Objective: To analyze the characteristics of diffusion tensor magnetic resonance imaging in patients with cerebral infarction and to explore the values of diagnosis and predicting prognosis of diffusion tensor imaging (DTI) in patients with cerebral infarction in different stages. Methods: Forty patients with cerebral infarction in different stages and 40 healthy volunteers were examined by magnetic resonance imaging (MRI), including conventional T1 and T2-weighted imaging, diffusion-weighted imaging and DTI. Fractional anisotropy (FA) images were reconstructed. The values of FA and apparent diffusion coefficient (ADC) were measured in the infarcted regions, corresponding contralateral normal regions and corresponding normal regions in normal control group. Results: DTI showed that the size of infarction foci was more accurate and clearer than that of the conventional MRI. The FA values of the infarcted regions, infarcted ipsilateral posterior limb of internal capsule, cerebral peduncle, and corticospinal tract in cerebral infarction group were 0.12 ± 0.01, 0.29 ± 0.03, 0.36 ± 0.12 and 0.35 ± 0.04, respectively. They were lower than those in the contralateral corresponding regions 0.35 ± 0.08, 0.50 ± 0.13, 0.53 ± 0.14 and 0.56 ± 0.07, and they all had significant differences (P < 0.05). There were no significant differences between the ADC and FA values at the uninjured sides in patients with cerebral infarction as compared with the corresponding regions in the normal control group (P > 0.05). The FA and ADC values in brain tissues changed regularly with the time of infarction after cerebral infarction. The FA values in the affected sides had no consistent changes as compared with the contralateral sides in the superacute phase. They increased or decreased slightly, then (during acute stage, subacute stage and chronic stage) decreased irreversibly; the ADC values in the affected sides changed with time regularly; they decreased significantly; then gradually returned to normal, and after that increased again. Conclusion: DTI examination contributes to the diagnosis of cerebral infarction. The combination of the ADC and FA values may more accurately conduct clinical stage and evaluate the time of the occurrence of cerebral infarction.

Adolescent ; Female ; Heart Septal Defects, Atrial ; complications ; Humans ; Hypertension, Pulmonary ; complications ; Scimitar Syndrome ; complications ; Tomography, X-Ray Computed

Cardia ; pathology ; surgery ; China ; epidemiology ; Esophageal Neoplasms ; diagnosis ; epidemiology ; surgery ; Esophagectomy ; Esophagoscopy ; Gastroscopy ; Humans ; Mass Screening ; Minimally Invasive Surgical Procedures ; Precancerous Conditions ; diagnosis ; surgery ; Stomach Neoplasms ; diagnosis ; epidemiology ; surgery

Puromycin-sensitive aminopeptidase (PSAP) belongs to the M1 family of aminopeptidases, characterized by the N-terminal substrate binding sequence GAMEN, the enzyme activity center HEXXH(X)₁₈E motif, and the C-terminal ERAP-1-like superfamily structural domain. Encoded by the gene NPEPPS located at 17q21.32, PSAP consists of 919 amino acids and is widely distributed throughout the human body, with the highest expression in the brain, followed by the heart and skeletal muscle. It is also found in the liver, renal tubular epithelium, small intestine, large intestine epithelium, and gastric epithelial cells. PSAP primarily relies on its aminopeptidase hydrolytic activity to remove toxic protein aggregates such as Tau, poly Q, and Cu, Zn-superoxide dismutase 1, making it an important factor in the development of diseases such as Alzheimer's disease, Huntington's chorea, and tumors. Existing PSAP inhibitors include bestatin, amastatin, leuhistin, actinonin, and purinomycin, some of which are already available or in clinical trials. This review provides an overview of the structural and biological functions of M1 family aminopeptidases, with a focus on PSAP, to facilitate further research and targeted drug development.

AlM: To evaluate the function of the microprobe dredging technology in the treatment of meibomian gland dysfunction ( MGD ) and to provide fast, efficient, economical and practical method of treatment for meibomian gland dysfunction ( MGD) .
METHODS:The 100μm diameter stainless steel wire was made as the microprobe with the total length of 3cm, which the needle was about 5mm and hand shank was about 2. 5cm. Selected 140 cases with dry eyes of meibomian gland dysfunction ( MGD ) , patients were divided into two groups and made them have comparability. Observation group ( n = 70 ) used microprobe to dredge meibomian gland pipe accompanied with drugs, hot compress and meibomian gland massage treatment. The control group (n=70) was given conventional drugs, hot compress and meibomian massage treatment. To compare the tear break-up time ( BUT) , efficient rate and the cure rate of the two groups after treatment of 1d, 1wk, 2wk, 1 mo, 2mo and 3mo.
RESULTS: BUT were significantly prolonged in observation group and control group after treatment, and the observation group improved more obviously; the efficient rate and cure rate of the observation group were significantly higher than that of the control group after 1d, 1wk, 2wk, 1mo, 2mo and 3mo treatment.
CONCLUSlON: Using microprobe to unclog the meibomian gland tube can provide the fast and efficient, economical and practical treatment for meibomian gland dysfunction ( MGD ) , which can be promoted in the clinical practice.

Objective To discuss the pathogenesis,diagnosis and treatment of delayed traumatic intracerebral hematoma.Methods The clinic data of traumatic delayed intracranial hematoma patients in this hospital were retro- spectively analyzed.According to clinic observation and CT re-examination,47 cases were diagnosed as delayed trau- matic intracranial hematoma(45 cases by operative treatment,and the other 2 by conservative treatment).Results There were 21 cases of recovery,10 cases of slight disability,8 cases of severe disability,8 cases of death.The total mortality rate was 17 %.Conclusion Brain contusion,subarachnoid hemorrhage and skull base fracture were impor- tant factors of DTICH.Fine-observation and prompt CT re-examination offered excellent results for DTICH.

Objective To determine the effect of mild hypothermia on neonatal piglet cardiac hemodynamic function after hypoxia-ischemia (HI).Method Twenty five 7-day-old piglets were used for hypoxic ischemic brain damage (HIBD) model by the method of temporary occlusion of the bilateral carotid arteries and followed by mechanical ventilation with low concentration of oxygen (FiO_2=6%) for 30 minutes.The piglets were randomly divided into three groups:group A (normothermia with body temperature to 39℃,n=9),group B (body temperature to 36℃for 72 hours,n=8),and group C (body temperature to 34℃for 72 hours,n=8).Mild hypothermia was initiated at 4 hours after HI,the systolic and diastole function were evaluated by Doppler echocardiography at pre-HI,post-Hi 4 hours and post-HI 72 hours.Results There were no significant differences in left ventrieular ejection time/left ventrieular ejection time (LPEP/LVEF),right ventricular ejection acceleration time/right ventricular ejection time (RACT/RVET) and CO at post-HI with hypothermia 72 hours in three groups,but the heart rate decreased in B and group C group.Compared with nonnothermia,mild hypothermia treatment showed no significant differences in MAP,LPEP/LVET,RACT/RVET,CO,SV at post-HI with hypothermia 72 hours.Conclusions Body temperature decreased by 3～5℃for 72 hours will not aggravate hemodynamic abnormity.

Objective To explore the relationship between the genesis of dyskinesia and the degree of substantia nigra lesion in Parkinson disease(PD).Methods The hemi-parkinsonian rat model was established by injecting 6-OHDA stereotaxically to right medial forebrain bundle(MFB). Then the hemi-parkinsonian rat was injected intraperitoneally with levodopa methylester(25 mg?kg~(-1)?d~(-1),twice a day)for 21 days,the abnormal involuntary movements were estimated.After being sacrificed,the midbrain was removed,and the injured degree of dopaminergic neurons at substantia nigra was observed by tyrosine hydroxylase immunohistochemistry staining.The relationship between the abnormal involuntary movement scores and dopaminergic neurons loss at substantia nigra was evaluated by sigmoid equation analysis by using Excel software.Results The apomorphine-induced rotation rate above 7 r/min was found in 10 of 25 rats,those rats were regarded as successful hemi-parkinsonian model rats.After the treatment with levodopa methylester,8 of 10 rats displayed abnormal involuntary movements,including stereotype and contralateral rotation,the types of movements varied.Abnormal involuntary movements were appeared in the rats with dopaminergic neurons loss above 90%.The positive relationship was observed between the degree of lesion in substantia nigra and the severity of abnormal involuntary movements.Conclusions The severe loss of dopaminergic neurons at substantia nigra probably plays a role in the development of levodopa-induced dyskinesia in patient with Parkinson disease.

Objective To investigate cellular and behavioural effects of 5-HT1A receptor agonist 8- OH-DPAT in a rat model of levodopa-induced motor complications.Methods The hemi-parkinsonian rat model was produced by stereotaxically injecting 6-OHDA to right medial forebrain bundle(MFB).Two sets of experiments were performed.First,rats were intrapefitoneally treated with levodopa 50 mg/kg plus benserazide 12.5 mg/kg twice a day for 22 days.On day 23,rats intraperitoneally received either 8-OH- DPAT(1 mg/kg)or 8-OH-DPAT plus WAY-100635(0.1 mg/kg)or dissolvent with each levodopa dose as controls.In the second set,rats were intraperitoneally treated either with levodopa(50 mg/kg)plus 8-OH- DPAT(1 mg/kg)or levodopa 50 mg/kg plus dissolvent,administered twice daily for 22 consecutive days. Rotational duration and frequency of off period were estimated.After sacrificed,subcellualr distribution of GluR1 and GluR1Ser845 phosphorylation was observed by Western blot.Results 8-OH-DPAT,reversing the shortened rotational duration induced by levodopa,prolonged the rotational duration by 27.8%?6.1% and reduced the frequency of failures to levodopa by 7.2%?1.7%.Co-administration of WAY-100635,a 5-HT1A receptor antagonist,with 8-OH-DPAT eliminated the effect of 8-OH-DPAT on motor complications, indicating that the observed 8-OH-DPAT responses were probably mediated via the 5-HT1A autoreceptor. Moreover,8-OH-DPAT could regulate subcellular distribution of GluR1 and reduce hyperphosphorylation of GluR1 Ser845 by 22.1%?3.5%,which was closely associated with levodopa-induced motor complications. Conclusions These results suggest that pharmaceuticals stimulating 5-HT1A receptors could be useful in the treatment and prevention of the motor complications in parkinsonian patients.

Ginsenoside Rb1 is an active component in ginseng. Previous in vitro experiments showed that ginsenoside Rb1, could inhibit lipolysis and promote glucose transporter in adipocytes. This study focused on the effect of ginsenoside Rb1 in insulin resistance and ectopic fat deposit in obese mice induced by high fat diet and its molecular mechanism. Obese male C57/L mice induced by high fat diet were randomly divided into the diet-induced obesity group (DIO group), the ginsenoside Rb1 group (Rb1 group) and the rosiglitazone group (Rog group), and continuously fed with high fat diet. In addition, male C57/L mice fed with normal diet were selected as the normal group (NC group). Mice in Rb1 group and Rog groups were intraperitoneally injected with ginsenoside Rb1 and rosiglitazone with the dosage of 20 mg x kg(-1) and 10 mg x kg(-1), respectively. NC and DIO groups were intraperitoneally injected with the same amount of saline. Two weeks later, the intraperitoneal glucose tolerance test (IPGTT) was performed. Three days later, the mice were killed, and their serum samples were collected to detect insulin and free fatty acid (FFA). Their livers were weighed to examine the triglyceride content, and a pathological detection was performed. Epididymal adipose tissues were weighed, and PDE3B, HSL and perilipin were detected by Western blotting. The results showed that the treatment with ginsenoside Rb1 for two weeks could improve the glucose tolerance of obese mice. Except for 0-120 min, the areas under the glucose tolerance curve (0-30 min, 0-60 min and 0-90 min) in the Rb1 group were less than that in the DIO group (P < 0.05, n = 5), with a much lower HOMA-IR (P < 0.05, n = 5). The fat level of obese mice was significantly reduced by Rbl (P < 0.05, n = 5), and so were liver weight/weight (P < 0.05, n = 8). The increased serum FFA of obese mice declined after the treatment of Rb1 (P < 0.05, n = 8). Rb1 could partially recover the expression of perilipin in adipose tissues, but without obvious change in the expressions of PDE3B and HSL and the phosphorylated activation. The above findings indicated that ginsenoside Rb1 could reduce the release of FFA and alleviate the ectopic deposit of triglyceride by up-regulating the expression of perilipin in adipose tissue, which may be one of its mechanisms for improving the insulin resistance and abnormal glucose metabolism of organisms.
Adipose Tissue ; drug effects ; pathology ; Animals ; Body Weight ; drug effects ; Diet, High-Fat ; adverse effects ; Dose-Response Relationship, Drug ; Fatty Acids, Nonesterified ; blood ; Gene Expression Regulation ; drug effects ; Ginsenosides ; pharmacology ; Glucose Tolerance Test ; Insulin ; blood ; Insulin Resistance ; Liver ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Obesity ; blood ; etiology ; metabolism ; pathology ; Organ Size ; drug effects ; Triglycerides ; metabolism