DOI: 10.37421/2795-6172.2022.6.160
DOI: 10.37421/2795-6172.2022.6.161
DOI: 10.37421/2795-6172.2022.6.159
DOI: 10.37421/2795-6172.2022.6.158
Naresh K. Reddy*, A. Pramod, P. Goverdhan and M. Hariprasad
DOI: 10.37421/2795-6172.2022.6.157
Aim of the study was to investigate the effect of voglibose on circadian pattern of blood glucose and enzymatic antioxidants in normal rats. Male albino wistar rats were selected, divided into eight groups, each group consist of six animals and subjected for investigation. Voglibose suppressed the postprandial rise of blood glucose in rats, when voglibose (0.3 mg/kg) was given 0.5hr before the administration of carbohydrates such as sucrose, maltose and starch (2 gm/kg each). Blood samples were collected from both the normal and treated animals at o hr, 1hr, 2 hr, 4 hr, 6 hr, and 8 hr respectively. This study showed that the treatment of rats with voglibose significantly suppressed the increase in plasma glucose level after loading with sucrose, maltose and starch at time intervals CT 1400 (8 pm) was significantly lower, against the time CT 2000 (2 am), CT and 0200 (8 am), CT 0800 (2 pm) and circadian pattern of antioxidants in normal rats before and after treatment with voglibose did not show any significant difference at time intervals 0200 CT (8 am), 0800 CT (2 pm), 1400 CT (8 pm), and 2000 CT (2 am).
Anita Arsovska*, Brola Waldemar, Frasineanu Armand Daniel, Marceanu Manuela, Reisz Daniela, Sarzyńska-Długosz Iwona, Serdahely Vlastimil, Simu Mihaela Adriana, Valkovič Peter and Narayanaswamy Venketasubramanian
DOI: 10.37421/2795-6172.2023.7.182
Objectives: The efficacy and safety of NeuroAiD™ is well-established in patients with ischemic stroke in the acute and chronic phase. It is an addon treatment to standard therapies and there were no reports of major interactions. However, there is currently no data on the use of NeuroAiDTM in combination with anticoagulants. We aimed to determine the safety of using MLC901 (NeuroAiD II) with anticoagulants among patients in the Eastern European Cohort.
Methods: We performed a subgroup analysis of patients enrolled in the NeuroAiD Safe Treatment Registry (NeST). Patient who were given anticoagulants were included. Data collected were baseline demographics, diagnosis, concomitant medications and adverse events.
Results: A total of 98 patients were included. There were 48 female (49%), median age 64 years IQR (50,71), baseline median NIHSS 16, IQR (11,20), median mRS 4, IQR (3.25,5). Diagnoses included: Ischemic Stroke -80%, Traumatic Brain Injury - 7%, Cerebral Venous Thrombosis - 3%, Global hypoxic encephalopathy - (2%), Venous infarct - 1 %, AV Malformation - 1%, Meningoencephalitis - 1%. Risk factors were: hypertension - 72%, diabetes mellitus - 21% and hyperlipidaemia - 31%. The presence of cardiac disease was seen in 38% of which 24% had non-valvular atrial fibrillation. The concomitant anticoagulants were used in 98% of patients and included: low-molecular-weight heparin (LMWH), direct acting oral anticoagulants (DOACs), and Vitamin K antagonist (VKA). Neither adverse events nor side effects were reported.
Conclusions: The study provides new evidence for the safe use of MLC901 when combined with anticoagulants in a real-world setting.
DOI: 10.37421/2795-6172.2023.7.183
About half of all cancers in humans have mutations in the tumor suppressor p53 (p53), most of which are missense mutations. Not only do p53 mutations impair its ability to suppress drugs, but they also give the missense mutant p53 (mutp53) oncogenic properties that are distinct from those of the wild-type p53. Restoring or stabilizing wtp53 conformation from mutp53, rescuing p53 nonsense mutations, depleting mutp53 proteins, and inducing p53 synthetic lethality or targeting vulnerabilities imposed by p53 deficiencies (activated retrotransposons) or mutations (enhanced YAP/TAZ) are some of the approaches that have been taken to develop novel cancer therapies because p53 mutations are specific to cancer. The mechanisms of action and activities of FDA-approved and clinically available drugs that target p53 mutations to stop the progression of cancer are summarized here Cancer spread is aided by mutations in the tumor suppressor p53 (p53).
DOI: 10.37421/2795-6172.2023.7.184
DOI: 10.37421/2795-6172.2023.7.185
DOI: 10.37421/2795-6172.2023.7.186
Journal of Clinical Research received 8 citations as per Google Scholar report
