2004年 · 第117卷第09期

Background Multislice helical computed tomography (MSCT) has been used to depict coronary anatomy noninvasively, and proved useful for evaluating ventricular function. The aim of our study was to assess the accuracy of ventricular volume as measured by MSCT. Methods Fourteen human left ventricular (LV) and 15 right ventricular (RV) casts were scanned by MSCT. A series of LV and RV short-axis images were reconstructed later with slice thickness of 2. 0 mm, 3.5 mm, 5.0 mm, 7.0 mm, and 10.0 mm. Ventricular volume was calculated by the multislice tomographic Simpson's method. True LV and RV cast volumes were determined by water displacement. Results Both calculated LV and RV volumes correlated highly with the corresponding true volumes (all r > 0. 95, P < 0. 01). But with slice thickness from 2. 0 mm to 10. 0 mm, MSCT scanning overestimated the corresponding true volume by (3.21 ±5.95) ml to (12.58 ±8.56) ml for LV and (10.22 ±8.45) ml to (23. 91 ± 12. 24) ml for RV (all P < 0. 01). There was a very high correlation between the overestimation and the selected slice thickness for both LV and RV volume measurements (r = 0. 998 and 0. 996, P < 0. 01, respectively). However, when slice thickness was reduced to 5. 0 mm, the overestimation for both LV and RV volume measurements became nonsignificant for slice thickness from 2. 0 mm to 5. 0 mm. Conclusions Both LV and RV volumes can be accurately estimated by MS CT. Thinner slice has more accurate calculated volume. However, 5.0 mm slice thickness is thin enough for an accurate measurement of LV or RV volume. Chin Me J 2004; 117(9):1283-1287

Background The Taq IB, Msp I and 1405V polymorphisms of cholesteryl ester transfer protein (CETP), an important regulatory factor of lipid metabolism, have been attracted much more attention by the researchers. In this study, we investigated the associations between these 3 polymorphisms of CETP gene and variations in plasma lipid and lipoprotein levels in patients with coronary heart disease (CHD). Methods Genomic DNA was extracted from leukocytes of 203 CHD patients and 100 control subjects using the salting out method. Genotyping of the CETP gene was performed using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) techniques. Statistical analysis was conducted using the SPSS 10. 0 software package. Results The distribution of allele and genotype frequencies of the Taq IB, Msp I, and I405V polymorphisms was similar in the CHD patient group and the control group. The B1B1 genotype of the Taq IB polymorphism was associated with significantly higher TC (P = 0. 039) and LDL-C (P = 0.044) levels than the B2B2 genotype in CHD patients, and with significantly higher LDL-C (P = 0.034) levels than the B2B2 genotype in controls. Homozygotes of the 1405V polymorphism exhibited significantly higher HDL-C levels than VV homozygotes among control subjects (P = 0.023). In male CHD patients with unambiguously assigned haplotypes, B2-M2-V/B2-M2-I patients demonstrated significantly higher HDL-C concentrations than B1-M2-V/B1-M2-I (P = 0.023) and B1-M2-V/B1-M2-V patients (P = 0.047). Conclusions Genetic variations in the CETP gene may account for a significant proportion of the differences in plasma lipid and lipoprotein concentrations among the general population. The B1B1 genotype of the Taq IB polymorphism is probably a genetic risk factor for CHD in the study population. Chin Med J 2004; 117(9):1288-1292

Background Atherosclerotic plaque rupture and coronary thrombosis are the main causes of acute coronary syndromes. However, there is no animal model of unstable atherosclerotic plaques. The presence of the p53 gene in advanced atherosclerotic plaques and the sensitivity to p53-induced apoptosis of smooth muscle cells isolated from these plaques prompted us to build an animal model of unstable atherosclerotic plaques using p53 gene transfer. Methods Sixty-four New Zealand white rabbits were randomly divided into two groups: group A (n = 54) and group B (n = 10). Rabbits in group A underwent balloon-induced abdominal aortic wall injury and were then given a diet of 1% cholesterol, while rabbits in group B were given a diet of 1% cholesterol without the induction of aortic wall injury. At the end of the eighth week, rabbits in group A were randomly divided into two subgroups: group A1 (n = 27) and group A2 (n = 27). Recombinant adenovirus carrying p53 or β-galactosidase (LacZ) genes were injected through a catheter into the aortic segments rich in plaques in groups A1 and A2, respectively. Two weeks later, 10 rabbits each from groups A1 and A2 were killed to observe the occurrence of spontaneous plaque ruptures, and the remaining rabbits in groups A1, A2, and B all underwent pharmacological triggering with an injection of Chinese Russell's viper venom (CRVV) and histamine. Results The over expression of p53 in group A1 [(32. 4 ±10. 2) % vs (15. 8 ±3. 6) % in group A2 and (16. 2 ±6. 7) % in group B, P < 0. 001, respectively] resulted in a marked increase in cellular apoptosis [(2. 5 ±0. 8) % vs (1.0 ±0. 3) % in group A2 and (0. 9 ±0. 4) % in group B, P <0.01, respectively], an accumulation of inflammatory cells withhin the plaques, and a significant decrease in vascular smooth muscle cells (VSMCs) and in the thhickness of the fibrous caps. Although spontaneous plaque rupture was rare in group A1, plaque ruptures and thrombosis occurred in 12 rabbits with a total of 20 lesions after pharmacological triggering. By contrast, pharmacological triggering led to plaque rupture and thrombosis in only 5 rabbits for a total of 7 lesions in group A2 and in none of the rabbits in group B. Conclusion After transfection with human wild-type p53 gene and pharmacological triggering, plaque rupture and thrombosis occur in most atherosclerotic lesions in rabbits, thus offering a reliable model for the further study of unstable atherosclerotic plaques. Chin Med J 2004; 117(9):1293-1298

Background Diffuse panbronchiolitis (DPB) was originally and is still primarily reported in Japan, rarely in other countries. As macrolide therapy is effective for this disease with once dismal prognosis, familiarity with its clinical features is urgently needed, especially for clinicians outside Japan. The objectives of this study were to investigate the clinical features of DPB in a Chinese population and propose diagnostic procedures that will lead to increased awareness of this treatable disease among clinicians, ultimately allowing for more rapid diagnosis. Methods After a literature review, the clinical features of DPB were histopathologically confirmed in a series of 9 cases either by open lung biopsy or video-assisted thoracic surgical biopsy, resulting in the largest series of confirmed DPB cases in a non-Japanese population. Here, the cases are retrospectively described and diagnostic procedures are discussed. Results Persistent cough, sputum, and exertion dyspnea occurred in 89 % of patients, a history of or current chronic sinusitis in 78 %, centrilobular micronodules appearing on chest CT scans in 100 %, coarse crackles in 78 %, FEV1/FVC < 70 % in 44 %, Pa02 < 80 mmHg in 56 %, and titer of cold hemagglutinin ≥1 64 in 11 %. According to its clinical diagnostic criteria, diagnosis was definitive in 44 %, suggested in 33 %, and excluded in 23 % at the time of diagnosis. However, DPB was clinically considered before confirmation in only 22 % of patients, with the remaining 78 % of cases missed or mistaken for other diseases. Of the 9 cases, 8 received transbronchial biopsies before confirmation of the diagnosis, but all showed non-specific inflammation. Conclusions Although its clinical features may vary with disease course and ethnic populations, most cases of DPB can be diagnosed or suggested according to clinical diagnostic criteria. However, underdiagnosis as a result of unfamiliarity with its clinical features and diagnostic criteria prevails, If difficulty in diagnosis arises, the diagnosis should be based on clinicopathological features and the exclusion of other diseases. Few cases can be confirmed by transbronchial biopsies; in these cases, either an open-lung biopsy or a video-assisted thoracic surgical lung biopsy should be recommended. Chin Med J 2004; 117(9):1299-1303

Background The major neuropathological symptoms of Parkinson's disease (PD) consist of a loss of pigmented doparminergic neurons in the substantia nigra and the presence of Lewy bodies. This study was to investigate the effects of bilateral subthalamic nucleus (SIN) stimulation on resting-state cerebral glucose metabolism in advanced PD, and investigate the mechanism of deep brain stimulation (DBS). Methods Seven consecutive advanced PD patients (4 men and 3 women, mean age 64 ±4 years, mean H-Y disability rating 4. 4 ±0. 65) receiving bilateral STN DBS underwent18F-fluorodeoxyglucose (18F-FDG)/positron-emission tomography (PET) examinations at rest both preoperatively and one month postoperatively, with SIN stimulation still on. The unified PD rating scale was used to evaluate the clinical state under each condition. Statistical parametric mapping (SPM) was used to investigate the regional cerebral metabolic rates of glucose (rCMR Glu) during STN stimulation, and to compare these values to rCMR Glu preoperation. Results STN stimulation clearly improved clinical symptoms in all patients. A significant increase in rCMR Glu was found in the bilateral lentiform nucleus, brainstem (midbrain and pons), bilateral premotor area (BA6), parietal-occipital cortex, and anterior cingulated cortex, and a marked decrease in rCMR Glu was noted in the left limbic lobe and bilateral inferior frontal cortex (P <0. 05). Conclusion Bilateral STN stimulation may activate the projection axon from the STN, improving clinical synptoms in advanced PD patients by improving both ascending and descending pathways from the basal ganglia and increasing the metabolism of higherorder motor control in the frontal cortex. Chin Med J 2004; 117(9):1304-1308

Background Functional magnetic resonance imaging (fMRI) has become a powerful tool for tracking human brain activity in vivo. This technique is mainly based on blood oxygenation level dependence (BOLD) contrast. In the present study, we employed this newly developed technique to characterize the neural representations of human portraits and natural sceneries in the human brain. Methods Nine subjects were scanned with a 1. 5 T magnetic resonance imaging (MRI) scanner using gradient recalled echo and echo-planar imaging (GRE-EPI) pulse sequence while they were visually presented with 3 types of white-black photographs: natural scenery, human portraits, and scrambled nonsense pictures. Multiple linear regression was used to identify brain regions responding preferentially to each type of stimulus and common regions for both human portraits and natural scenery. The relative contributions of each type of stimulus to activation in these regions were examined using linear combinations of a general linear test. Results Multiple linear regression analysis revealed two distinct but adjacent regions in both sides of the ventral temporal cortex. The medial region preferentially responded to natural scenery, whereas the lateral one preferentially responded to the human portraits. The general linear test further revealed a distribution gradient such that a change from portraits to scenes shifted areas of activation from lateral to medial. Conclusions The boundary between portrait-associated and scenery-associated areas is not as clear as previously demonstrated. The representations of portraits and scenes in ventral temporal cortex appear to be continuous and overlap. Chin Med J 2004; 117(9):1309-1312

Background Cubital tunnel syndrome is a well-recognized clinical condition and is the second most common peripheral compression neuropathy. This study was designed to investigate the causes of cubital tunnel syndrome by surgical means and to assess the clinical value of the neurophysiological diagnosis of cubital tunnel syndrome. Methods Twenty-one patients (involving a total of 22 limbs from 16 men and 5 women, aged 22 to 63, with a mean age of 49 years) with clinical symptoms and signs indicating a problem with their ulnar nerve underwent motor conduction velocity examinations at different sites along the ulnar nerve and examinations of sensory conduction velocity in the hand, before undergoing anterior transposition of the ulnar nerve. Results Electromyographic abnormalities were seen in 21 of 22 limbs [motor nerve conduction velocity (MCV) range (15. 9 - 47.5) m/s, mean 32. 7 m/s] who underwent motor conduction velocity examinations across the elbow segment of the ulnar nerve. Reduced velocity was observed in 13 of 22 limbs [MCV (15. 7 - 59. 6) m/s, mean 40. 4 m/s] undergoing MCV tests in the forearms. An absent or abnormal sensory nerve action potential following stimulation was detected in the little finger of 14 of 22 limbs. The factors responsible for ulnar conpression based on observations made during surgery were as follows: 15 cases involved compression by arcuate ligaments, muscle tendons, or bone hyperplasia; 2 involved fibrous adhesion; 3 involved compression by the venous plexus or a concurrent thick vein; 2 involved compression by cysts. Conclusions Factors inducing cubital tunnel syndrome include both common factors that have been reported and rare factors, involving the venous plexus, thick veins, and cysts. Tests of motor conduction velocity at different sites along the ulnar nerve should be helpful in diagnosis cubital tunnel syndrome, especially MCV tests indicating decreased velocity across the elbow segment of the ulnar nerve. Chin Med J 2004; 117(9):1313-1316

Background Diabetic neuropathy is common in diabetes mellitus. The early stage of diabetic neuropathy is often symptomless and difficult to be treated. The aim of this study was to assess the correlation between the results of the sympathetic skin response (SSR) test and the development of diabetic neuropathy, and explore the use of SSR as an objective basis for the early diagnosis of diabetic neuropathy. Methods The latencies and amplitudes of initiation and of the N and P waves were determined by SSR testing of the extremities of 80 diabetic patients and 30 healthy controls. Results The latencies of initiation and of the N and P waves were significantly (P < 0. 001) longer in diabetic patients than in the controls, while there was no significant difference in the amplitudes (P >0. 05). All but two patients (97. 5%) demonstrated abnormal SSR in at least one limb. Conclusions SSR can detect early dysfunction of the small sympathetic fibers in people affected by diabetes mellitus, and may be a useful electrophysiological test for the early diagnosis of diabetic neuropathy. Chin Med J 2004; 117(9):1317-1320

Background Nowadays it is now a focus topic in schistosomiasis research to find ideal vaccine candidates and new drug targets for developing anti-schistosomiasis vaccine. We cloned a new gene, casein kinase Ⅱbeta subunit, of Schistosoma japonicum (S. japonicum) and express it in Escherichia coli (E. coli). Methods The ESTs obtained in our laboratory were analyzed by homologous searching, and a new gene was recognized. The full-length cDNA of the new gene was obtained by joining the 3'RACE PCR fragment and the EST clone. To express the new gene, the cDNA was cloned into pGEX-4T-1 vector and then transformed into E. coli JM109. The recombinant protein was analyzed by SDS-PAGE and Western-blot. Results A 908 bp cDNA was isolated from S. japonicum and identified to be casein kinase Ⅱ beta subunit gene by sequence analysis. The open reading frame of the gene encodes a protein of 217 amino acids exhibiting 75.8 %, 75.8%, 73.9%, 68.2%, 51.6% identity to the amino acids sequence of the corresponding genes of Homo sapiens (H. sapiens), Xenopus laevi (X. laevi), Drosophila melanogaster (D. melanogaster), Caenorhabditis elegan (C. elegan), and Schizosaccharomyces pombe (S. promber) respectively. The predicted molecular weight of the protein was 24. 921 kDa. The new cDNA sequence had been submitted to GenBank, and its accession number is AY241391. This cDNA was subcloned into the pGEX-4T-1 vector and expressed in E. coli JM109. The recombinant protein could be recognized by the S. japonicum infected rabbit serum. Conclusion The full-length cDNA sequences encoding S. japonicum casein kinase Ⅱ beta subunit were firstly sequenced, cloned, and expressed in E. coli. Chin Med J 2004; 117(9):1321-1325

Background Recently congenital infection with Schistosoma japonicum (S. japonicum) has been demonstrated in pigs, rabbits, mice and dogs. We explored the rabbit as an animal model for the congenital infection of schistosomiasis japonica and assessed the effect of a congenital S. japonicum infection on the resistance of rabbit kittens to a postnatal challenge infection. Methods Sixteen pregnant New Zealand white rabbits were infected with a single dose of S. japonicum cercariae. The exposed animals were divided into three groups according to the gestation age at the time of infection. Diagnosis of prenatally acquired S. japonicum infection in the rabbit kittens was primarily based on serological tests in combination with parasitological and histopathological findings. Congenitally infected kittens were challenged percutaneously with 100 S. japonicum cercariae to assess the effect of a congenital S. japonicum infection on kitten resistance to a postnatal challenge infection. Results The overall prevalence of congenital infection in off spring of infected mothers was 20 % (12/ 60). The congenital infection rate in group L (late gestation) was much higher than in group E (early gestation) and group M (mid-gestation) (P < 0. 05). After a postnatal challenge infection, prenatally infected kittens had a 54. 66 % worm reduction rate, 41. 45 % egg reduction rate, and 51. 76 % granuloma size reduction rate compared to naïve kittens. Conclusions This study demonstrates the possibility of congenital infection of S. japonicum in rabbits and the resistance of congenitally infected kittens to a postnatal challenge infection. These results have important implications not only for epidemiological investigations, but also in designing government control programs for schistosomiasis. Chin Med J 2004; 117(9):1326-1329

Objective To review the recent developments in and research into binding receptors of hepatitis C virus (HCV) and especially the role of dendritic cell-specitic adhesion receptor (DC-SIGN) in HCV. Data sources Both Chinese- and English-languge literature was searched using MEDLINE (2000-2003) and the databank of Chinese-language literature (2000-2003). Study selection Relevant articles on DC-SIGN and HCV binding receptors in recent domestic and foreign literature were selected. Data extraction Data were mainly extracted from 40 articles which are listed in the references section of this review. Results DC-SIGN, a dendritic cell-specific adhesion receptor and a type Ⅱ transmembrane mannose-binding C-type lectin, is very important in the function of dendritic cells (DC), both in mediating naïve T cell interactions through ICAM-3 and as a rolling receptor that mediates the DC-specific ICAM-2-dependent migration processes. It can be used by HCV and other viral and bacterial pathogens including human immunodeficiency virus (HIV), Ebola virus, CMV and Mycobacterium tuberculosis to facilitate infection. Both DC-SIGN and DC-SIGNR can act either in cis, by concentrating virus on target cells, or in trans, by transmission of bound virus to a target cell expressing appropriate entry receptors. Recent report showed that DC-SIGN not only plays a role in entry into DC, HCV E2 interaction with DC-SIGN might also be detrimental to the interaction of DC with T cells during antigen presentation. Conclusions DC-SIGNs are high-affinity binding receptors for HCV. The clinical strategies that target DC-SIGN may be successful in restricting HCV dissemination and pathogenesis as well as directing the migration of DCs to manipulate appropriate immune responses in autoimmunity and tumorigenic situations. Chin Med J 2004; 117(9):1395-1400

Background Corneal dystrophy is a group of inherited blinding diseases of the cornea. This study was to identify the mutations of the keratoepithelin (KE) gene for proper diagnosis of corneal dystrophy. Methods Three families with corneal dystrophy were analysed. Thirteen individuals at risk for corneal dystrophy in family A, the proband and her son in family B, and the proband in family C were examined after their blood samples were obtained. Mutation screening of human transforming growth factor β-induced gene (BIGH3 gene) was performed. Results Five individuals in family A were found by clinical evaluation to be affected with granular corneal dystrophy and carried the BIGH3 mutation W555R. However, both probands in families B and C, also diagnosed with granular corneal dystrophy, harboured the BIGH3 mutation R124H. Conclusion Molecular genetic analysis can improve accurate diagnosis of corneal dystrophy. Chin Med J 2004; 117(9):1418-1421