THE EFFECTS OF A PRAGMATIC SET OF INTERVENTIONS ON THE SHOULDER RANGE OF MOTION IN MALES AND FEMALES WITH SHOULDER PAIN: A CLINICAL TRIAL

Background and Aim: The effects of novel set of interventions are known but their effects with respect to gender are not known. This study aim to determine the effects of novel set of interventions on shoulder range of motion in males and females with shoulder pathology. Methodology: This study was of quasive experimental design. Thirty subjects of mean age (±SD) of 43. 23±10 years with shoulder pathology and restricted ROM were recruited. The major criteria for recruitment were 18-60 years of age. The general contraindications of manual therapy were the exclusion criteria. Shoulder functional movement and range of motion were the outcome measures.  Results: The mean % (SD) change for RUBB was 15.04±11.57for males and  14.49±10.44 for males. The change for RDBN was also significant (<0.00) from baseline and the % change in mean was 14.93±11.0 for males and 12.60±9.06 for females. The changes were well above the highly clinical meaningful difference (>0.8). It is further observed that the differences in gender were non-significant (P>0.05). Conclusion: The pragmatic set of interventions affect both the genders equally and improve shoulder range of motion and functional movements.  However, the results must be interpreted cautiously because of the inadequate sample size.

Pharmacological Screening of Different Extracts of Tribulus Terrestris for Neurodegenerative Disorders and Other Potential Activities

Oxidative stress is predominantly involved in pathogenesis of neurodegeneration. Conventional treatments are linked to harmful after-effects. Revolutionary herbal therapeutic agents are unmet clinical need to target neurodegeneration. Steroidal saponins, alkaloid and flavonoids are key phytochemicals of Tribulus terrestris (T. terrestris) accountable for its neuroprotective medicinal peculiarity. The objective of current study was to ensure the safety and to explore neuroprotective potential of T. terrestris. Physicochemical, phytochemical and GCMS analyses were carried out for characterization of plant. Acute toxicity, sub-acute toxicity and in vitro antioxidant activity were investigated. We measured the effect of T. terrestris methanol extract in aluminum chloride induced Alzheimer’s disease model and haloperidol induced parkinsonian rats by estimating behavioral and biochemical parameters. Open field test for locomotion and exploration, passive avoidance task for learning and memory, Y-maze and elevated plus maze for spontaneous behavior, memory and anxiety , hole board test for exploratory behavior and wire hanging test for neuromuscular coordination estimation were performed in anti-Alzheimer study. Catalepsy, head dipping, ladder climbing, foot printing and wire hanging behavioral task were carried out in anti-Parkinson’s study. The level of antioxidant enzymes and acetylcholinesterase inhibitory activity were estimated on brain homogenates of both neuroprotective studies. mRNA expression of pathological biomarkers was evaluated by RTPCR. GC-MS analysis showed highest % peak area (64.19) of benzene dicarboxylic acid. Toxicity signs and mortality were not observed during toxicity studies. TTME exhibited antioxidant properties by DPPH scavenging and by reduction potential. The results showed that TTME at a dose of 1000 mg/kg significantly improved (p ˂ 0.05) aluminum chloride, haloperidol induced neurotoxicity by modulating motor dysfunctions and cognitive disabilities, normalized the biochemical alteration of antioxidant enzymes and acetylcholinesterase. Histopathological analysis revealed that TTME significantly reversed the degenerative changes, neurofibrillary tangles, neuroinflmmation and neuronal loss in the brain architecture. TTME significantly downregulated (p ˂ 0.001) the level of BACE-1, IL-1α, IL-1β, TNFα and alpha synuclein mRNA expression. We concluded that Tribulus terrestris improved behavioral and biochemical parameters and therefore it will be effective in treatment of neurodegenerative disorders via myriad underlying mechanistic pathways.