Royal Prince Alfred Hospital

About: Royal Prince Alfred Hospital is a healthcare organization based out in Sydney, New South Wales, Australia. It is known for research contribution in the topics: Population & Transplantation. The organization has 7424 authors who have published 14798 publications receiving 550338 citations. The organization is also known as: RPAH & RPA.

The prevalence and management of diabetes in rural India.

Abstract: Very high levels of diabetes have been reported in urban areas of India (1), but few data are available for rural regions where >70% of the population lives. Data from a new large-scale survey done in 2005 suggest rural India may soon experience the same epidemic of diabetes. A total of 4,535 individuals aged ≥30 years (response rate 81%, mean age 46.8 years) were sampled at random age and sex strata from 20 villages representative of Godavari, a developing rural area of Andhra Pradesh. Data were collected using a structured questionnaire and a …

Differences in activity-dependent hyperpolarization in human sensory and motor axons

Abstract: The present study was undertaken to determine whether activity-dependent changes in axonal excitability are greater in motor axons than cutaneous afferents for the same impulse load. In nine healthy subjects, supramaximal stimulation at 8 Hz was delivered to the median nerve at the wrist. Changes in the threshold current required to generate compound motor and sensory potentials approximately 50% of maximum and other indices of axonal excitability were tracked before and after repetitive stimulation for 10 min. The long-lasting stimulation produced a prolonged depression in the excitability of both cutaneous afferents and motor axons, with gradual recovery to control levels over 15-20 min. These changes in threshold were associated with a reduction in refractoriness, an increase in supernormality and a decrease in the strength-duration time constant, changes consistent with axonal hyperpolarization. Greater changes in threshold occurred in motor axons: threshold increased by 9.9% and 16.4% for test stimulus durations of 0.1 and 1 ms, respectively, for motor axons and by 5.4% and 8.3% for cutaneous afferents. With higher stimulus frequencies and thereby greater impulse loads, greater threshold changes could be induced in cutaneous afferents. It is argued that the hyperpolarization resulted from activity of the electrogenic Na(+)-K+ pump, that it requires > 125 ms to restore the resting state following an action potential, and that significant intracellular Na+ accumulation occurs during a steady 8-Hz train. These findings imply that physiological discharge rates will activate the pump and thereby produce axonal hyperpolarization, the extent of which will vary with impulse load. A plausible explanation is that greater activity-dependent hyperpolarization in motor axons is due to less inward rectification as a result of less activity of the hyperpolarization-activated cation conductance (IH) than in cutaneous afferents.

Mannitol as a challenge test to identify exercise-induced bronchoconstriction in elite athletes

Abstract: Bronchial provocation tests provide objective criteria for asthma and exercise-induced bronchoconstriction (EIB) and were recommended to justify the use of inhaled beta2-agonists by athletes at the Winter Olympics 2002. Eucapnic voluntary hyperpnea (EVH) was one test recommended to identify EIB. Provocation with EVH requires a special dry gas mixture limiting its availability. Provocation tests with osmotic aerosols require less expensive equipment that is easily portable. We assessed the sensitivity of a challenge with mannitol to identify responsiveness to EVH in 50 elite summer sport athletes who were unselected if they had respiratory symptoms. Asthma was previously diagnosed by a doctor in 27 subjects, and 21 subjects were currently under treatment for EIB or asthma. The mean predicted FEV1 was 103.6 +/- 10.8%, FVC was 99 +/- 13.3%, and mean forced expiratory flow during the middle half of the FVC was 104 +/- 22.7%. A total of 25 subjects were positive to EVH challenge (mean percentage of fall in FEV1 was 25.4 +/- 15% SD), and 26 subjects had a positive mannitol challenge (geometric mean [95% confidence interval] provoking dose causing a 10% fall in forced expiratory volume in one second [PD10] was 202 mg [134, 300], with 24 of the subjects positive to both challenges). Mannitol had a sensitivity of 96% and specificity of 92% to identify a positive response to EVH and, as such, could be used as an alternative to EVH to identify EIB.

Pathogenesis of alcohol‐induced liver disease: Classical concepts and recent advances

Abstract: Alcoholic liver disease (ALD) is a primary consequence of heavy and prolonged drinking ALD contributes to the bulk of liver disease burden worldwide Progression of ALD is a multifactorial and multistep process that includes many genetic and environmental risk factors The molecular pathogenesis of ALD involves alcohol metabolism and secondary mechanisms such as oxidative stress, endotoxin, cytokines and immune regulators The histopathological manifestation of ALD occurs as an outcome of complex but controlled interactions between hepatic cell types Hepatic stellate cells (HSCs) are the key drivers of fibrogenesis, but transformation of hepatocytes to myofibroblastoids also implicate parenchymal cells as playing an active role in hepatic fibrogenesis Recent discoveries indicate that lipogenesis during the early stages of ALD is a risk for advancement to cirrhosis Other recently identified novel molecules and physiological/cell signaling pathways include fibrinolysis, osteopontin, transforming growth factor-β-SMAD and hedgehog signaling, and involvement of novel cytokines in hepatic fibrogenesis The observation that ALD and non-alcoholic steatohepatitis share common pathways and genetic polymorphisms suggests operation of parallel pathogenic mechanisms Future research involving genomics, epigenomics, deep sequencing and non-coding regulatory elements holds promise to identify novel diagnostic and therapeutic targets for ALD There is also a need for adequate animal models to study pathogenic mechanisms at the molecular level and targeted therapy