least 24 hours after the intrathecal administration of a single dose of dexmedetomidine 3 µg and 10 µg. Dexmedetomidine added to bupivacaine for spinal block improves analgesia and prolongs block duration.