Accuracy and reliability of continuous blood glucose monitor in post-surgical patients

Background: The STG-22^™ is the only continuous blood glucose monitoring system currently available. The aim of this study is to determine the accuracy and reliability of the STG-22^™ for continuously monitoring blood glucose level in post-surgical patients.
Methods: Fifty patients scheduled for routine surgery were studied in surgical intensive care unit (ICU) of a university hospital. After admission to the ICU, the STG-22^™ was connected to the patients. An attending physician obtained blood samples from a radial arterial catheter. Blood glucose level was measured using the ABL^™800FLEX immediately after blood collection at 0, 4, 8, and 16 h post-admission to the ICU (total of 200 blood glucose values).
Results: The correlation coefficient ( R ²) was 0.96. In the Clarke error grid, 100% of the paired measurements were in the clinically acceptable zone A and B. The Bland and Altman analysis showed that bias±limits of agreement (percent error) were 0.04(0.7)±0.35(6.3) mmol (mg/dl) (7%), −0.11(−2)±1.22(22) (15%) and −0.33(−6)±1.28(23) (10%) in hypoglycemia (<70(3.89) mmol (mg/dl), normoglycemia (3.89(70)–10(180) mmol (mg/dl), and hyperglycemia (>10(180) mmol (mg/dl), respectively.
Conclusions: The STG-22^™ can be used for measuring blood glucose level continuously and measurement results are consistent with intermittent measurement (percentage error within 15%). Therefore, the STG-22^™ is a useful device for monitoring in blood glucose level in the ICU for 16 h.     

散发性阿尔茨海默病早老素2 基因的新突变

 目的检测早老素2（PSEN2）基因的外显子序列,探索基因外显子可能的突变与散发性阿尔茨海默病（SAD）发
病的相关性。方法所有被试者均来自日本人群。选择300 例符合NINCDS-ADRDA诊断标准的无阳性家族史的SAD 患者,其
中男120 例,女180 例,平均年龄（72.57±7.56）岁。选择与患者组年龄、性别相匹配的正常对照300 例,其中男120 例,女180 例,
平均年龄（70.97±6.73）岁。从被试者外周血中提取基因组DNA,采用聚合酶链式反应、DNA测序方法,进行基因外显子
序列测定。结果PSEN2基因外显子3上发现100G>A（G34S）的突变, 基因外显子4 上发现1915C>T（87H）的突变。结
论此次发现的2个基因突变均位于PSEN2 蛋白非功能区N 端片段,可能与SAD发病无关。     

Severe neurological abnormalities associated with a mutation in the zinc-finger domain in a group A xeroderma pigmentosum patient

All the reported Japanese patients with group A xeroderma pigmentosum (XP) have two or three mutations at codon 116 in exon 3, codon 228 in exon 6, and the splicing acceptor site of intron 3 of XP group A complementing (XPAC) gene. A homozygote (XP390S) with a nonsense mutation at codon 228 has less severe neurological abnormalities than patients with the splicing mutation at the acceptor site of intron 3. As homozygotes for the nonsense mutation at codon 116, which truncates a carboxyl-terminal site of XPAC protein at an early part of its zinc-finger domain, have not been reported previously, the possible severity of associated neurological abnormalities was not known. We report a group A XP patient, XP180S, who had neurological abnormalities which were more severe than those in patients homozygous for the splicing mutation. The polymerase chain reaction product from exon 3 of the patient's XPAC gene was digested completely into three fragments by MseI restriction endonuclease. Thus, the patient was homozygous for the mutation at codon 116.     

Circumscribed myxoedema of lichen myxoedematosus as a sign of faulty formation of the proteoglycan macromolecule

Using a new method devised by our laboratory, the ultrastructure of dermal glycosaminoglycan in an involved area of lichen myxoedematosus was examined. Although histochemical and biochemical studies have indicated simply an accumulated deposition of hyaluronic acid in the lesion, the glycosaminoglycan ultrastructure within it was distinaly different from that in normal skin. The glycosaminoglycan structure of normal skin was similar to the proteoglycan aggregate model described by Rosenberg (1975). As confirmed by the enzymatic digestion procedure, it represents the ultrastructure of hyaluronic acid bound to glycosaminoglycans such as dermatan sulphate or chondroitin sulphate. In contrast, hyaluronic acid filaments observed in lesions of lichen myxoedematosus contained no glycosaminoglycan subunits.     

Elevated tissue factor expression contributes to exacerbated diabetic nephropathy in mice lacking eNOS fed a high fat diet

Summary. Background: Human eNOS (NOS3) polymorphisms that lower its expression are associated with advanced diabetic nephropathy (DN), and the lack of eNOS accelerates DN in diabetic mice. Diabetes is associated with fibrin deposition. Lack of nitric oxide and fatty acids stimulates the NF‐kB pathway, which increases tissue factor (TF). Objectives: To test the hypothesis that TF contributes to the severity of DN in the diabetic eNOS^?/? mice fed a high‐fat diet (HF). Methods: We made eNOS^?/? and wild‐type mice diabetic with streptozotocin. Half of them were placed on HF. Results: Blood glucose levels were not affected by either the diet or eNOS genotype. Lack of eNOS in the diabetic mice increased urinary albumin excretion, glomerulosclerosis, interstitial fibrosis, and glomerular basement membrane thickness. HF by itself did not affect DN in the wild‐type mice, but significantly enhanced DN in eNOS^?/? mice. More than half of diabetic eNOS^?/? mice on HF died prematurely with signs of thrombotic complications. Diabetic kidneys contained fibrin and TF, and their levels were increased by the lack of eNOS and by HF in an additive fashion. The HF diet increased the kidney expression of inflammatory genes. The increase in TF preceded DN, and administration of an anti‐mouse TF antibody to diabetic mice reduced the expression of inflammatory genes. Conclusion: Together, these data indicate a causal link between TF and the exacerbation of DN in eNOS^?/? mice. The condition is significantly worsened by enhanced inflammatory responses to an HF diet via TF.     

Treatment with a novel lipid A analogue, FS-112, and partial hepatectomy causes submassive liver necrosis and impaired liver regeneration in mice

A novel experimental model of submassive liver necrosis with impaired regeneration has been established. A novel lipid A analogue, FS-112, was injected intravenously into male BALB/c mice, followed 2 days later by a 70% partial hepatectomy. Over the next 9 days, mice became severely jaundiced, with a peak total bilirubin (TBil) concentration of (mean±s.d.) 12.9±2.1 mg/dL 7 days postoperatively. In contrast, the TBil concentration in vehicle-treated mice remained less than 2 mg/dL. Significant elevations of L-alanine:2-oxoglutarate aminotransferase (ALT) were also observed 3–7 days after the operation in mice pretreated with FS-112, compared with mice pretreated with the vehicle. Submassive liver necrosis was observed with extensive mononuclear cell infiltration in mice treated with FS-112 and subjected to partial hepatectomy. Furthermore, both the BrdU and the proliferating cell nuclear antigen (PCNA) labelling index (LI) 1 day following partial hepatectomy in mice pretreated with FS-112 (8.6±4.3 and 7.9±4.2%, respectively) were significantly lower than levels in vehicletreated mice (25.8±3.8 and 26.5±10.5%, respectively). The time course of changes in the BrdU LI in liver specimens from mice treated with both FS-112 and partial hepatectomy did not increase, even 3, 5, and 7 days postoperatively. Excellent liver regeneration with a PCNA LI 10-fold higher than the resting level was observed in mice treated with D-galactosamine hydrochloride. These results strongly suggest that this animal model of submassive liver necrosis may be suitable for clarifying the mechanisms of impaired liver cell regeneration often seen in fulminant hepatitis.     

Tissue characterization of uterine myometrium using the ultrasound gray-level histogram width

Purpose The purpose of this study was to clarify the usefulness of the gray-level histogram width for tissue characterization of the uterine myometrium. Methods Thirty-five patients with uterine fibroids, 5 patients with adenomyosis, and 9 patients with extensive myometrial invasion by endometrial carcinoma were studied. The gray-level histogram width was determined by transvaginal ultrasonography. The Mann–Whitney U test was used for statistical analysis. Receiver operating characteristic curves were generated for use in tissue characterization. Results Significant differences in the gray-level histogram width were found between normal myometrium (54.2% ± 4.2%) and carcinoma (58.2% ± 3.9%), normal myometrium and fibroid (64.3% ± 5.2%), and carcinoma and fibroid. However, it was difficult to identify adenomyosis. The cutoff values to distinguish normal myometrium from carcinoma, normal myometrium from fibroid, and carcinoma from fibroid are 56, 58, and 64, respectively. Conclusion The gray-level histogram width is useful for tissue characterization of the uterine myometrium.     

Epidemiological and clinical features of idiopathic pulmonary alveolar proteinosis in Japan

Abstract:   Idiopathic pulmonary alveolar proteinosis (IPAP) is a rare disease characterized by excessive amounts of lipoproteinaceous material in the alveolus. This report presents an interim analysis of nationwide epidemiological data from Japanese patients with pulmonary alveolar proteinosis, and the roles of serum markers for IPAP. (i) The nationwide demographic data from 166 Japanese patients with IPAP are shown. The female to male ratio was 1:2, and the average age was 51 ± 14 years old (age range: 15–79 years) at registration or diagnosis. A total of 30% of patients with IPAP have a poor clinical course. In total, 30% of patients were treated with whole lung lavage therapy (WLL). Under WLL, the patients significantly improved in the short term, but 40% of the patients who underwent WLL worsened again. A new strategy such as granulocyte-macrophage colony-stimulating factor (GM-CSF) therapy for intractable PAP is required. (ii) The correlation of serum KL-6, carcinoembryonic antigen, surfactant proteins D and A, and LDH with disease severity suggests their potential as disease markers. In contrast, serum anti-GM-CSF antibody did not correlate with disease severity, but is a specific marker for the diagnosis of IPAP. The combined measurements of the serum markers may well prove very useful for both the diagnosis and the management of IPAP patients.