Search PubMed⌕ Search

Biomedical subjects

John H Newman

Publications and source records attributed to John H Newman.

4 recordsLinked to original sources
PubMed2003

When should we do knee replacements?

It is not known whether it is better to perform total knee replacements early or late in the course of arthritis. To examine the determinants of patient-related outcomes after knee replacement, we examined 812 patients in the Avon knee registry, in whom pre-operative and 5-year post-operative American Knee Society Scores were available. Ninety percent had a good outcome at 5 years. Women had significantly more severe disease at the time of surgery than men. Older people (>79 years) had the worst disease at the time of surgery, and made the least health gain, although their overall outcomes were still good. Those with the most severe disease at the time of operation made greater gains to those with less disease, but remained in worse health at 5 years, suggesting that earlier surgery may be preferable.

Aged↗
PubMed2002

Pulmonary veno-occlusive disease caused by an inherited mutation in bone morphogenetic protein receptor II.

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension in which the vascular changes originate in the small pulmonary veins and venules. The pathogenesis is unknown and any link with primary pulmonary hypertension (PPH) has been speculative. Mutations in the bone morphogenetic protein receptor II (BMPR2) gene have been identified in at least 50% of familial cases and in 25% of sporadic cases of PPH. We report a patient with documented PVOD whose mother had severe pulmonary hypertension. Sequencing of the patient's BMPR2 coding region revealed a del44C mutation in Exon 1 that is predicted to encode for a truncated protein. Analysis of DNA from family members suggests that this mutation was transmitted by the proband's mother to two of her four children. The finding of PVOD associated with a BMPR2 mutation reveals a possible pathogenetic connection with PPH.

Adult↗
PubMed2002

Inhibition of endogenous nitric oxide during endotoxemia in awake sheep - effects of Nomega-nitro-l-arginine on the distribution of pulmonary vascular resistance and prostanoid products.

We examined the effects of endogenous nitric oxide (NO) inhibition on the longitudinal distribution of pulmonary vascular resistance and on arachidonic acid metabolism during endotoxemia in awake sheep. Mean pulmonary artery (Ppa), left atrial (Pla), and systemic artery pressure (Psa) were continuously measured, and cardiac output (CO) was continuously monitored by an implanted ultrasonic flow probe. We advanced a 7-French Swan-Ganz catheter into distal pulmonary artery and measured the pulmonary microwedge pressure (Pmw) with the balloon deflated, allowing calculation of upstream pulmonary vascular resistance (PVRup = [Ppa - Pmw]/CO) and down-stream PVR (PVRdown = [Pmw - Pla]/CO), respectively. In paired studies, endotoxin (1 micro g/kg) was infused over 30 minutes with and without N(omega)-nitro-L-arginine (NLA) treatment. NLA (20 mg/kg) was administered 30 minutes before endotoxin infusion. Endotoxin caused increases in PVRup and PVRdown. Pretreatment with NLA increases PVRup at baseline and enhanced increases in both PVRup and PVRdown during endotoxemia. Plasma level of thromboxane B(2) (TxB(2)) and prostacyclin (6-keto = PGF(1alpha)) significantly increased 1 hour after endotoxin administration (TxB(2), 308.3 +/- 94.8 [SE] to 2163.5 +/- 988.5 pg ml(-1), P <.05; 6-keto=PGF(1alpha), 155.6 +/- 91.4 to 564.9 +/- 131.8 pg ml(-1), P <.05), but the increased levels were similar to those in the NLA-pretreated animals. We conclude that endogenous NO mainly regulates precapillary vascular tone at baseline, and that NO modulated pre- and postcapillary vascular constriction during endotoxemia in sheep. It appears that cyclooxygenase production in response to endotoxin is unaffected by NO and its vascular effects.

6-Ketoprostaglandin F1 alpha↗