Objective: Spinal cord injury (SCI), one of the major disabilities concerning central nervous system injury, results in permanent tissue loss and neurological impairment. The existing therapeutic options for SCI are limited and predominantly consist of chemical compounds. In this study, we delved into the neuroprotective effects of myricetin, a natural flavonoid compound, and the underlying mechanisms, specifically in the context of SCI, utilizing an in vivo model. Previously, our investigations revealed an elevation in the phosphorylated form of Lin-11, Isl-1, and Mec-3 kinase1 (LIMK1) at chronic time points postinjury, coinciding with neuronal loss and scar formation. Our primary objective here was to assess the potential neuroprotective properties of myricetin in SCI and to ascertain if these effects were linked to LIMK inhibition, a hitherto unexamined pathway to date. Methods: Computational docking and molecular dynamics simulation studies were performed to assess myricetin’s potential to bind with LIMK. Then, using a rat contusion model, SCI was induced and different molecular techniques (Western blot, Evans Blue assay, quantitative reverse transcription polymerase chain reaction and immunohistochemistry) were performed to determine the effects of myricetin. Results: Remarkably, computational docking models identified myricetin as having a better interaction profile with LIMK than standard. Subsequent to myricetin treatment, a significant downregulation in phosphorylated LIMK expression was observed at chronic time points. This reduction correlated with a notable decrease in glial and fibrotic scar formation, and enhanced neuroprotection indicating a positive outcome in vivo. Conclusion In summary, our findings underscore myricetin’s potential as a bioactive compound capable of attenuating SCI-induced injury cascades by targeting the LIMK pathway.

Background/Aims: A Helicobacter pylori (H. pylori) infection is the most common cause of chronic gastritis (CG), with approximately 50% of the world’s population infected. Long-term infection increases the risk of progression to gastric cancer. This study evaluated the histopathological changes in CG using the Updated Sydney System (USS) to estimate the prevalence and correlation of H. pylori gastritis with other histological variables. Methods: This research was a prospective observational study conducted in the Department of Pathology of a tertiary care teaching hospital in Central India. The study was conducted between Feb 2017 to April 2018. Two antral biopsies were taken per patient, one for a Rapid Urease Test and the second for routine histopathology. All samples were analyzed according to the USS. Results: CG was found in 83.84% of total dyspeptic patients. The most common age group was 31–40 years, with a male preponderance. Of 109 gastric antral biopsies with histopathological evidence of chronic gastritis, neutrophilic activity, intestinal metaplasia, atrophy, and lymphoid aggregates were present in 50 (45.87%), 10 (9.2%), 23 (21.10%), and 11(10.09%) cases, respectively.The prevalence of H. pylori was 46.78%, and its association with the degree of chronic inflammation and intestinal metaplasia was statistically significant. Conclusions H. pylori was significantly associated with the degree of chronic inflammation and intestinal metaplasia. Hence, this study suggests a vigorous search for H. pylori should be initiated if chronic inflammation and intestinal metaplasia are seen in antral gastric biopsies.

Background: Pre-operative ilioinguinal-iliohypogastric nerve block (II-IHNB) has a proven role in lessening acute postoperative pain and opioid consumption following hernia repair. However, its role in preventing post-herniorrhaphy groin pain (PHGP) is still unknown. The current study aims to assess pre-operative II-IHNB's impact on PHGP three and six months after open inguinal hernia repair under spinal anesthesia. Methods: Seventy patients posted for inguinal hernia surgery were randomly allocated into group A (received ultrasound-guided II-IHNB with 10 mL of 0.5% ropivacaine and 4 mg [1 mL] dexamethasone) and group B (received ultrasound-guided II-IHNB with 11 mL of 0.9% normal saline). The time to first analgesic request, pain scores, opioid consumption, DN4 score, and PHGP at 3 and 6 months were analyzed using appropriate statistical tests. Results: The numerical pain rating scale at movement in group A was significantly reduced at all the time intervals of 3, 6, 12, and 24 hours compared to group B. Total opioid usage was lower in group A (3.71 mg [3.90]) versus group B (12.14 mg [4.90]) with a mean difference of –8.43 mg (95% CI –10.54, –6.32), P < 0.001. The time required for the first rescue analgesic was significantly longer in group A (360 min [180–360]) versus (180 min [180–360]) in group B (P < 0.001). However, there was no difference in the incidence of PHGP at three and six months between the two groups. Conclusions Pre-operative ultrasound-guided II-IHNB reduces postoperative analgesic requirement but does not reduce the incidence of chronic PHGP following hernia surgery at 6 months.

Objective: Spinal cord injury (SCI), one of the major disabilities concerning central nervous system injury, results in permanent tissue loss and neurological impairment. The existing therapeutic options for SCI are limited and predominantly consist of chemical compounds. In this study, we delved into the neuroprotective effects of myricetin, a natural flavonoid compound, and the underlying mechanisms, specifically in the context of SCI, utilizing an in vivo model. Previously, our investigations revealed an elevation in the phosphorylated form of Lin-11, Isl-1, and Mec-3 kinase1 (LIMK1) at chronic time points postinjury, coinciding with neuronal loss and scar formation. Our primary objective here was to assess the potential neuroprotective properties of myricetin in SCI and to ascertain if these effects were linked to LIMK inhibition, a hitherto unexamined pathway to date. Methods: Computational docking and molecular dynamics simulation studies were performed to assess myricetin’s potential to bind with LIMK. Then, using a rat contusion model, SCI was induced and different molecular techniques (Western blot, Evans Blue assay, quantitative reverse transcription polymerase chain reaction and immunohistochemistry) were performed to determine the effects of myricetin. Results: Remarkably, computational docking models identified myricetin as having a better interaction profile with LIMK than standard. Subsequent to myricetin treatment, a significant downregulation in phosphorylated LIMK expression was observed at chronic time points. This reduction correlated with a notable decrease in glial and fibrotic scar formation, and enhanced neuroprotection indicating a positive outcome in vivo. Conclusion In summary, our findings underscore myricetin’s potential as a bioactive compound capable of attenuating SCI-induced injury cascades by targeting the LIMK pathway.

Background/Aims: A Helicobacter pylori (H. pylori) infection is the most common cause of chronic gastritis (CG), with approximately 50% of the world’s population infected. Long-term infection increases the risk of progression to gastric cancer. This study evaluated the histopathological changes in CG using the Updated Sydney System (USS) to estimate the prevalence and correlation of H. pylori gastritis with other histological variables. Methods: This research was a prospective observational study conducted in the Department of Pathology of a tertiary care teaching hospital in Central India. The study was conducted between Feb 2017 to April 2018. Two antral biopsies were taken per patient, one for a Rapid Urease Test and the second for routine histopathology. All samples were analyzed according to the USS. Results: CG was found in 83.84% of total dyspeptic patients. The most common age group was 31–40 years, with a male preponderance. Of 109 gastric antral biopsies with histopathological evidence of chronic gastritis, neutrophilic activity, intestinal metaplasia, atrophy, and lymphoid aggregates were present in 50 (45.87%), 10 (9.2%), 23 (21.10%), and 11(10.09%) cases, respectively.The prevalence of H. pylori was 46.78%, and its association with the degree of chronic inflammation and intestinal metaplasia was statistically significant. Conclusions H. pylori was significantly associated with the degree of chronic inflammation and intestinal metaplasia. Hence, this study suggests a vigorous search for H. pylori should be initiated if chronic inflammation and intestinal metaplasia are seen in antral gastric biopsies.

Background: Pre-operative ilioinguinal-iliohypogastric nerve block (II-IHNB) has a proven role in lessening acute postoperative pain and opioid consumption following hernia repair. However, its role in preventing post-herniorrhaphy groin pain (PHGP) is still unknown. The current study aims to assess pre-operative II-IHNB's impact on PHGP three and six months after open inguinal hernia repair under spinal anesthesia. Methods: Seventy patients posted for inguinal hernia surgery were randomly allocated into group A (received ultrasound-guided II-IHNB with 10 mL of 0.5% ropivacaine and 4 mg [1 mL] dexamethasone) and group B (received ultrasound-guided II-IHNB with 11 mL of 0.9% normal saline). The time to first analgesic request, pain scores, opioid consumption, DN4 score, and PHGP at 3 and 6 months were analyzed using appropriate statistical tests. Results: The numerical pain rating scale at movement in group A was significantly reduced at all the time intervals of 3, 6, 12, and 24 hours compared to group B. Total opioid usage was lower in group A (3.71 mg [3.90]) versus group B (12.14 mg [4.90]) with a mean difference of –8.43 mg (95% CI –10.54, –6.32), P < 0.001. The time required for the first rescue analgesic was significantly longer in group A (360 min [180–360]) versus (180 min [180–360]) in group B (P < 0.001). However, there was no difference in the incidence of PHGP at three and six months between the two groups. Conclusions Pre-operative ultrasound-guided II-IHNB reduces postoperative analgesic requirement but does not reduce the incidence of chronic PHGP following hernia surgery at 6 months.

Objective: Spinal cord injury (SCI), one of the major disabilities concerning central nervous system injury, results in permanent tissue loss and neurological impairment. The existing therapeutic options for SCI are limited and predominantly consist of chemical compounds. In this study, we delved into the neuroprotective effects of myricetin, a natural flavonoid compound, and the underlying mechanisms, specifically in the context of SCI, utilizing an in vivo model. Previously, our investigations revealed an elevation in the phosphorylated form of Lin-11, Isl-1, and Mec-3 kinase1 (LIMK1) at chronic time points postinjury, coinciding with neuronal loss and scar formation. Our primary objective here was to assess the potential neuroprotective properties of myricetin in SCI and to ascertain if these effects were linked to LIMK inhibition, a hitherto unexamined pathway to date. Methods: Computational docking and molecular dynamics simulation studies were performed to assess myricetin’s potential to bind with LIMK. Then, using a rat contusion model, SCI was induced and different molecular techniques (Western blot, Evans Blue assay, quantitative reverse transcription polymerase chain reaction and immunohistochemistry) were performed to determine the effects of myricetin. Results: Remarkably, computational docking models identified myricetin as having a better interaction profile with LIMK than standard. Subsequent to myricetin treatment, a significant downregulation in phosphorylated LIMK expression was observed at chronic time points. This reduction correlated with a notable decrease in glial and fibrotic scar formation, and enhanced neuroprotection indicating a positive outcome in vivo. Conclusion In summary, our findings underscore myricetin’s potential as a bioactive compound capable of attenuating SCI-induced injury cascades by targeting the LIMK pathway.