[Characteristics and risk factors of spinal epidural hematoma after unilateral biportal endoscopic lumbar interbody fusion].

Objective: To investigate the incidence, characteristics and risk factors of spinal epidural hematoma after unilateral biportal endoscopic (UBE) lumbar spine surgery. Methods: The clinical data of 105 patients who underwent lumbar spine surgery under UBE in Guangdong Provincial People's Hospital from February 2020 to March 2021 were retrospectively reviewed. Of the patients, 48(45.7%) were male and 57(54.3%) were female, the mean age was (60.1±11.4) years (ranged 26 to 85 years). The MRI images at the third day post-surgery were observed, and the occurrence of hematoma was counted. Patients were assigned to normal group and hematoma group based on the presence of hematoma or not. The related clinical indicators of each patients were collected and used for comparison between two different groups. Logistic stepwise regression model was used to analyze whether each index was a risk factor for hematoma after the UBE lumbar fusion. Results: The total hematoma incidence rate was 28.6%(30/105), the symptomatic hematoma rate was 6.7%(7/105), and the hematoma reoperation rate was 0.9%(1/105). Univariate logistic regression analysis showed that hypertension (OR=3.368, 95%CI: 1.389-8.171), diabetes (OR=3.589, 95%CI: 1.230-10.476), admission systolic blood pressure>140 mmHg (1 mmHg=0.133 kPa,OR=3.687, 95%CI: 1.493-9.017), platelets<200×109/L (OR=0.300, 95%CI: 0.119-0.785), preoperative blood calcium<2.25 mmol/L (OR=0.340, 95%CI: 0.142-0.818), spinal stenosis grade D (OR=4.462, 95%CI: 1.810-10.996) were possible risk factors for spinal hematoma after UBE lumbar fusion. Multivariate logistic regression analysis showed that admission blood pressure systolic blood pressure>140 mmHg (OR=3.788, 95%CI:1.055-13.606), preoperative blood calcium<2.25 mmol/L (OR=78.544, 95%CI:3.895-1 584.058) and spinal stenosis grade D (OR=3.698, 95%CI:1.110-12.325) were risk factors for spinal hematoma after UBE lumbar fusion (all P<0.05). Conclusion: The types of spinal canal hematoma after UBE lumbar fusion include localized and extended type. The risk factors for hematoma include high systolic blood pressure on admission, low preoperative blood calcium and severe spinal stenosis.

A strong association between thyrotropin receptor-blocking antibody-positive atrophic autoimmune thyroiditis and HLA-DR8 and HLA-DQB1*0302 in Koreans.

We investigated whether the associations between HLA alleles of patients with autoimmune hypothyroidism varied according to the presence or absence of TSH receptor-blocking antibody (TRBab). We analyzed the HLA-A, -B, -C, and -DR antigens by serotyping and the DQA1 and DQB1 genes using both enzymatic DNA amplification and sequence-specific oligonucleotide hybridizations. The patient population consisted of 47 Korean patients with atrophic autoimmune thyroiditis and 62 patients with goitrous autoimmune thyroiditis. The antigen frequency of HLA-DR8 was significantly increased in 23 atrophic autoimmune thyroiditis patients that were positive for TSH binding inhibitor immunoglobulin (TBII) compared to 136 controls [52% vs. 16%; chi 2 = 13.1; Pc (corrected P value) = 0.003]. This relative risk was 5.7; the etiological fraction was 0.43. HLA-DQB1*0302 was also increased in patients with TBII-positive atrophic autoimmune thyroiditis (24% vs. 7%; chi 2 = 11.2; Pc = 0.012; relative risk = 4.4; etiological fraction = 0.19). No specific DR antigens or DQB1 alleles were increased in either TBII-negative atrophic autoimmune thyroiditis or goitrous autoimmune thyroiditis. A significant decrease in the frequency of HLA-DR6 antigen was observed in both TBII-positive atrophic autoimmune thyroiditis (0% vs. 32%; chi 2 = 8.4; Pc = 0.03) and goitrous autoimmune thyroiditis (0% vs. 32%; chi 2 = 23.2; Pc < 0.001) patients. The frequency of the HLA-Cw1 antigen was significantly increased in all patient groups. We conclude that TRBab-positive atrophic autoimmune thyroiditis is immunogenetically different from both goitrous autoimmune thyroiditis and TRBab-negative atrophic autoimmune thyroiditis. It is possible that HLA-DR8 and/or DQB1*0302 may be related to the susceptibility genes involved in the production of TRBab in Koreans.

Human histocompatibility leukocyte antigen-DQA1*0501 allele associated with genetic susceptibility to Graves' disease in a Caucasian population.

Graves' disease (GD) is an autoimmune disease of the thyroid gland. Genes of, or closely associated to, the HLA complex are assumed to contribute to the genetic predisposition to GD. We have previously reported an increased frequency of HLA-DR3/DQ2 in Caucasian patients with GD, and recently the importance of Dw24 encoded by DRB3 gene has been suggested. To further investigate the associations of GD and these genes, 94 unrelated patients with GD and 75 control subjects were typed for HLA-DRB3, -DRB1, -DQA1, and -DQB1, using sequence-specific oligonucleotide probes to analyze polymerase chain reaction amplified DNA (PCR-SSO). Three findings emerged from these studies. 1) The frequency of subjects positive for DQA1*0501 (GD, 73.4% vs. control 42.7%, P = 0.0001, Pc < 0.001, RR = 3.71) was significantly increased among patients. The frequency of DR3 (GD, 34.0% vs. control 17.3%, P = 0.0146, RR = 2.46), which is in tight linkage disequilibrium with DQA1*0501, was also increased; however, it was not significant when the P value was corrected for the number of antigens tested. Neither DQB1 nor DRB3 alleles were significantly increased in frequency. 2) After exclusion of DR3-positive subjects, DQA1*0501 was still significantly increased (GD, 59.7% vs. control 30.6%, P = 0.0012, Pc < 0.01, RR = 3.35) among patients. 3) The distributions of Dw24 and Dw25,26 (Dw25 or Dw26) did not differ between patients and controls on either DR3 positive or negative groups. These findings suggest that DQA1*0501, or a closely associated unknown gene, confers susceptibility to GD, while Dw24 is not directly involved. The importance of DR3, however, remains to be elucidated, because of the fixed linkage with DQA1*0501.

HLA class II genes in Graves' disease.

Inheritance of Graves' disease has been linked to the HA-DR3 gene product which may function in some specific way in antigen presentation. To determine whether the first extracellular domain of this protein, which is specifically involved in antigen presentation, has the same sequence in patients with Graves' disease and in normal individuals, we have amplified the second exon using the polymerase chain reaction, and then cloned and sequenced the DNA segment. In eight subjects with Graves' disease, sequences identical to prototypic reported sequence for DRB1*0301 were recovered, and in two individuals sequences varied by a few nucleotides, leading to 1-3 amino acid substitutions which did not occur in a pattern. Sequences identical to the prototypic sequence known as DRB3*0101, also previously known as DRw52, were also recovered. Thus the HLA-DRB1 and B3 genes present in patients with autoimmune disease appear to be the same as those present in the general population. These observations indicate that a unique allele is not present in patients with autoimmune disease, but rather that the normal DR3 allele itself, in a manner yet to be described, increases the probability of developing autoimmune thyroid disease.

Sources of pancreatic pathogens in acute pancreatitis in cats.

The source(s) of pancreatic pathogens is uncertain, although the colon is usually implicated. We studied whether pathogens may spread from different sites in a feline model of the disease. Acute pancreatitis was induced using a standard technique and a distinctive clinical strain of Escherichia coli as the marker bacterium. E. coli were placed in the colon, gall bladder, main pancreatic duct, or obstructed renal pelvis of control cats (no pancreatitis) and acute pancreatitis cats. Pancreases were colonized from each source, whether or not pancreatitis was present. The pancreatic colonization rate was greater in acute pancreatitis only when E. coli had been placed in the colon. In conclusion, E. coli may spread to the pancreas from different sources. The high rate of pancreatic colonization in both control and inflamed glands suggested that, clinically, bacteria may spread to the pancreas more frequently than is currently thought.

Pituitary atrophy in Korean (epidemic) hemorrhagic fever: CT correlation with pituitary function and visual field.

Eleven patients with Korean (epidemic) hemorrhagic fever were each studied three times with high-resolution CT in order to demonstrate necrosis of the pituitary gland and to correlate the CT findings with the patients' pituitary function and visual fields. Seven of the 11 patients showed varying degrees of progressive decrease in the height of the pituitary gland: one severe, two moderate, and four mild. The visual fields of all the patients were checked at the time of the third (last) follow-up CT. Six of the 11 patients had bitemporal superior quadrantanopsia. In five patients, the decreased height (atrophic change) of the pituitary gland and the visual-field defect were coincidental. The visual-field defects in those patients were not improved on follow-up examination 5 weeks later. Two patients in whom a 1-year follow-up examination was performed showed no interval changes in the defects. Pituitary function tests were performed in nine of the 11 patients (six with atrophic pituitary glands and three without atrophic changes) at the time of the third CT. Five of the six patients with atrophy showed decreased pituitary reserve function for follicle-stimulating hormone, cortisol, or human growth hormone, while only one patient showed decreased reserve function for cortisol among the three patients without atrophic change. The pituitary atrophic changes observed on follow-up sellar CT are thought to be the result of the ischemic necrosis of the gland. The high probability (five of seven) of visual-field defects in those patients with atrophic glands suggests optochiasmatic and pituitary ischemia as the basic pathogenesis.

Magnetic resonance imaging of human melanoma xenografts in vivo: proton spin-lattice and spin-spin relaxation times versus fractional tumour water content and fraction of necrotic tumour tissue.

Proton nuclear magnetic resonance (1H-nmr) imaging is used routinely in clinical oncology to provide macroscopic anatomical information, whereas its potential to provide physiological information about tumours is not well explored. To evaluate the potential usefulness of 1H-nmr imaging in the prediction of tumour treatment resistance caused by unfavourable microenvironmental conditions, possible correlations between proton spin-lattice and spin-spin relaxation times (T1 and T2) and physiological parameters of the tumour microenvironment were investigated. Tumours from six human melanoma xenograft lines were included in the study. 1H-nmr imaging was performed at 1.5 T using spin-echo pulse sequences. T1- and T2-distributions were generated from the images. Fractional tumour water content and the fraction of necrotic tumour tissue were measured immediately after 1H-nmr imaging. Significant correlations across tumour lines were found for T1 and T2 versus fractional tumour water content (p < 0.001) as well as for T1 and T2 versus fraction of necrotic tumour tissue (p < 0.05). Tumours with high fractional water contents had high values of T1 and T2, probably caused by free water in the tumour interstitium. Fractional water content is correlated to interstitial fluid pressure in tumours, high interstitial fluid pressure being indicative of high vascular resistance. Tumours with high fractional water contents are thus expected to show regions with radiobiologically hypoxic cells as well as poor intravascular and interstitial transport of many therapeutic agents. T1 and T2 decreased with increasing fraction of necrotic tumour tissue, perhaps because complexed paramagnetic ions were released during development of necrosis. Viable tumour cells adjacent to necrotic regions are usually chronically hypoxic. Tumours with high fractions of necrotic tissue are thus expected to contain significant proportions of radiobiologically hypoxic cells. Consequently, quantitative 1H-nmr imaging has the potential to be developed as an efficient clinical tool in prediction of tumour treatment resistance caused by hypoxia and/or transport barriers for therapeutic agents. However, much work remains to be done before this potential can be adequately evaluated. One problem is that high fractional tumour water contents result in longer T1 and T2 whereas high fractions of necrotic tumour tissue result in shorter T1 and T2; i.e. the two parameters which are indicative of treatment resistance contribute in opposite directions. Another problem is that the correlations for T1 and T2 versus fraction of necrotic tumour tissue are not particularly strong.

The interference effects of hexadecylphosphocholine on proliferation and membrane phospholipid metabolism in human myeloid leukemia cell lines.

Membrane phospholipids are important regulators of cellular function. The phospholipid activities, such as lipid composition and transportation, contribute to cellular homeostasis in the lifespan of cells. Alterations in phospholipids result in the movement of bilayer lipids and the initiation of coagulation, recognition and internalization. Hexadecylphosphocholine (HePC) exerts antitumor potencies and represents a new class of antitumor agents targeted to the cellular membrane. Human myeloid leukemia cell lines HL-60 and K562 employed in this study were inhibited by HePC in vitro. The results indicate that the HL-60 cell line was sensitive, while K562 was resistant to HePC. Synthetic HePC is an alkyllysophospholipid analog which interacted with the cell membrane, thereby altering lipid composition and metabolism of membrane phospholipids and modulating intracellular calcium in human myeloid leukemia HL-60 and K562 cell lines. The contents of membrane phospholipids, including phosphatidylinositol (PI), phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE), were determined quantitatively with high performance liquid chromatography. The sensitivity of myeloid leukemia HL-60 and K562 cell lines to HePC probably depends on the different distribution of these four phospholipids in the cellular membrane, or on the response of these phospholipids to HePC. The cytosolic free calcium ([Ca++]i) concentration increased by HePC confirmed that [Ca++]i was released from the intracellular calcium pool and is associated with cell differentiation and apoptosis. We investigated the hypothesis that the antiproliferative effect of HePC was mediated through the interference with cellular membrane phospholipids, including choline-containing phospholipids (PC), aminophospholipids (PE and PS) and PI, in eukaryotic cells.

Low dose dopamine protects against hemorrhagic pancreatitis in cats.

Acute hemorrhagic pancreatitis (HP) is probably associated with decreased blood flow in its early phases, as well as with an increase in microvascular permeability. Dopamine (DOP; 5 micrograms/kg-min) is a splanchnic vasodilator, and also has beta-adrenergic effects that can prevent increases in microvascular permeability. We hypothesized that low dose dopamine might have beneficial effects on both blood flow and microvascular permeability, thus ameliorating the severity of the disease. We studied its actions in an animal model of HP. In anesthetized cats, intragastric ethanol (20 ml/40% solution) rendered the main pancreatic duct permeable to pancreatic enzymes. Then the duct was perfused from tail to head with 0.5 ml of activated pancreatic enzymes for 1 hr. To create HP, 16,16-dimethyl prostaglandin E2 (2 micrograms/kg-hr, iv) was given for 2 hr to increase blood flow and microvascular permeability. Seven of eight cats developed HP in 24 hr. Control cats received no additional drugs. Two experimental groups received DOP (6 hr infusion) begun either (1) at the onset of enzyme perfusion or (2) 12 hr later. Each pancreas was examined after 24 hr and graded (1-4) histologically for edema, hemorrhage, polymorphonuclear cell infiltrate, and architectural loss. An inflammatory score (IS) from 0 to 16 was thus created (higher scores = greater damage). The results showed an IS of 10.9 +/- 1.8 for the controls, 3.3 +/- 0.5 for the immediate treatment group, and 7.2 +/- 1.8 for the delayed treatment group. Both treated groups had a significantly better IS (t tests, P less than 0.001 and P less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The antiinflammatory effect of dopamine in alcoholic hemorrhagic pancreatitis in cats. Studies on the receptors and mechanisms of action.

Hemorrhagic pancreatitis was induced in cats by perfusing pancreatic enzymes through a pancreatic duct after the administration of intragastric ethanol. Dimethyl prostaglandin E2 was administered concurrently. In the first study, dopamine's antiinflammatory effect on the pancreas was determined in the presence of haloperidol, propranolol, or both. Next, dopamine's effects on blood flow in the normal and inflamed pancreas were compared using a hydrogen gas-clearance technique. In the final study, the effect of dopamine on fluorescein isothiocyanate-labeled dextran leakage from the pancreatic duct to portal venous blood was investigated. It was found that blockade of either dopamine or beta-adrenergic receptors reduced, and blockade of both receptors completely eliminated, the antiinflammatory effect. Dopamine had no effect on pancreatic blood flow in normal cats. In pancreatitis, although dopamine transiently reduced blood flow, after an hour flow had returned to normal. Dopamine reversed the leakage of fluorescein isothiocyanate-labeled dextran from the pancreatic duct caused by ethanol and by ethanol and prostaglandin E2. It was concluded that dopamine ameliorated pancreatitis by reducing pancreatic ductal and/or microvascular permeability rather than by altering pancreatic blood flow. The antiinflammatory effect was mediated by both dopamine and beta-adrenergic receptors.