Ventricular fibrillation after exposure to air freshener-death just a breath away

A case of ventricular fibrillation due to butane toxicity after unintentional inhalation of air freshener is reported for its rarity and to create awareness among practitioners and the public. A 25-year-old woman collapsed in the supermarket after unintended exposure to air freshener sprayed into her nostrils. Her husband started cardiopulmonary resuscitation immediately, and she was brought to the hospital. She had coarse ventricular fibrillation. Defibrillation with 360 J was given, and the rhythm reverted to normal sinus rhythm after the third shock. Epinephrine was not administered, and she was treated with esmolol infusion for ventricular ectopy. The patient recovered completely without any sequelae and was discharged on the fifth hospital day. On thin layer chromatography, the chemical content of the spray was identified to be isobutane. Avoiding epinephrine and administering β-adrenergic blockers may protect the catecholamine-sensitized heart early during resuscitation in butane exposure cases.     

Non-mechanical traumatic gas gangrene: forgotten but not gone

We report a case of gas gangrene (GG) in a non-diabetic HIV seronegative man who died within 60 hours following an intramuscular injection in rural India. The occurrence of GG after intramuscular injection is rare and only a few cases have been reported in the published literature.     

Chemopreventive efficacy of gallic acid,an antioxidant and anticarcinogenic polyphenol,against 1,2-dimethyl hydrazine induced rat colon carcinogenesis

Colon cancer is a major cause of morbidity and mortality in developed and developing countries and its etiology is known to be a combination of hereditary, environmental, dietary factors and lack of physical activity. Chemoprevention offers a novel approach to control the incidence of colon cancer. Gallic acid (GA) is a polyphenol widely present in tea and other plants which is popularly used in the traditional medicine of China. The present study was to evaluate the efficacy of GA supplementation on tissue lipid peroxidation and antioxidant defense system in 1,2-dimethyhydrazine (DMH) induced colon carcinogenesis in male Wistar rats. The rats were assorted into six groups, viz., group1 control rats received modified pellet diet; group 2 rats received GA (50 mg/kg body weight) orally along with modified pellet diet; group 3 rats received DMH (20 mg/kg body weight) subcutaneously once a week for the first 15 weeks; groups 4, 5 and 6 rats received GA along with DMH during the initiation, post- initiation stages and the entire period of study respectively. All the rats were sacrificed at the end of 30 weeks and the tissues were evaluated biochemically. We observed decreased lipid peroxidation (LPO) products such as thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) and diminished levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione reductase (GR) and glutathione peroxidase (GPx) in the tissues of DMH treated rats, which were elevated significantly on GA supplementation. Moreover, enhanced activity of ascorbic acid and α-tocopherol levels were also observed in DMH alone treated rats which were significantly reduced on GA supplementation. Our results suggest that GA could exert a significant chemopreventive effect on DMH induced colon carcinogenesis.     

Nano-TiO2 particles impair adhesion of airway epithelial cells to fibronectin

Titanium dioxide engineered nanoparticles (nano-TiO₂) are widely used in the manufacturing of a number of products. Due to their size (<100 nm), when inhaled they may be deposited in the distal lung regions and damage Clara cells. We investigated the mechanisms by which short-term (1-h) incubation of human airway Clara-like (H441) cells to nano-TiO₂ (6 nm in diameter) alters the ability of H441 cells to adhere to extracellular matrix. Our results show that 1 h post-incubation, there was a 3-fold increase of extracellular H₂O₂, increased intracellular oxidative stress as demonstrated by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) oxidation, and a 5-fold increase of phosphor-ERK1/2 as measured by Western blotting. These changes were accompanied by a 25% decrease of H441 adherence to fibronectin (p < 0.05 compared to vehicle incubated H441 cells). Pretreatment with the ERK1/2 inhibitor U0126 for 3 h, partially prevented this effect. In conclusion, short-term exposure of H441 cells to nano-TiO₂ appears to reduce adherence to fibronectin due to oxidative stress and activation of ERK1/2.     

Expression of common chromosomal fragile site genes, WWOX/FRA16D and FHIT/FRA3B is downregulated by exposure to environmental carcinogens, UV, and BPDE but not by IR

Common chromosomal fragile sites are unstable genomic loci susceptible to breakage, rearrangement, and are highly recombinogenic. Frequent alterations at these loci in tumor cells led to the hypothesis that they may contribute to cancer development. The two most common chromosomal fragile sites FRA16D and FRA3B which harbor WWOX and FHIT genes, respectively, are frequently altered in human cancers. Here we report that environmental carcinogens, ultraviolet (UV) light, and Benzo[a]pyrene diol epoxide (BPDE), significantly downregulate expression of both genes. On the other hand, we observe that ionizing radiation (IR) does not affect expression of these genes, suggesting that the effect of repression exerted by UV and BPDE is not just a consequence of DNA damage but may be a result of different signaling pathways triggered by specific DNA lesions. Such downregulation correlates with an induction of an S-phase delay in the cell cycle. Treatment of UV-irradiated cells with caffeine abrogates the S-phase delay while concomitantly overcoming the repression phenomenon. This suggests the involvement of unique cell cycle checkpoint mechanisms in the observed repression. Therefore, it is hypothesized that protracted downregulation of the putative tumor suppressor genes WWOX and FHIT by environmental carcinogens may constitute an additional mechanism of relevance in the initiation of tumorigenesis.     

Bronchopulmonary dysplasia: new insights

The pathology of BPD has changed over time, with the old BPD characterized by airway injury, inflammation, and parenchymal fibrosis giving way to the new BPD manifesting less fibrosis but with decreased alveolar and vascular development. The pathogenesis of BPD involves factors affecting the severity and management of RDS, alterations in lung development and maturation, alveolar-vascular interactions, and extracellular matrix remodeling. These factors in pathogenesis are mediated and modulated by hyperoxic lung injury, antioxidants, NO, the pulmonary neuroendocrine system and peptide growth factors, the immune system, and various genetic polymorphisms and predispositions. Future therapeutic interventions are likely to target one or more of these abnormalities in lung development, maturation, and response to injury.     

Preschool hearing screening: pass/refer rates for children enrolled in a head start program in eastern North Carolina

This 4-year project investigated the pass/refer rates of preschool children in a hearing screening program. Three- and 4-year-old children who attended Head Start centers in rural, traditionally medically underserved, eastern North Carolina participated (n = 1,462). Screening procedures and pass/refer criteria were based on the Guidelines for Audiologic Screening (American Speech-Language-Hearing Association [ASHA], Panel on Audiologic Assessment, 1997). Only 54% (n = 787) of children passed the initial screening (i.e., passed all three of the screening components, which included pure-tone audiometry, tympanometry, and otoscopy), and an additional 22% (n = 323) passed the rescreening, for an overall pass rate of 76%. The initial pass rate was 90%, 71%, and 71% for otoscopy, tympanometry, and pure-tone audiometry, respectively. After the initial screening, 675 children were referred (i.e., 83%, 2%, and 15% for audiologic rescreening, medical evaluation, or both, respectively). About 71% (n = 478) received the recommended evaluation. Follow-up assessment compliance after the rescreening was poor. Slightly more than 10% of children were evaluated. The hearing status of 267 (i.e., 18.3%) children was never determined. Six (i.e., 0.5%) of the 1,195 children who completed the audiologic screening and/or received diagnostic audiologic assessment were confirmed to have hearing loss. Methodological factors that may have contributed to this high refer rate include the use of all screening techniques (pure tones, tympanometry, and otoscopy), procedural considerations in testing protocol and pass/refer criteria, and the demographic characteristics of the children screened.