Sensitization to various minor house dust mite allergens is greater in patients with atopic dermatitis than in those with respiratory allergic disease.

BACKGROUND: Various allergenic proteins are produced by house dust mites (HDM). However, the allergenicity and clinical implications of these allergens are unknown. OBJECTIVE: The purpose of this study was to identify allergens in Dermatophagoides farinae and elucidate the sensitization profiles to these in Korean patients suffering from respiratory (allergic rhinitis and/or asthma) and atopic dermatitis symptoms. METHODS: IgE reactivities in sera from 160 HDM allergy patients were analysed by one- and two-dimensional gel electrophoresis and immunoblotting. IgE-reactive components were identified by liquid chromatography-coupled electrospray ionization-tandem mass spectrometry. Nine recombinant mite allergens (Der f 1, Der f 2, Der f 10, Der f 11, Der f 13, Der f 14, Der f 30, Der f 32 and Der f Alt a 10) were produced, and the IgE reactivity in sera to each was determined by ELISAs. RESULTS: Der f 1 and Der f 2 were recognized by IgE in serum samples from 88.1% and 78.1% of all patients, respectively. Patients with respiratory allergies were mainly sensitized to these major allergens, whereas patients with atopic dermatitis symptoms showed polysensitization to major and minor allergen components (including Der f 11, Der f 13, Der f 14, Der f 32 and Der f Alt a 10). CONCLUSIONS: Patients with respiratory allergic disease sensitize to major allergen components of HDM. Those with atopic dermatitis were sensitized to a broader range of minor allergen components of HDM (Der f 11, Der f 13, Der f 14, Der f 32 and Der f Alt a 10).

DOCK8: regulator of Treg in response to corticotropin-releasing hormone.

BACKGROUND: Atopic dermatitis (AD) is exacerbated by psychological factors, such as stress. We previously reported that corticotrophin-releasing hormone (CRH) treatment in AD patients decreased the proportion of IL-10(+) Tr1 cells, a subset of inducible regulatory T cells (Tregs). However, changes in the function of Tregs in response to CRH have yet to be studied. METHODS: We analyzed the total proteins taken from CRH-treated and untreated Tregs from AD mice model (NC/Nga mice) using a quantitative proteomic analysis for the different protein expressions. RESULTS: We found a statistically decreased protein level of DOCK8 in CRH-treated Tregs from AD mice. In human, DOCK8 protein levels were also significantly decreased in CRH-treated Tregs from AD patients. Moreover, the expression of DOCK8 in Tregs was inversely correlated with the anxiety levels in the AD patients. In addition to the clinical correlation of DOCK8 with the stress level of AD patients, the knockdown of DOCK8 in Tregs reduced the inhibitory cytokines, IL-10 and TGF-ß, and inhibited the regulatory function of Tregs to suppress the proliferation and TNF-α release of CD4(+) T cells in vitro. CONCLUSION: This study provides new insights on the mechanisms of stress-induced AD aggravation by showing that CRH downregulated DOCK8 expression in Tregs that not only clinically correlates with anxiety levels of AD patients but also regulates suppressive function of Tregs on CD4(+) T cells.

Does prevalence of migraine and Raynaud's phenomenon also increase in Korean patients with proven variant angina?

BACKGROUND: The incidence of coronary artery spasm in oriental patients is higher than that in western patients. Oriental patients with variant angina (VA) frequently show normal or insignificant coronary artery stenosis by angiogram, compared with western patients. The prevalence of migraine and Raynaud's phenomenon in oriental patients with VA has not yet reported. OBJECTIVE: We did a prospective study on the prevalence of migraine and Raynaud's phenomenon in patients with proven VA compared with those in two control groups using a radioisotope technique following ice water exposure. Simultaneously, we studied lipid profiles of each group. METHODS AND RESULTS: migraine was diagnosed if the score in part A totalled 7 or more of 26, and Raynaud's phenomenon was diagnosed if the score in part B totalled 4 or more of 11 by Miller et al. Technetium-99m-labeled red blood cells (99mTc-RBC) radionuclide angiography was performed in all patients. Patients were included in a prospective protocol. Patients were grouped as follows: Group I: 20 patients with proven VA; Group II: 30 patients with coronary artery disease; Group III: 31 patients without heart disease. Age and sex of patients were not statistically different among the three groups. Migraine was diagnosed in 8 patients (40.0%) of group I and in 6 patients (20.0%) of group II and in 12 patients (38.7%) of group III. Raynaud's phenomenon was reported in 2 (10.0%) of the patients in group I and in 5 (16.1%) of the patients of group III. The mean index ratio of the digital blood flow of right over left hand on static image was 0.85 +/- 0.07 (mean +/- S.E.M.) of the patients of group I, 0.73 +/- 0.03 of the patients of group II and 0.74 +/- 0.04 of the patients of group III. The mean flow index ratio of right over left hand of the digital blood flow on dynamic study was 0.51 of the patients of group I, 0.43 of the patients of group II and 0.43 of the patients of group III. The score of migraine did not differ significantly among the three groups. The score of Raynaud's phenomenon of patients with variant angina did not differ significantly from that of patients in the non-coronary control group, although it differed significantly from that of patients in the coronary control group. But, the prevalence of migraine and Raynaud's phenomenon (questionnaire and radionuclide angiography) in patients of group I did not differ significantly from that in groups II and III. In the end, more patients with variant angina than coronary or non-coronary control group did not reach the predetermined point level for the diagnosis of migraine and Raynaud's phenomenon. Lipid profiles were not significantly different among three groups. CONCLUSIONS: This result suggests that variant angina may not be a manifestation of a generalized vasospastic disorder in Korean patients.

Diurnal variation in lumbar MRI. Correlation between signal intensity, disc height, and disc bulge.

There have been no reports indicating diurnal variations in MRI at different portions of each lumbar disc. Eight asymptomatic healthy volunteers between 22 and 29 years old had MRI of their lumbar spine, twice on the same day (in the morning and evening). Forty lumbar discs were studied and the signal intensity change was measured from three portions of each disc (a total of 120 portions). No visible changes could be detected between scans by blinded observers. However, the calculated signal intensity changes showed an average loss of -20.0% (ant., 5 cases), -19.0% (mid, 2 cases), and -17.5% (post., 1 case). Height loss of the disc showed an average loss of -9.9% (ant., 4 cases), -8.3% (mid., 2 cases), and -10.4% (post., 2 cases). An increase of disc bulge at L4-5 level (18.3%) was pronounced, but L5-S1 level was less than others. Loss of body height averaged a loss of 7 mm (0.39% of body height). There was no correlation between reduced signal intensity and height loss at the ant./post. portion (p = 0.42), but there was a close relation at the mid. portion (p = 0.008). Diurnal change of the disc bulge was not correlated with reduced signal intensity (p = 0.48) or height loss (p = 0.16). Intradiscal fluid change was not necessarily influenced by the disc height loss, and height loss did not necessarily have an effect on disc bulge. But diurnal change showed a trend that was reflected in reduced signal intensity, height loss, and an increase of disc bulge which was more apparent from the ant. portion to the post, portion on moving down to the lower levels. Loss of disc height was one factor in the reduction of body height. These changes occurred randomly throughout 5 lumbar disc levels in each case.

The effects of methylprednisolone on prevention of brain edema after experimental moderate diffuse brain injury in rats--comparison between dosage, injection time, and treatment methods.

Our study was designed to determine whether methylprednisolone exerts a beneficial effect after experimental moderate diffuse brain injury and whether this possible beneficial effect is affected by the dosage, the timing of administration, and the methods of treatment. A total of 200 anesthetized adult rats were injured utilizing a weight-drop device through a Plexiglas guide tube. These rats were divided into eight groups: Group 1 (n = 35) was assigned to receive no methylprednisolone after impact (control group), Group 2 (n = 25) received an initial intraperitoneal administration of methylprednisolone with a dose of 5 mg/kg at 1 hour after cranial impact, followed by administration with a maintenance dose of 5 mg/kg/4 hours. Group 3 (n = 25), group 5 (n = 25), and group 7 (n = 20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours, respectively without a maintenance dose. Group 4 (n = 25), group 6 (n = 25), and group 8 (n = 20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours after impact, with a maintenance dose of 15 mg/kg/4 hours. Measured water content of brain tissue expressed the amount of water as the difference between fresh and dry weight. At 48 hours after impact, the water content in group 4 and 6 were significantly lower than group 1. Mean +/- SD was 61.4 +/- 0.37% in group 4 (p < 0.03), 61.5 +/- 0.34% in group 6 (p < 0.001), and 63.6 +/- 0.48% in group 1. Compared to group 1, the difference was not statistically significant in group 2 (p > 0.1), group 3 (p > 0.5), group 5 (p > 0.6), group 7 (p > 0.1), and group 8 (p > 0.5). Groups treated with mega dose before 4 hours after head injury, including maintenance dose, showed beneficial effects. Our study suggests that the efficacy of methylprednisolone in head injury was related to the dosage, the timing of administration, and method of treatment.

Clinical analysis of 34 diffuse axonal injured (DAI) patients below GCS 8.

A consecutive series of 34 severe head-injured patients (DAI) were studied prospectively. Patients were categorized according to a new, simple classification system comprised of four lesion types according to the compression or obliteration of the ventricles or cisterns. Five patients belonged to type II and 19 patients to type IV. Each type was further subdivided into two GCS score ranges (5 to 8 and below 5). The distribution of the posttraumatic infarction was mainly in the frontal and temporal lobes (60% of all cases). Our data demonstrated that the ICP was significantly lower at a 30 degrees head elevation than at 0 degree (18.6 +/- 7.21 mmHg vs 23.0 +/- 10.60 mmHg. t = 4.22 P < 0.001), but head position did not statistically affect CPP (69.4 +/- 19.86 mmHg vs 68.2 +/- 19.87 mmHg. t = -0.54, P < 0.59). The effect of intensive therapy on ICP, CPP and AVDO2 was studied in all cases, employing steroids and diuretics in a modified intensive care scale. In cases where barbiturates were employed, there were statistically significant changes in ICP and AVDO2 (P < 0.001), but CPP was not affected (P < 0.59). Surviving patients were analyzed by using the GOS and the neurological grading score (NGS, Nihon University) of the persistent vegetative state. Our data suggests that head elevation of 30 degrees and barbiturate therapy are more effective on ICP and AVDO2, and NGS more exact than GOS in vegetative patients.

Apoptotic change and NOS activity in the experimental animal diffuse axonal injury model.

Although nitric oxide (NO) plays an important role in the pathophysiological process of cerebral ischemia or severe traumatic brain injury, its contribution to the pathogenesis of moderate diffuse axonal injury (mDAI) remains to be clarified. The alterations in nitric oxide synthase (NOS) activity and the histopathological response after mDAI was investigated. Forty anesthetized Sprague-Dawley adult rats were injured with a Marmarou's weight-drop device through a Plexiglas guide tube. These rats were divided into 8 groups (control, 1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 48 hr after trauma). The temporal pattern of apoptosis in the adult rat brain after mDAI was characterized using TUNEL histochemistry. In addition, the cDNA for NOS activity was amplified using RT-PCR. The PCR products were electrophoresed on a 2% agarose gel. eNOS activity was not detected, but nNOS activity was expressed after 3 hr and continuously 48 hr after impact, which was approximately double that of the control group at 12 and 24 hr. Subsequently, there was a decrease in activity after 48 hr. The iNOS activity increased dramatically after 12 hr and was constant for a further 12 hr followed by a dramatic decrease below the level of the control group. Significant apoptotic changes occurred 12 and 24 hr. after insult. nNOS and iNOS activity were affected after moderate diffuse axonal injury in a time-dependent manner and there was a close relation between the apoptotic changes and NOS activity. Although the nNOS activity was expressed early, its activity was not stronger than iNOS, which was expressed later.

Prediction of newly developed acute renal failure using serum phosphorus concentrations after living-donor liver transplantation.

OBJECTIVE: This retrospective study investigated the predictive role of serum phosphorus concentration for acute renal failure (ARF), defined by the Risk Injury Failure Loss End-stage kidney disease (RIFLE) criteria, after living-donor liver transplantation (LDLT). METHODS: Perioperative factors, including serum phosphorus concentrations, in LDLT recipients without pre-existing renal dysfunction were retrospectively analysed and compared between patients with or without post-LDLT ARF. RESULTS: A total of 45 patients out of 350 (12.9%) met the RIFLE ARF criteria and experienced significantly higher postoperative mortality, longer intensive care unit stay and more frequent graft dysfunction than those patients without post-LDLT ARF. Multivariate logistic regression analyses showed that a serum phosphorus concentration ≥ 4.5 mg/dl on postoperative day 1 (relative risk [RR] 5.31; 95% confidence interval [CI] 2.56, 11.03), a preoperative model for end-stage liver disease score 20 points (RR 4.17, 95% CI 2.04, 8.52), and packed red blood cell transfusion 10 units (RR 2.55, 95% CI 1.13, 5.88) were independent risk factors for post-LDLT ARF. CONCLUSIONS: Hyperphosphataemia on postoperative day 1 could be an early and simple indicator of ARF occurrence after LDLT.

Nonextraction treatment of a Class II Division 1 malocclusion.

A case report is presented of a Class II, Division 1 malocclusion with a considerable amount of maxillary arch length deficiency and a significant anterior posterior discrepancy. The patient was treated without extraction to the standards of the American Board of Orthodontics. [This case was presented to the American Board of Orthodontics in partial fulfillment of the requirements for the certification process conducted by the Board.]

Changes in intracellular Na+ and pH in rat heart during ischemia: role of Na+/H+ exchanger.

The role of the Na+/H+ exchanger in rat hearts during ischemia and reperfusion was investigated by measurements of intracellular Na+ concentration ([Na+]i) and intracellular and extracellular pH. Under our standard conditions (2-Hz stimulation), 10 min of ischemia caused no significant rise in [Na+]i but an acidosis of 1.0 pH unit, suggesting that the Na+/H+ exchanger was inactive during ischemia. This was confirmed by showing that the Na+/H+ exchange inhibitor methylisobutyl amiloride (MIA) had no effect on [Na+]i or on intracellular pH during ischemia. However, there was a short-lived increase in [Na+]i of 8.2 +/- 0.6 mM on reperfusion, which was reduced by MIA, showing that the Na+/H+ exchanger became active on reperfusion. To investigate the role of metabolic changes, we measured [Na+]i during anoxia. The [Na+]i did not change during 10 min of anoxia, but there was a small, transient rise of [Na+]i on reoxygenation, which was inhibited by MIA. In addition, we show that the Na+/H+ exchanger, tested by sodium lactate exposure, was inhibited during anoxia. These results show that the Na+/H+ exchanger is inhibited during ischemia and anoxia, probably by an intracellular metabolic mechanism. The exchanger activates rapidly on reperfusion and can cause a rapid rise in [Na+]i.