Grain boundary widening controls siderite (FeCO3) replacement of limestone (CaCO3).

The microstructure of minerals and rocks can significantly alter reaction rates. This study focuses on identifying transport paths in low porosity rocks based on the hypothesis that grain boundary widening accelerates reactions in which one mineral is replaced by another (replacement reaction). We conducted a time series of replacement experiments of three limestones (CaCO3) of different microstructures and solid impurity contents using FeCl2. Reacted solids were analyzed using chemical imaging, small angle X-ray and neutron scattering and Raman spectroscopy. In high porosity limestones replacement is reaction controlled and complete replacement was observed within 2 days. In low porosity limestones that contain 1-2% dolomite impurities and are dominated by grain boundaries, a reaction rim was observed whose width did not change with reaction time. Siderite (FeCO3) nucleation was observed in all parts of the rock cores indicating the percolation of the solution throughout the complete core. Dolomite impurities were identified to act as nucleation sites leading to growth of crystals that exert force on the CaCO3 grains. Widening of grain boundaries beyond what is expected based on dissolution and thermal grain expansion was observed in the low porosity marble containing dolomite impurities. This leads to a self-perpetuating cycle of grain boundary widening and reaction acceleration instead of reaction front propagation.

Effects of essential oils on symptoms and course (duration and severity) of viral respiratory infections in humans: A rapid review.

Oral doses of certain essential oils may reduce symptoms of acute respiratory infections of viral origin. It is likely that the commercially available essential oil capsules Myrtol® (a mixture of essential oils of eucalyptus Eucalyptus globulus, sweet orange Citrus sinensis, myrtle Myrtus communis and lemon Citrus limonum) and Tavipec® (spike lavender Lavandula latifolia) could also provide mild to moderate symptom relief in patients with viral respiratory diseases. Myrtol® may also improve the course (duration and severity) of acute bronchitis of viral origin, in humans. Both products were well tolerated, with most of the mild to moderate side-effects affecting the gastrointestinal tract. This review found no research evidence describing the clinical effect of inhalation of essential oils for acute respiratory viral infections.

Clinical evidence from published clinical trials identified in this rapid review suggests that oral administration of blends of certain essential oils (EO) can reduce symptoms of acute respiratory infections of viral origin in humans, namely acute sinusitis and acute bronchitis.There is clinical evidence for orally administered Lavandula latifolia essential oil (Tavipec®) (n = 2) and a blend of essential oils of Eucalyptus globulus, Citrus sinensis, Myrtus communis and lemon Citrus limonum (Myrtol® and its successors GeloMyrtol® and GeloMyrtol®Forte) (n = 3) to reduce symptoms of acute sinusitis and acute bronchitis of viral origin(s) [[1], [2], [3], [4], [5]]. All five clinical trials relied mostly on (subjective) symptom scores to determine the treatment effect. Differences between treatment and placebo symptom scores in these clinical trials were statistically significant, although the differences in absolute numbers were small. Furthermore, clinical evidence suggests that Myrtol® is also able to improve the course (duration and severity) of acute bronchitis of viral origin, in humans [3,5].No clinical evidence was found on whether EO can also improve symptoms and/or course of other acute respiratory infections, like influenza or acute respiratory distress syndrome caused by viruses of the coronavirus class. Further clinical trials with these and other EO (or blends of EO), and other administration forms, like steam inhalation or personal inhalers, are warranted to further elucidate the potential of commonly available EOs in treating acute respiratory infections of viral origin, especially influenza and COVID-19.

Human melanoma cells express functional receptors for thyroid-stimulating hormone.

We have reported a high prevalence of hypothyroidism in the cutaneous melanoma population, suggesting that the pathologic hormonal environment of hypothyroidism promotes melanoma growth. The objective of this study was to test the hypothesis that TSH, which circulates at elevated levels in hypothyroid individuals, stimulates the growth of melanoma cells. Our results show that TSH receptors (TSHR) are expressed by virtually all cutaneous melanocytic lesions, including benign nevi, dysplastic nevi, and melanomas, with higher expression found in malignant and pre-malignant lesions. The finding of TSHR expression by human tumors is confirmed in cultured melanoma cells and melanocytes, in which TSHR expression is demonstrated by immunofluorescent staining, western blotting, and reverse transcriptase-PCR. Melanoma TSHR are functional, as evidenced by the ability of TSH to induce the formation of cAMP and to activate the mitogen-activated protein kinase (MAPK) pathway. Cultured melanoma cells, but not melanocytes, are induced to proliferate at a physiologically relevant concentration of TSH. Taken together, these data support the hypothesis that TSH is a growth factor for human melanoma. Our findings have broad clinical implications for the prevention of melanoma and the management of established disease.

Delay in the diagnosis of testicular tumours - changes over the past 18 years.

BACKGROUND: Delay in the diagnosis of testicular cancer is associated with greater morbidity and poorer prognosis. While the national agenda relates to reducing time to referral and diagnostic delay, delay in presentation has previously been recognised as a major cause of delay in the diagnosis of this patient group. AIMS: To evaluate changes in referral times and patient awareness among men with testicular cancer in Yorkshire over the past 18 years. DESIGN OF STUDY: Prospective cohort study. Comparison was made with a similar study in Yorkshire in 1985. SETTING: Leeds Cancer Centre Testicular Germ Cell Outpatient Clinic. METHOD: Three hundred and thirty-one men, newly diagnosed with testicular cancer between August 1998 and October 2002, were asked to complete a questionnaire. The time taken from when the patient first noticed symptoms to their first visit to their general practitioner (GP), from their first GP visit to their first hospital visit, and from their first hospital visit to orchidectomy were recorded. We also asked patients about the treatment they were offered at their first GP visit. RESULTS: Questionnaires were completed by 180 (54%) men. The median time that men took between when they first noticed symptoms and first visited their GP has decreased compared with 1985 (5 versus 2 weeks, respectively). No improvement was observed in referral times (mean = 3.55 versus 4.8 weeks). Ninety-one per cent of responders had heard of testicular cancer prior to diagnosis. CONCLUSION: Patient performance has improved over the past 18 years. The data lends support to the effectiveness of national health education initiatives aimed at increasing public awareness and self-examination. GPs performed well in this study, assessing and referring men appropriately and urgently into secondary care.

Clinical correlates of NRAS and BRAF mutations in primary human melanoma.

PURPOSE: NRAS and BRAF mutations are common in cutaneous melanomas, although rarely detected mutually in the same tumor. Distinct clinical correlates of these mutations have not been described, despite in vitro data suggesting enhanced oncogenic effects. This study was designed to test the hypothesis that primary human cutaneous melanomas harboring mutations in NRAS or BRAF display a more aggressive clinical phenotype than tumors wild type at both loci. EXPERIMENTAL DESIGN: Microdissection of 223 primary melanomas was carried out, followed by determination of the NRAS and BRAF mutational status. Genotypic findings were correlated with features known to influence tumor behavior including age, gender, Breslow depth, Clark level, mitotic rate, the presence of ulceration, and American Joint Committee on Cancer (AJCC) staging. RESULTS: Breslow depth and Clark level varied significantly among the genotypes, with NRAS mutants showing the deepest levels and wild-type tumors the least depth. Ulceration also differed significantly among the genotypes, with BRAF mutants demonstrating the highest rate. In addition, tumors with mutated NRAS were more likely to be located on the extremities. Patients whose tumors carried either mutation presented with more advanced AJCC stages compared with patients with wild-type tumors, and specifically, were more likely to have stage III disease at diagnosis. Overall survival did not differ among the 3 groups. CONCLUSIONS: Distinct clinical phenotypes exist for melanomas bearing NRAS and BRAF mutations, whether considered together or separately, and are associated with features known to predict aggressive tumor behavior. The impact of these mutations is most evident at earlier stages of disease progression.

Promotion of melanoma growth by the metabolic hormone leptin.

We have previously shown that melanoma cells proliferate in response to the metabolic hormones TRH and TSH. The objective of the present study was to test the hypothesis that a third metabolic hormone, leptin, serves as a growth factor for melanoma. Using western blotting, indirect immunofluorescence, and RT-PCR, leptin receptors were found to be expressed by human melanoma cells. In contrast, cultured melanocytes expressed message for the receptor without detectable protein. Melanoma cells responded to treatment with leptin by activating the MAPK pathway and proliferating. Melanoma cells but not melanocytes, also expressed leptin protein, creating a potential autocrine loop. Examination of human melanoma tumors by immunohistochemistry revealed that melanomas and nevi expressed leptin at a high frequency. Melanomas also strongly expressed the leptin receptor, whereas nevi expressed this receptor to a much lesser degree. We conclude that leptin is a melanoma growth factor and that a leptin autocrine-loop may contribute to the uncontrolled proliferation of these cells.