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Biomedical subjects

L W Chu

Publications and source records attributed to L W Chu.

At least 37 records · Page 2Linked to original sources

Risk factors for falls in hospitalized older medical patients.

BACKGROUND: The incidence of falls among older hospitalized patients is higher than that of community-dwelling older persons. Prevention is important, but factors associated with these falls are less well studied than falls occurring in the community or nursing homes. METHODS: This study was conducted in an acute-care general hospital in Hong Kong. During November 1995 to March 1997, all older inpatients who fell during hospitalization were assessed by a geriatrician, a physiotherapist, and an occupational therapist. A standardized protocol to study the clinical and performance-oriented functional factors was employed. A sex- and age-matched hospital control was recruited for each case. In total, 51 cases and controls (mean ages 77.8 +/- 7.3 years and 77.5 +/- 7.0 years, respectively) were studied. RESULTS: Among the multiple clinical and functional risk factors for falls identified, lower limb weakness (i.e., power less than MRC grade 4 in one or both lower limbs) and poor tandem walk ability emerged as two significant predictive factors for falls in the hospital. The overall classification accuracy of fallers and nonfallers was 79%. The sensitivity was 84% and specificity was 75%. Clinical factors were the underlying causes for the lower limb weakness and poor tandem walk performance. CONCLUSIONS: Among clinical and functional risk factors for falls in the older medical patient, lower limb weakness and poor tandem walk ability were most predictive. Falls prevention programs in hospitals should employ these two tests as screening instruments.

Accidental Falls↗

Age-related osteoporosis in Chinese: an evaluation of the response of intestinal calcium absorption and calcitropic hormones to dietary calcium deprivation.

BACKGROUND: Age-related osteoporosis may be associated with inefficient intestinal calcium absorption and bone remodeling. OBJECTIVE: We investigated the pathogenesis of age-related osteoporosis in Chinese women with habitual low calcium intakes. DESIGN: We studied the response of intestinal calcium absorption, calcitropic hormones, and biochemical bone markers to graded dietary calcium deprivation. RESULTS: The osteoporotic subjects (n = 25) had higher urinary calcium excretion (P < 0.05) and lower plasma 1,25-dihydroxyvitamin D concentrations (P < 0.02) than did age-matched control women (n = 25). Parathyroid hormone was not significantly different from that in age-matched control women but was significantly higher than in young women (n = 15, P < 0.05). Fractional 45Ca absorption was approximately 61% in all 3 groups when the diet was unmodified and increased to 71%, 69%, and 68% in the osteoporotic subjects, age-matched control women, and young women, respectively, when dietary calcium was reduced to 300 mg/d. When the osteoporotic women were calcium deprived, serum 1,25-dihydroxyvitamin D failed to increase but urinary calcium excretion persisted. In contrast, supplementation with 1200 mg Ca resulted in a lowering of parathyroid hormone (P < 0.005 compared with the unmodified diet) and 1,25-dihydroxyvitamin D (P < 0.01) and decreased fractional 45Ca absorption (P < 0.01), suggesting that the increased calcium intake was associated with a potent compensatory ability of the intestine and calcitropic hormones to adapt. Calcium supplementation lowered osteocalcin (P < 0.05) but not alkaline phosphatase, which remained elevated in the osteoporotic subjects at all stages. CONCLUSIONS: Elderly osteoporotic women had reduced 1,25-dihydroxyvitamin D production, excessive urinary calcium loss, and high bone turnover. The Chinese women had exceptionally potent intestinal calcium absorption.

Adult↗

Frequency dependent sympathetic modulation of vasomotor tone in the anesthetized rat.

The hypothesis that sympathetic nerve system modulates a specific frequency range of blood pressure fluctuation was tested by electrical stimulation of the medullary sympathetic excitatory sites in anesthetized, paralyzed, vagotomized, cardiac sympathetic blocked, baroreceptor transected and angiotensin II converting enzyme inhibited rats. The frequency tested ranged from 0.02 to 1.7 Hz. For blood pressure fluctuation within this range there was no specific sympathetic reactive zone. Instead, low frequency fluctuation of sympathetic flow produced blood pressure fluctuation of the same frequency. Transfer magnitude of renal sympathetic activity to blood pressure decrease logarithmically with the increase of stimulation frequency. The relationship between the sympathetic spectral power (P(SND), (microV.s)2/Hz) and the blood pressure spectral power (P(BP), mmHg2/Hz) was found as P(BP)=10(1.3) x P(SND) x 10(-4.7x(frequency)). This transfer function demonstrates that when blood pressure fluctuation is used to estimate the sympathetic activity, it should be frequency weighted.

Anesthesia, General↗

Morbidity patterns of persons waiting for infirmary care in Hong Kong.

Ageing of the Hong Kong population is associated with an increased prevalence of physical and mental disability. For persons with severe disability, infirmary care is needed. In the present study, the morbidity pattern of persons waiting for infirmary service in Hong Kong was studied. Two hundred and four consecutive Central Infirmary Waiting List persons were included in the study. Clinical assessment was based on history review and physical examination. The commonest diagnoses giving rise to severe disability in this population, 89.2% of whom were elderly (aged greater-than-or-equal65 years), in descending order of prevalence were stroke (40.2%), dementia (27.0%), proximal femoral fracture (7.4%), and parkinsonism (5.9%); 67.5% of subjects were dependent physically. For cognitive function, 87.3% had a subnormal Abbreviated Mental Test score of less-than-or-equal5. Approximately 80% had urinary incontinence and/or bowel incontinence. For the outcome of assessment, 93.6% needed infirmary care, while 6.4% did not. More adequate provision of infirmary beds, innovative medical, nursing, and social home-support programmes, and effective prevention and rehabilitation programmes for patients with these disabling diseases are urgently needed in Hong Kong.

Journal Article↗

Genetic aberrations detected by comparative genomic hybridization predict outcome in node-negative breast cancer.

Breast cancer progression is determined by a complex pattern of multiple genetic aberrations the association of which with patient prognosis is unknown. In this study, we have undertaken a genome-wide screening to detect genetic changes associated with clinical outcome in node-negative breast cancer. Comparative genomic hybridization was used to screen for DNA sequence gains and losses across all human chromosomes in 23 tumors from node-negative breast cancer patients with no disease recurrence after at least 5 years of follow-up and in 25 node-negative patients with recurrence during the first 5 years of follow-up. The total number of genetic aberrations (copy number gains and losses) per tumor was significantly greater in the recurrence group (P = 0.019) and in the subgroup of these patients who died as a result of breast cancer (P = 0.0022). When copy number losses and gains were analyzed separately, only losses were significant (P = 0.013 for recurrence and P = 0.002 for overall survival). Of the individual loci involved, a high level gain of the long arm of chromosome 8 was significantly associated with recurrence (P = 0.01, Fisher's exact test). Furthermore, amplification of DNA sequences at chromosome 20q12-13 was found in 7 cases (15%), 6 of which had early recurrence within 32 months of diagnosis. This genome-wide overview by comparative genomic hybridization suggests that genetically advanced node-negative breast cancers having a high overall number of genetic aberrations may have a poor prognosis and that increased copy number of two specific regions, 8q and 20q13, may confer a more aggressive phenotype. Results of this pilot study suggest that determination of the total number of DNA sequence copy number aberrations may help therapeutic decision making. Specific probes should be developed to test the prognostic value of 8q and 20q12-13 amplifications in large numbers of patients.

Aged↗

Rods are selectively altered by lead: II. Ultrastructure and quantitative histology.

Electroretinographic and cyclic nucleotide metabolism studies have established that low-level lead exposure during early postnatal development results in long-term selective rod deficits. To determine whether there was a corresponding selective rod photoreceptor cell degeneration we examined retinas of adult rats exposed to low-level lead during development using light and electron microscopy. In all retinal regions, a rod but not cone cell degeneration was observed. Overall, 20% of the rod cells were lost. Moreover, two specific regional differences were found. Degeneration was much greater in the inferior (-25%) than superior (-15%) retina and greater in the posterior (-22%) than peripheral (-17%) retina. The latter pattern indicates a central-peripheral gradient of degeneration. Total retinal thickness decreased 15-20%, which reflects cell loss in the outer and inner nuclear layers. Ultrastructurally, the most obvious lead-induced alterations were swollen and disorganized rod outer segments and large accumulations of beta-glycogen particles in rod photoreceptor mitochondria. Glycogen accumulations were heaviest in rod inner segment mitochondria followed by rod axon and synaptic terminal mitochondria. Possible cellular mechanisms of action responsible for these lead-induced retinal alterations include an inhibition of retinal cyclic GMP phosphodiesterase and the resultant elevation of cyclic GMP, an inhibition of intermediary metabolism, and/or an alteration in calcium metabolism. In addition, the thinning of the inner nuclear layers could be due to transneuronal degeneration. As noted in our preceding paper, the first possibility has been demonstrated in rats similarly exposed to lead. These quantitative histological results, in combination with the ERG and biochemical results in the preceding paper, demonstrate that low-level lead exposure during early postnatal development produces long-term selective rod functional deficits and degeneration.

3',5'-Cyclic-GMP Phosphodiesterases↗

Protection from harmful UV radiation by contact lenses.

Ultraviolet radiation (UVR) has been demonstrated to be harmful to the cornea, the lens and the retina. Recent research has indicated that, in addition to the epithelial trauma found in UVR-induced keratitis, the deeper corneal layers are also involved. Since trauma to keratocytes and endothelial cells can result in permanent damage or cell loss, it is imperative to protect eyes against excessive dosages of UVR. Standard hydrogel contact lenses (Vistamarc normal) and newly developed UV-filtering hydrogel lenses (Vistakon UV-BLOC) were fitted on five rabbits and compared in protection from harmful UVR (300 nm). The eyes that wore the UV-filtering lens maintained normal corneas; however, the eyes that wore the standard hydrogel lens showed pronounced epithelial, stromal and endothelial changes. We concluded that the UV-filtering lens effectively absorbed the hazardous UV radiation while the standard soft lens provided little protection.

Animals↗

Ultrastructural analysis of corneal exposure to UV radiation.

The primate cornea was exposed to 300 nm UVR with five levels of radiant exposure from 0.08 to 0.6 Jcm-2. All cellular layers of the cornea were damaged at the 0.08 Jcm-2 exposure, and damage became more severe as the exposure level was increased. The corneal cells showed variable response in that essentially normal cells were found among damaged cells. Eight days post-exposure using the 0.6 Jcm-2 level, the epithelium had regained its normal thickness and was populated largely by normal appearing cells; however, the stroma showed damaged keratocytes and the loss of keratocytes. The corneal basement membranes (the epithelial basement membrane and the posterior limiting lamina) and the anterior limiting lamina were not damaged at any exposure level except for an isolated area along the epithelial basement membrane in one cornea. Therefore, one is lead to conclude that basement membranes are unaffected by UVR. The endothelium continued to demonstrate the loss of mitochondria, endoplasmic reticulum and some vacuoles at 8 days after exposure. However, the endothelium appeared to have resumed its physiological function as demonstrated by the reduced stromal oedema. This research gives the first complete description of UV-B induced corneal damage and repair of the full, in-depth cornea of the primate using the EM.

Animals↗

The efficacy of a UV-blocking soft contact lens in protecting cornea against UV radiation.

Recently, it has been shown that UV keratitis is more serious than previously thought because it is not limited to the corneal epithelium but also involves the stroma and the endothelium. It is, therefore, very important to avoid ultraviolet radiation (UVR) damage, and the purpose of the present study was to examine the ability of a UV absorbing hydrogel lens to filter such wavelengths. Ultrastructural observations of rabbit corneas showed that a regular soft (Vistamarc normal) contact lens offered no protection, and since wearing one adds stress to the cornea it seems possible that the cornea may be more vulnerable to UVR trauma. A UV absorbing soft contact lens (Vistakon UV-BLOC) provided complete protection to all corneal layers. Subepithelial nerve fibres in the traumatized corneas were mostly of normal morphology and may explain why UV keratitis is a very painful experience. It was concluded that a UV absorbing soft contact lenses with acceptable clinical performance may be prescribed on a routine basis.

Animals↗

Epithelial morphological response to soft hydrogel contact lenses.

Hydrogel (HEMA) contact lenses of increased thickness were worn by owl monkeys (Aotus tivergatus) under open and closed eye conditions to study ultrastructurally the corneal epithelial response to increased stress. The 0.07 mm thick lens with a calculated Dk/L of 4.2-2.2 caused an epithelial thinning without oedema. This thinning was due to a loss of superficial cells and a flattening of the remaining ones. Factors in the mechanism of epithelial thinning without oedema may include anoxia, trauma, lid pressure, and lens weight. The 0.4 mm thick lens offers negligible gas transmission in the closed eye, and after 48 hours much of the epithelium was stripped, while oedema and degenerative cytoplasmic changes were prominent in areas of surviving cells. In such areas the thickness of the epithelium was reduced to one or two layers of cells. The basement membrane was in all experiments unharmed by hydrogel contact lens wear. The epithelial innervation was maintained in all corneas except those of the closed eye, and finding correlates well with the good corneal touch threshold in soft contact lens wearers.

Animals↗

Ultrastructural observations on (pseudo-) exfoliation of the lens capsule: a re-examination of the involvement of the lens epithelium.

One lens each from 2 separate patients suffering from pseudoexfoliation and one lens from a normal eye were examined ultrastructurally. The normal lens capsule was internally lamellar in places and externally of a somewhat reduced electron density but otherwise of a homogeneous appearance and free of inclusions. Observations on the abnormal lenses revealed an electron dense and mainly granular but sometimes fibrillar material along the surface of the peripheral one-third of the capsule. Material of similar ultrastructural appearance was also found deeper in the capsule and in the immediately underlying epithelium. Since the capsule close to the pole of the lens was completely free of these abnormal inclusions and the underlying epithelium also lacked this material, it is concluded that the lens epithelium is a source of the surface debris in pseudoexfoliation. These findings therefore support previous authors who proposed a lenticular involvement in this disease. The present study does, however, not rule out the possibility of a uveal contribution of abnormal material but disputes its exclusive involvement in this disease, as has previously been postulated. Build-up of exfoliated material close to the capsular surface caused an apparent peeling of the lens capsule. It is therefore concluded that the anomalous lenses suffered from a true exfoliative process that may be more correctly termed 'exfoliation of the lens capsule.'

Epithelium↗

Corneal epithelial response of the primate eye to gas permeable corneal contact lenses: a preliminary report.

The comparative corneal epithelial effects of rigid gas permeable and soft contact lenses are reported in the present preliminary study using two bush baby monkeys (Galago senegalensis). Both types of lenses produced early cell death among the surface squamous cells while internally the epithelium and its nerve fibers remained normal. Sporadically small abnormal groups of cells involving two to three of the surface layers were observed in both the hard and soft lens wearing corneas. It was concluded that this represented superficial punctate keratitis (SPK). Small superficial intracellular epithelial cysts with membranous contents were infrequently noted in the gas permeable lens wearing cornea and it is suggested here that they were mild forms or precursors of those seen clinically in human corneas. Since the gas permeable lens met the corneal oxygen requirement it is postulated that the traumatic effect of the rigidity of the lens caused the cystic formation to occur. The relative hypoxia induced by the soft contact lens resulted in a mild superficial epithelial edema.

Animals↗

Rabbit eye exposure to broad-spectrum fluorescent light.

Two F40CW fluorescent lamps mounted in an EYS-2404 fixture and 300 nm, 5 nm waveband UV radiation were used to expose pigmented rabbit eyes. The results of the exposures to the eye were evaluated with the biomicroscope, ophthalmoscope, light microscope and electron microscope. The following conclusions were reached: The adverse ocular responses to fluorescent radiation exposure were due to long-duration, broadband radiation. These reactions were more generalized for fluorescent exposures when the cornea and lens are compared to UV exposures. The differences between the levels of threshold exposure needed to cause damage for the fluorescent source and UV radiation were attributed to exposure duration and the rate of delivery of the radiation. Corneal and lenticular damage was mild when compared with UV 300 nm exposures, and the threshold occurred after 8 h to 12 h of exposure. The effect of the radiation was to interfere with the normal functions of the cell while changes to the inert materials in the tissues was secondary to injury to the cell. The damage was mild in the corneal epithelium, somewhat more severe in the corneal endothelium, but minimal in the corneal stroma. Early retinal changes were found after 8 h of exposure to the fluorescent source. These induced changes were evident in the neural retina as spaces and were assumed to represent oedema. The retinal oedema was initially found only in the receptor cell, outer nuclear and nerve fibre layers. Many vacuoles or spaces were located in the junctional area between the ganglion cell and nerve fibre layers while smaller spacing occurred also within the nerve fibre layer. Twelve h of exposure to the fluorescent source produced a further increase in the oedema in the retina. The outer segments of the receptor cells appear to disintegrate and significant open spaces are evident among the inner and outer segments of the receptors. The inner plexiform layer shows an increased number of spaces within and among the neural elements, and the mitochondria appeared to be undergoing changes. The 20-h and longer exposure induced severe changes affecting all layers of the retina. These changes include massive retinal oedema with degenerative signs in all retinal neurons. A sympathetic reaction of the unexposed, contralateral eye occurred as the result of the damage to the exposed eye. Minimal sympathetic responses to the cornea and the lens began at exposure durations at or above 12 h, while the retina showed the sympathetic reaction beginning at 8 h.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Contact lens-induced corneal epithelial injury.

Rigid contact lenses were fitted on primates to study the subsequent corneal epithelial injury. This trauma was compared to corneal abrasions produced by a blunt object. The traumatic abrasion caused a rupture of the basal cells, which were identified as the most vulnerable part of the corneal epithelium for such an injury. The internal plasmalemma of the basal cell remained adherent to the epithelial basement membrane due to the strong hemidesmosomes along the cell membrane. Contact lenses were capable of producing similar injuries which did not penetrate the basement membrane and therefore did not involve the anterior limiting lamina (Bowman's membrane). We concluded that contact lenses produce a self-limiting trauma and even a severe case of contact lens overwear, although it causes deep corneal abrasions, seldom results in permanent scar formation.

Animals↗

Corneal response to rigid contact lens wear.

Three adult rhesus monkeys were subjected to 2 and 24 hours of polymethylmethacrylate (PMMA) contact lens wear. The induced corneal changes were examined with the electron microscope. Mild epithelial oedema as well as early degenerative cell changes was present already after 2 hours' wear. Rigid lens wear for 24 hours produced more severe oedema and cell alterations together with premature cell loss and ultimately, in areas of lens bearing, corneal denuding. Only the monkeys wearing contact lenses for 24 hours had significant stromal swelling, which was primarily evident in the posterior region, while the anterior limiting lamina remained unaffected. The stromal swelling was patchy and mainly around keratocytes and between lamellae, while fluid within the lamellae was evident only occasionally in posterior stroma. Changes among keratocytes were evident, especially posteriorly, where reaction was frequently severe. Endothelial reaction was restricted to a limited fluid uptake in the 24-hour-wear experiment. In addition there was in these monkeys an apparent loosening of the endothelial adhesion to the posterior limiting lamina. It is concluded that the oedematous epithelium undergoes cell shrinkage and flattening, which is compensated for by an uptake of fluid. The uptake of fluid maintains the overall normal thickness of the epithelium. The conclusion is supported by other studies, where the normal thickness of oedematous epithelium has been shown by pachometry. The results in the present study further suggest that stromal oedema in the contact lens wearer is a result of a relative loss of endothelial function, leading to a swelling that moves in a posterior to anterior direction.

Animals↗

Cerebral tissue response to electrode implantation.

Tissue response to platinum electrodes was assessed after an eight-day implantation period. The regions of study included the cortical areas at the opercular gyri and at the sulcus parieto-occipitalis externus, as well as the sub-cortical white matter in these cases. Perivascular and intraparenchymal hemorrhagic lesions as well as edematous changes characterized both by extensive intra and extracellular swelling were noted. Numerous phagocytic elements and degenerative strucutres were present at the electrode/parenchymal interface. Tissue alterations were asymmetrical as observed both around and at the tip of the implanted electrode. The parenchymal alterations extended from 0.2mm to 3.5mm distance from the electrode path/parenchymal interface. Greater tissue involvement was found in the subcortical white matter as compared to the adjacent cortical gray matter.

Animals↗

Cerebral tissue response to reserpine: a morphological study.

The acute influence of reserpine injection on cerebral tissue was studied in baboon and rat models. Five h after the infusion of reserpine, bilateral cortical areas were found to contain perivascular changes only, whereas basal ganglia regions contained advanced oedematous responses. Mitochondrial swelling was commonly found in the latter regions, as were loci containing microvascular crenation with accompanying pericytic changes.

Animals↗

Acute tissue response to cerebral ischemia in the gerbil. An ultrastructural study.

The Mongolian gerbil, because of the uniqueness of the anatomical features of its circle of Willis, has become an increasingly useful model in the study of cerebrovascular disease. The present work defines acute changes at the ultrastructural level following ischemic insult. The pathomorphological responses include initial astrocytic involvement and, when the degree of insult is increased, a progression of morphological changes is evident in neuronal and other parenchymal elements. Animals with vessels occluded for more than 3 hr without neurological signs suggestive of ischemia exhibited limited perivascular edema. Contralateral changes (perivascular astrocytic) were observed in the basal ganglia at 24 hr in animals with neurological deficit. Astrocytic and basal ganglia susceptibility to ischemia was consistent with previous findings in primate models. An additional association was found in that limited edematous involvement could exist in animals without neurological deficit but neuronal changes were only present in animals with signs of ischemic neurological deficit.

Animals↗