Zika virus (ZIKV) disease is caused by a virus transmitted by Aedes mosquito. It presents as flu-like symptoms lasting for 5–7 days and shows potential association with neurological and autoimmune complications such as congenital microcephaly and adult paralysis disorder, Guillain–Barré syndrome. Treatment measures are conservative as the disease is self-limiting. ZIKV earlier affected several tropical regions of Africa and Asia from 1951 to 2006. Subsequently, it moved out from these regions to land as outbreaks in Yap Island, French Polynesia, South America, and most recently in Brazil. The WHO declared it as an international public health emergency in 2016 and an extraordinary event with recommendations for improving communications, tightening vigil on ZIKV infections, and improving mosquito control measures. The authors in this article aim to briefly discuss ZIKV infection, its epidemiology, clinical manifestations, management, and prevention.
An outbreak of febrile illness occurred in Kolkata (formerly Calcutta), India, which led to an increased utilization of treatment centre facilities during August – September 2005. The etiological agent was confirmed to be dengue by analysing 308 acute-phase clinical specimens for virus-specific IgM antibodies.
The mandibular third molar is the most frequently impacted tooth with incidence varies from 9.5% to 68% in different populations. Hence, the aim was to study the prevalence and pattern of mandibular impacted third molar among Delhi-National Capital Region (NCR) population.The study was conducted with data collected from registered hospitals and dental clinics of Delhi NCR region. The study represents a retrospective analysis of panoramic radiographs and intraoral periapical radiograph of patients at these centers from June 2014 to June 2016.Out of 960 patients with the third molar investigated, a total of 250 patients having impacted mandibular third molar (152 [60.8%] males and 98 [39.2%]) females between June 2014 and June 2016 were included in the study. The age ranged from 20 to 55 years, with a mean age of 27.6 years and the standard deviation was 5.8 years. The prevalence of impacted mandibular third molars for this study was 26.04%.This study demonstrated that males (60.8%) were more likely to present with impacted mandibular third molars than females (39.2%). The prevalence of third molar impactions was almost the same on both the left (45.8%) and right (54.2%) sides. This study also noted that mesioangular impactions (49.2%) were the most common type of impaction. The least common form of impactions was the transverse types (2%). The prevalence of impacted mandibular third molars for this study was 26.04%.
Botulinum neurotoxins, causative agents of botulism in humans, are produced by Clostridium botulinum, an anaerobic spore-former Gram-positive bacillus. Botulinum neurotoxin poses a major bioweapon threat because of its extreme potency and lethality; its ease of production, transport, and misuse; and the need for prolonged intensive care among affected persons. This paper aims at discussing botulinum neurotoxin, its structure, mechanism of action, pharmacology, its serotypes and the reasons for wide use of type A, the various indications and contraindications of the use of botulinum neurotoxin and finally the precautions taken when botulinum neurotoxin is used as a treatment approach. We have searched relevant articles on this subject in various medical databases including Google Scholar, PubMed Central, ScienceDirect, Wiley Online Library, Scopus, and Copernicus. The search resulted in more than 2669 articles, out of which a total of 187 were reviewed. However, the review has been further constricted into only 54 articles as has been presented in this manuscript keeping in mind the page limitation and the limitation to the number of references. A single gram of crystalline toxin, evenly dispersed and inhaled, can kill more than one million people. The basis of the phenomenal potency of botulinum toxin (BT) is enzymatic; the toxin is a zinc proteinase that cleaves neuronal vesicle-associated proteins responsible for acetylcholine release into the neuromuscular junction. A fascinating aspect of BT research in recent years has been the development of the most potent toxin into a molecule of significant therapeutic utility. It is the first biological toxin which is licensed for the treatment of human diseases. The present review focuses on both warfare potential as well as medical uses of botulinum neurotoxin.
Background/Aims: Serotonin (5-hydroxytryptamine; 5-HT) released from enterochromaffin (EC) cells in gastric mucosa inhibits gastric acidity by increasing the gastric mucus secretion. In the present study, we evaluated the effect of aqueous extract of Aegle marmelos (AM) ripe fruit pulp (250 mg/kg body weight) on mean ulcer index (MUI), EC cells, 5-HT content, and adherent mucosal thickness of ulcerated gastric tissue in adult albino rats. Material and Methods: Ulceration was induced by using aspirin (500 mg/kg, p.o.), cerebellar nodular lesion and applying cold-restraint stress. Results: In all cases increased MUI in gastric tissue along with decreased EC cell count was observed with concomitant decrease of 5-HT content and adherent mucosal thickness (P < 0.05). Pretreatment with AM for 14 days decreased MUI, increased EC cell count, and 5-HT content as well as adherent mucosal thickness in all ulcerated group (P < 0.05). Conclusion: AM produces gastric mucosal protection mediated by increased EC cell count and 5-HT levels.
17β-estradiol (E2) via its cytochrome P450 (CYP) 1B1 generated metabolite 2-methoxyestradiol (2ME) protects from angiotensin (Ang) II-induced hypertension in female mice. Gene disruption of 12/15 lipoxygenase (LOX) that metabolizes arachidonate (A) into 12(S)- and 15(S)-HETE minimizes Ang II-induced hypertension in male mice. We performed this study to determine if 2-ME generated by CYP1B1 from E2 mediates its protective effect against Ang II-induced hypertension via LOX inhibition in female mice. Systolic blood pressure (SBP, mmHg, tail-cuff) in response to Ang II (700 ng/Kg/min, sc, miniosmotic pump, 2 weeks) was greater ( P <0.05, n=4-5) in ovariectomized (OVX) than intact Cyp1b1 +/+ / Alox15 +/+ (174±2 vs 135±5), and intact or OVX- Cyp1b1 +/+ / Alox15 –/– (120±4 and 125±5) mice. Moreover, SBP in response to Ang II was greater in trans-2,3',4,5'-tetramethoxystilbene (CYP1B1 inhibitor, 300 μg/Kg, every 3rd day, ip)-treated intact Cyp1b1 +/+ / Alox15 +/+ than Cyp1b1 +/+ / Alox15 –/– (164±3 vs 132±3, n=6-8, P <0.05) mice. Also, mean arterial pressure (MAP, mmHg, radiotelemetry) and low frequency to high-frequency oscillation ratio (LF/HF ratio, power spectral analysis), the index of baroreflex sensitivity impairment, in response to Ang II was greater ( P <0.05, n=4) in OVX- Cyp1b1 +/+ / Alox 15 +/+ (160±3; 2.9±0.1) than in OVX- Cyp1b1 +/+ / Alox15 –/– (119±7; 2±0.1) mice. However, MAP and LF/HF ratio in response to Ang II was lower in 2ME (1.5 mg/g, every 3rd day, ip)-treated OVX- Cyp1b1 +/+ / Alox15 +/+ (108±3; 1.6±0.1) and OVX- Cyp1b1 +/+ / Alox 15 –/– (107±2; 1.6±0.1) mice (n=4). Plasma12(S)-HETE level (ELISA), and renal injury assessed by urine albumin/creatinine ratio in response to Ang II was lower in 2ME than its vehicle (dimethyl sulfoxide)-treated OVX- Cyp1b1 +/+ / Alox 15 +/+ mice (1616±30 vs 2162±55, pg/mL, and 2.7±0.3 vs 1.9±0.1; n=4, P <0.05). Ang II did not increase 12(S)-HETE or albumin/creatinine ratio in Cyp1b1 +/+ / Alo x 15 –/– mice. These data suggest that that E2-CYP1B1 generated metabolite 2ME by inhibiting A-LOX signaling protects against Ang II-induced hypertension, impaired baroreflex, and renal injury in female mice. Therefore, LOX inhibitors could be useful in the treatment of Ang II-induced hypertension and associated renal injury in females.