OBJECTIVE: Conization is used for diagnosis and treatment of cervical neoplasia. Our purpose of this investigation is to determine the efficacy of loop conization for the treatment of cervical dysplasia and the significance of the clinical and histological factors used to predict residual dysplasia after loop conization. METHODS: We reviewed the charts of patients who were received conization and subsequently total hysterectomy at Kangnam St Mary Hospital during 1989 and 2000. Logistic regression and Chi-square test were used for analysis. RESULTS: Total 257 patients were included. The mean age of the patients was 44.7 years. Of these patients, 87 (33.8%) had residual disease in the hysterectomy specimens. Age, the involvement of cut surface of endocervix and exocervix, severity and extent of the lesion, and scattering lesion were associated with the residual disease. But preoperative HPV infection, which is known as the cause of cervical neoplasia was not associated with the residual disease. CONCLUSION: When the high risk factors are present, the validity of conservative treatment should be considered and more careful follow up with pap smear, HPV test and colposcopy is necessary. Because about one thirds of patient has residual disease after conization, LEEP conization should be used for diagnosis of cervical neoplasia rather than treatment.
Colposcopy ; Conization* ; Diagnosis ; Follow-Up Studies ; Humans ; Hysterectomy ; Logistic Models ; Risk Factors*

Nimopidine, one of dihydropyridine derivatives, has been widely used to pharmacologically identify L-type Ca currents. In this study, it was tested if nimodipine is a selective blocker for L-type Ca currents in sensory neurons and heterologous system. In mouse dorsal root ganglion neurons (DRG), low concentrations of nimodipine (<10 muM), mainly targeting L-type Ca currents, blocked high-voltage-activated calcium channel currents by apprx38%. Interestingly, high concentrations of nimodipine (>10 muM) further reduced the "residual" currents in DRG neurons from alpha1E knock-out mice, after blocking L-, N- and P/Q-type Ca currents with 10 muM nimodipine, 1 muM omega-conotoxin GVIA and 200 nM omega-agatoxin IVA, indicating inhibitory effects of nimodipine on R-type Ca currents. Nimodipine (>10 muM) also produced the inhibition of both low-voltage-activated calcium channel currents in DRG neurons and alpha1B and alpha1E subunit based Ca channel currents in heterologous system. These results suggest that higher nimodipine (>10 muM) is not necessarily selective for L-type Ca currents. While care should be taken in using nimodipine for pharmacologically defining L-type Ca currents from native macroscopic Ca currents, nimodipine (>10 muM) could be a useful pharmacological tool for characterizing R-type Ca currents when combined with toxins blocking other types of Ca channels.
Animals ; Calcium Channels ; Calcium* ; Diagnosis-Related Groups ; Ganglia, Spinal ; Mice ; Mice, Knockout ; Neurons ; Nimodipine* ; omega-Agatoxin IVA ; omega-Conotoxin GVIA ; Sensory Receptor Cells

Pulpitis (toothache) is a painful inflammation of the dental pulp and is a prevalent problem throughout the world. This pulpal inflammation occurs in the cells inside the dental pulp, which have host defense mechanisms to combat oral microorganisms invading the pulp space of exposed teeth.This innate immunity has been well studied, with a focus on Toll-like receptors (TLRs). The function of TLR4, activated by Gram-negative bacteria, has been demonstrated in trigeminal ganglion (TG) neurons for dental pain. Although Gram-positive bacteria predominate in the teeth of patients with caries and pulpitis, the role of TLR2, which is activated by Gram-positive bacteria, is poorly understood in dental primary afferent (DPA) neurons that densely innervate the dental pulp. Using Fura-2 based Ca2+ imaging, we observed reproducible intracellular Ca2+ responses induced by Pam3 CSK 4 and Pam2 CSK 4 (TLR2-specific agonists) in TG neurons of adult wild-type (WT) mice. The response was completely abolished in TLR2 knock-out (KO) mice. Single-cell RT-PCR detected Tlr2 mRNA in DPA neurons labeled with fluorescent retrograde tracers from the upper molars. Using the mouse pulpitis model, real-time RT-PCR revealed that Tlr2 and inflammatory-related molecules were upregulated in injured TG, compared to non-injured TG, from WT mice, but not from TLR2 KO mice. TLR2 protein expression was also upregulated in injured DPA neurons, and the change was corresponded with a significant increase in calcitonin gene-related peptide (CGRP) expression. Our results provide a better molecular understanding of pulpitis by revealing the potential contribution of TLR2 to pulpal inflammatory pain.

Dentin hypersensitivity is an abrupt intense pain caused by innocuous stimuli to exposed dentinal tubules. Mechanosensitive ion channels have been assessed in dental primary afferent neurons and odontoblasts to explain dentin hypersensitivity. Dentinal fluid dynamics evoked by various stimuli to exposed dentin cause mechanical stress to the structures underlying dentin. This review briefly discusses three hypotheses regarding dentin hypersensitivity and introduces recent findings on mechanosensitive ion channels expressed in the dental sensory system and discusses how the activation of these ion channels is involved in dentin hypersensitivity.
Dental Physiological Phenomena ; Dentin Sensitivity ; Dentin ; Dentinal Fluid ; Hydrodynamics ; Ion Channels ; Mechanoreceptors ; Neurons, Afferent ; Odontoblasts ; Stress, Mechanical

Subdiaphragmatic vagotomy (SDV) is known to produce analgesic effect in various pain conditions including not only visceral pain but also somatic pain. We aimed to determine brain mechanisms by which SDV induces analgesic effect in somatic pain condition by using formalin-induced acute inflammatory pain model. We identified brain regions that mediate SDV-induced analgesic effect on acute inflammatory pain by analyzing cFos expression in the whole brain. We found that c-Fos expression was specifically increased in the anterior insular cortex (aIC) among subregions of the insular cortex in acute inflammatory pain, which was reversed by SDV. These results were not mimicked in female mice, indicating sexualdimorphism in SDV-induced analgesia. SDV decreased c-Fos expressions more preferentially in glutamatergic neurons rather than GABAergic neurons in the aIC, and pharmacological activation of glutamatergic neurons with NMDA in the aIC inhibited SDV-induced analgesic effect. Furthermore, chemogenetic activation of glutamatergic neurons in the aIC reversed SDV-induced analgesia. Taken together, our results suggest that the decrease in the neuronal activity of glutamatergic neurons in the aIC mediates SDV-induced analgesic effect, potentially serving as an important therapeutic target to treat inflammatory pain.

Somatostatin (SOM) is a widely distributed peptide in the central nervous system and exerts a variety of hormonal and neural actions. Although SOM is assumed to play an important role in spinal nociceptive processing, its exact function remains unclear. In fact, earlier pharmacological studies have provided results that support either a facilitatory or inhibitory role for SOM in nociception. In the current study, the effects of SOM were investigated using anesthetized cats. Specifically, the responses of rostrally projecting spinal dorsal horn neurons (RPSDH neurons) to different kinds of noxious stimuli (i.e., heat, mechanical and cold stimuli) and to the A delta-and C-fiber activation of the sciatic nerve were studied. Iontophoretically applied SOM suppressed the responses of RPSDH neurons to noxious heat and mechanical stimuli as well as to C-fiber activation. Conversely, it enhanced these responses to noxious cold stimulus and A delta-fiber activation. In addition, SOM suppressed glutamate-evoked activities of RPSDH neurons. The effects of SOM were blocked by the SOM receptor antagonist cyclo-SOM. These findings suggest that SOM has a dual effect on the activities of RPSDH neurons; that is, facilitation and inhibition, depending on the modality of pain signaled through them and its action site.
Animals ; Cats ; Central Nervous System ; Cold Temperature ; Hot Temperature ; Neurons ; Nociception ; Posterior Horn Cells ; Sciatic Nerve ; Somatostatin ; Spinal Cord

BACKGROUND/AIMS: The benefit of oral antiviral therapy in preventing hepatocellular carcinoma (HCC) in the general population is not well understood. We used a novel prediction method to estimate the risk of HCC in the Korean population based on various treatment guidelines. METHODS: The 5-year risk of HCC following antiviral therapy was calculated using an HCC risk prediction model. A virtual cohort that represented Koreans (>40 years old) with chronic hepatitis B virus (HBV) infection was established using the fifth National Health and Nutrition Examination Survey. The antiviral indications tested were the Korean National Health Insurance (NHI) and European Association for the Study of the Liver (EASL) guidelines as well as a new extended indication (serum HBV DNA >2,000 IU/mL regardless of serum aminotransferase level). RESULTS: A total of 993,872 subjects were infected with HBV in the general Korean population. Over a 5-year period, 2,725 HCC cases were predicted per 100,000 persons (0.55%/yr). When the cohort was treated based on the Korean NHI, the EASL, and the newly extended indications, HCC risks decreased to 2,531 (−7.1%), 2,089 (−23.3%), and 1,122 (−58.8%) cases per 100,000 persons, respectively (p<0.0001). CONCLUSIONS: Simulated risk prediction suggests that extending of oral antiviral indication may reduce the HCC risk in the general population.
Carcinoma, Hepatocellular* ; Cohort Studies ; DNA ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Liver ; Methods ; National Health Programs ; Nutrition Surveys

BACKGROUND AND OBJECTIVES: Osteoprotegerin (OPG) is a decoy receptor for receptor nuclear factor-kB ligand (RANKL). We sought to evaluate the association between the serum OPG level and the target lesion calcium (TLC) in those patients suffering with coronary artery disease (CAD). SUBJECTS AND METHODS: We assayed the serum OPG levels in 65 CAD patients (mean age: 62+/-10 yrs, M : F=46 : 19) with using enzyme immunoassay, and these patient underwent intravascular ultrasound (IVUS) examinations of their target lesions. The degree of TLC was estimated by the maximum arc of calcium and also the calcified plaque surface area that was calculated from the serial cross-section IVUS images. RESULTS: The median serum OPG levels were greater in the subjects with TLC than in the subjects without TLC (1.36 vs 0.95 ng/mL, respectively, p<0.05). Significant correlation was noted between the serum OPG levels and the maximum arc of calcium (r=0.274, p=0.027). The median serum OPG levels were significantly increased more in the subjects who had a maximum arc of calcium ranging from 90 to 180 degrees than in those subjects who had a maximum arc of calcium less than 90 degrees (1.63 vs 1.14 ng/mL, respectively, p<0.05) and the median serum OPG levels were also increased more in the subjects who fell within the second tertile of the calcified plaque surface area than that in those subjects who fell within the first and third tertile (0.96, 1.53, 1.40 ng/mL for the first, second, third tertile, respectively, p<0.05). On the stepwise multivariate logistic regression analysis, the serum OPG level remained a risk factor for TLC after adjustment was made for the other risk factors such as age, diabetes mellitus, HbA1C and a smoking history (p=0.019, odds ratio 5.208 [95% confidence interval: 1.308-20.744]). CONCLUSION: In patients with CAD, an increased serum OPG level is associated with target lesion calcification.
Calcium* ; Coronary Artery Disease* ; Coronary Vessels* ; Diabetes Mellitus ; Humans ; Immunoenzyme Techniques ; Logistic Models ; Odds Ratio ; Osteoprotegerin* ; Risk Factors ; Smoke ; Smoking ; Ultrasonography

The long belief that dental primary afferent (DPA) neurons are entirely composed of nociceptive neurons has been challenged by several anatomical and functional investigations. In order to characterize non-nociceptivepopulation among DPA neurons, retrograde transport fluorescent dye was placed in upper molars of rats and immunohistochemical detection of peripherin and neurofilament 200 in the labeled trigeminal ganglia was performed. As the results, majority ofDPA neurons were peripherin-expressing small-sized neurons, showing characteristic ofnociceptive C-fibers. However, 25.7% of DPA were stained with antibody against neurofilament 200, indicating significant portion of DPA neurons are related to large myelinated Abeta fibers. There were a small number of neurons thatexpressed both peripherin and neurofilament 200, suggestive of Adelta fibers. The possible transition of neurochemical properties by neuronal injury induced by retrograde labeling technique was ruled out by detection of minimal expression of neuronal injury marker, ATF-3. These results suggest that in addition to the large population of C-fiber-related nociceptive neurons, a subset of DPA neurons is myelinated large neurons, which is related to low-threshold mechanosensitive Abeta fibers. We suggest that these Abeta fiber-related neurons might play a role as mechanotransducers of fluid movement within dentinal tubules.
Animals ; Dentin ; Intermediate Filament Proteins ; Membrane Glycoproteins ; Molar ; Myelin Sheath ; Nerve Tissue Proteins ; Neurofilament Proteins ; Neurons ; Neurons, Afferent ; Nociceptors ; Rats ; Trigeminal Ganglion

No abstract available.
Aneurysm* ; Coronary Vessels* ; Stents*