Conservative treatments for fracture repair

Conservative treatments for fractures are basic technique. We introduced the basic concepts of following methods:bandage, plaster casting, traction, cast-brace, pinning and external fixation. Then we summarized the indications of these techniques.     

Comparison of five-day Helicobacter pylori eradication regimens: rabeprazole-based and omeprazole-based regimens with and without omeprazole pretreatment

Background: The onset of antisecretory activity of rabeprazole is faster than that of omeprazole.Objective: This study was performed to compare the efficacy of short-term rabeprazole-based triple therapy with that of omeprazole-based triple therapy and to determine the influence of omeprazole pretreatment in omeprazole-based short-term triple therapy.Methods: This was a 2-center, open-label, prospective, randomized study. Patients who tested positive for Helicobacter (formerly Campylobacter) pylori were randomized to one of three 5-day regimens: (1) rabeprazole 20 mg BID, amoxicillin 500 mg TID, and clarithromycin 400 mg BID (RAC group); (2) omeprazole 20 mg BID, amoxicillin 500 mg TID, and clarithromycin 400 mg BID without omeprazole pretreatment (OAC1 group); and (3) omeprazole 20 mg BID, amoxicillin 500 mg TID, and clarithromycin 400 mg BID with 5 days of omeprazole pretreatment 20 mg BID (OAC2 group). Eradication was assessed by ¹³C-urea breath test and rapid urease test ∼1 month after completion of treatment. All patients who entered this study were included in the intent-to-treat (ITT) analysis, patients who completed the study were included in the per-protocol (PP) analysis, and patients who did not undergo the ¹³C-urea breath test and rapid urease test were included in the all-patients-treated (APT) analysis.Results: A total of 120 patients (86 men, 34 women; mean [SD] age, 55.8 [14.3] years; range, 19-86 years) were assigned to the RAC, OAC1, or OAC2 group (40 patients in each group). ITT, PP, and APT eradication rates in the RAC group were 90%, 92%, and 90%, respectively; in the OAC1 group, 75%, 83%, and 75%; and in the OAC2 group, 85%, 90%, and 87%. These eradication rates were not significantly different between groups.Conclusions: Eradication rates did not differ significantly between the three 5-day proton pump inhibitor-based triple therapies in this study population. However, 5-day rabeprazole-based triple therapy tends to be more effective than 5-day omeprazole-based triple therapy in the eradication of H pylori, and treatment with omeprazole before eradication therapy may improve the eradication rates of 5-day omeprazole-based therapy.     

Characterization of Klebsiella pneumoniae and Escherichia coli strains that produce CTX-M-2-type broad spectrum beta-lactamase isolated from a child with leukemia

An 8-year-old girl with acute leukemia had bacteremia caused by Klebsiella pneumoniae producing CTX-M-2-type broad spectrum beta-lactamase. K. pneumoniae and Escherichia coli strains producing the same enzyme and harboring identical conjugative plasmids were recovered from stoor culture. Patients with frequent episodes of neutropenia and prophylactic administration of beta-lactams are at risk of harboring colonizing strains that produce broad spectrum beta-lactamases.     

Molecular alterations of h-warts/LATS1 tumor suppressor in human soft tissue sarcoma

h-warts/LATS1 is a human homolog of the Drosophila warts tumor suppressor gene, which functions as a component of the mitotic apparatus. LATS1-deficient (Lats1(-/-)) mice have been reported to develop ovarian stromal tumors and soft tissue sarcomas. We investigated the status of the h-warts/LATS1 in 50 human soft tissue sarcomas to address its potential function as a tumor suppressor in human sarcoma development. In our RT-PCR assay, 7 (14%) (3 of 4 myxoid liposarcomas, 3 of 7 leiomyosarcomas, 1 of 9 malignant fibrous histiocytomas) of 50 sarcomas examined had no or a reduced expression of the h-warts/LATS1, indicating down-regulated gene expression. We further analyzed alterations of the h-warts/LATS1 in these seven sarcomas. Using microsatellite markers for chromosome 6q23-25.1, to which the h-warts/LATS1 is localized, an allelic loss of this locus was detected in one leiomyosarcoma, in which a missense point mutation of the h-warts/LATS1 was detected by PCR single-strand conformation polymorphism. Clusters of CpG dinucleotides in a 5' putative promoter region were hypermethylated in the other six sarcomas. Our data suggest that the molecular alterations of the h-warts/LATS1 could be of pathologic importance in human sarcomagenesis.     

A case of amelanotic melanoma of the nasal cavity

A 68-year-old male visited Hospital A for treatment of epistaxis, his chief complaint. He was told that he had an easily-bleeding tumor in the nasal cavity. Based of biopsy, a diagnosis of amelanotic melanoma was made. Operation was performed for removal of the tumor. About 8 months after discharge, he visited Hospital B with complaints of lumbar pain and epistaxis. After biopsy at Hospital B, malignant lymphoma (diffuse large cell) was diagnosed, and the patient was referred to our hospital. On bone marrow puncture and biopsy, tumor cell infiltration was observed. Flow cytometric surface marker analysis revealed that these tumor cells were negative for CD45. Results of HE staining of the nasal cavity tumor were insufficient for diagnosis, and staining by immunohistochemistry was necessary to confirm the diagnosis. On immunohistochemical staining of the nasal cavity tumor tissue and bone marrow biopsy tissue, LCA, L26 and UCHL-1 were negative, and S-100 and HMB-45 positive. Recurrence of amelanotic melanoma accompanied by bone marrow infiltration was therefore diagnosed. The incidence of amelanotic melanoma with primary lesions in the nasal cavity is low. However, in making the diagnosis of a nasal cavity lesion, the possibility of such a melanoma should be kept in mind. In many cases, it is difficult to diagnose amelanotic melanoma with HE staining alone, and immunohistochemistry must be used.     

A novel TRH-PFTAIRE protein kinase 1 pathway in the cerebellum: subtractive hybridization analysis of TRH-deficient mice

TRH has been reported to possess several neurophysiological actions in the brain. To gain insights into the molecular mechanisms underlying these effects, particularly in the cerebellum, we attempted to clone a cDNA that was regulated by TRH using TRH knockout mice and subtractive cDNA analysis. Over 100 clones obtained by subtractive hybridization analysis between the wild-type and TRH-1-cerebellum were analyzed. Four clones among them were identical and cdc2-related kinase (PFTAIRE protein kinase 1 (PFTK1)) cDNA, which was previously reported to be expressed only in the brain and testis. PFTK1 mRNA levels in the euthyroid TRH-1- cerebellum supplemented with thyroid hormone were significantly decreased compared with those in the wild-type. Induction of PFTK1 mRNA by TRH was also observed in a time- and dose-dependent manner in human medulloblastoma-derived HTB-185 cells that expressed TRH receptor subtype I mRNA. In addition, treatment of 8-Br-cGMP significantly increased PFTK1 mRNA levels, and a specific inhibitor of cGMP production, ODQ, completely blocked TRH-induced expression of PFTK1 mRNA. Furthermore, induction of PFrK1 mRNA by TRH was significantly inhibited by a NOS specific inhibitor, L-NAME, but not by a MEK inhibitor, PD98059 or a calcium channel inhibitor, nimodipine. These findings demonstrated, for the first time, a novel pathway between a neuropeptide and a cell cycle related peptide in the brain, and PFTK1 may be a key regulator for TRH action in t he cerebellum through t he NO-cGMP pathway.     

De novo germinoma in the brain in association with Klinefelter's syndrome: case report and review of the literature

BACKGROUND: There are no previous reports about de novo germ cell tumors without any past history of germ cell tumor. We describe a case of de novo cerebral germinoma in association with Klinefelter's syndrome. CASE DESCRIPTION: A boy had undergone growth hormone therapy for dwarfism because of hypopituitarism from 10 to 17 years old. The result of karyotyping at the age of 13 was 47,XXY. Magnetic resonance images (MRI) of the brain at the age of 17 years showed no lesions. Two years later, at the age of 19, the patient noticed onset of mild right hemiparesis. MR imaging revealed the existence of a brain tumor in the left temporal lobe and hypothalamus. The patient underwent an operation and the histologic diagnosis of the lesion was germinoma. After postoperative chemotherapy and radiation therapy, the lesion disappeared and the patient was discharged uneventfully. CONCLUSIONS: To the best of the authors' knowledge, this is the first reported case of a germ cell tumor to be de novo without any past history of other germ cell tumor and the seventh case in which it occurred in association with Klinefelter's syndrome.     

Upregulation of osteopontin expression in rat spinal cord microglia after traumatic injury

Osteopontin is a noncollagenous extracellular matrix protein that is expressed in various tissues. Recent studies have shown the upregulation of osteopontin expression in the ischemic cortex after cerebral infarction. We demonstrate here the upregulation of osteopontin expression in the spinal cord after compression injury. Laboratory rats were used in a compression model of spinal cord injury (30-g load for 5 min). Northern blot analysis showed that osteopontin mRNA expression levels reached a peak 3 days after injury (sevenfold; p < 0.05). In situ hybridization demonstrated osteopontin mRNA expression in necrotic areas from 24 h, peaking 3 days after injury. Immunohistochemistry detected osteopontin protein immunoreactivity from 12 h, peaking at 3 days. The peak time and distribution of osteopontin protein expression were coincident with those of osteopontin mRNA expression. Osteopontin expression in our model preceded that shown in the previously reported cerebral infarction models. Osteopontin protein was found in the cytoplasm at 3 days and secreted into the extracellular matrix at 7 days. Triple immunolabeling showed that osteopontin was localized in activated microglia surrounded by astrocytes.