12 research outputs found
Polyphenols, Flavonoids, Mineral Elements, and Biological Activities of Ginger and Cinnamon Essential Oil and Extracts as Regulated by Their Isolation Procedures
Our research compared the chemical make-up of wild Ginger and cinnamon, including their essential oils (EOs), total phenol, and total flavonoid, for their antioxidant and antibacterial effects in vitro. The mineral (nutritional and poisonous) components of the plant were also identified in this investigation. Hydro distillation (HD), steam distillation (SD), and microwave-assisted distillation (MAD) were used to extract the EOs, and gas chromatography with flame ionization detection (GC-FID) and mass spectrometry detection (GC-MS) were used to examine them. 2,2-diphenyl-1-picrylhydrazyl (DPPH) was used to evaluate the EOs' antioxidant properties. The essential oil was analyzed, and twenty-six components were found to make up 97.73% of the oil with a yield of 0.202%. The primary components were pulegone (74.81%), menthone (13.01%) and piperitone (3.82%). Neutron activation analysis (INAA) and inductively coupled plasma optical emission spectrometry (ICP-OES) were used to detect twenty-one elements, including macro- and micro-elements (Ba, Br, Ca, Cl, Co, Cr, Cs, Eu, Fe, K, Mg, Mn, Mo, Na, Rb, Sb, Sc, Sr, Th, U, and Zn), with the mineral element concentration being very close to the FAO recommendation
Frequency of \u3b2-thalassemia trait and other hemoglobinopathies in northern and western India
Introduction : India is an ethnically diverse country with an
approximate population of 1.2 billion. The frequency of
beta-thalassemia trait (\u3b2TT) has variously been reported from <
1% to 17% and an average of 3.3%. Most of these studies have been
carried out on small population groups and some have been based on
hospital-based patients. There is also a variation in the prevalence of
hemoglobinopathies in different regions and population groups in the
country. A high frequency of Hb D has been reported from the North in
the Punjabi population, Hb E in the eastern region of India and Hb S is
mainly reported from populations of tribal origin from different parts
of the country. Objectives: To study the gene frequency of \u3b2TT
and other hemoglobinopathies in three regions East (Kolkata), West
(Mumbai) and North (Delhi) in larghe population group (schoolchildren)
for a more accurate assessment of gene frequency for planning of
control programmes for haemoglobinopathies. Materials and Methods:
This study included 5408 children from 11 schools in Delhi, 5682 from
75 schools in Mumbai and 957 schoolchildren from Kolkata who were
screened for \u3b2TT and haemoglobinopathies. These included 5684
children from 75 schools in Mumbai and 5408 children from 11 schools in
Delhi. Children were 11-18 years of age of both sexes. The final report
is, however, only on 11090 schoolchildren from Mumbai and Delhi as data
from Kolkata was restricted both in numbers and objectives and could
not be included for comparison. Results: The overall gene frequency of
\u3b2TT in Mumbai and Delhi was 4.05% being 2.68% and 5.47% in
children of the two cities respectively. In Mumbai, the gene frequency
was evenly distributed. Majority of the children with \u3b2TT from
Mumbai were from Marathi (38.9%) and Gujarati (25%) speaking groups.
Gene frequency was> 5% in Bhatias, Khatris, Lohanas and Schedule
Castes. In Delhi, a higher incidence was observed in schoolchildren of
North and West Delhi (5.8-9.2%). The schoolchildren of North and West
Delhi comprised predominantly of Punjabi origin compared to children in
the South of the city (2.2%, 2.3%). When analyzed state-wise, the
highest incidence was observed in children of Punjabi origin (7.6%) and
was> 4% from several other states. Majority of the traits from
Mumbai were anemic (95.1% male and 85.6% in female). The prevalence of
anemia was lower (62.7% male and 58.4% female) children with \u3b2TT
from Delhi. This was a reflection of the higher prevalence of anemia in
children without hemoglobinopathy in Mumbai than in Delhi. Nutritional
deficiency was probably more severe and rampant in children Mumbai.
Gene frequency of Hb D was greater in schoolchildren from Delhi (1.1%)
than in Mumbai (0.7%). Hb S trait (0.2%) was observed exclusively in
children from Mumbai. A low incidence of Hb E trait (0.04%) was seen in
children in Mumbai. A higher incidence is reported from the East. The
number of cases studied from the eastern region was small as the data
from the East (Kolkata) could not be included in the analysis.
Conclusion: This study comprises a larger number of children studied
for the gene frequency of \u3b2TT and other hemoglobinopathies from
India. Population groups with higher gene frequencies require screening
programmes and facilities for antenatal diagnosis as well as increased
awareness and educational programmes to control the birth of
thalassemic homozygotes. The overall carrier frequency of \u3b2TT was
4.05% and reinforces the differential frequency of \u3b2-thalassemia
trait in schoolchildren from Delhi and Mumbai and the higher incidence
of hemoglobin D in Punjabis as reported previously. The birth incidence
calculated thereof for homozygous thalassemics would be 11,316 per year
which are added each year to the existing load of homozygous
thalassemics. This is much higher than the previously reported number
of births annually. Hence suitable control measures need to be
undertaken urgently in India
Somatic mutations in facial skin from countries of contrasting skin cancer risk
The incidence of keratinocyte cancer (basal cell and squamous cell carcinomas of the skin) is 17-fold lower in Singapore than the UK1-3, despite Singapore receiving 2-3 times more ultraviolet (UV) radiation4,5. Aging skin contains somatic mutant clones from which such cancers develop6,7. We hypothesized that differences in keratinocyte cancer incidence may be reflected in the normal skin mutational landscape. Here we show that, compared to Singapore, aging facial skin from populations in the UK has a fourfold greater mutational burden, a predominant UV mutational signature, increased copy number aberrations and increased mutant TP53 selection. These features are shared by keratinocyte cancers from high-incidence and low-incidence populations8-13. In Singaporean skin, most mutations result from cell-intrinsic processes; mutant NOTCH1 and NOTCH2 are more strongly selected than in the UK. Aging skin in a high-incidence country has multiple features convergent with cancer that are not found in a low-risk country. These differences may reflect germline variation in UV-protective genes
Selection of Oncogenic Mutant Clones in Normal Human Skin Varies with Body Site
Skin cancer risk varies substantially across the body, yet how this relates to the mutations found in normal skin is unknown. Here we mapped mutant clones in skin from high- and low-risk sites. The density of mutations varied by location. The prevalence of NOTCH1 and FAT1 mutations in forearm, trunk, and leg skin was similar to that in keratinocyte cancers. Most mutations were caused by ultraviolet light, but mutational signature analysis suggested differences in DNA-repair processes between sites. Eleven mutant genes were under positive selection, with TP53 preferentially selected in the head and FAT1 in the leg. Fine-scale mapping revealed 10% of clones had copy-number alterations. Analysis of hair follicles showed mutations in the upper follicle resembled adjacent skin, but the lower follicle was sparsely mutated. Normal skin is a dense patchwork of mutant clones arising from competitive selection that varies by location.
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Significance: Mapping mutant clones across the body reveals normal skin is a dense patchwork of mutant cells. The variation in cancer risk between sites substantially exceeds that in mutant clone density. More generally, mutant genes cannot be assigned as cancer drivers until their prevalence in normal tissue is known
Comprehensive sequencing of the myocilin gene in a selected cohort of severe primary open-angle glaucoma patients
Primary open-angle glaucoma (POAG) is the most common form of glaucoma, prevalent in approximately 1-2% of Caucasians in the UK over the age of 40. It is characterised by an open anterior chamber angle, raised intraocular pressure (IOP) and optic nerve damage leading to loss of sight. The myocilin gene (MYOC) is the most common glaucoma-causing gene, accounting for ∼2% of British POAG cases. 358 patients were selected for next generation sequencing (NGS) with the following selection criteria: Caucasian ethnicity, intraocular pressure (IOP) 21-40 mm Hg, cup:disc ratio ≥ 0.6 and visual field mean deviation ≤ -3. The entire MYOC gene (17,321 bp) was captured including the promoter, introns, UTRs and coding exons. We identify 12 exonic variants (one stop-gain, five missense and six synonymous variants), two promoter variants, 133 intronic variants, two 3’ UTR variants and 23 intergenic variants. Four known or predicted pathogenic exonic variants (p.R126W, p.K216K, p.Q368* and p.T419A) were identified across 11 patients, which accounts for 3.07% of this POAG cohort. This is the first time that the entire region of MYOC has been sequenced and variants reported for a cohort of POAG patients
Comprehensive sequencing of the myocilin gene in a selected cohort of severe primary open-angle glaucoma patients.
Primary open-angle glaucoma (POAG) is the most common form of glaucoma, prevalent in approximately 1-2% of Caucasians in the UK over the age of 40. It is characterised by an open anterior chamber angle, raised intraocular pressure (IOP) and optic nerve damage leading to loss of sight. The myocilin gene (MYOC) is the most common glaucoma-causing gene, accounting for ~2% of British POAG cases. 358 patients were selected for next generation sequencing (NGS) with the following selection criteria: Caucasian ethnicity, intraocular pressure (IOP) 21-40 mm Hg, cup:disc ratio ≥0.6 and visual field mean deviation ≤-3. The entire MYOC gene (17,321 bp) was captured including the promoter, introns, UTRs and coding exons. We identify 12 exonic variants (one stop-gain, five missense and six synonymous variants), two promoter variants, 133 intronic variants, two 3' UTR variants and 23 intergenic variants. Four known or predicted pathogenic exonic variants (p.R126W, p.K216K, p.Q368* and p.T419A) were identified across 11 patients, which accounts for 3.07% of this POAG cohort. This is the first time that the entire region of MYOC has been sequenced and variants reported for a cohort of POAG patients
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Somatic mutations in facial skin from countries of contrasting skin cancer risk.
Acknowledgements: This work was supported by grants from the Wellcome Trust to the Wellcome Sanger Institute (grant nos. 098051 and 296194). P.H.J. is supported by a Cancer Research UK Programme Grant (grant no. C609/A27326). B.A.H. acknowledges support from the Royal Society (grant no. UF130039).The incidence of keratinocyte cancer (basal cell and squamous cell carcinomas of the skin) is 17-fold lower in Singapore than the UK1-3, despite Singapore receiving 2-3 times more ultraviolet (UV) radiation4,5. Aging skin contains somatic mutant clones from which such cancers develop6,7. We hypothesized that differences in keratinocyte cancer incidence may be reflected in the normal skin mutational landscape. Here we show that, compared to Singapore, aging facial skin from populations in the UK has a fourfold greater mutational burden, a predominant UV mutational signature, increased copy number aberrations and increased mutant TP53 selection. These features are shared by keratinocyte cancers from high-incidence and low-incidence populations8-13. In Singaporean skin, most mutations result from cell-intrinsic processes; mutant NOTCH1 and NOTCH2 are more strongly selected than in the UK. Aging skin in a high-incidence country has multiple features convergent with cancer that are not found in a low-risk country. These differences may reflect germline variation in UV-protective genes
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