Pharmacology teaching in dental education in India: Time for a reappraisal.

India has a unique position with its vast population and rapidly increasing healthcare demand. Dental health is integral to a holistic health care need, and a robust dental education system is necessary. Dental education in India is mainly regulated by the Dental Councilof India, setting broad guidelines. Universities having dental colleges and institutes develop fine curriculum development and evaluation details. General and Dental Pharmacology and Therapeuticsis a crucial subject taught to undergraduate dental students during the second year of a 4-year duration course. A dental graduate should be well trained in general and systemic pharmacology and rational therapeutics principles. This has been set as an objective by the Dental Council of India. Sound knowledge of the drug action mechanisms, indications, adverse drug reactions, drug interactions and contraindications, evidence-based medicine, and rational use of adrug is core to the allopathic system. The practical exercises on human simulation or computer-assisted learning are critical for understanding pharmacology. The subject of pharmacology for dental graduates has been allotted 70 hours of theory and 20 hours of practicals with almost the same syllabus as medical graduates. This article highlights the areas of concern concerning the deficiency of teaching hours and needed improvement in the curriculum to make it competent to achieve its objective. The authors bring this much-needed topic for discussion among academicians and for the attention of regulatory authorities.

Tannic Acid Provides Neuroprotective Effects Against Traumatic Brain Injury Through the PGC-1α/Nrf2/HO-1 Pathway.

The present research was conducted to elucidate a possible molecular mechanism related to neuromodulatory effects of tannic acid (TA) supplementation against traumatic brain injury (TBI) in a rodent model. Oxidative damage and neuroinflammation play a critical role in TBI and lead to behavioral alterations and neuronal dysfunction and death. These changes suggest a potential avenue in neurotherapeutic intervention. The aim of the present study was to investigate the neuroprotective effects of TA and potential mechanism of these effects in a controlled cortical impact injury model of TBI in Wistar rats that were treated with TA (50 mg/kg body weight. i.p.) before 30 min and 6 and 18 h after TBI. TBI-induced rats were examined after 24 h for behavioral dysfunction, Nissl stain, lipid peroxidation rate, glutathione level, activities of antioxidant enzymes (catalase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase), the expression level of 4-hydroxynonenal, pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-1 beta, as well as brain edema and immunoreactivity of glial fibrillary acidic protein. Results indicated that TA supplementation significantly modulated above mentioned alterations. Moreover, TA treatment effectively upregulated the protein expression of peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) and nuclear factor-E2-related factor-2 (Nrf2) as well as mitochondrial transcription factor A and heme oxygenase-1 (HO-1) following TBI. Overall, our results suggest that TA effectively ameliorates the behavioral alterations, oxidative damage, mitochondrial impairment, and inflammation against TBI that may be attributed to activation of PGC-1α/Nrf-2/HO-1 signaling pathway.

Melatonin pre-treatment mitigates SHSY-5Y cells against oxaliplatin induced mitochondrial stress and apoptotic cell death.

Oxaliplatin (Oxa) treatment to SH-SY5Y human neuroblastoma cells has been shown by previous studies to induce oxidative stress, which in turn modulates intracellular signaling cascades resulting in cell death. While this phenomenon of Oxa-induced neurotoxicity is known, the underlying mechanisms involved in this cell death cascade must be clarified. Moreover, there is still little known regarding the roles of neuronal mitochondria and cytosolic compartments in mediating Oxa-induced neurotoxicity. With a better grasp of the mechanisms driving neurotoxicity in Oxa-treated SH-SY5Y cells, we can then identify certain pathways to target in protecting against neurotoxic cell damage. Therefore, the purpose of this study was to determine whether one such agent, melatonin (Mel), could confer protection against Oxa-induced neurotoxicity in SH-SY5Y cells. Results from the present study found Oxa to significantly reduce SH-SY5Y cell viability in a dose-dependent manner. Alternatively, we found Mel pre-treatment to SH-SY5Y cells to attenuate Oxa-induced toxicity, resulting in a markedly increased cell viability. Mel exerted its protective effects by regulating reactive oxygen species (ROS) production and reducing superoxide radicals inside Oxa-exposed. In addition, we observed pre-treatment with Mel to rescue Oxa-treated cells by protecting mitochondria. As Oxa-treatment alone decreases mitochondrial membrane potential (Δψm), resulting in an altered Bcl-2/Bax ratio and release of sequestered cytochrome c, so Mel was shown to inhibit these pathways. Mel was also found to inhibit proteolytic activation of caspase 3, inactivation of Poly (ADP Ribose) polymerase, and DNA damage, thereby allowing SH-SY5Y cells to resist apoptotic cell death. Collectively, our results suggest a role for melatonin in reducing Oxa induced neurotoxicity. Further studies exploring melatonin's protective effects may prove successful in eliciting pathways to further alter the neurotoxic pathways of platinum compounds in cancer treatment.

[Urodynamic results of the treatment of urinary incontinence with peripheral electric stimulation]. / Resultados urodinámicos del tratamiento de la incontinencia urinaria con estimulación eléctrica periférica.

OBJECTIVES: To evaluate the urodynamic results achieved by electrostimulation in patients with different types of urinary incontinence. METHODS: 37 patients (32 females and 5 males) with urinary incontinence were treated with peripheral electrical stimulation. The urodynamic diagnosis were: detrusor instability (24.3%), stress urinary incontinence (24.3%), mixed urinary incontinence (48.6%), and bladder hyper-reflexia (2.7%). Rectal and vaginal electrodes were utilized. The therapeutic frequencies were 10 Hz, 20 Hz and 50 Hz. RESULTS: Detrusor instability disappeared in the cases treated with the 10 Hz frequency (79%) and in one case treated with the 50 Hz frequency. A significantly increased bladder capacity and decreased first micturition sensation were observed in this patient group. All patients with stress urinary incontinence were treated with high frequency (50 Hz), which achieved positive results in 44%. In the group of patients with mixed urinary incontinence. 45% remained unchanged. Treatment failed to achieve satisfactory results in the single case of detrusor hyperreflexia in this series. CONCLUSION: Peripheral electrical stimulation is a valid alternative in the treatment of male and female incontinence. Satisfactory results were achieved with the 10 Hz frequency in 89% of the patients with bladder instability and with the 50 Hz frequency in 44% of the patients with stress urinary incontinence.

[Clinical results of the treatment of urinary incontinence with peripheral electric stimulation]. / Resultados clínicos del tratamiento de la incontinencia urinaria con estimulación eléctrica periférica.

A series of 126 patients, 98 women (78%) and 29 male (22%), average 50.2 years old, with different types of urinary incontinence (incontinence at cough, urge-incontinence, post-prostatectomy incontinence and nocturnal enuresis), has been treated with periferic electrostimulation to evaluate the clinical value of this type of treatment. Extrahospitalary management with electrostimulation by vaginal in 39 cases (30.9%) or rectal in 87 cases (69.1%) electrodes was performed. Frequencies has been different in urge-incontinence (10 Hz) and urinary incontinence at coughing (50 Hz). Average treatment duration was 3.3 months. Incontinence intensity decreased significantly with electrostimulation treatment (51-62%). Non statistical differences between other parameters (age, sex, clinical features, clinical incompetence type, cistocele grade) was observed. Positive results in larger period treatment (over 3 months) was obtained (p < 0.005). Best results were obtained with 10 Hz and 50 Hz frequencies (p < 0.05). Therapeutic results, good tolerance (89%), easy application for the patient and absence of secondary effects could made electrostimulation as an alternative therapy in all type of urinary incontinence.