No abstract available.
Arthrography* ; Wrist*

BACKGROUND: We evaluated the role and effects of prolotherapy in patients presenting with lower back pain and detected sacral asymlocation, by retrospectively analyzing the results of prolotherapy performed at our institute. METHODS: Twenty-three patients with referred pain in the lower back rather than distinct radiculopathy, were detected to have sacral asymlocation by simple X-ray from May 2004 through July 2005. The patients were treated with prolotherapy and manipulation by the Ongley's method around the lumbosacral junction, iliolumbar ligament, and sacroiliac joint. They were treated for approximately one to two week intervals, and during this period were rechecked by X-ray and evaluated using the visual analogue scale (VAS). RESULTS: A total of 23 patients were included in the study (10 male and 13 female), and the average age was 41 years. The average VAS at the time of visit was 8.5, the average treatment time was 4.7 days, and the average VAS after treatment was 2.1. CONCLUSIONS: Back pain, and associated leg and buttock pain, originate from several causes. In these case analyses, instability around the lumbosacral area and sacral asymlocation might have been important causes of patient back pain and associated buttock and leg pain. We therefore applied prolotherapy as well as manipulation techniques devised by Ongley to these patients, and obtained good results.
Back Pain* ; Buttocks ; Diagnosis* ; Humans ; Leg ; Ligaments ; Low Back Pain ; Male ; Pain, Referred ; Radiculopathy ; Retrospective Studies ; Sacroiliac Joint

No abstract available.
Shoulder*

PURPOSE: Thyroid transcription factor-1 (TTF-1) has been known to regulate the transcriptional activity of thyroid-specific genes. Ki-67 has been known as a marker for indicating tumor growth. This study was designed to campare the expressions of TTF-1 and Ki-67 on non- neoplastic and neoplastic thyroid tissues. METHODS: The surgically resected specimens of various histological types of thyroid tumor, from the files of the Dept. of surgery, Chung-Ang University Pil-Dong Hospital, between January 1998 and June 2002 were reviewed, and 55 cases selected for immunohistochemical studies. The materials consisted of tissues from 10 nodular hyperplasias, 28 papillary carcinomas, 15 follicular adenomas and 12 follicular carcinomas. All specimens were routinely processed, and paraffin blocks were available in all cases. Immunohistochemical stains for TTF-1 and Ki-67 were also performed. RESULTS: In all the cases, including the nodular hyperplasias, papillary carcinomas, follicular adenomas and follicular carcinomas, expressions of the TTF-1 were observed. The properties of the TTF-1 expression, including staining intensity, extent and index were not related to the tumor type. The expression of TTF-1 was inversely correlated with the tumor proliferation fraction, as assessed by the Ki-67 staining index. CONCLUSION: TTF-1 was expressed in almost all the benign lesions and well differentiated carcinomas, and correlated with the tumor proliferation fraction.
Adenoma ; Carcinoma, Papillary ; Coloring Agents ; Hyperplasia ; Paraffin ; Thyroid Gland* ; Thyroid Neoplasms*

The spontaneous regression of herniated cervical discs is not a well established phenomenon. However, we encountered the 3 cases of spontaneous regression of severe radiculopathic herniated cervical discs that were treated using a non-surgical method. Each of the patients were treated with a combination of manipulation, dry needling and analgesics. In each case, the symptoms improved within 12 months of treatment and magnetic resonance imaging (MRI) conducted at that time revealed marked regression of the herniated disc in all cases. These cases provide additional examples of spontaneous regression of herniated cervical discs documented by MRI following non-surgical treatment.
Analgesics ; Humans ; Intervertebral Disc Displacement ; Magnetic Resonance Imaging

In cancer genome studies, the annotation of newly detected oncogene/tumor suppressor gene candidates is a challenging process. We propose using concept lattice analysis for the annotation and interpretation of genes having candidate somatic mutations in whole-exome sequencing in acute myeloid leukemia (AML). We selected 45 highly mutated genes with whole-exome sequencing in 10 normal matched samples of the AML-M2 subtype. To evaluate these genes, we performed concept lattice analysis and annotated these genes with existing knowledge databases.
DNA Mutational Analysis ; Genes, Suppressor ; Genome ; Leukemia, Myeloid, Acute ; Oncogenes ; Sequence Analysis, DNA

The funding acknowledgment in this article was partially omitted as published.

BACKGROUND: Allodynia, one of the most debilitating symptoms of neuropathic pain syndromes, can be defined as `pain due to a stimulus that does not normally provoke pain'. Subsets of dorsal root ganglion (DRG) neurons involved in nociception are characteristically expressed capsaicin sensitivity and high proportion of tetrodotoxin resistant sodium current (TTX-R INa). We performed an experiment to elucidate whether nerve injury induced mechanical allodynia could be resulted from elctrophysiological modulation of large, nonnociceptive afferent neurons to nociceptors. METHODS: Whole cell patch clamp recordings were made from acutely dissociated dorsal root ganglion (DRG) neurons of normal and experimental neuropathic rats. We compared the proportion of capsaicin sensitive neurons which responded to capsaicin (1micrometer) with an inward current > or = 100 pA in amplitude and the proportion of sodium channel subtypes measured in the absence and presence of tetrodotoxin (1micrometer), in small and large DRG neurons. RESULTS: The proportion of capsaicin sensitive cells to total number of cells tested was not changed by nerve injury in both small and large cell populations. In large cell population of nerve injured rats, the proportion of TTX-R INa was significantly increased as compared with normal group (p <0.05), and in small cell population of nerve injured rats, TTX-S INa was increased, but there was no statistical significance. CONCLUSIONS: These data indicate that expression of the sensitivity to capsaicin in DRG neurons would not be altered by nerve injury and increased TTX-R INa in large cell population of nerve injured DRG may underlie increased excitability.
Animals ; Capsaicin* ; Diagnosis-Related Groups ; Ganglia, Spinal* ; Hyperalgesia ; Neuralgia ; Neurons ; Neurons, Afferent ; Nociception ; Nociceptors ; Rats* ; Sodium Channels ; Sodium* ; Spinal Nerve Roots* ; Tetrodotoxin

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.

Background: Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor erythroid- 2-related factor 2 (NRF2) pathway is a major regulator protecting cells from oxidative and metabolic stress. Studies have revealed that this pathway is involved in mediating resistance to cytotoxic chemotherapy and immunotherapy; however, its implications in oncogene-addicted tumors are largely unknown. This study aimed to elucidate whether this pathway could be a potential therapeutic target for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Methods: We measured the baseline expression of NRF2 using EGFR-mutant parental cells and acquired gefitinib resistant cells. We investigated whether NRF2 inhibition affected cell death in vitro and tumor growth in vivo using a xenograft mouse model, and compared the transcriptional changes before and after NRF2 inhibition. Results: Baseline NRF2 expression was enhanced in PC9 and PC9 with gefitinib resistance (PC9/GR) cells than in other cell lines, with a more prominent expression in PC9/ GR. The NRF2 inhibitor induced NRF2 downregulation and cell death in a dose-dependent manner. Cotreatment with an NRF2 inhibitor enhanced osimertinib-induced cell death in vitro, and potentiated tumor growth inhibition in a PC9/GR xenograft model. Finally, RNA sequencing revealed that NRF2 inhibition resulted in the altered expression of multiple genes involved in various signaling pathways. Conclusion We identified that NRF2 inhibition enhanced cell death and inhibited tumor growth in tyrosine kinase inhibitor (TKI)-resistant lung cancer with EGFR-mutation. Thus, NRF2 modulation may be a novel therapeutic strategy to overcome the resistance to EGFR-TKIs.