Association of socioeconomic inequality in cardiovascular disease risk with economic development across 57 low- and middle-income countries: Cross-sectional analysis of nationally representative individual-level data.

Background: According to epidemiological transition theory, cardiovascular disease (CVD) risk shifts down the socioeconomic distribution with economic development.

Methods: We tested this hypothesis using nationally representative data on 88,559 individuals aged 40-80 years from 57 low- and middle-income countries (LMICs). We used measured risk factors to estimate the 10-year probability of a CVD event (CVD risk) and proxied socioeconomic status (SES) by years of education.

Preclinical development and characterisation of PP353, a formulation of linezolid for intradiscal administration.

Introduction: Bacterial infection of the intervertebral disc can lead to vertebral endplate edema known as Modic changes, with associated chronic low back pain. Oral antimicrobial therapy has shown efficacy but relies on prolonged dosing and may not be optimal in terms of patient outcome, side effects, or antibiotic stewardship. There is no antibiotic formulation approved for intradiscal administration.

Pharmacokinetics of PP353, a formulation of linezolid for intervertebral disc administration, in patients with chronic low back pain and Modic change Type 1: A first-in-human, Phase 1b, open-label, single-dose study.

Background: Bacterial infection of the intervertebral disc is difficult to treat because the tissue is usually not vascularized and systemic antibiotic therapy may not reach optimal antibacterial exposure. Here we characterize the safety, tolerability, and pharmacokinetics of PP353, a suspension of micronized linezolid, formulated for direct intervertebral disc administration.

Methods: The safety, tolerability, and pharmacokinetics of an intradiscal administration of PP353, was assessed in Part A of a Phase 1b study and consisted of a single injection of study drug (3 mL of PP353 and 150 mg linezolid).

Deep postnatal phenotyping of a new mouse model of nonketotic hyperglycinemia.

Nonketotic hyperglycinemia due to deficient glycine cleavage enzyme activity causes a severe neonatal epileptic encephalopathy. Current therapies based on mitigating glycine excess have only limited impact. An animal model with postnatal phenotyping is needed to explore new therapeutic approaches.

Deep postnatal phenotyping of a new mouse model of nonketotic hyperglycinemia.

Unlabelled: Nonketotic hyperglycinemia due to deficient glycine cleavage enzyme activity causes a severe neonatal epileptic encephalopathy. Current therapies based on mitigating glycine excess have only limited impact. An animal model with postnatal phenotyping is needed to explore new therapeutic approaches.