Osteonecrosis has been found in association with non-traumatic pathological conditions such as alcoholism, sickle cell hemoglobinopathies, Gaucher's disease and decompression sickness. It is also a major compcation in surviving renal transplantation patients where it is generally believed to be a result of immunosupressive systemic corticosteroid administration. The precise etiology of osteonecrosis is still unknown, but many hypotheses have presented; interruption of the blood supply, direct cytotoxic effect, incresed intraosseous pressure and decreased venous return. Whatever the caused or the starting point, and whatever the pathologic process, blockage of the osseous microcirculation with intramedullary stasis appears to be the common denominator. In the present study, our purpose is to examine the microvascular structural changes and corresponding pathological changes of rabbit's femoral head by disturbance of lipid metabolism resulting from the administration of a large dose of the steroid. The results were as follows:1. In the study group (steroid-treated);there was a relatively increased empty lacuna within the rabbit's femoral head suchondral bone at 3 weeks in contrast with the control group. (control:10.72%, study:20.8%,P<0.01.). 2. Early definite marrow necrosis was found since 3 wekks, a marrow focal osteonecrosis since 5 weeks, and roentgenographically osteoporosis since 5 weeks in the study group. 3. In the histological study, the more degenerative vascular changes were found in the subchondral plate as weekly time was relapsed (H & E), and the subchondral vessels were filled with fat in most of the steroid-treated group (Oil-red 0). 4. In the microangiographic study, the chnges of vascular pattern of the subchondral area was found in the more steroid treated group. ie, it was shown to be dissimilar in size, irregulary spaced and not orderly arranged side by side in a line with disappearing focal vascular shadow.
Adult ; Alcoholism ; Bone Marrow ; Decompression Sickness ; Gaucher Disease ; Head ; Hemoglobinopathies ; Humans ; Kidney Transplantation ; Lipid Metabolism ; Microcirculation ; Necrosis ; Osteonecrosis ; Osteoporosis

BACKGROUND/AIMS: Clevudine is a pyrimidine analogue with potent activity against hepatitis B virus (HBV) replication in vitro. In a previous pivotal phase III clinical study, 24 weeks treatment with clevudine 30 mg has been shown to profoundly suppress HBV replication and normalize serum alanine aminotransferase level. METHODS: In this study, we compare the efficacy and safety of clevudine (30 mg daily) versus lamivudine (100 mg daily) for 48 weeks in treatment-naive chronic hepatitis B e antigen (HBeAg) positive patients. RESULTS: Ninety-two chronic HBeAg positive patients were randomized to receive clevudine 30 mg daily or lamivudine 100 mg daily in a 1:1 ratio. The clevudine group demonstrated greater viral suppression at week 48 when compared with the lamivudine group (median reduction: 4.27 vs. 3.17 log(10) copies/ml at week 48, p<0.0001). At week 48, serum HBV DNA level was below 300 copies/mL in 73% and 40% in the clevudine and lamivudine groups, respectively (p=0.001). HBeAg seroconversion occurred in 18% of patients in the clevudine group versus 12% in the lamivudine group at week 48. Lamivudine-resistant mutations were detected in 11 (24%) patients in the lamivudine group, who showed viral rebound during lamivudine therapy but no resistance was found in the clevudine group during 48-week treatment period. CONCLUSIONS: A 48-week dosing with clevudine 30 mg daily was superior to lamivudine 100 mg daily in suppressing HBV replication, with no emergence of viral breakthrough in patients with HBeAg positive chronic hepatits B.
Adult ; Alanine Transaminase/blood ; Antiviral Agents/*administration & dosage ; Arabinofuranosyluracil/administration & dosage/*analogs & derivatives ; DNA, Viral/blood ; Double-Blind Method ; Drug Administration Schedule ; Drug Resistance, Viral ; Female ; Genotype ; Hepatitis B e Antigens/blood ; Hepatitis B, Chronic/*drug therapy ; Humans ; Lamivudine/*administration & dosage ; Male ; Middle Aged

Peripheral chemoreceptors in the carotid body play important roles in the transduction of chemical stimuli in the arterial blood to the central for eliciting the chemoreflex, which mediates the ventilatory and circulatory responses to hypoxia. The activity of carotid chemoreceptor is modulated and significantly contributes to the ventilatory acclimatization at high altitude. In addition, the carotid chemoreceptor activity is augmented in patients with sleep-disordered breathing, notably in central or obstructive sleep apnea, and also in experimental animals. Thus, the carotid body functions to maintain the oxygen homeostasis, whereas anomalous carotid chemoreceptor activities could be both adaptive and pathogenic in sleep apnea. This review aims to summarize the cellular and molecular mechanisms that could mediate the augmented chemoreceptor activity induced by intermittent hypoxia. Our recent findings suggest a pathogenic role of inflammation mediated by an upregulation of renin-angiotensin system in the carotid body in the over-activity of the chemoreflex. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body function, which could play a role in the pathophysiology of sleep apnea.
Acclimatization ; Animals ; Carotid Body ; cytology ; Chemoreceptor Cells ; pathology ; Humans ; Hypoxia ; physiopathology ; Renin-Angiotensin System ; Sleep Apnea Syndromes ; physiopathology

Type 2 diabetes mellitus (T2DM) and sarcopenia (low skeletal muscle mass and function) share a bidirectional relationship. The prevalence of these diseases increases with age and they share common risk factors. Skeletal muscle fat infiltration, commonly referred to as myosteatosis, may be a major contributor to both T2DM and sarcopenia in older adults via independent effects on insulin resistance and muscle health. Many strategies to manage T2DM result in energy restriction and subsequent weight loss, and this can lead to significant declines in muscle mass in the absence of resistance exercise, which is also a first-line treatment for sarcopenia. In this review, we highlight recent evidence on established treatments and emerging therapies targeting weight loss and muscle mass and function improvements in older adults with, or at risk of, T2DM and/or sarcopenia. This includes dietary, physical activity and exercise interventions, new generation incretin-based agonists and myostatin-based antagonists, and endoscopic bariatric therapies. We also highlight how digital health technologies and health literacy interventions can increase uptake of, and adherence to, established and emerging treatments and therapies in older adults with T2DM and/or sarcopenia.

Cardiac ion channelopathies encompass a set of inherited or acquired conditions that are due to dysfunction in ion channels or their associated proteins, typically in the presence of structurally normal hearts. They are associated with the development of ventricular arrhythmias and sudden cardiac death. The aim of this review is to provide a historical perspective and recent advances in the research of the cardiac ion channelopathies, Brugada syndrome, long QT syn‑ drome and catecholaminergic polymorphic ventricular tachycardia, in Hong Kong, China. In particular, recent works on the development of novel predictive models incorporating machine learning techniques to improve risk strati‑ fication are outlined. The availability of linked records of affected patients with good longitudinal data in the public sector, together with multidisciplinary collaborations, implies that ion channelopathy research efforts have advanced significantly.

The clinical application of triptolide (TPL) in tumor therapy has been greatly limited by its toxicity and inefficient delivery. Herein, a localized and sustained-release thermo-sensitive hydrogel was developed for the intra-tumor administration of TPL. Based on the amphiphilic structure of poly (