Tissue parasites in patients with chronic urticaria

Chronic urticaria is an important diagnostic and therapeutic problem. We aimed to investigate the sero-prevalence of tissue parasites causing toxocariasis and fasciolosis in patients with chronic urticaria. All cases were analyzed for antibodies against Toxocara canis and Fasciola hepatica by modified (homemade) ELISA. The excretory/secretory products of Toxocara and Fasciola were used as antigens (ES-ELISA) in the test. In this study, the highest toxocariasis seropositivity (29.0%) rate and the highest fasciolosis seropositivity (14.5%) rate were found in patients with chronic urticaria. Fasciolosis seropositivity and total seropositivity of toxocariasis and fasciolosis in patients with chronic urticaria was significantly higher than in healthy controls (p<0.05). Toxocariasis seropositivity in patients with chronic urticaria was not significantly higher than that in healthy controls (p>0.05). We suggest that parasitic infections should be considered as an important cause of chronic urticaria. Serological methods should be used to expose the diagnosis of tissue parasites in such cases.     

The effects of articaine hydrochloride on wound healing: an experimental study

PURPOSE: The aim of the study was to examine the effect of articaine hydrochloride (AH) on the healing of surgical wounds and to compare healing with that of lidocaine. MATERIALS AND METHODS: Forty rats were used in this study. The rats were randomly separated into 4 groups. Three groups were given 2% lidocaine, 4% AH, or injectable saline, and the fourth was a control group. Skin specimens underwent the breaking strength test (BST) and histologic examination at 1 week after the surgical procedure. The skin specimens of the rats were subjected to a pulling force of 10 mm/min across the incision line. The strength value at the moment of breaking in the tissue was expressed in Newtons. Histologic examination was performed as well, and wound healing was graded. RESULTS: Both the histologic grade and BST values in the lidocaine and AH groups were significantly lower than those of the control and saline groups (P <.01). Similarly, the histologic and BST values of the AH and lidocaine groups were statistically significant (P <.05, P <.001). Some necrotic regions were observed at the incision region in 2 samples from the AH group. CONCLUSION: The results of the study showed that AH is as safe a local anesthetic agent as lidocaine from the standpoint of wound response.     

Vertical growth changes after adenoidectomy

The purpose of this retrospective investigation is to compare vertical growth component of craniofacial structure of subjects with early and late adenoidectomy history. The study consisted of 93 lateral cephalometric radiographs of three groups of randomly selected patients. The first group was made up of 12 patients (10 male and two female) with an average age of 11.16 +/- 2.08 years, who had been operated upon between 1.5-4 years of age. The second group was made up of 54 patients (25 maleand 29 female) with an average age of 12.18 +/- 2.6 years, who had been operated upon after four years of age. The third group of 27 patients (7 male and 20 female) with clear airway with an average age of 11.18 +/- 2.35 years was used as the control. The data obtained from two adenoidectomy groups were compared and because no statistically significant difference was found except for ANSMe/NMe, the two groups were pooled and compared with the growth pattern in the control sample. There were statistically significant differences in the following parameters: SNGoMe, PPGoMe angle, Gonial angle, Gonial ratio, sigma of inner angles, ANSMe/NMe ratio, Jarabak ratio, PNS-adl distance, PNS-ad2 distance, OAW1 distance. When compared with the control group, the adenoidectomy group showed a more vertically directed growth pattern, however, there were no vertical growth pattern differences between the two groups of children who had adenoidectomy before and after four years of age.     

C-Jun N-terminal kinase is required for phorbol ester- and thapsigargin-induced apoptosis in the androgen responsive prostate cancer cell line LNCaP

In early, androgen dependent stages of prostate cancer, androgen withdrawal, the major course of therapy in prostate cancer, leads to a rapid regression of the tumor as a result of apoptosis. However, prostate cancer invariably progresses to an androgen independent and apoptosis resistant stage for which no curative treatment is available. The molecular details of regression upon androgen withdrawal and progression to a resistant state are largely unknown. Here we show that c-Jun N-terminal Kinase (JNK) is activated strongly and in a sustained fashion by 12-O-tetradecanoylphorbol 13-acetate (TPA) and thapsigargin (TG), two agents which were previously shown to lead to apoptosis in the androgen responsive prostate cancer cell line LNCaP. The time course of JNK induction by both compounds correlated very well with the onset and progression of apoptosis in LNCaP cells. Inhibition of either ERK or p38 pathways did not affect TPA-induced cell death. In the androgen-independent prostate cancer cell lines DU-145 and PC-3, and in the cervical carcinoma cell line HeLaS3, TPA did not lead to apoptosis and there were no significant changes in JNK activity upon TPA treatment. The failure of TPA to induce JNK activity in PC-3, DU-145, and HelaS3 cells was not due to a general defect in JNK signaling since ultraviolet (UV) irradiation dramatically increased JNK activity in all four cell lines. Specific inhibition of JNK by expression of the JNK Inhibitory Protein (JIP) dramatically inhibited both TPA- and TG-induced apoptosis. Furthermore, apoptosis induced by both agents was completely blocked by ectopic expression of the baculovirus caspase-inhibitor P35. Surprisingly, ZVAD-fmk, a cell-permeable fluoromethylketone inhibitor of caspases, had no effect on TPA-induced apoptosis, whereas it completely inhibited TG-induced cell death; JNK activity was not affected in either case. This indicates that ZVAD-fmk does not inhibit some of the caspases involved in TPA-induced apoptosis, and that despite the common requirement of JNK activation, TPA- and TG-induced cell death are mechanistically different. Furthermore, it also suggests that JNK is either upstream or independent of caspases in LNCaP cells. Collectively, these results indicate that apoptosis in LNCaP cells requires a sustained increase in JNK activity and caspase activation; components of these signaling pathways may be defective in the androgen independent prostate cancer cell lines.     

Nitric oxide reverses endotoxin-induced inflammatory hyperalgesia via inhibition of prostacyclin production in mice.

We examined whether nitric oxide (NO), derived from constitutive NO synthase (NOS) and/or inducible NOS (iNOS), could contribute to endotoxin-induced inflammatory hyperalgesia via interacting with nuclear factor-kappaB (NF-kappaB), inducible cyclooxygenase (COX-2) and/or polyADP-ribose synthase (PARS). Injection of endotoxin (10 mg kg(-1), i.p.) to mice elicited hyperalgesia, determined by hot plate test, which is prevented by NO precursor (L-arginine), cNOS/iNOS inhibitor (N(G)-nitro-L-arginine methyl ester; L-NAME), NF-kappaB inhibitor (N-acetylserotonin), COX inhibitor (indomethacin), COX-2 inhibitor (DFU) and PARS inhibitor (3-aminobenzamide). Endotoxin caused a decrease in serum nitrite levels prevented by N-acetylserotonin, L-arginine, indomethacin, DFU or 3-aminobenzamide. Endotoxin increased serum 6-keto-PGF(1alpha) levels diminished by L-arginine or aminoguanidine (iNOS inhibitor). L-Arginine, L-NAME, aminoguanidine, DFU or 3-aminobenzamide prevented endotoxin-induced decrease in heart, lungs, kidneys and brain nitrite and malonedialdehyde levels and myeloperoxidase activity. In conclusion, NO reverses endotoxin-induced inflammatory hyperalgesia via inhibition of prostacyclin production, and also contributes to the analgesic effect of NF-kappaB, COX or PARS inhibitors.     

Thrombin activatable fibrinolysis inhibitor activity (TAFIa) levels in neonates with meconium-stained amniotic fluid

OBJECTIVE: Meconium-stained amniotic fluid (MSAF) is thought to be a sign of fetal hypoxia, which causes activation of coagulation and inhibition of fibrinolysis. Inflammation is also seen in MSAF. On the other hand, thrombin activatable fibrinolysis inhibitor (TAFI) is an inhibitor of fibrinolysis and a regulator of vascular inflammation. For this reason, in this study we aimed to evaluate the relation between hypoxia, fibrinolysis, and inflammation by determining the levels of TAFI activity (TAFIa) in MSAF where inflammation was also thought to have a role in the pathogenesis. METHODS: The MSAF group consisted of 22 neonates; 20 neonates served as the control group. Plasma TAFIa levels were evaluated in all neonates in the first six hours of life. RESULTS: TAFIa levels were significantly higher in the MSAF group when compared with the control group and the levels correlated negatively with cord blood pH levels. CONCLUSIONS: Increased TAFIa levels in neonates with MSAF might be due to hypoxia. Inflammation observed in MSAF may also play an additional role in increased TAFIa expression. Although no clinical complication that can be attributed to this increase was seen, one should be alert to the complications of depressed fibrinolysis that might be observed in these neonates.     

Maturation-related changes in tolerance development to hexobarbital after short term treatment with diazepam in the rat

Male rats at six different ages received diazepam on a 4-day treatment schedule. Cross-tolerance to hexobarbital was tested several times during withdrawal period with an anaesthesia threshold technique. Pattern of cross-tolerance was different at different ages. Thus, age and maturation of the rat is a variable which must be considered in studies of tolerance to diazepam.     

High nitrate intake impairs liver functions and morphology in rats; protective effects of α-tocopherol

The aim of this study was to determine the effect of high dose nitrate ingested in drinking water, on liver enzymes and histopathology, liver weight/body weight (lw/bw) ratio, serum and liver malondialdehyde (MDA) levels and osmotic fragility in Sprague-Dawley rats. These parameters were compared on 40 rats divided into four groups; control animals (group A) drank filtered tap water containing maximum 10mg/L nitrate while treatment groups drank 200mg/L (group B), 400mg/L (group C) and α-tocopherol plus 400mg/L (group D) nitrate containing water ad libitum for 60 days. As a result, lw/bw ratio increased significantly (p<0.05) among rats that consumed water with 400mg/L nitrate. Osmotic fragility increased significantly in treatment groups (p<0.05 versus control). Liver but not serum MDA levels increased in group C (p<0.05 versus control). Group A showed normal hepatic lobular architecture and histology. After nitrate administration, there was hepatocellular degeneration with increased intercellular space of the liver cells in groups B and C. Liver MDA, osmotic fragility and liver histology have returned to nearly normal in group D. These findings show clearly that high nitrate ingestion can cause pathological changes in liver histology and functions. Moreover, α-tocopherol can prevent these effects, possibly through antioxidant properties.     

Surgical treatment of a huge cavernous hemangioma surrounding the right coronary artery

Hemangioma of the heart is an extremely rare benign cardiac tumor. A 61-year-old woman presented with a huge hemangioma on the right ventricle. The tumor was completely surrounding the right coronary artery. Under cardiopulmonary bypass, the right coronary artery was transected from the aortic sinus and the supplying arteries of the tumor were divided. The tumor was successfully resected, and the right coronary artery was reanastomosed to the aortic sinus.     

The effects of selective nitric oxide synthase blocker on survival, mesenteric blood flow and multiple organ failure induced by zymosan

BACKGROUND: Circulatory failure in multiple organ dysfunction syndromes (MODS) is characterized with systemic vasodilation, diminished blood flow to various vascular beds. The aim of this study was to investigate the effects of selective inhibition of nitric oxide on the mesenteric arterial blood flow (MABF), survival and organ injury of the liver, kidney, lung and spleen in zymosan-induced MODS. MATERIALS AND METHODS: Forty Swiss albino mice (20-40 g), 7 to 9 weeks old, were obtained. Animals were randomly divided into four groups. The first group were treated intraperitoneally (i.p) with vehicle (saline) and served as a sham group for aminoguanidine (AG) (n=10). The second group was treated with zymosan (500 mg/kg, suspended in saline solution, i.p). The mice in the third and fourth group received AG (15 mg/kg) 1 h and 6 h after zymosan or saline administration, respectively. Eighteen hours after the administration of zymosan, animals were assessed for MODS described subsequently. The signals from the flowmeter were also recorded on mesenteric arterial blood flow values. RESULTS: In zymosan-treated animals, the MABF was significantly lower than that of solvent (saline)-treated controls (ml min(-1), controls: 4.6 +/- 0.6; zymosan: 1.6 +/- 0.9, P <0.05). When animals were treated with AG, there were no significant differences in MABF values between AG group and solvent (saline)-treated control group. However AG prevented zymosan-induced mesenteric MABF decrease. Treatment with aminoguanidine also decreased mortality. CONCLUSION: AG is capable of inhibiting both the induction and the activity of the already iNOS; it remains a potential therapeutic agent in patients with MODS.