Capsaicin, the pungent principle of hot peppers, is a neurotoxin that depletes unmyelinated primary sensory neurons (polymodal nociceptors) of neuropeptides like tachykinins. However, the role of capsaicin-sensitive sensory nerve in the production of cytokines, penicillin V (PEV)-induced active fatal anaphylaxis and other immune responses is not yet fully established. Neonatal mice were pretreated s.c. with a single injection of 10 ug of capsaicin per mouse in volume of 20 ul within 5 days of age. Using 5-8 week old mice pretreated as neonates with capsaicin, the capsaicin- pretreated and vehicle-treated control mice were examined for various parameters of immune responses described above. For the induction of active fatal anaphylaxis with PEV, 8 week old mice pretreated as neonates and age-matched capsaicin- untreated control mice were sensitized i.p. with 500 ug of PEV-ovalbumin conjugate plus 2*10(9) B. pertussis and 1.0 mg alum and challenged i.v. with PEV-bovine serum albumin conjugate 14 days later. It was found that neonatal capsaicin-pretreatment significantly enhanced contact hypersensitivity to TNCB and hemagglutination response to SRBC, but significantly inhibited the proliferation response of rnurine splenocyte to Con A and LPS. Interestingly, neonatal capsaicin pretreatment significantly inhibited the intensity of PEV-induced active fatal anaphylaxis and decreased the mortality due to anaphylactic shock. It also significantly inhibited LPS- induced production of cytokines such as TNF-a, IL-1B, IL-6, IL-10, and IL-12. The capsaicin-pretreatment also resulted in an inhibition of the activation of NF-kB. Taken together, these data showed for the first time that neonatal capsaicin-pretreatment significantly inhibited an antibiotic (PEV)-induced anaphylaxis and production of various cytokines, and suggest that capsaicin-sensitive primary sensory nerve may play an important regulatory role in active fatal anaphylaxis and cytokine production, thus potentially presenting tools for immune intervention. In particular, the data presented also indicated the possibility to selectively down-modulate cytokine production and NF-kB activation may offer a broad application for therapeutic intervention in neuroimmunological diseases and other pathological situations.
Anaphylaxis ; Animals ; Capsaicin* ; Cytokines ; Denervation* ; Dermatitis, Contact ; Hemagglutination ; Humans ; Infant, Newborn ; Interleukin-10 ; Interleukin-12 ; Interleukin-6 ; Mice ; Mortality ; Neuropeptides ; NF-kappa B ; Penicillin V ; Sensory Receptor Cells ; Serum Albumin ; Tachykinins ; Whooping Cough

Osteoclasts are a major component of bone metabolism in physiologic condition and in rheumatoid arthritis (RA). RA is a chronic, autoimmune, inflammatory disease primarily affecting the joints. Joint inflammation leads to cartilage and bone destruction by osteoclast activation. This osteoclast activation leads to typical RA symptoms and is the therapeutic target. Several kinds of drugs are used for preventing bone loss by osteoclasts in RA patients. However, the bone destructive action of osteoclasts is not the only mechanism in RA pathogenesis. Recent research suggests that the osteoclasts regulate hematopoietic stem cell niches and invoke immune responses in bone. Osteoclasts are derived from bone marrow hematopoietic stem cells, and maintain the hematopoietic stem cell niches contract with osteoblasts. Osteoclasts secret several cytokines to regulate inflammation and T cell differentiation, and present antigen to T cells via major histocompatibility complex class I and class II molecules. Osteoclast concepts in both origins and functions are under major reconsideration and research. In this review, we will discuss these new insights.
Arthritis, Rheumatoid* ; Bone Marrow ; Cartilage ; Cell Differentiation ; Cytokines ; Hematopoietic Stem Cells ; Humans ; Inflammation ; Joints ; Major Histocompatibility Complex ; Metabolism ; Osteoblasts ; Osteoclasts* ; RANK Ligand ; T-Lymphocytes

No abstract available.
Aneurysm* ; Arteriovenous Fistula* ; Hypertension, Renovascular* ; Renal Artery*

No abstract available.
Thioacetamide*

PURPOSE: This study examined relationships among stress, stress coping strategies, and somatization in mothers-in-law from multi-cultural families in a rural area. METHODS: Elderly mothers-in-law (n=227) living with foreign daughters-in-law completed a self-reporting questionnaire. Data were collected from April to August 2009. Questions related to stress (Visual Analog Scale, VAS), coping strategies (Coping Strategy Scale) for stress, and somatization (Symptom Check List 90, Revised). SPSS/WIN 12.0 program was used for descriptive analysis, t-test, one-way ANOVA, Pearson correlation, and multiple regression analyses. RESULTS: Subjects had a moderate level of stress (5.03). There were significant differences in stress level according to age, educational level, religion, chronic disease, health status, number of children, agreement of an international marriage of her sons, satisfaction in living with a foreign daughter-in-law, and family conflict. Stress showed a significant positive correlation with offensive coping strategy, passive strategy, and somatization. Stress, offensive coping strategy, and passive coping strategy affected the level of somatization. CONCLUSION: In a family situation involving co-habitation of mother- and foreign daughter-in-law, increased stress experienced by the mother-in-law can lead to increased offensive and passive coping strategies, and increased somatization. More effective means of stress reduction are needed for mothers-in-law from multi-cultural families.
Adaptation, Psychological ; Aged ; Child ; Chronic Disease ; Family Conflict ; Humans ; Marriage ; Somatoform Disorders ; Surveys and Questionnaires

BACKGROUND: To investigate the role of alpha-adrenergic receptors in the development of delayed afterdepolarization, the effect of alpha-adrenoceptor stimulation and blockade on ouabain induced delayed afterdepolarization(DDAD) was examined in rabbit heart Purkinje fibers. METHODS: Purkinje fibers, taken from adult rabbit(1.8 - 2.0kg) heart anesthetized with penobarbital, were mounted in a Luicite chamber and superfused with Tyrode's solution. The transmembrane potentials were measured by the conventional microelectrode technique while the fibers were being stimulated with rectangular pulses of 50% above threshold voltage. The delayed afterdepolarizations were induced by overdrive excitation in the presence of ouabain. RESULTS: Delayed afterdepolarizations were not observed during superfusion of the control Tyrode's solution containing propranolol(5x10(-7)M). However, the addition of ouabain in the presence of propranolol elicited DADs which were dose-, time- and drive cycle length- dependent. Phenylephrine(PE ; 10(-7)M), and alpha-adrenoceptor agonist, potentiated the ouabain-induced DAD during the initial superfusion(for 10 or 20 min) of the test Tyrode's solution. However, it was followed by attenuating-effects after a superfusion time of 50 to 60 min. Both effects showed ouabain dose-dependence. Ouabain(2x10(-7)M), in the presence of propranolol, depolarized the maximum diastolic potential and shortened the action potential duration, and the addition of PE(10(-7)M) did not affect the characteristics of action potential except a decrease in velocity of phase 0 depolarization. Prazosin, an alpha1-adrenoceptor antagonist, inhibited the PE's enhancing effects of ouabaininduced DDAD at 20 min superfusion, but did not affect the attenuating-effects of PE at 60 min superfusion. On the other hand, yohimbine, an alpha2-adrenoceptor antagonist, did not affect the PE's DAD potentiating-effects at 20 min superfusion, but inhibited the attenunating-effects of PE at 60 min superfusion. CONCLUSION: It is inferred that alpha-adrenergic stimulation induce delayed afterdepolarization and triggered activity in the rabbits, being responsible for the arrhythmia development, and the effects are mainly due to the action of alpha1-subtpe adrenoceptor stimulation.
Action Potentials ; Adult ; Arrhythmias, Cardiac ; Hand ; Heart ; Humans ; Membrane Potentials ; Microelectrodes ; Ouabain ; Prazosin ; Propranolol ; Purkinje Fibers ; Rabbits ; Receptors, Adrenergic, alpha* ; Yohimbine

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.
Acetylcholine ; Action Potentials ; Adenosine ; Animals ; Atropine ; Carbachol ; Cholinergic Agonists* ; Hand ; Ischemia ; Microelectrodes ; Myocardium* ; Rats*

STUDY DESIGN: Case report OBJECTIVES: We report a case of surgically proven tophaceous gout of the lumbar spine at the L5-S1 level in a 43-year-old man that mimicked infectious spondylodiscitis and epidural abscess on magnetic resonance (MR) images. SUMMARY OF LITERATURE REVIEW: Some patients have chronic back pain with an epidural mass. Among the many causes of epidural masses, tophaceous gout of the lumbar spine is very rare. MATERIALS AND METHODS: A 43-year-old man presented with fever and chronic back pain with radiating pain. In an MR image of L4-5, an abnormal subcutaneous mass was found in the posterior epidural space. The subcutaneous mass was isointense on T1-weighted images compared with the intervertebral disc, and focally and strongly hyperintense and heterogeneous on T2-weighted images. After the intravenous administration of gadolinium contrast, the mass was fairly homogenous, with a low signal intensity and without enhancement. With the diagnosis of infective spondylitis with epidural abscess, we performed a decompressive mass resection. RESULTS: The pathologic examination revealed multinuclear giant cells and amorphous crystalline fibrous tissue. The lesion was diagnosed as tophaceous gout. CONCLUSIONS: This case underscores the importance of considering tophaceous gout in the differential diagnosis of an epidural mass in a patient with chronic back pain.
Administration, Intravenous ; Adult ; Back Pain ; Crystallins ; Diagnosis ; Diagnosis, Differential ; Discitis ; Epidural Abscess ; Epidural Space ; Fever ; Gadolinium ; Giant Cells ; Gout ; Humans ; Intervertebral Disc ; Magnetic Resonance Imaging ; Spine ; Spondylitis

OBJECTIVES: We report a case of surgically proven tophaceous gout of the lumbar spine at the L5-S1 level in a 43-year-old man that mimicked infectious spondylodiscitis and epidural abscess on magnetic resonance (MR) images.SUMMARY OF LITERATURE REVIEW: Some patients have chronic back pain with an epidural mass. Among the many causes of epidural masses, tophaceous gout of the lumbar spine is very rare. MATERIALS AND METHODS: A 43-year-old man presented with fever and chronic back pain with radiating pain. In an MR image of L4-5, an abnormal subcutaneous mass was found in the posterior epidural space. The subcutaneous mass was isointense on T1-weighted images compared with the intervertebral disc, and focally and strongly hyperintense and heterogeneous on T2-weighted images. After the intravenous administration of gadolinium contrast, the mass was fairly homogenous, with a low signal intensity and without enhancement. With the diagnosis of infective spondylitis with epidural abscess, we performed a decompressive mass resection. RESULTS: The pathologic examination revealed multinuclear giant cells and amorphous crystalline fibrous tissue. The lesion was diagnosed as tophaceous gout. CONCLUSIONS This case underscores the importance of considering tophaceous gout in the differential diagnosis of an epidural mass in a patient with chronic back pain.

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*