No abstract available.

BACKGROUND: Nitric oxide (NO) is known to play causative role in the development of neuropathic pain following peripheral nerve injury. However, it is yet to be investigated whether the role of NO differs in pain modalities, such as mechanical and thermal stimuli. Also, it has not been investigated whether NO has different roles in the stages of neuropathic pain - its development and maintenance. METHODS: Neuropathic pain was induced by a resection of the lumbar dorsal root 5, 6 (L 5, 6). After N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor was injected intrathecally or locally around the dorsal root, we observed the behavioral response to the mechanical and thermal stimuli. RESULTS: Mechanical and thermal allodynia was inhibited by the application of L-NAME before the dorsal root injury. However, L-NAME did not affect the mechanical and thermal allodynia during the maintenance of neuropathic pain. CONCLUSIONS: We suggest that NO in the spinal cord or injured perineural site may play an important role in the induction of neuropathic pain, and may be associated with mechanical and thermal allodynia.
Animals ; Hyperalgesia* ; Neuralgia* ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase ; Nitric Oxide* ; Peripheral Nerve Injuries ; Rats* ; Spinal Cord ; Spinal Nerve Roots

STATEMENT OF PROBLEM: Macroscopic and especially microscopic properties of implant surfaces play a major role in the osseous healing of dental implants. Dental implants with modified surfaces have shown stronger osseointegration than implants which are only turned (machined). Advanced surface modification techniques such as anodic oxidation and Ca-P application have been developed to achieve faster and stronger bonding between the host bone and the implant. PURPOSE: The purpose of this study was to investigate the effect of surface treatment of titanium dental implant on implant stability after insertion using the rabbit tibia model. MATERIAL AND METHODS: Three test groups were prepared: sandblasted, large-grit and acid-etched (SLA) implants, anodic oxidized implants, and anodized implants with Ca-P immersion. The turned implants served as control. Twenty rabbits received 80 implants in the tibia. Resonance frequencies were measured at the time of implant insertion, 2 weeks and 4 weeks of healing. Removal torque values (RTV) were measured 2 and 4 weeks after insertion. RESULTS: The implant stability quotient (ISQ) values of implants for resonance frequency analysis (RFA) increased significantly (P < .05) during 2 weeks of healing period although there were no significant differences among the test and control groups (P > .05). The test and control implants also showed significantly higher ISQ values during 4 weeks of healing period (P < .05). No significant differences, however, were found among all the groups. All the groups showed no significant differences in ISQ values between 2 and 4 weeks after implant insertion (P > .05). The SLA, anodized and Ca-P immersed implants showed higher RTVs at 2 and 4 weeks of healing than the machined one (P < .05). However, there was no significant difference among the experimental groups. CONCLUSION: The surface-modified implants appear to provide superior implant stability to the turned one. Under the limitation of this study, however, we suggest that neither anodic oxidation nor Ca-P immersion techniques have any advantage over the conventional SLA technique with respect to implant stability.
Dental Implants ; Imidazoles ; Immersion ; Nitro Compounds ; Osseointegration ; Rabbits ; Tibia ; Titanium ; Torque

No abstract available.
Aneurysm, False* ; Embolization, Therapeutic* ; Hepatic Artery*

Common adverse effects due to topical therapy with DPCP(Diphenyprone) are severe contact dermatitis, dermographism, urticaria, generalized pruritus, lymphadenoiathy, and dermatitis on the remote areas. Rarely, DPCP can induce vitiligo or dyschromia in confetias side effects on the pigmentary system. It is not clear yet whither DPCP induced the vitiligcbatoxic effect of phenol ring in DPCP or by koebner phenomenon clue to repeated contact dermatitis in cases where vitiligo was in latent subclinical condition. We describe a patient with alopecia areatairho developed vitiligo due to topical therapy with DPCP. A 20-year-old woman developed alopecia areata with a loss of eye shows and eyelashes. After sensitization, DPCP was topically applieid to the scalp every week. Vitiligo, confirmed by electron microscopic study, appeared 4 month. after the beginning of treatment and was localized only to the areas of topical application. Both alogecia aieata and vitiligo are improving now under systemic and topical corticosteroid therapy.
Alopecia Areata* ; Alopecia* ; Dermatitis ; Dermatitis, Contact ; Eyelashes ; Female ; Humans ; Phenol ; Pruritus ; Scalp ; Urticaria ; Vitiligo ; Young Adult

No abstract available.
Cesarean Section* ; Cicatrix* ; Endometriosis* ; Female ; Pregnancy

No abstract available.

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

BACKGROUND: Pustular eruptions due to drugs are uncommonly reported. We studied the characteristics of clinical and histopathologic findings of pustular drug eruption. OBJECTIVE: We observed th.e causative agents, clinical featurs and histopathologic findings of pustular drug eruption and identified differential points of generlized pustular eruption. METHODS: We evaluated t,he clinical and histopathologic findings of 8 patients with pustular drug eruption and reviewed the literatures reported cases of pustular drug eruption. RESULTS: All patients diagnosed pustular drug eruption suffered from generalized pustular eruption associated with systemic symptoms such as fever, headachened myagia one to three days after treatment with causative agents. The causative agents of putular drug eruption are antibiotics such as ceftriaxone, analgesics and antipyretics. The pustule resolved after a few days of treatment with systemic corticosteroids and antihistamines. Laboratory findings revealed leukocytosis, neutrophilia, and analevated erythrocyte sedimentation rate, On histopatologic findings, we observed subcorneal pustuls containing neutrophils, eosinophils and some lymphocytes and spongiosis, exocytosis of acute iiflammatory cells. Perivascular infiltration of lymphocyte ancl edema of papillary dermis was also bserved in the dermis. CONCLUSION: Pustular drug eruption is characterized by generalized pustular eruption associated with systemic symptoms and histopathologic findings of that are sterile subcorneal pustules. Therefore differential diagnosis of other generalized pustular erupticns are relatively easy by careful history of medication, clinical and histopathologic findings.
Adrenal Cortex Hormones ; Analgesics ; Anti-Bacterial Agents ; Antipyretics ; Blood Sedimentation ; Ceftriaxone ; Dermis ; Diagnosis, Differential ; Drug Eruptions* ; Edema ; Eosinophils ; Exocytosis ; Fever ; Histamine Antagonists ; Humans ; Leprosy ; Leukocytosis ; Lymphocytes ; Neutrophils