Biomedical subjects
Publications and source records attributed to W H Chen.
A left rostral thalamic hematoma was found in a 52-year-old hypertensive man who suffered from a 10-h episode of transient global amnesia (TGA). A neuropsychological study revealed no cognitive impairment in a follow-up period for 5 years. The left rostral part of the thalamus appears to be responsible for his TGA, due probably to an interference of the mamillothalamic tract, ventroamygdalofugal pathway or dorsal noradrenergic bundle.
The purpose of this study was to evaluate the effects of reperfusion or in vivo pretreatment with a lipid peroxidation inhibitor, lazaroid (U74389G), on attenuating systolic and diastolic alterations occurring during myocardial stunning in isolated rat hearts. Male Sprague-Dawley rats (350-400 g) were randomized into three groups: control animals (n = 13) received no drugs; hearts from reperfused animals (n = 11) received 5 microM U74389G in the reperfusion solution; pretreated animals (n = 11) received 6 mg/kg U74389G by i.v. infusion 30 min before killing. Isolated, isovolumic rat hearts were subjected to 20 min of ischemia at 37 degrees C and subsequent reperfusion for 30 min. Left ventricular isovolumic developed pressure (LVDP), its first derivative (LVDPdP/dt), end-diastolic pressure (LVEDP), and the time constant of diastolic relaxation (tau) were measured. At baseline, no statistically significant differences were detected in systolic or diastolic function in hearts of rats with or without U74389G treatment. After reperfusion, LVDP stabilized at 87 and 92% in both drug-treated groups compared with 52% in the control group (p < 0.01) and dP/dtmax recovered to 101 and 110% of baseline compared with 58% in the control group (p < 0.01). Diastolic dysfunction showed significant improvement in both U74389G pretreatment groups. The increases in LVEDP and tau were 2.0- and 1.2-fold in pretreated hearts and 2,8-fold and 1.5-fold in drug-reperfused hearts, respectively (compared with 6-fold increases in LVEDP and a 2.5-fold increase in tau in controls; p < 0.05). In conclusion, whether administered before ischemia or during reperfusion, U74389G effectively attenuated the systolic and diastolic dysfunction in this model of myocardial stunning, probably protecting cell membranes from peroxidation by oxygen-derived metabolites.
In the present study the effect of pressure overload on the expression of protooncogene c-fos in the left ventricle was investigated in rats with abdominal aorta constriction. It was found that a remarkable expression of c-fos was induced by pressure overload and the expression was greatly attenuated by angiotensin converting enzyme inhibitor captopril. In the pressure overload group the angiotensinogen mRNA level was found increased. The above results suggest that angiotensin II is involved in the expression of c-fos due to pressure overload.
In order to elucidate the relationship between the lipoprotein profile and large cerebral artery atherosclerosis in the young adults living in developing Asian countries, the serum lipoprotein profile and the luminal diameter of large cerebral arteries (internal carotid, middle/anterior cerebral and vertebrobasilar arteries) were measured and correlated in 67 young Taiwanese with non-embolic cerebral infarct (CI). Totally 23 (21.9%) patients had atherosclerotic stenosis. A significant elevation of the serum total cholesterol (TC), triglyceride, total lipids, beta-lipoprotein (beta-LP) and pre-beta-LP level was found in atherosclerotic CI patients. But multiple regression analysis showed only the serum beta-LP (p = 0.0041) and TC (p = 0.0324) level to be the independent risk factors for atherosclerosis. Secondary dyslipoproteinemia is the main cause for hyperlipoproteinemia in our atherosclerotic patients. Therefore, an abnormal lipoprotein profile is linked to large cerebral artery atherosclerosis in young Asians regardless of ethnic group. A tailored program is recommended to modify the life style and dietary habit, as well as to gain access to secondary control for large cerebral atherosclerosis prevention in developing countries.
Typical bilateral cheiro-oral syndrome was encountered in a 74-year-old man who had bilateral subdural hematoma after a minor head injury. The delayed grave neurologic deficits occurred 1 month later without expansion of the hematoma. Removal of the lesions reversed both cheiro-oral syndrome and his late-onset neurological disabilities.
Insulin-like growth factor I (IGF I) plays a key role in the regulation of cell proliferation. Progression of the cell cycle is regulated by stimulatory and inhibitory pathways. In order to understand the mechanisms through which IGF I regulates cardiac muscle growth, we have studied the effects of IGF I on inhibitory pathways involving p53 and WAF1 in cultured cardiac muscle cell line H9C2. The onset of DNA synthesis in response to IGF I stimulation was preceded by activation of p53 expression. In addition, IGF I increased p53-dependent and p53-independent induction of WAF1 in H9C2 cells. Dose-response studies showed that IGF I effects on p53-dependent and p53-independent induction of WAF1 occur at physiological concentrations of IGF I. These data indicate that IGF I coordinately regulates inhibitory pathways of cell cycle progression, and that p53-dependent and p53-independent induction of WAF1 may provide negative control mechanisms to regulate stimulatory pathways of cell cycle progression activated by IGF I.
A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Using in situ hybridisation and computerised image analysis we show here that in ct/ct embryos, RAR-beta transcripts are deficient in the hindgut endoderm, a tissue whose proliferation rate is abnormal in the ct mutant, and RAR-gamma transcripts are deficient in the tail bud and posterior neuropore region. The degree of deficiency of RAR-gamma transcripts is correlated with the severity of delay of posterior neuropore closure. As early as 2 hours following RA treatment at 10 days 8 hours post coitum, i.e. well before any morphogenetic effects are detectable, RAR-beta expression is specifically upregulated in the hindgut endoderm, and the abnormal expression pattern of RAR-gamma is also altered. These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway.
44 oral cavity malignant cancer patients who underwent operation and chemotherapy are taken as the Experiment Group,using a mixture liquid of Calcii Folinas and Gentamycin to rinse out the mouth.48 patients using single drug gargle as the Comparison Group,The comparison between the two gargles' effects on oral ulcer and infection shows that the incidence of oral ulcer in the Comparison Group(P<0.05),and there is a significant difference.The oral infection incidence is lower too (P>0.05).There is no statistical difference.The expeiment suggests that gargling with mixture liquid is superior to using single drug liquid.
A 43-year-old male was diagnosed as having cryptococcal meningitis based on his clinical condition, cerebrospinal fluid (CSF) profile and high titer CSF cryptococcal antigen. The patient received intravenous amphotericin B at a total dose of 91 mg over 5 days. The therapy was then abandoned due to acute hepatorenal failure. The patient's neurologic status remained stable for 2 months, after which he began experiencing somnolence, confusion and a personality change. Cranial computed tomography revealed multifocal white matter lesions, and a brain biopsy showed a demyelination change with concurrent IgM and C1q deposition. A clinical diagnosis of amphotericin B-induced leukoencephalopathy was made. The patient's clinical condition was partially reversed after low-dose steroid therapy.
We present a 74-year-old woman who developed a sudden onset of vertigo, vomiting, and axial retropulsion without limb ataxia. A clinical diagnosis of acute peripheral labyrinthine lesion was made initially. However, magnetic resonance imaging demonstrated a small infarct area involving the caudal part of the cerebellar vermis and medial cerebellar hemispheres on both sides. We emphasize that a cautious attitude should be taken in managing patients with isolated vestibular dysfunction, especially in aged person or those associated with stroke risk factor.
In the present study, the effects of angiotension II on the expression of protooncogene c-fos and c-myc in the left ventricle were investigated on Langedorff heart preparations. It was observed that angiotensin induced both c-fos and c-myc expression in a dose-dependent manner and the c-fos expression showed an earlier appearance than c-myc. All these induced expressions were blocked by a Angiotensin II receptor antagonist saralasin. The Angiotensin II induced expression of c-fos was also blocked by TTX, but the c-myc gene expression was unaffected.
Using a unilateral, focal, cortical, ischemia-reperfusion rat model, c-fos mRNA and Fos immunoreactivity in the brain were investigated. The study was divided into a series of reperfusion intervals which were carried out for a period of up to 7 days. The c-fos mRNA peaked in the ischemic cortex (about 15-fold) after 30 minutes of ischemia followed by 1 hour of reperfusion and dropped to baseline level after 1 day of reperfusion. Increased expression switched to the bilateral retrosplenial and frontal cortex, as well as the left (nonischemic) parietal cortex, at 3- or 5-days of reperfusion (about three- to fourfold). Fos immunohistochemical staining correlated positively with the surge of c-fos mRNA. Nuclear run-off transcription assays further indicated that the increase in c-fos mRNA was regulated at the transcriptional level not only in the ischemic cortex (30 min of ischemia, followed by 1 h of reperfusion) but also in the contralateral counterpart (30 min of ischemia, followed by 3 d of reperfusion). A link between altered gene expression and diaschisis is suggested. The distant/delayed c-fos expression is probably caused by loss of inhibition from the ischemic cortex through a polysynaptic transneural pathway.
Although the correlation between fibromuscular dysplasia (FMD) and intracranial aneurysm is well established, the combination of FMD with a giant aneurysm is rare. This paper reports a patient with extracranial FMD associated with a giant intracavernous aneurysm compromising the trigeminal and abducens nerve. A review of the literature uncovered only four documented cases of FMD with concurrent giant intracranial aneurysms. The present case adds further weight to the argument for including FMD in the differential diagnosis list when confronted with a patient with a giant intracranial aneurysm. Absence of adequate collaterals in this patient eliminated ligation as a treatment strategy for the aneurysm.
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During mammalian neurulation regional differences are evident between the cranial region, in which neurulation is most complex, the trunk as far as the caudal neuropore and the secondary neurulation region of the caudal trunk plus tail. Differences among these three regions are characterized by specific patterns of morphogenesis and by specific patterns of gene expression. During cranial neurulation distinct regions develop in the brain and the presomitic hindbrain forms seven rhombomeric divisions. The first clear morphological boundary is the preotic sulcus (later transformed into the gyrus between rhombomeres 2 and 3), which may limit cell movement as neuroepithelial cells rostral to it flow towards and into the rapidly expanding forebrain region. The formation of rhombomeres as morphological entities and the development of a normal rhombomere-specific pattern of homeobox and other gene expression domains depend on relatively low levels of retinoic acid. Retinoic acid receptors, which are retinoic acid-activated transcription factors, and retinoid binding proteins, which control the availability of retinoic acid to the receptors, show regional patterns of expression in the cranial, trunk and caudal regions of the neuroepithelium during neurulation. These patterns suggest a possible mechanism for region-specific gene expression during neurulation.
Curly tail mouse mutant embryos (ct/ct) develop spinal neural tube defects (NTD) in 54% of cases, comprising isolated tail flexion defects and spinal bifida with tail flexion defects. Both types of spinal NTD result from delayed closure of the posterior neuropore (PNP). Previous studies (Seller et al. [1979] Proc. R. Soc. Lond. Biol. 206:95-107; Seller and Perkins [1982] Prenat. Diagn. 2:297-300) described a paradoxical effect of retinoic acid (RA) on the phenotypic expression of the ct mutation: Treatment with low doses of RA on day 8 of gestation increased the incidence of total NTD, whereas low doses of RA administered on day 9 resulted in reduced incidence of total NTD. In order to investigate further the reported preventive effect of RA, we have carried out detailed analyses of the effects of maternal treatment with 5 mg/kg RA on the incidence of NTD at different developmental stages, and on the development and growth of ct/ct embryos. We found that 5 mg/kg RA reduces the incidence of spinal NTD in a stage-specific manner, without increasing the incidence of cranial NTD. The effect of RA is specific: There were no other alterations in morphogenesis, growth, development, resorption rate, or litter size. RA was more effective in the prevention of isolated tail flexion defects than of spina bifida. Prevention of isolated tail flexion defects was maximal (50% reduction) when RA was administered between 10 days 4 hours and 10 days 8 hours post coitum (p.c.) inclusive (24 to 34 somite stage).(ABSTRACT TRUNCATED AT 250 WORDS)
This experimental study was undertaken to evaluate the hypothesis that cardioplegic arrest at 37 degrees C is superior to 10 degrees C cardioplegic arrest in the myocardial protection of an acutely injured heart. The hypothesis was tested using Sprague-Dawley rat hearts that were excised and retroperfused with Krebs-Henseleit buffer as isolated, isovolumic heart preparations. After 15 min of equilibration and baseline readings, ischemic injury of the myocardium was established by cessation of perfusion for 20 min, followed by 30 min of reperfusion to obtain cardiac measurements and verify uniformity of ventricular dysfunction. All hearts were then arrested for 30 min with continuous cardioplegia (oxygenated crystalloid cardioplegia, 4 ml/min) followed by 30 min of reperfusion. In one group (N = 12), temperature of cardioplegia was 10 degrees C. In the second group (N = 12), cardioplegia temperature was 37 degrees C. The experiments showed that in acutely injured hearts, cardioplegic arrest at 10 degrees C resulted in further deterioration in ventricular dysfunction (P < 0.01). In contrast, similarly injured hearts which underwent cardioplegic arrest at 37 degrees C showed a modest deterioration in ventricular dysfunction which did not reach statistical significance (P > 0.05). The experimental findings suggest that in the presence of acute myocardial injury, cardioplegic arrest at normothermia may provide better myocardial protection.
OBJECTIVE: The heart of the young Syrian cardiomyopathic hamster (CMH) displays discrete patches of active myocytolytic necrosis and it has been hypothesised that these lesions are triggered by arteriolar spasm. Accordingly, we tested the theory that the coronary vasoconstrictor response to arginine vasopressin (AVP) infusion is more vigorous in the actively necrotising young (2-3 month old) CMH than in age matched normal hamsters, 5-6 month old CMHs in the histologically quiescent phase of the disease, or 5-6 month old normal hamsters. METHODS: An isovolumetric isolated heart preparation was used in which the coronary arteries were perfused with Krebs-Henseleit buffer at constant flow by a syringe pump. Coronary vascular resistance was determined by the ratio of measured perfusion pressure to flow rate during extended diastoles. RESULTS: There were no significant differences in baseline coronary vascular resistance among the four groups. The increase in resistance with AVP infusion (0.54 pressor units.min-1) was significantly greater (p < 0.01) in the young CMH [6.66(SEM 4.75) mm Hg.ml-1.min-1] than in the old CMH [1.66(0.78)], the young normal [1.10(1.07)], and the old normal [2.72(1.86)] groups. CONCLUSIONS: There is increased vasoconstrictive responsiveness in the young CMH coronary vasculature. The results suggest a broader coronary abnormality in this myopathic model and are consistent with the microvascular spasm hypothesis of myocytolytic lesion formation.