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"Daughters"
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Toni Erdmann
Not only is Conradi an inveterate practical joker, he has a social conscience unlike Ines, who seems able to discount the impact of her proposal upon the ordinary Romanian people.
Journal Article
The salt marsh
It is a year since Sam's father died, but she cannot lay his ghost to rest. Jim was an undercover agent living a double life, and Sam has quit university to find out the truth about his work. Her journey will take her from the nightclubs of 80s Soho to the salt marshes and shingle spits of Norfolk and Kent. Here, in a bleak windswept landscape dotted with smugglers' huts and buried bones, Jim's secret past calls to her like never before. Now Sam must decide. Will she walk away and pick up her own life? Or become an undercover operative herself and continue her father's work in the shadows ...
Book
Little jewel
One day in the corridors of the metro, nineteen-year-old Thérèse glimpses a woman in a yellow coat. Could this be the mother who long ago abandoned her? Is she still alive? Desperate for answers to questions that have tormented her since childhood, Thérèse pursues the mysterious figure on a quest through the streets of Paris. In classic Modiano style, this book explores the elusive nature of memory, the unyielding power of the past, and the deep human need for identity and connection.
Book
Familial gain-of-function Nav1.9 mutation in a painful channelopathy
ObjectiveGain-of-function mutations in Nav1.9 have been identified in three families with rare heritable pain disorders, and in patients with painful small-fibre neuropathy. Identification and functional assessment of new Nav1.9 mutations will help to elucidate the phenotypic spectrum of Nav1.9 channelopathies.MethodsPatients from a large family with early-onset pain symptoms were evaluated by clinical examination and genomic screening for mutations in SCN9A and SCN11A. Electrophysiological recordings and multistate modelling analysis were implemented for functional analyses.ResultsA novel Nav1.9 mutation, p.Arg222His, was identified in patients with early-onset pain in distal extremities including joints and gastrointestinal disturbances, but was absent from an asymptomatic blood relative. This mutation alters channel structure by substituting the highly conserved first arginine residue in transmembrane segment 4 (domain 1), the voltage sensor, with histidine. Voltage-clamp recordings demonstrate a hyperpolarising shift and acceleration of activation of the p.Arg222His mutant channel, which make it easier to open the channel. When expressed in dorsal root ganglion neurons, mutant p.Arg222His channels increase excitability via a depolarisation of resting potential and increased evoked firing.ConclusionsThis study expands the spectrum of heritable pain disorders linked to gain-of-function mutations in Nav1.9, strengthening human validation of this channel as a potential therapeutic target for pain.
Journal Article