Cauda equina syndrome caused by delayed traumatic spinal subdural haematoma.
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Biomedical subjects
Publications and source records attributed to K Lu.
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Non-traumatic cerebrospinal fluid rhinorrhea indirectly caused by a remote brain tumor has rarely been reported. Here we describe a case of non-traumatic cerebrospinal fluid rhinorrhea that occurred as the initial symptom of a posterior falx meningioma. In addition, based on the period of occurrence of cerebrospinal fluid rhinorrhea before or after the tumor operation, we introduced a novel classification for these cases into pre-treatment and post-treatment types. The findings of the present case and the results of our literature research suggest that different treatments should be used for patients with these two types of non-traumatic cerebrospinal fluid rhinorrhea resulting from remote brain tumor. After tumor excision, patients of the pre-treatment type may receive conservative management or cerebrospinal fluid shunting, while patients of the post-treatment type need direct repair of the fistula.
Absorption of dietary cholesterol from the intestine is an important part of cholesterol homeostasis and represents the first step that allows dietary cholesterol to exert its metabolic effects. Although the role of bile salts in the initial absorption of dietary cholesterol, by the formation of emulsions, is readily appreciated, the recognition that other molecular mechanisms might govern this process is only recently gaining momentum. Not only does the intestine regulate the amount of dietary cholesterol that enters the body; it is very selective with regard to the sterols that are allowed in. The human intestine is responsible for absorbing a significant amount of cholesterol each day. In addition to approximately 0.5 g d(-1) of dietary cholesterol, many other sterols are also present in almost equal abundance in the normal diet. Approximately 0.4 g of plant sterols, such as sitosterol, brassicasterol and avanesterol, are also present. However, the human body seems to allow only cholesterol to enter and remain in the body, with almost negligible amounts of plant sterols being retained. That specific molecular mechanisms are responsible for this behavior is supported by the identification of the genetic defect(s) in a rare disorder, beta-sitosterolemia (MIM 210250), where this process is disrupted. Such studies are now beginning to throw light on sterol absorption and excretion and elucidate the molecular mechanisms that govern these processes.
OBJECTIVES: The independent predictors of aphasia outcome for patients with left basal ganglia hemorrhage were evaluated. PATIENTS AND METHODS: We included 140 patients of 1,036 patients with spontaneous intracerebral hemorrhage admitted to our hospital from January 1993 through December 1997. Aphasia was assessed using the aphasia scale of the Scandinavian stroke scale. Univariate and step-wise logistic regression analyses were performed to assess the relationships between the initial aphasia score, age, gender, blood volume, locations of hematoma and aphasia outcome. RESULTS: Step-wise logistic regression analysis revealed that the following two factors were independently associated with the final aphasia outcome: initial aphasia score (P < 0.0001) and location of hematoma involving the posterior limb of the internal capsule (P = 0.004). CONCLUSIONS: A particularly high likelihood of poor aphasia outcomes of patients with left basal ganglia hemorrhage are predicted in those who have poor initial aphasia score and whose brain computed tomography shows the hematoma involves the posterior limb of the internal capsule.
PURPOSE: Internuclear ophthalmoplegia is a syndrome produced by a lesion in the medial longitudinal fasciculus. Head trauma is a rare cause. We describe an unusual case of bilateral internuclear ophthalmoplegia as an isolated sequela following a minor head injury that resolved completely 3 months later. METHODS: Case report. Magnetic resonance images. RESULTS: A 34-year-old male developed typical bilateral internuclear ophthalmoplegia after closed head injury. Attempted convergence was normal. Magnetic resonance imaging clearly delineated the focal hemorrhage in the medial longitudinal fasciculus region by showing a small bright lesion in the pontomesencephalic junction in the midline on both T2-weighted and T1-weighted images. The diplopia resolved 4 weeks later. Three months after the accident, his versions were completely normal. CONCLUSION: Isolated internuclear ophthalmoplegia should be considered in the differential diagnosis when one encounters an adduction deficit in a recently traumatized patient. Magnetic resonance images enhance the ability to correlate the clinical findings with the anatomic lesion.
The molecular mechanisms regulating the amount of dietary cholesterol retained in the body, as well as the body's ability to exclude selectively other dietary sterols, are poorly understood. An average western diet will contain about 250-500 mg of dietary cholesterol and about 200-400 mg of non-cholesterol sterols. About 50-60% of the dietary cholesterol is absorbed and retained by the normal human body, but less than 1% of the non-cholesterol sterols are retained. Thus, there exists a subtle mechanism that allows the body to distinguish between cholesterol and non-cholesterol sterols. In sitosterolemia, a rare autosomal recessive disorder, affected individuals hyperabsorb not only cholesterol but also all other sterols, including plant and shellfish sterols from the intestine. The major plant sterol species is sitosterol; hence the name of the disorder. Consequently, patients with this disease have very high levels of plant sterols in the plasma and develop tendon and tuberous xanthomas, accelerated atherosclerosis, and premature coronary artery disease. We previously mapped the STSL locus to human chromosome 2p21 and further localized it to a region of less than 2 cM bounded by markers D2S2294 and D2S2291 (M.-H.L. et al., manuscript submitted). We now report that a new member of the ABC transporter family, ABCG5, is mutant in nine unrelated sitosterolemia patients.
Sitosterolaemia (phytosterolaemia) is an autosomal recessive disorder characterised by the presence of tendon xanthomas in the face of normal or mildly elevated plasma cholesterol levels, premature atherosclerotic disease and has diagnostically elevated plasma and tissue plant sterol concentrations. Affected individuals show an increased absorption of both cholesterol and sitosterol from the diet, decreased bile clearance of these sterols and their metabolites resulting in markedly expanded whole body cholesterol and sitosterol pools. The defective gene is therefore hypothesised to play a crucial role in regulating dietary cholesterol absorption, and its elucidation may shed light on these molecular processes. We have previously localised the defective gene to human chromosome 2p21, between microsatellite markers D2S1788 and D2S1352, a distance of approximately 15 cM. Recently, the disease locus interval has been narrowed to lie between D2S2294 and D2S2291/D2S2174. We have constructed a high-resolution YAC and BAC contigs by using known STSs and generating novel STSs from the minimal interval. Eight previously identified genes and 60 ESTs were mapped to these contigs. The BAC contig contains 60 BAC clones and 108 STSs and encompasses a physical distance of approximately 2.0 cM between microsatellite markers D2S2294 and D2S2291. These results will not only facilitate cloning of the sitosterolaemia gene, but also other disease genes located in this region, and accelerate sequencing of the corresponding genomic clones.
Sitosterolaemia (also known as phytosterolaemia, MIM 210250) is a rare recessive autosomal inherited disorder, characterised by the presence of tendon and tuberous xanthomas, accelerated atherosclerosis and premature coronary artery disease. The defective gene is hypothesised to play an important role in regulating dietary sterol absorption and biliary secretion, thus defining a molecular mechanism whereby this physiological process is carried out. The disease locus was localised previously to chromosome 2p21, in a 15 cM interval between microsatellite markers D2S1788 and D2S1352 (based upon 10 families, maximum lodscore 4.49). In this study, we have extended these studies to include 30 families assembled from around the world. A maximum multipoint lodscore of 11.49 was obtained for marker D2S2998. Homozygosity and haplotype sharing was identified in probands from non-consanguineous marriages from a number of families, strongly supporting the existence of a founder effect among various populations. Additionally, based upon both genealogies, as well as genotyping, two Amish/Mennonite families, that were previously thought not to be related, appear to indicate a founder effect in this population as well. Using both homozygosity mapping, as well as informative recombination events, the sitosterolaemia gene is located at a region defined by markers D2S2294 and Afm210xe9, a distance of less than 2 cM.
OBJECTIVE: Ischemic preconditioning combined with potassium cardioplegia does not always confer additive myocardial protection. This study tested the hypothesis that the efficacy of ischemic preconditioning under potassium cardioplegia is dependent on protein kinase C isoform. METHODS: Isolated and crystalloid-perfused rat hearts underwent 5 cycles of 1 minute of ischemia and 5 minutes of reperfusion (low-grade ischemic preconditioning) or 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion (high-grade ischemic preconditioning) or time-matched continuous perfusion. These hearts received a further 5 minutes of infusion of normal buffer or oxygenated potassium cardioplegic solution. The isoform nonselective protein kinase C inhibitor chelerythrine (5 micromol/L) was administered throughout the preischemic period. All hearts underwent 35 minutes of normothermic global ischemia followed by 30 minutes of reperfusion. Isovolumic left ventricular function and creatine kinase release were measured as the end points of myocardial protection. Distribution of protein kinase C alpha, delta, and epsilon in the cytosol and the membrane fractions were analyzed by Western blotting and quantified by a densitometric assay. RESULTS: Low-grade ischemic preconditioning was almost as beneficial as potassium cardioplegia in improving functional recovery; left ventricular developed pressure 30 minutes after reperfusion was 70 +/- 15 mm Hg (P <.01) in low-grade ischemic preconditioning and 77 +/- 14 mm Hg (P <.001) in potassium cardioplegia compared with values found in unprotected control hearts (39 +/- 12 mm Hg). Creatine kinase release during reperfusion was also equally inhibited by low-grade ischemic preconditioning (18.2 +/- 10.6 IU/g dry weight, P <.05) and potassium cardioplegia (17.6 +/- 6.7 IU/g, P <.01) compared with control values. However, low-grade ischemic preconditioning in combination with potassium cardioplegia conferred no significant additional myocardial protection; left ventricular developed pressure was 80 +/- 17 mm Hg, and creatine kinase release was 14.8 +/- 11.0 IU/g. In contrast, high-grade ischemic preconditioning with potassium cardioplegia conferred better myocardial protection than potassium cardioplegia alone; left ventricular developed pressure was 121 +/- 16 mm Hg (P <.001), and creatine kinase release was 8.3 +/- 5.8 IU/g (P <.05). Chelerythrine itself had no significant effect on functional recovery and creatine kinase release in the control hearts, but it did inhibit the salutary effects not only of low-grade and high-grade ischemic preconditioning but also those of potassium cardioplegia. Low-grade ischemic preconditioning and potassium cardioplegia enhanced translocation of protein kinase C alpha to the membrane, whereas high-grade ischemic preconditioning also enhanced translocation of protein kinase C delta and epsilon. Chelerythrine inhibited translocation of all 3 protein kinase C isoforms. CONCLUSIONS: These results suggest that myocardial protection by low-grade ischemic preconditioning and potassium cardioplegia are mediated through enhanced translocation of protein kinase C alpha to the membrane. It is therefore suggested that activation of the novel protein kinase C isoforms is necessary to potentiate myocardial protection under potassium cardioplegia.
The molecular mechanisms regulating the amount of dietary cholesterol retained by the body, as well as the body's ability to exclude other dietary sterols selectively, are poorly understood. An average Western diet will contain approximately 250-500 mg of dietary cholesterol and approximately 200-400 mg of non-cholesterol sterols, of which plant sterols are the major constituents. Approximately 50-60% of dietary cholesterol is absorbed and retained by the normal human body, but less than 1% of the non-cholesterol sterols are retained. There thus exists a subtle mechanism that allows the body to distinguish between cholesterol and non-cholesterol sterols. In sitosterolemia, a rare autosomal recessive disorder, affected individuals hyperabsorb and retain not only cholesterol but also all other sterols, including plant and shellfish sterols from the intestine. Consequently, patients with this disease have very high levels of plant sterols in the plasma, and develop tendon and tuberous xanthomas, accelerated atherosclerosis, and premature coronary artery disease. The STSL locus has been mapped to human chromosome 2p21. Mutations in two tandem ABC genes, ABCG5 and ABCG8, encoding sterolin-1 and -2, respectively, are now known to be mutant in sitosterolemia. The identification of these genes should now lead to a better understanding of the molecular mechanism(s) governing the highly selective absorption and retention of cholesterol by the body. Indeed, it is the very existence of this disease that has given credence to the hypothesis that there is a molecular pathway that regulates dietary cholesterol absorption and sterol excretion by the body.
We propose a method to estimate the regression coefficients in a competing risks model where the cause-specific hazard for the cause of interest is related to covariates through a proportional hazards relationship and when cause of failure is missing for some individuals. We use multiple imputation procedures to impute missing cause of failure, where the probability that a missing cause is the cause of interest may depend on auxiliary covariates, and combine the maximum partial likelihood estimators computed from several imputed data sets into an estimator that is consistent and asymptotically normal. A consistent estimator for the asymptotic variance is also derived. Simulation results suggest the relevance of the theory in finite samples. Results are also illustrated with data from a breast cancer study.
Previous models combining the human cardiovascular and pulmonary systems have not addressed their strong dynamic interaction. They are primarily cardiovascular or pulmonary in their orientation and do not permit a full exploration of how the combined cardiopulmonary system responds to large amplitude forcing (e.g., by the Valsalva maneuver). To address this issue, we developed a new model that represents the important components of the cardiopulmonary system and their coupled interaction. Included in the model are descriptions of atrial and ventricular mechanics, hemodynamics of the systemic and pulmonic circulations, baroreflex control of arterial pressure, airway and lung mechanics, and gas transport at the alveolar-capillary membrane. Parameters of this combined model were adjusted to fit nominal data, yielding accurate and realistic pressure, volume, and flow waveforms. With the same set of parameters, the nominal model predicted the hemodynamic responses to the markedly increased intrathoracic (pleural) pressures during the Valsalva maneuver. In summary, this model accurately represents the cardiopulmonary system and can explain how the heart, lung, and autonomic tone interact during the Valsalva maneuver. It is likely that with further refinement it could describe various physiological states and help investigators to better understand the biophysics of cardiopulmonary disease.
OBJECT: Transthoracic endoscopic T2-3 sympathectomy is currently the treatment of choice for palmar hyperhidrosis. Compensatory sweating of the face, trunk, thigh, and sole of the foot was found in more than 50% of patients who underwent this procedure. The authors conducted this study to investigate the associated intraoperative changes in plantar skin temperature and postoperative plantar sweating. METHODS: One hundred patients with palmar hyperhidrosis underwent bilateral transthoracic endoscopic T2-3 sympathectomy. There were 60 female and 40 male patients who ranged in age from 13 to 40 years (mean age 21.6 years). Characteristics studied included changes in palmar and plantar skin temperature measured intraoperatively, as well as pre- and postoperative changes in plantar sweating and sympathetic skin responses (SSRs). In 59 patients (59%) elevation of plantar temperature was demonstrated at the end of the surgical procedure. In this group, plantar sweating was found to be exacerbated in three patients (5%); plantar sweating was improved in 52 patients (88.1%); and no change was demonstrated in four patients (6.8%). In the other group of patients in whom no temperature change occurred, increased plantar sweating was demonstrated in three patients (7.3%); plantar sweating was improved in 20 patients (48.8%); and no change was shown in 18 patients (43.9%). The difference between temperature and sweating change was significant (p = 0.001). Compared with the presympathectomy rate, the rate of absent SSR also significantly increased after sympathectomy: from 20 to 76% after electrical stimulation and 36 to 64% after deep inspiration stimulation, respectively (p < 0.05). CONCLUSIONS: In contrast to compensatory sweating in other parts of the body after T2-3 sympathetomy, improvement: in plantar sweating was shown in 72% and worsened symptoms in 6% of patients. The intraoperative plantar skin temperature change and perioperative SSR demonstrated a correlation between these changes.
The authors describe a patient with ossiculum terminale. Thin-section three-dimensional computerized tomography reconstructions, magnetic resonance images, and radiographs of the cervical spine were obtained to evaluate the atlantoaxial stability and structures of the ossiculum terminale. Bone had formed between the ossicles and the body of the odontoid process, and good atlantoaxial stability was clearly demonstrated.
Gliomatosis cerebri (GC) is a rare disease loosely defined as a diffusely infiltrating glioma involving extensive areas of the brain. The prognosis is poor and no definite treatment has proven effective for GC. Little information exists regarding the role of radiation therapy (RT) for GC, but some researchers have suggested that it is a good choice of treatment from their limited experience. In this report, we present a case with imaging and histological diagnosis of GC and demonstrate the treatment results of RT. The patient was a 39-year-old woman with progressive symptoms of dizziness, unsteady gait, headache, vomiting, and consciousness disturbance for 6 months. She received a series of radiographic examinations and surgical interventions for diagnosis. The definite diagnosis of GC was made by a combination of magnetic resonance imaging (MRI) findings and histological examinations. Forty Gray (Gy) of whole brain irradiation followed by 14 Gy reduced-field boosts were given to her. The MRI, following treatment, showed regressive changes, and clinical symptoms were slightly improved. The patient survived 19 months after the diagnosis, which is longer than the average survival time of patients without treatment.
BACKGROUND: Telomerase activity and telomere length have been shown to be involved in controlling cell proliferation and regulating cell senescence. The authors examined telomerase activity and telomere length in intracranial tumors to determine the clinicopathological behavior of primary intracranial tumors with respect to telomerase expression and alteration of telomere length. METHODS: Telomerase activity was examined in 139 brain tumor samples. Telomere length was examined in 138 of the 139 samples. These tumors included 61 meningiomas, 27 schwannomas, 19 high-grade neuroepithelial tumors, and 32 low-grade neuroepithelial tumors. Telomerase activity was measured with a telomerase polymerase chain reaction, enzyme-linked immunosolvent assay kit. Telomere length was examined by Southern blot analysis for the terminal restriction fragment length. RESULTS: Telomerase activity was detected in 39.2% (20/51) of the neuroepithelial tumors. Detection rates were 47.4% (9/19) for anaplastic astrocytomas and glioblastomas and 34.4% (11/32) for low-grade neuroepithelial tumors. However, detectable telomerase activity was found in 30.8% (4/13) of atypical or malignant meningiomas, but was not detected in any schwannomas. There was a highly significant difference in the telomerase detection rate in neuroepithelial or non-neuroepithelial tumors (p = 0.001). Telomere elongation was found in 11.7% (7/60) of all meningiomas, 46.1% (6/13) of atypical or malignant meningiomas, and 14.8% (4/27) of schwannomas. Elongation of telomere length was detected in 12.6% (11/87) of the cases and 23.5% (12/51) in neuroepithelial tumors. This difference was also significant (p < 0.05). Telomere length was reduced in the majority, (75%, 3/4) of malignant or atypical meningiomas with detectable telomerase activity, but only 45% (9/20) of the neuroepithelial tumors. CONCLUSION: These results indicate that telomerase activation may be a critical step in the pathogenesis of intracranial tumors. Telomere length elongation also indicates a high potential for malignant behavior in these tumors.
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OBJECTIVE: To study the mechanism of calcium channel antagonist Verapamil on the treatment of hypertrophic scar and explore the possibility of further clinical application. METHODS: After six strains of HSFB were cultured in vitro, we investigated HSFB proliferation by MTT method, investigated HSFB collagen synthesis by 3H-proline uptaken and Hydroxyproline colorimetric analysis, and investigated collagen gene expression by Northern Blot. RESULTS: Verapamil can inhibit HSFB proliferation, collagen synthesis and gene expression by a dose-depended manner, especially treated with 100 mumol/L Verapamil. CONCLUSION: By inhibiting I, III procollagen gene expression, Verapamil can inhibit the formation of hypertrophic scar.