Rosae Multiflorae Fructus Hot Water Extract Inhibits a Murine Allergic Asthma Via the Suppression of Th2 Cytokine Production and Histamine Release from Mast Cells.

Mast cell-mediated anaphylactic reactions are involved in many allergic diseases, including asthma and allergic rhinitis. In Korea, where it has been used as a traditional medicine, Rosae Multiflorae fructus (RMF) is known to have potent antioxidative, analgesic, and anti-inflammatory activities and to have no obvious acute toxicity. However, its specific effect on asthma is still unknown. In this study, we evaluated whether or not RMF hot water extracts (RMFW) could inhibit ovalbumin (OVA)-induced allergic asthma and evaluated compound 48/80-induced mast cell activation to elucidate the mechanisms of asthma inhibition by RMFW. Oral administration of RMFW decreased the number of eosinophils and lymphocytes in the lungs of mice challenged by OVA and downregulated histological changes such as eosinophil infiltration, mucus accumulation, goblet cell hyperplasia, and collagen fiber deposits. In addition, RMFW significantly reduced T helper 2 cytokines, TNF-α, IL-4, and IL-6 levels in the BAL fluid of mice challenged by OVA. Moreover, RMFW suppressed compound 48/80-induced rat peritoneal mast cell degranulation and inhibited histamine release from mast cells induced by compound 48/80 in a dose-dependent manner. These results suggest that RMFW may act as an antiallergic agent by inhibitingTh2 cytokine production from Th2 cells and histamine release from mast cells, and could be used as a therapy for patients with Th2-mediated or mast cell-mediated allergic diseases.

Morphology of the human xiphoid process: dissection and radiography of cadavers and MDCT of patients.

PURPOSE: The purpose of this study was to evaluate the morphology of xiphoid process by dissection and using radiography of cadavers and multidetector computed tomography (MDCT) in patients. METHODS: The xiphoid processes of 41 cadavers were dissected and taken by radiography. Other 902 patients examined by MDCT were revealed by image post-processing used with multiple planar reconstruction, maximum intensity projection and volume rendering. RESULTS: Xiphoid processes displayed pointed shape in 422 cases (44.75 %), oval shape in 387 cases (41.04 %), and forked shape in 134 cases (14.21 %). The sagittal shape of the xiphoid process was observed as ventrally deviated in 217 cases (23.01 %), dorsally deviated in 191 cases (20.25 %), S-shaped (ahead ventral, then dorsal) in 21 cases (2.23 %), and resembling a hook in 14 of ventral deviated patients and in 19 of those dorsal deviated patients. The foramen of xiphoid processes was found in 544 cases (57.69 %). The pattern L (a large foramen with a diameter of more than 5 mm) appeared in 302 cases (55.51 %), pattern S (a small foramen with a diameter of no more than 5 mm) in 155 cases (28.49 %), pattern LS (a mixture of a large and a small foramina) in 37 cases (6.80 %), and pattern SS (two or more small foramina) in 50 cases (9.19 %). CONCLUSION: Human xiphoid process appeared in morphological diversity. The anatomic structure and ossification degree of xiphoid process was well evaluated by MDCT. Our data may be used for diagnosis and surgical treatment of xiphoid process-related diseases.

Right-sided aortic arch with the retroesophageal left subclavian artery as the fourth branch.

We present a rare variation of the right-sided aortic arch with the retroesophageal left subclavian artery as the forth branch found in a cadaver of an 89-year-old Korean woman during a routine dissection. In this case, the first branch that arose from the ascending aorta was the left common carotid artery, which crossed ventral to the trachea in a left cephalic direction, followed by the right common carotid artery and then the right subclavian artery. Distal to these branches the aortic arch ran dorsally, passing between the esophagus and the vertebra. The left subclavian artery arose from the descending portion of the aortic arch, crossing over to the left upper extremity behind the esophagus. This anomaly was not accompanied by congenital heart disease. Accurate information regarding this variation is of great importance to surgeons for its early identification and preservation during interventions and to radiologists for precise interpretation of angiograms.

The effect of continuous epidural electrical stimulation on neuronal proliferation in cerebral ischemic rats.

OBJECTIVE: To investigate the effect of electrical stimulation (ES) on the recovery of motor skill and neuronal cell proliferation. METHODS: The male Sprague-Dawley rats were implanted with an epidural electrode over the peri-ischemic area after photothrombotic stroke in the dominant sensorimotor cortex. All rats were randomly assigned into the ES group and control group. The behavioral test of a single pellet reaching task (SPRT) and neurological examinations including the Schabitz's photothrombotic neurological score and the Menzies test were conducted for 2 weeks. After 14 days, coronal sections were obtained and immunostained for neuronal cell differentiation markers including bromodeoxyuridine (BrdU), neuron-specific nuclear protein (NeuN), and doublecortin (DCX). RESULTS: On the SPRT, the motor function in paralytic forelimbs of the ES group was significantly improved. There were no significant differences in neurological examinations and neuronal cell differentiation markers except for the significantly increased number of DCX+ cells in the corpus callosum of the ES group (p<0.05). But in the ES group, the number of NeuN+ cells in the ischemic cortex and the number of NeuN+ cells and DCX+ cells in the ischemic striatum tended to increase. In the ES group, NeuN+ cells in the ischemic hemisphere and DCX+ cells and BrdU+ cells in the opposite hemisphere tended to increase compared to those in the contralateral. CONCLUSION: The continuous epidural ES of the ischemic sensorimotor cortex induced a significant improvement in the motor function and tended to increase neural cell proliferation in the ischemic hemisphere and the neural regeneration in the opposite hemisphere.

Effects of Anemarrhena asphodeloides on IgE-mediated passive cutaneous anaphylaxis, compound 48/80-induced systemic anaphylaxis and mast cell activation.

BACKGROUND: We investigated the effect of Anemarrhena asphodeloides Bunge (Liliaceae) water extract (AAWE) on mast cell-mediated anaphylactic reactions. Mast cell-mediated anaphylactic reaction is involved in many allergic diseases, including asthma and allergic rhinitis. In Korea, where it has been used as a traditional medicine, AAWE is known to have antioxidant and anticancer activity. However, its specific effect on mast cell-mediated anaphylactic reactions is still unknown. METHODS: We examined whether or not AAWE could inhibit IgE-mediated passive cutaneous anaphylaxis (PCA), compound 48/80-induced systemic anaphylaxis, and mast cell activation. RESULTS: Oral administration of AAWE inhibited compound 48/80-induced systemic anaphylaxis in mice. AAWE also inhibited the local allergic reaction, PCA, activated by anti-dinitrophenyl IgE antibody in rats. AAWE reduced compound 48/80-induced degranulation of rat peritoneal mast cells (RPMCs). Moreover, AAWE inhibited histamine release and calcium uptake of RPMCs induced by compound 48/80 in a dose-dependent manner. AAWE also significantly inhibited secretion of tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 in phorbol 12-myristate 13-acetate plus calcium ionophores A23187-stimulated RPMCs. CONCLUSIONS: These results suggest that AAWE suppresses compound 48/80-induced mast cell activation by inhibition of cellular mechanisms in signaling pathways, and would be beneficial for treatment of mast cell-mediated anaphylactic response.

Choline acetyltransferase expression in rat prefrontal cortex and hippocampus after acute and chronic exposure to amisulpride, haloperidol, and risperidone.

Recently, there has been an increasing concern that atypical antipsychotics as well as typical ones may cause detrimental effects on cognitive function. Supporting evidence comes from many preclinical studies demonstrating that long-term administration of haloperidol, risperidone, and ziprasidone reduced choline acetyltransferase (ChAT) expression in rat hippocampus (HIP). However, to the best of our knowledge, no studies have examined the effects of amisulpride on ChAT expression in rats. Therefore, the aim of this study was to investigate the effects of acute and chronic administration of amisulpride, haloperidol, and risperidone on ChAT expression in the rat prefrontal cortex (PFC) and HIP. Animals received daily intraperitoneal (i.p.) injections of amisulpride (5 or 100mg/kg), haloperidol (1 or 2mg/kg), risperidone (1 or 2mg/kg) or vehicle for 7 or 45 days. One day after the last injection, rats were sacrificed. ChAT immunoreactivity was assessed with immunofluorescence staining. Target areas of brain were PFC and HIP (CA1, CA3 and DG). The short-term administration of haloperidol and risperidone produced significant decrease of ChAT immunoreactivity in the PFC and HIP compared to vehicle whereas amisulpride had no effects on ChAT immunoreactivity in the PFC and HIP. In long-term study, haloperidol and risperidone decreased ChAT-positive cells and/or fiber pixel density in the PFC and HIP whereas amisulpride decreased ChAT-positive cells in the PFC and had no effects on fiber pixel density of ChAT in the HIP. The results suggest that both short-term and long-term administration of haloperidol and risperidone, and long-term administration of amisulpride may produce detrimental effects on cognitive function by reducing ChAT expression in the PFC and/or HIP.

Fetal topographical anatomy of the upper abdominal lymphatics: its specific features in comparison with other abdominopelvic regions.

Using semiserial sections from 19 human fetuses of 8-30 weeks gestation, we examined the topohistology of the upper abdominal lymphatics and compared it with that of the lower abdominal and pelvic lymphatics. The upper abdominal lymphatics were characterized by an intimate relationship with the peritoneal lining, a common mesentery for the celiac trunk and superior mesenteric artery (SMA). Lymphatic connections from the upper abdominal viscera to the paraaortic and paracaval areas followed two routes: (1) from the intestinal mesentery, along the peritoneum on the left aspect of the proximal SMA, via the chain of lymph follicles (LFs) lying along the retropancreatic fusion fascia, to drain into the LFs around the left renal vein; (2) from sites along the peritoneum on the posterior wall of the omental bursa, via the root of the hepatoduodenal ligament, to drain into LFs around the vena cava. The development of these two posterior drainage routes seemed to be promoted by the peritoneum or a peritoneal remnant (i.e., fusion fascia) attaching to the great vessels, and inhibited or impeded by the developing nerves and diaphragm. No paraaortic, paracaval, or pelvic LFs lay along the peritoneum. The pelvic LFs were usually located along the bundle of lymphatic vessels originating from the femoral canal.

Effects of Aripiprazole and Haloperidol on Fos-like Immunoreactivity in the Prefrontal Cortex and Amygdala.

OBJECTIVE: Aripiprazole, a dopamine system stabilizer, shows efficacy against both negative symptoms and positive symptoms in patients with schizophrenia. The aim of this study was to investigate the effects of aripiprazole and haloperidol on c-FOS expression in rat brain. METHODS: Aripiprazole (1, 10 and 30 mg/kg, i.p.) and haloperidol (0.1 and 1 mg/kg, i.p.) were administered to adult Male Sprague-Dawley rats. After 2 h of drug or vehicle administration, the rats were killed and their brains were removed and perfused with fixative, then cut into 40 µm slices on a freezing microtome. Brain regions of interest were the medial prefrontal cortex (mPFC), the nucleus accumbens core and shell (NAC-C and NAC-S), the hippocampus (CA1, CA3 and DG), the central amygdala (Ce), the basolateral amygdala (BL) and the temporal cortex (Tc). Immunohistochemistry was performed to label cell bodies containing c-FOS. RESULTS: The administration of aripiprazole at all doses (1, 10 or 30 mg/kg) resulted in greater Fos-like immunoreactivity (FLI) in the investigated brain areas, as compared to the vehicle. Comparable increases in FLI were demonstrated in the NAC-C and NAC-S in response to both aripiprazole and haloperidol treatment. The administration of haloperidol (0.1 or 1 mg/kg) also resulted in greater FLI in the investigated brain areas, except the mPFC, where no changes were observed. In the Ce and BL, a significant increase in Fos-positive neurons was observed only with 0.1 mg/kg of haloperidol. CONCLUSION: Both aripiprazole and haloperidol increased FLI in limbic areas, which are considered important targets of antipsychotic drugs. The differential action of aripiprazole on FLI in the amygdala and mPFC as compared to haloperidol may be a good way to differentiate atypical from typical antipsychotics.

The role of mast cells in atrial natriuretic peptide-induced cutaneous inflammation.

Atrial natriuretic peptide (ANP) is widely distributed throughout the heart, skin, gastrointestinal and genital tracts, and nervous and immune systems. ANP acts to mediate vasodilation and induces mast cell activation in both human and rats in vitro. However, the mechanisms of ANP-induced mast cell activation, the extent to which ANP can induce tissue swelling, mast cell degranulation, and granulocyte infiltration in mouse skin are not fully understood. This issue was investigated by treatment with ANP in rat peritoneal mast cells (RPMCs) and mouse peritoneal mast cells (MPMCs) in vitro and by injection of ANP into the skin of congenic normal WBB6F1/J-Kit+/Kit+ +/+, genetically mast cell-deficient WBB6F1/J-Kit(W)/Kit(W-v) (W/W(v)) and mast cell-engrafted W/W(v) (BMCMC→W/W(v)) mice in vivo. ANP induced the release of histamine and TNF-α from RPMCs and enhanced serotonin release from MPMCs, in a dose-dependent fashion, as well as reduced cAMP level of RPMCs in vitro. In +/+ mice, ANP induced significant tissue swelling, mast cell degranulation, and granulocyte infiltration in a dose-dependent manner, whereas not in genetically mast cell-deficient W/W(v) mice. However, ANP-induced cutaneous inflammation has been restored in BMCMC→W/W(v) mice. These data indicate that mast cells play a key role in the ANP-induced cutaneous inflammation.

Mast cells play a key role in Th2 cytokine-dependent asthma model through production of adhesion molecules by liberation of TNF-α.

Mast cells are well recognized as key cells in allergic reactions, such as asthma and allergic airway diseases. However, the effects of mast cells and TNF-α on T-helper type 2 (Th2) cytokine-dependent asthma are not clearly understood. Therefore, an aim of this study was to investigate the role of mast cells on Th2 cytokine-dependent airway hyperresponsiveness and inflammation. We used genetically mast cell-deficient WBB6F1/J-Kitw/Kitw-v (W/Wv), congenic normal WBB6F1/J-Kit+/Kit+ (+/+), and mast cell-reconstituted W/Wv mouse models of allergic asthma to investigate the role of mast cells in Th2 cytokine-dependent asthma induced by ovalbumin (OVA). And we investigated whether the intratracheal injection of TNF-α directly induce the expression of ICAM-1 and VCAM-1 in W/Wv mice. This study, with OVA-sensitized and OVA-challenged mice, revealed the following typical histopathologic features of allergic diseases: increased inflammatory cells of the airway, airway hyperresponsiveness, and increased levels of TNF-α, intercellular adhesion molecule (ICAM)-1, and vascular cellular adhesion molecule (VCAM)-1. However, the histopathologic features and levels of ICAM-1 and VCAM-1 proteins in W/Wv mice after OVA challenges were significantly inhibited. Moreover, mast cell-reconstituted W/Wv mice showed restoration of histopathologic features and recovery of ICAM-1 and VCAM-1 protein levels that were similar to those found in +/+ mice. Intratracheal administration of TNF-α resulted in increased ICAM-1 and VCAM-1 protein levels in W/Wv mice. These results suggest that mast cells play a key role in a Th2 cytokine-dependent asthma model through production of adhesion molecules, including ICAM-1 and VCAM-1, by liberation of TNF-α.

Human primitive meninges in and around the mesencephalic flexure and particularly their topographical relation to cranial nerves.

Development of the meninges in and around the plica ventralis encephali has not been well documented. A distinct mesenchymal structure, the so-called plica ventralis encephali, is sandwiched by the fetal mesencephalic flexure. We histologically examined paraffin-embedded sections from 18 human embryos and fetuses at 6-12 weeks of gestation. In the loose tissues of the plica, the first meninx appeared as a narrow membrane along the oculomotor nerve at 7-8 weeks. Subsequently, the plica ventralis evolved into 3 parts: bilateral lateral mesenchymal condensations and a primitive membranous meninx extending between. Notably, the topographical anatomy of the oculomotor, trochlear and trigeminal nerves did not change: the oculomotor nerve ran along the rostral aspect of the membranous meninx, the trigeminal nerve ran along the caudal side of the lateral mesenchymal condensation, and the trochlear nerve remained embedded in the lateral condensation. Up to 9-10 weeks, the lateral mesenchymal condensations became tongue-like folds; i.e., the primitive form of the tentorium cerebelli, while the membranous meninx became the diaphragma sellae. The falx cerebri seemed to develop from the tongue-like folds. Overall, the final tentorium cerebelli corresponded to the regressed plica ventralis, while the parasellar area originated from the base of the plica and other tissues along the ventral aspects of the basisphenoid and basioccipital.

Effects of 6-hydroxydopamine lesioning of the medial prefrontal cortex on social interactions in adolescent and adult rats.

Bilateral depletion of dopamine (DA) in the medial prefrontal cortex (mPFC) following local infusions of 6-hydroxydopamine (6-OHDA) was reported to affect mesolimbic DA neurotransmission and augment spontaneous and amphetamine-induced locomotion. However, the effects of 6-OHDA lesioning of the mPFC of adolescent rats have never been investigated. Given that dopaminergic neurons reach the peak of maturation during adolescence, we hypothesized that 6-OHDA lesioning of the mPFC during adolescence would have greater impact on subsequent behavioral parameters than would such lesioning during adulthood. The aim of this study was to investigate the effects of 6-OHDA lesioning of the mPFC on the open-field activities and novel investigative and socially interactive behaviors of adolescent and adult rats. Using a stereotaxic apparatus, 6-OHDA (8.0 microg) was injected bilaterally into the mPFC of adolescent and adult rats. After a 1-week recovery period, rats were placed in an open-field chamber, and spontaneous locomotion and other behaviors were monitored. Next, a novel toy was place in the center and behavioral responses were observed. One day later, socially interactive behaviors were measured by placing the lesioned rats into a cage with four unfamiliar rats matched for age. The tests of locomotor activity and novel investigative behaviors revealed no significant differences between the lesioned and sham groups of adolescent or adult rats. Grooming and socially interactive behaviors were significantly lower in the adolescent and adult lesioned groups than in each sham group. Interestingly, we observed more extensive impairment in socially interactive behaviors among the adolescent lesioned rats compared to the adult lesioned rats. The present study indicates that DA depletion in the mPFC causes significantly reduced grooming and socially interactive behaviors; this phenomenon may be comparable to the negative symptoms observed in schizophrenia. Further research is warranted to investigate the mechanisms underpinning the detrimental effects of 6-OHDA lesioning of the mPFC on social behaviors.

Lipoic acid suppresses compound 48/80-induced anaphylaxis-like reaction.

Alpha-lipoic acid (LA), a naturally occurring dithiol compound, is an essential cofactor in metabolic reactions involved in energy utilization. LA improves glycemic control, reduces diabetic polyneuropathies, atherosclerosis, and allergic inflammation. The effects of LA on mast cell-mediated anaphylactic reactions, however, are unknown. LA dose-dependently inhibited systemic and passive cutaneous anaphylaxis-like reactions in mice induced by compound 48/80, a condensation product of N-methyl-p-methoxyphenethylamine and formaldehyde. Pretreatment with LA, prior to induction of the systemic anaphylaxis-like reaction with compound 48/80, reduced plasma histamine levels in a dose-dependent manner. In our in vitro study, LA decreased histamine release from rat peritoneal mast cells (RPMCs) triggered by compound 48/80. Moreover, an increase in calcium uptake activated by compound 48/80 was inhibited by LA. LA also significantly elevated intracellular cyclic adenosine-3',5' monophosphate (cAMP) levels in RPMCs. This inhibition of mediator release from RPMCs may be due to inhibition of calcium uptake and augmentation of intracellular cAMP levels. Based on these results, we suggest that LA may be a potential remedy for allergy-related diseases.

Inhibition of anaphylaxis-like reaction and mast cell activation by water extract from the fruiting body of Phellinus linteus.

Mast cell-mediated anaphylactic reaction is involved in many allergic diseases such as asthma and allergic rhinitis. Phellinus linteus has been used as a traditional herb medicine in oriental countries and is known to have anti-tumor, immunomodulatory, anti-inflammatory, and anti-allergic activities. However, roles of Phellinus linteus in the mast cell-mediated anaphylactic reactions have not fully been examined. In the present study, we have investigated the effects of water extract from the fruiting body of Phellinus linteus (WEPL) on mast cell-mediated anaphylaxis-like reactions. Oral administration of WEPL inhibited the compound 48/80-induced systemic anaphylaxis-like reaction and ear swelling response. WEPL also inhibited the anti-dinitrophenyl (DNP) IgE-mediated passive systemic and cutaneous anaphylaxis. WEPL had no cytotoxicity on rat peritoneal mast cells (RPMC). WEPL dose-dependently reduced histamine release from RPMC activated by compound 48/80 or anti-DNP IgE. Moreover, WEPL decreased the compound 48/80-induced calcium uptake into RPMC. Furthermore, WEPL increased the level of intracellular cAMP and significantly inhibited the compound 48/80-induced cAMP reduction in RPMC. These results suggest that WEPL may serve as an effective therapeutic agent for allergic diseases.

Inhibitory effects of Agaricus blazei on mast cell-mediated anaphylaxis-like reactions.

Agaricus blazei is a medicinal mushroom native to Brazil. It used to be a source of anti-tumor and immunmoactive compounds and considered a health food in many countries. However, its specific effect against mast cell-mediated anaphylactic reactions is still unknown. In the present study, we investigated the effect of Agaricus blazei water extract (ABWE) on mast cell-mediated anaphylaxis-like reactions. We examined whether ABWE could inhibit systemic anaphylaxis-like reaction, ear swelling response, passive cutaneous anaphylaxis, and mast cell activation. ABWE inhibited compound 48/80-induced systemic anaphylaxis-like reaction, ear swelling response, and passive cutaneous anaphylaxis-like reaction in mice. ABWE also inhibited anti-dinitrophenyl (DNP) IgE-mediated passive cutaneous anaphylaxis. ABWE dose-dependently inhibited compound 48/80-induced or anti-DNP IgE-mediated histamine release from rat peritoneal mast cells (RPMC). Moreover, pretreatment with ABWE reduced compound 48/80-induced calcium uptake into RPMC. When ABWE was added, the level of intracellular cAMP in RPMC showed a significant increase compared with that of control cells. In addition, ABWE significantly inhibited compound 48/80-induced cAMP reduction in RPMC. These results propose that ABWE may be beneficial in the treatment of mast cell-mediated anaphylactic reactions.

Roles of TNF-alpha and IgE in the late phase of contact hypersensitivity induced by trimellitic anhydride.

Trimellitic anhydride (TMA) is widely used industrially to make epoxy and alkyd resins, plasticizers and surfactants. The purpose of this study was to investigate whether contact hypersensitivity (CHS) is induced by repeated TMA challenge and the role of TNF-alpha and IgE in the TMA-induced CHS. The repetition of the challenge enlarged the extent of an early and a late phase of CHS in TNF-alpha+/+ (B6129SF2/J) and Balb/c mice. In the late phase of TMA-induced CHS, the peak of ear swelling responses by single challenge showed at 24 h after challenge, but the peak was observed at 8 h after repeated challenge. In the TNF-alpha knockout TNF-alpha-/- (B6;129S-Tnftm1Gk1) mice, the repetition of the TMA challenges enlarged the extent of the late phase of CHS, but less than those in TNF-alpha+/+ mice. Injection of anti-TNF-alpha antibody into the peritoneal cavity of Balb/c mice significantly decreased the extent of the late phase of CHS. Subcutaneous injection of anti-IgE antibody into Balb/c mice also decreased the extent of the late phase of CHS in dose-dependent manner. Histologically, infiltration of polymorphonuclear leukocytes and eosinophils was more pronounced in repeatedly TMA-challenged TNF-alpha+/+ and Balb/c mice than in the TNF-alpha-/- mice and anti-TNF-alpha or anti-IgE antibodies treated Balb/c mice. These results indicate that mice sensitized by TMA could possibly offer a useful model to study the mechanism of CHS, and TNF-alpha and IgE may act as potential modulators in the late phase of TMA-induced CHS. Neutralization of TNF-alpha and IgE by anti-TNF-alpha or anti-IgE antibodies may provide therapeutic tools for the treatment of TMA-induced CHS.

Inhibitory effects of Morus alba on compound 48/80-induced anaphylactic reactions and anti-chicken gamma globulin IgE- mediated mast cell activation.

We investigated the effects of hot-water extract from the root bark of Morus alba (HEMA) on anaphylactic reactions. Using in vitro and in vivo experiments, we examined whether HEMA could inhibit compound 48/80-induced systemic anaphylactic shock and anti-chicken gamma globulin (CGG) IgE-mediated rat peritoneal mast cell activation. HEMA significantly inhibited systemic anaphylaxis induced by the compound 48/80 in mice. HEMA also significantly inhibited the passive cutaneous anaphylaxis activated by anti-CGG IgE. HEMA had no cytotoxicity on rat peritoneal mast cells (RPMC). Moreover, HEMA dose-dependently inhibited mast cell degranulation, histamine release and calcium uptake into RPMC induced by the compound 48/80 or anti-CGG IgE. When HEMA was added, the level of intracellular cAMP in RPMC showed a transient and significant increase (5-fold) compared with that of control cells. HEMA also inhibited significantly the compound 48/80-induced cAMP reduction in RPMC. These results suggested that HEMA inhibits the compound 48/80- or anti-CGG IgE-induced mast cell activation and its inhibitory effects on mast cell activations were favorably comparable to disodium cromoglycate. And HEMA is a candidate for effective therapeutic tools of allergic diseases.

Inhibitory effects of Houttuynia cordata water extracts on anaphylactic reaction and mast cell activation.

The present study was investigated the effect of Houttuynia cordata THUNB water extract (HCWE) on mast cell-mediated anaphylactic reactions. The mast cell-mediated anaphylactic reaction is involved in many allergic diseases such as asthma and allergic rhinitis. HCWE has been used as a traditional medicine in Korea and is known to have an antioxidant and anti-cancer activities. However, its specific effect of mast cell-mediated anaphylactic reactions is still unknown. We examined whether HCWE could inhibit compound 48/80-induced systemic anaphylaxis, IgE-mediated passive cutaneous anaphylaxis (PCA), and mast cell activation. The oral administration of HCWE inhibited compound 48/80-induced systemic anaphylaxis in mice. HCWE also inhibited the local allergic reaction, PCA, activated by anti-dinitrophenyl (DNP) IgE antibody in rats. HCWE reduced the compound 48/80-induced mast cell degranulation and colchicine-induced deformation of rat peritoneal mast cells (RPMC). Moreover, HCWE dose-dependently inhibited histamine release and calcium uptake of RPMC induced by compound 48/80 or anti-DNP IgE. HCWE increased the level of intracellular cAMP and inhibited significantly the compound 48/80-induced cAMP reduction in RPMC. These results suggest that HCWE may be beneficial in the treatment of mast cell-mediated anaphylactic responses.

Hypoplasia of the left portal vein territory of the human liver: a case study.

Although reports of hypoplasia or absence of the liver of left lobe are not few, descriptions of the intrahepatic vessels are rare but valuable for discussion of the pathogenesis. The present report demonstrates a case of the left surgical lobe hypoplasia that is characterized by 1) the scar-like lobe with few parenchymal tissue and dilated bile ducts, 2) no Spiegel's lobe with the portal vein stuck to the inferior vena cava, 3) unusual configurations of the right hepatic vein and the 8th segmental portal vein branch, 4) the hepatic groove on S8, and 5) the trifurcation pattern of the portal vein primary division. According to the macroscopic and histological observations, we hypothesized that the secondary abnormal peritoneal fusion occurred in utero and/or during the postnatal growth, and that it involved the left portal vein and other adjacent structures, resulting in severe atrophy of the left surgical lobe.