High‐resolution computed tomography of ‘hot tub’ pneumonitis

A case of pneumonitis following exposure to Mycobacterium avium intracellulare in an indoor home spa (hot tub) is presented. The patient complained of recurrent dyspnoea and wheezing. High‐resolution CT showed centrilobular ground‐glass nodules. Pathological correlation showed interstitial and bronchiolocentric granulomata. Biopsy cultures grew M. avium intracellulare. The patient condition improved following cessation of hot tub use.     

Mutation screen of the brain derived neurotrophic factor gene (BDNF): identification of several genetic variants and association studies in patients with obesity, eating disorders, and attention-deficit/hyperactivity disorder.

Several lines of evidence indicate an involvement of brain derived neurotrophic factor (BDNF) in body weight regulation and activity: heterozygous Bdnf knockout mice (Bdnf(+/-)) are hyperphagic, obese, and hyperactive; furthermore, central infusion of BDNF leads to severe, dose-dependent appetite suppression and weight loss in rats. We searched for the role of BDNF variants in obesity, eating disorders, and attention-deficit/hyperactivity disorder (ADHD). A mutation screen (SSCP and DHPLC) of the translated region of BDNF in 183 extremely obese children and adolescents and 187 underweight students was performed. Additionally, we genotyped two common polymorphisms (rs6265: p.V66M; c.-46C > T) in 118 patients with anorexia nervosa, 80 patients with bulimia nervosa, 88 patients with ADHD, and 96 normal weight controls. Three rare variants (c.5C > T: p.T2I; c.273G > A; c.*137A > G) and the known polymorphism (p.V66M) were identified. A role of the I2 allele in the etiology of obesity cannot be excluded. We found no association between p.V66M or the additionally genotyped variant c.-46C > T and obesity, ADHD or eating disorders. This article contains supplementary material, which may be viewed at the American Journal of Medical Genetics website at http://www.interscience.wiley.com/jpages/0148-7299:1/suppmat/index.html.     

ETHANOL-INDUCED SUPEROXIDE RADICALS IN FETAL CORTICAL NEURONS: CELLULAR ROS NETWORK

Alcohol exposure to the developing brain compromises both neurons and glial functions. While neurons are considered the primary targets, microglia may play a neurotoxic role in this process. Previous studies demonstrated that neuron death is due to oxidative stress and mitochondrially mediated (Intrinsic). These studies showed a rapid increase (within minutes) in reactive oxygen species (ROS). Due to the diffusive nature of ethanol and multiple sources of free radicals, we sought to determine the primary source of superoxide targeted by ethanol. Confocal studies of neurons suggest that the superoxide radicals may originate from the mitochondria. Using whole neurons in a luminol-based chemiluminescence assay (Diogenes) we detected superoxide radicals in the extracellular mileu. We observed a two-three fold transient increase in the steady state generation of superoxide radicals between 20 minutes to one hour of ethanol exposure (4mg/ml). However, the presence of Rotenone (mitochondrial complex I inhibitor) and DPI (an inhibitor of all flavinoids) blocked the release of these superoxide radicals. Interestingly, cortical microglia treated identically with ethanol, showed a greater than five fold increase in superoxide generation with a maximum at one hour. Moreover, since ethanol is known to induce hydrogen peroxide generation, it was used as a mimetic. Hydrogen peroxide also induced the production of superoxide different time kinetics. Thus, together these data demonstrate that ethanol induces the steady state production of superoxide radicals in the extracellular mileu in a mitochondrial dependent manner. Since NOX2 an NADPH oxidase is expressed in neurons, it is a potential candidate for the secondary sites of superoxide generation. The ROS network between mitochondria and the plasma membrane highlights new therapeutical targets to counter ethanol toxicity.     

Contemporary management of drug-packers

There has been an increasing amount of work worldwide in search for tests not only to be able to absolutely diagnose acute pancreatitis, but more importantly to prognosticate patients at admission. While the tests are still within the realm of research laboratories and involve complex computing and analytical methods, we believed that the already widely practiced methods of scoring needed to be verified in the Indian context. And, hence, the study.     

Proof of Direct Radiogenic Destruction of Collagen in Vitro

BACKGROUND: Fibroses of vessels and soft tissue are side effects of radiotherapy. The authors assumed that there was an immediate direct radiogenic damage of collagen of bone, periosteum and skin. MATERIAL AND METHODS: 15 porcine jaws samples (group 1) were exposed to a total dose of 60 Gy (cobalt-60, 2 Gy/day, five fractions/week). 15 jaws samples were stored accordingly (group 2, no irradiation, control). Collagen fragments of bone, periosteum and skin samples of groups 1 and 2 were isolated by ultrafiltration. Collagen types were characterized by SDS-PAGE measurement of the mature collagen cross-links hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP) by high-performance liquid chromatography (HPLC) and analysis of hydroxyproline (Hyp) was used to determine the ratio of the amount of collagen fragments from irradiated as opposed to nonirradiated samples. RESULTS: The concentrations of HP, LP and Hyp in ultrafiltrates of probes of irradiated bone, periosteum and skin were markedly increased (average factors for bone: 3.69, 1.84, and 3.40, respectively; average factors for periosteum: 1.55, 1.41, and 1.77, respectively; average factors for skin: 1.55, 1.60, and 2.23, respectively) as compared to nonirradiated probes. SDS-PAGE did show collagen types I and V in nonirradiated bone, I and III in nonirradiated skin, and I in nonirradiated periosteum samples. In irradiated samples, smeared bands illustrated fragmentation of the collagen molecule. CONCLUSION: The increased concentrations of HP, LP and Hyp in ultrafiltrates indicated increased concentrations of split collagen. Direct and instant radiogenic damage of (extracellular matrix of) bone, periosteum and skin tissue collagen could be demonstrated.     

Huiles essentielles antibactériennes chez des patients à tumeurs cancéreuses malodorantes

Malodorous necrotic ulcers in cancer patients are of major concern as it leads to social isolation and poor quality of life. Current medications and topical therapies have proven inadequate in their ability to reduce foul smell to acceptable levels. We report the positive experience we have had in using antibacterial essential oils in patients with incurable head and neck cancer and associated malodorous necrotic ulcers. All patients received a standard course of therapy with oral or systemic antibiosis. In addition, we rinsed the ulcers with an antibacterial essential oil mix (mainly based on eucalyptus oil) twice a day. All patients experienced complete resolution of the foul smell by only the third or fourth day of therapy. As a secondary effect we saw that besides smell reduction the oils had anti-inflammatory effects on cancer ulcers. In some patients ulcers started to heal and achieved complete re-epithiliazation. The patients experienced great personal relief upon resolution of their malodorous conditions. Quality of life improved significantly with the resulting reintroduction of social contact with friends and relatives.     

Early operative mortality after surgical treatment of bronchogenic carcinoma

Background A retrospective analysis of the results of pulmonary resection over a 7 years period for bronchogenic carcinoma was performed. Methods Three hundred and eleven patients with primary bronchogenic carcinoma were operated upon at Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Kashmir, between January 1996 to June 2002. There were 62 pneumonectomies (19.93%), 174 lobectomies (55.94%) and 75 lesser resections (24.11%). Results The overall operative mortality was 4.82%. The mortality rate for pneumonectomy, lobectomy and lesser resections were 9.6%, 4.5% and 1.3% respectively. There was no significant difference in operative mortality between pneumonectomy and lobectomy, and between lobectomy and lesser resections. Post operative mortality rate increased as the age of patient increased. Mortality was 2.3;2.9;5.0;7.41; and 14.2 in the age groups of <50 years, 50–59 years, 60–69 years, 70–79 years and 80 years and above respectively. Pneumonia and respiratory failure caused most deaths (46.66%). Conclusions Pulmonary resections can be performed with satisfactory mortality and morbidity in bronchogenic carcinoma.     

DNA adducts, mutant frequencies and mutation spectra in lambda lacZ transgenic mice treated with N-nitrosodimethylamine

Groups of lambda lacZ transgenic mice were treated i.p. with N- nitrosodimethylamine (NDMA) as single doses of 5 mg/kg or 10 mg/kg or as 10 daily doses of 1 mg/kg and changes in DNA N7- or O6-methylguanine or the repair enzyme O6-alkylguanine-DNA alkyltransferase (AGT) were followed for up to 14 days in various tissues. Adduct induction in the liver exceeded by at least one order of magnitude than observed in the next nearest target tissue (lung), and was approximately linearly related to dose, except for O6-methylguanine after the first dose of 1 mg/kg which was lower than expected. Substantial induction of lambda lacZ mutagenesis was observed only in the liver, where the mutant frequency was already maximal within 7 days after 5 mg/kg NDMA and remained unchanged thereafter up to 49 days. Small but marginally significant increases in mutant frequency were consistently observed in the spleen after all three modes of treatment. A lack of proportionality between mutation induction and the administered dose or the corresponding adduct levels was observed, probably reflecting the importance of toxicity-related cell proliferation caused by NDMA at higher doses. Twenty eight days after a dose of 10 mg/kg (causing a 3.6- fold increase in mutant frequency), NDMA was found to increase the frequency of GC-->AT mutations (with a concomitant shift of their preferential location from CpG sites to GpG sites), which made up approximately 60% of the induced mutations. Surprisingly, NDMA also caused a significant increase in deletions of a few (up to 11) base- pairs (22%).