Increased Serum Levels of Epidermal Growth Factor in Children with Autism

The etiology of autism is unclear, however autism is considered as a multifactorial disorder that is influenced by neurological, environmental, immunological and genetic factors. Growth factors, including epidermal growth factor (EGF), play an important role in the celluler proliferation and the differentiation of the central and peripheral nervous system. In this study we hypothesized that EGF may play a role in the pathophysiology of autism and examined serum EGF levels in children with autism. We measured serum levels of EGF in the 27 autistic children and 28 age- matched normal controls. The serum levels of EGF in the subjects with autism were significantly higher than those of normal control subjects. However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. This is the first report demonstrating the increased serum levels of EGF in children with autism. This study suggests that increased levels of EGF might have an importance in the pathophysiology of autism.     

Morphologic Evidence of Apoptosis in Childhood Acute Myeloblastic Leukemia Treated with High-Dose Methylprednisolone

We have previously demonstrated that various subtypes of AML children respond to high-dose methylprednisolone (HDMP; 20-30 mg/kg/day) which could induce in vivo differentiation of myeloid leukemic cells to mature granulocytes. In this study we have evaluated whether apoptosis occurs in AML cells of patients treated by HDMP using morphological criteria. For light and electronmicro-scopic examination bone marrow aspirates were obtained four days and two weeks after methylprednisolone (30 mg/kg/day) treatment from two children with newly diagnosed AML (AML-M3 and AML-M4). In both patients maturation of leukemic cells has previously been reported four days (in patient with AML-M3) and two weeks (in patient with AML-M4) after HDMP treatment. Electronmicroscopy revealed the characteristic ultrastructural changes of various stages of apoptosis four days after HDMP treatment in a case with AML-M3. Morphologic evidence of apoptosis induced by HDMP were also detected on Wright-stained and toluidine blue stained semithin sections of BM preparations in a patient with AML-M4 and AML-M3 respectively. These findings suggest that HDMP which could induce in vivo terminal differentiation in myeloid leukemic cells is also able to induce apoptosis in patients with AML. The possibility of HDMP-induced apoptosis should be evaluated in a larger series of patients with AML and other types of malignant tumors.     

Psoas abscess twenty-one years after ipsilateral nephrectomy

We report an unusual case of psoas abscess,which developed twenty-one years afteripsilateral nephrectomy and was caused byinfrequent pathogen, Proteus mirabilis.It was diagnosed by computed tomography andwas drained percutaneously with a nephrostomytube guided by ultrasonography.     

Ceruloplasmin levels in antineutrophil cytoplasmic antibody-positive patients

Anti-myeloperoxidase (MPO) antibodies are associated with the development of anti-neutrophil cytoplasmic antibody (ANCA)-related vasculitis. The imbalance between the protease-antiprotease activity in the neutrophils has been implicated in the pathogenesis of ANCA-related vasculitis. Ceruloplasmin is an acute-phase protein that has antiproteinase and antioxidant properties and inhibits MPO activity. We attempted to study the association between serum ceruloplasmin and ANCA in childhood vasculitis. Forty-five ANCA-related diseases were included in the study. The age range was 4-16 years. Patients were divided into two groups based on indirect immunofluorescence and/or ELISA specificity (MPO). Twenty-six patients had p-ANCA- and 19 patients had c-ANCA-positive disease. Nine patients with Henoch-Sch?nlein purpura were studied as an ANCA-negative control group. Serum ceruloplasmin levels in p-ANCA-, c-ANCA-positive patients, and controls were 125.85+/-93.48 mg/dl, 59.79+/-17.60 mg/dl, and 64.34+/-18.77 mg/dl, respectively, and were significantly higher in patients with p-ANCA ( P<0.05). Ceruloplasmin levels were significantly decreased in remission ( P<0.05). Median MPO level in p-ANCA-positive patients was 15.2 (5-250) and was negative in all c-ANCA-positive patients. There was a significant positive correlation between MPO and ceruloplasmin levels ( r=0.70, P<0.05). Of 26 patients (53.8%) in the p-ANCA-positive group, 14 had renal involvement. The patients with renal disease had significantly higher ceruloplasmin levels than others (151.17+/-92.14 and 134.64+/-95.16 mg/dl respectively, P<0.05). In conclusion, the increase in ceruloplasmin levels during the acute phase suggests that this might be an activation criterion or a response to neutrophil-mediated tissue injury. Increased ceruloplasmin levels together with p-ANCA positivity may be predictive for renal involvement and a serious clinical course. The correlation between ceruloplasmin and MPO levels supports their association. Further studies are necessary to elucidate whether genetic and/or functional alterations in ceruloplasmin are effective in the pathogenesis of vasculitis.     

National Patterns of Depression Treatment in Primary Care

BACKGROUND: While past studies suggest that primary care physicians underdiagnose and undertreat depression, little is known about recent national patterns of depression treatment. METHOD: Using the 1995 and 1996 National Ambulatory Medical Care Surveys, we analyzed 1322 primary care office visits by patients reported to have depression. Rates of psychotherapy/mental health counseling, antidepressant use, and benzodiazepine use were assessed. Independent predictors of depression therapy were examined using multiple logistic regression. Where instructive, we compared the practices of primary care physicians with those of psychiatrists (2418 depression visits). RESULTS: Primary care physicians reported depression in 7.8% of their office visits. For these depression visits, antidepressants (42%) were the most common form of treatment, followed by psychotherapy/mental health counseling (28%) and benzodiazepines (21%). Among specific antidepressants, selective serotonin reuptake inhibitors were most often prescribed by primary care physicians (26% of depression visits). Rates of antidepressant and benzodiazepine use varied significantly by primary care specialty. In addition, geographic region and health insurance status influenced the likelihood of receiving benzodiazepines. In their depression visits, psychiatrists reported psychotherapy/mental health counseling (88%) most frequently, followed by antidepressants (64%) and benzodiazepines (25%). CONCLUSION: The predominant use of selective serotonin reuptake inhibitors suggests that primary care physicians have begun to adopt new therapeutic strategies for depression. The modest rate of antidepressant therapy for a clinical population specifically identified by primary care physicians as having depression may indicate undertreatment of depression in primary care settings. Furthermore, high rates of benzodiazepine use are inconsistent with treatment guidelines, and variations in treatment patterns suggest that nonclinical factors influence depression management.     

Effects of topical application of mitomycin-C and 5-fluorouracil on myringotomy in rats.

OBJECTIVE: The effects of topical application of Mitomycin-C (MMC) and 5-fluorouracil (5-FU) for maintaining myringotomy patency were investigated in this experimental study. STUDY DESIGN: We performed simple myringotomy with a knife on 140 tympanic membranes of 70 rats. Rats were divided in two study groups and a control group. Each study group had 60 tympanic membranes, and the control group had 20. We applied Mitomycin-C (0.4 mg/ml) in Group A, 5-fluorouracil (50 mg/ml) in Group B topically, and sterile saline in the control group for 10 minutes. Examination was made with otoendoscope on days 1, 3, 5, 7, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, and 70, and patency rates were recorded. RESULTS: MMC and 5-FU Groups remained open for a mean of 46.17 days and 14.62 days, respectively. The control ears healed within 10.4 days. Fibrosis of the MMC-treated group was the same as that of 5-FU-treated groups. Fibrosis of both study groups was significantly lower than that of the control group. CONCLUSIONS: MMC is more effective than 5-FU, which is more effective than the simple myringotomy procedure in extending the patency of myringotomies in rat tympanic membranes (p < 0.05). Both medications are useful as an adjunct in preventing myringotomy closure.     

Effects of imatinib vary with the types of KIT-mutation in gastrointestinal stromal tumor cell lines

Mutations of proto-oncogene c-kit in gastrointestinal stromal tumors (GISTs) are considered to cause a constitutive activation of KIT responsible for their oncogenesis. Imatinib has therapeutic potential for GISTs because of its inhibitory effect on KIT kinase activity. However, no study has been published concerning the effects of imatinib on GIST cells with various types of KIT mutation. To investigate the effects of imatinib on various c-kit mutations found in GISTs, cell proliferation and apoptosis assays were performed in two GIST cell lines with different KIT mutations. One of the cell lines, GIST-T1, revealed a heterozygous deletion of exon 11 in the c-kit, while the other cell line, GIST882, possessed a homozygous missense mutation of exon 13 in the c-kit gene. Imatinib inhibited proliferation and induced apoptosis in both cell lines. Imatinib potently suppressed proliferation of the GIST882 cell line at the concentration of 1.0 microM, whereas it inhibited the GIST-T1 at 0.1 microM. In two types of activating mutant KIT, imatinib could inhibit the constitutive activation of both types of KIT mutant, although the antiproliferative effect on GIST882 was weaker than on GIST-T1. Western blot analysis revealed that apoptosis related proteins were activated or suppressed by imatinib in both cell lines in the respective manner. Our results suggest that the apoptotic signal trans-duction caused by imatinib in GISTs is susceptible to various types of KIT mutation.