A brother of murdered Natalie McNally says their family has been assured that detectives are 'throwing everything' at the investigation to find her killer
The family of Natalie McNally have said they are confident in the police investigation into her murder.
"We're very confident in the police," Mr McNally told BBC Radio Ulster's Good Morning Ulster programme.A 32-year-old man arrested on 19 December was released the next day and is no longer a suspect.A funeral service was held at Natalie McNally's parents' home in Craigavon last week. Police have previously said she may have known her killer and it is believed that she died on the night of Sunday 18 December."People say it's your worse nightmare but you would never have a nightmare like this - it's just unbelievable," he said.The charity Crimestoppers has also offered a £20,000 reward for information about the murder.
"We can't reiterate enough that if anyone has any information whatsoever, even if it seems insignificant, bring it to police or bring it to Crimestoppers."CCTV footage shows a man leaving Natalie McNally's street on the night she was killedThey had previously released CCTV footage of a suspect near her home.
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Calculating variant penetrance from family history of disease and average family size in population-scale data - Genome MedicineBackground Genetic penetrance is the probability of a phenotype when harbouring a particular pathogenic variant. Accurate penetrance estimates are important across biomedical fields including genetic counselling, disease research, and gene therapy. However, existing approaches for penetrance estimation require, for instance, large family pedigrees or availability of large databases of people affected and not affected by a disease. Methods We present a method for penetrance estimation in autosomal dominant phenotypes. It examines the distribution of a variant among people affected (cases) and unaffected (controls) by a phenotype within population-scale data and can be operated using cases only by considering family disease history. It is validated through simulation studies and candidate variant-disease case studies. Results Our method yields penetrance estimates which align with those obtained via existing approaches in the Parkinson’s disease LRRK2 gene and pulmonary arterial hypertension BMPR2 gene case studies. In the amyotrophic lateral sclerosis case studies, examining penetrance for variants in the SOD1 and C9orf72 genes, we make novel penetrance estimates which correspond closely to understanding of the disease. Conclusions The present approach broadens the spectrum of traits for which reliable penetrance estimates can be obtained. It has substantial utility for facilitating the characterisation of disease risks associated with rare variants with an autosomal dominant inheritance pattern. The yielded estimates avoid any kinship-specific effects and can circumvent ascertainment biases common when sampling rare variants among control populations.
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