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1.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-695655

ABSTRACT

Objective·To investigate therapeutic effect of gastrin on steroid-associated osteonecrosis (SAON) in rat model. Methods·Twenty-four SD rats were randomly divided into three groups i.e. normal control group (normal group), SAON control group (SAON group) and SAON treatment group (treatment group). SAON group and treatment group were intravenously injected with lipopolysaccharide 1 time per day (600 μg/kg) for 2 d and meanwhile intramuscularly injected with methylprednisolone 1 time per day (50 mg/kg) for 3 d. Normal group was injected with normal saline of the same volumns. After steroid injections, treatment group was injected with gastrin 1 time per day (800 μg/kg) for 14 d, while SAON group was injected with normal saline of the same volumns. After the treatment, bone trabeculas below femoral head growth plate were dissected in the rats for bone histology. Hematoxylin-eosin (H-E) staining, immunohistochemistry, fluorescence staining and Goldner's trichrome staining were applied in this study. Results·SAON model in rats was successfully established. The result of H-E staining showed that compared with SAON group, thrombus area, number and area of fat cells in the bone marrows of treatment group obviously decreased (all P<0.05). Immunohistochemistry showed that osteogenic transcription factor (Sp7) positive cells in treatment group were more than those in SAON group (P<0.01). Compared with SAON group, osteoid length and area (Goldner′s trichrome staining), and bone formation rate and bone mineralization deposition rate (fluorescence staining) all significantly increased in treatment group (all P<0.01). Conclusion·Gastrin can effectively treat SAON in rats by suppressing thrombus and lipid formation and enhancing bone-formation.

2.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-695604

ABSTRACT

Objective·To study the correlation between KRAS,NRAS and BRAF mutations and the clinicopathological features in patients with coloreetal cancer (CRC).Methods·The 461 paraffin-embedded CRC tissues were collected.The mutations in hotspot region of KRAS,NRAS and BRAF genes were investigated using amplification refractory mutation system.The relationship between the mutation rates of each gene and the clinicopathological characteristics in CRC patients were analyzed.TheKRAS and BRAF mutation profile and the impact on promoter methylation of the downstream genes were further investigated in both CRC tissues and cell lines through literatures and the American Type Culture Collection.Results·KRAS,NRAS and BRAF mutation rates in CRC tissues were 44.0%,6.1% and 5.2%,respectively.KRAS mutations in the right colon were remarkably higher than the left colon (P=0.000).NRAS mutations were more likely to occur in male patients than female patients (P=0.002).BRAF mutation was closely correlated with age,tumor differentiation,tumor location and nerve invasion,but was exclusive of 203 KRAS mutated samples.Contusion·KRAS,NRAS and BRAF mutations were significantly correlated with the clinicopathological features of CRC,and the mutation incompatibility was observed between KRAS and BRAF genes.

3.
J Neurogenet ; 23(4): 395-404, 2009.
Article in English | MEDLINE | ID: mdl-19863270

ABSTRACT

The cell-surface-signaling protein Notch, is required for numerous developmental processes and typically specifies which of two adjacent cells will adopt a non-neuronal developmental fate. It has recently been implicated in long-term memory formation in mammals and Drosophila. Here, we investigated whether activity-dependent synaptic plasticity at the neuromuscular junctions (NMJs) of third instar Drosophila larvae depends on Notch signaling. The length and number of axonal branches and number of presynaptic sites (boutons) in NMJ vary with the level of synaptic activity, so we increased activity at the NMJ by two complementary methods: increasing the chronic growth temperature of third instar larvae from 18 to 28 degrees C and using the double-mutant ether-a-gogo,Shaker (eagSh), both of which increase NMJ size and bouton count. Animals homozygous for the functionally null, temperature-sensitive Notch alleles, N(ts1) and N(ts2), displayed no activity-dependent increase in NMJ complexity when reared at the restrictive temperature. Dominant-negative Notch transgenic expression also blocked activity-dependent plasticity. Ectopic expression of wild-type Notch and constitutively active truncated Notch transgenes also reduced activity-dependent plasticity, suggesting that there is a "happy medium" level of Notch activity in mediating NMJ outgrowth. Last, we show that endogenous Notch is primarily expressed in the presynaptic cell bodies where its expression level is positively correlated with motor neuron activity.


Subject(s)
Drosophila Proteins/physiology , Neuromuscular Junction/physiology , Neuronal Plasticity/physiology , Receptors, Notch/physiology , Signal Transduction/physiology , Animals , Animals, Genetically Modified , Axons/physiology , Calcium , Drosophila , Drosophila Proteins/genetics , Electric Stimulation/methods , Horseradish Peroxidase , Larva , Motor Neurons/physiology , Muscle Fibers, Skeletal/physiology , Mutation/genetics , Neuromuscular Junction/cytology , Neuromuscular Junction/growth & development , Neuronal Plasticity/genetics , Patch-Clamp Techniques , Receptors, Notch/genetics , Signal Transduction/genetics , Temperature
4.
Chinese Journal of Pathology ; (12): 366-369, 2009.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-249111

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the discrepancies between clinical and autopsy diagnoses in hospitals of different grades and with respect to duration of hospitalization.</p><p><b>METHODS</b>A total of 188 autopsy cases collected from hospitals of different grades were retrospectively reviewed and the discrepancies between clinical and autopsy diagnoses were analyzed.</p><p><b>RESULTS</b>The overall rate of misdiagnosis was 48.9% (92/188). The misdiagnosis rate in grade I hospitals (75.8%, 25/33) was significantly higher than that in grade III (39.6%, 38/96; chi(2) = 12.861, P = 0.000) and grade II hospitals (49.2%, 29/59; chi(2) = 6.179, P = 0.016 ). The misdiagnosis rate of patients beyond 24 hours of admission was lower than that admitted within 24 hours (chi(2) = 20.991, P = 0.000). The overall rate of missed diagnosis was 34.6% (65/188). The rate of missed diagnosis in grade I hospitals was remarkably higher than that of the grade III hospitals (chi(2) = 8.241, P = 0.006). There was no difference between grades I and III hospitals on the rate of missed diagnosis within 24 hours of admission, however, this rate was lower in grade III hospitals in comparing with that of grade I hospitals in patients admitted beyond 24 hours (chi(2) = 5.181, P = 0.047). The distribution of disease entities commonly encountered in patients of both misdiagnosis and missed diagnosis were heart problems, infections, arterial diseases and pulmonary embolism.</p><p><b>CONCLUSIONS</b>The rate of discrepancies between clinical and autopsy diagnoses is relatively high. The misdiagnosis and missed diagnosis rate in grade I hospitals was significantly higher than that in grade III hospitals and was closely related with the duration of hospitalization. Autopsy study thus still remains an important measure in clinical audit.</p>


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Aortic Aneurysm , Diagnosis , Pathology , Autopsy , Cause of Death , Diagnostic Errors , Hospitals, Community , Hospitals, General , Hospitals, Teaching , Infections , Diagnosis , Pathology , Length of Stay , Myocardial Infarction , Diagnosis , Pathology , Myocarditis , Diagnosis , Pathology , Pulmonary Embolism , Diagnosis , Pathology , Retrospective Studies
5.
J Neurosci ; 27(25): 6852-7, 2007 Jun 20.
Article in English | MEDLINE | ID: mdl-17581973

ABSTRACT

Neurofibromatosis type 1 (NF1) is a dominant genetic disorder that causes tumors of the peripheral nervous system. In addition, >40% of afflicted children have learning difficulties. The NF1 protein contains a highly conserved GTPase-activating protein domain that inhibits Ras activity, and the C-terminal region regulates cAMP levels via G-protein-dependent activation of adenylyl cyclase. Behavioral analysis indicates that learning is disrupted in both Drosophila and mouse NF1 models. Our previous work has shown that defective cAMP signaling leads to the learning phenotype in Drosophila Nf1 mutants. In the present report, our experiments showed that in addition to learning, long-term memory was also abolished in Nf1 mutants. However, altered NF1-regulated Ras activity is responsible for this defect rather than altered cAMP levels. Furthermore, by expressing clinically relevant human NF1 mutations and deletions in Drosophila Nf1-null mutants, we demonstrated that the GAP-related domain of NF1 was necessary and sufficient for long-term memory, whereas the C-terminal domain of NF1 was essential for immediate memory. Thus, we show that two separate functional domains of the same protein can participate independently in the formation of two distinct memory components.


Subject(s)
Drosophila Proteins/physiology , Memory, Short-Term/physiology , Nerve Tissue Proteins/physiology , Neurofibromin 1/physiology , Retention, Psychology/physiology , ras GTPase-Activating Proteins/physiology , Animals , Drosophila , Drosophila Proteins/chemistry , Drosophila Proteins/genetics , Humans , Memory/physiology , Mutation , Nerve Tissue Proteins/chemistry , Nerve Tissue Proteins/genetics , Neurofibromin 1/chemistry , Neurofibromin 1/genetics , Protein Structure, Tertiary/genetics , ras GTPase-Activating Proteins/chemistry , ras GTPase-Activating Proteins/genetics
6.
J Neurosci ; 26(15): 4004-14, 2006 Apr 12.
Article in English | MEDLINE | ID: mdl-16611817

ABSTRACT

Drosophila larval neuromuscular junction (NMJ) is a well established preparation enabling quantitative analyses of synaptic physiology at identifiable synapses. Here, we report the first characterization of synaptic long-term depression (LTD) at the Drosophila NMJ. LTD can be reliably induced by specific patterns of tetanic stimulation, and the level of LTD depends on both stimulus frequency and Ca2+ concentration. We provide evidence that LTD is likely a result of presynaptic changes. Through screening of targeted mutants with defects in memory or signal transduction pathways, we found that LTD is strongly reduced in the akt mutants. This defect can be rescued by acutely induced expression of the normal akt transgene, suggesting that altered LTD is not attributable to developmental abnormalities and that Akt is critical for the induction of LTD. Our study also indicates that the molecular mechanisms of LTD are distinct from that of short-term synaptic plasticity, because akt mutants showed normal short-term facilitation and posttetanic potentiation, whereas LTD was unaffected in mutants that exhibit defective short-term synaptic plasticity, such as dunce and rutabaga. The characterization of LTD allows genetic analysis of the molecular mechanisms of long-term synaptic plasticity in Drosophila and provides an additional assay for studying functions of genes pertaining to synaptic and behavioral plasticity.


Subject(s)
Leukotriene D4/physiology , Neuromuscular Junction/physiology , Proto-Oncogene Proteins c-akt/physiology , Animals , Calcium/physiology , Calcium Chloride/pharmacology , Drosophila/growth & development , Larva/physiology , Neuromuscular Junction/drug effects , Proto-Oncogene Proteins c-akt/drug effects
7.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-640829

ABSTRACT

Objective To observe the abnormality on behavioral ability of transgenic mice for HRX-EEN fusion gene.Methods Transgenic mice for HRX-EEN fusion gene(transgenic group,n=12)and C57/BL mice(control group,n=12)were tested in hidden platform training(day 1 to day 4)and probe trial testing(day 5)in Morris water maze in which ability of spatial learning and retention was assessed.Results In hidden platform training,the latencies of transgenic group were longer than those in control group,and significant differences were observed between the two groups for day 2,3 and 4(P

8.
J Neurosci ; 24(29): 6507-14, 2004 Jul 21.
Article in English | MEDLINE | ID: mdl-15269261

ABSTRACT

To study the representation of olfactory information in higher brain centers, we expressed a green fluorescent protein-based Ca2+ sensor, G-CaMP, in the Drosophila mushroom body (MB). Using two-photon microscopy, we imaged odor-evoked G-CaMP fluorescence transients in MB neurons [Kenyon cells (KCs)] with single-cell resolution. Odors produced large fluorescence transients in a subset of KC somata and in restricted regions of the calyx, the neuropil of the MB. In different KCs, odor-evoked fluorescence transients showed diverse changes with odor concentration: in some KCs, fluorescence transients were evoked by an odor at concentrations spanning several orders of magnitude, whereas in others only at a narrow concentration range. Different odors produced fluorescence transients in different subsets of KCs. The spatial distributions of KCs showing fluorescence transients evoked by a given odor were similar across individuals. For some odors, individual KCs with fluorescence transients evoked by a particular odor could be found in similar locations in different flies with spatial precisions on the order of the size of KC somata. These results indicate that odor-evoked activity can have remarkable spatial specificity in the MB.


Subject(s)
Calcium/metabolism , Drosophila/metabolism , Green Fluorescent Proteins/analysis , Luminescent Agents/analysis , Mushroom Bodies/metabolism , Neurons/metabolism , Odorants , Animals , Calcium/analysis , Drosophila/cytology , Microscopy, Fluorescence, Multiphoton , Mushroom Bodies/cytology , Neurons/chemistry
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