小鼠模型中伯氏疏螺旋体组织载量的定量研究

目的用实时荧光定量PCR确定伯氏疏螺旋体感染小鼠模型不同组织的病原体载量。方法培养低传代伯氏疏螺旋体至对数生长期,稀释为1×10^5／ml。为建立伯氏疏螺旋体感染小鼠模型,于每只小鼠皮内注射菌液100μl,在证实感染成功后,于第12天和第18天分别取不同组织,提取总DNA,用实时荧光定量PCR分别测定组织中的螺旋体flaB基因拷贝数,并标准化为每10^6β-肌动蛋白所对应的flaB拷贝数（螺旋体数）。对不同组织的螺旋体载量进行统计学处理,确定不同组织螺旋体载量差异是否有统计学意义。结果在所检测的4种代表性组织中,膀胱螺旋体载量在两个典型时间点均最高,皮肤和关节次之,心脏最低。结论伯氏疏螺旋体感染小鼠后,不同组织螺旋体载量差异有统计学意义。组织螺旋体载量与组织损伤程度无密切关系。     

The effect of diltiazem on the healing of traumatic urethral inflammation

OBJECTIVE: To investigate the effect of diltiazem, a calcium channel blocker, on healing of the traumatic urethral inflammation when applied systemically or locally. MATERIALS AND METHODS: 21 adult male Wistar rats (230-250 g) were assigned to group 1 (n = 7) = control, group 2 (n = 7) = local application or group 3 (n = 7) = systemic application. In group 1, only a urethral injury was achieved at the 12-o'clock position by gently introducing and drawing a tiny hook in the urethra until urethral bleeding occurred. In group 2, after the same procedure, 10 mg/kg diltiazem was applied retrogradely via a 22-gauge Angiocath intraurethrally for 5 consecutive days, while the same account of the drug was administered intraperitoneally in group 3. After 21 days, the rats were sacrificed for urethrectomy. Pathologically, the thickness of connective tissue, the regularity of the epithelial lining, the presence of the inflammation and the density of collagen were evaluated with Masson's trichrome staining. The Mann-Whitney U test was used for statistical analyses. RESULTS: The mean connective tissue thickness was 0.77 +/- 0.39, 1.01 +/- 0.77 and 0.93 +/- 0.53 microm in groups 1, 2 and 3, respectively. The differences between the groups were insignificant (p > 0.05). The hyperplastic epithelial lining in the study groups, with both systemic and local applications, was markedly infrequent and the inflammation was less prominent. However, these differences did not reach statistical significance. CONCLUSIONS: Diltiazem appears not to have any preventive effect on connective tissue formation when applied locally or systemically in our urethral injury model.     

Are clinical characteristics of familial benign prostatic hyperplasia different than in sporadic cases?

OBJECTIVE: Familial benign prostatic hyperplasia (BPH) is a recently popularized entity with yet uncertain clinical and pathological features. In the present study we investigated whether there was any difference between clinical characteristics of familial and sporadic BPH in a series of 148 surgically treated BPH patients. MATERIALS AND METHODS: A retrospective analysis was performed in 148 patients subjected to transvesical or transurethral prostatectomy to determine the clinical features of familial BPH. Patients were categorised as having familial BPH when 3 or more (including the patient) first-degree family members gave a history of BPH. Accordingly 23 cases who fit this criterion were accepted as having familial BPH and the rest of the cases were taken as the control group. The two groups were compared with respect to age, International Prostate Symptom Score (IPSS), quality of life score, prostate specific antigen (PSA), maximum urinary flow rate and the weight of the surgical prostate specimen. RESULTS: The mean age, IPSS, quality of life score, total PSA, maximum urinary flow rate and the weight of the surgical prostate specimen were found as 65.13 +/- 5.51 years, 23.13 +/- 4.82, 4.78 +/- 0.95, 6.0 +/- 4.1 ng/ml, 6.9 +/- 2.7 ml/s and 62.96 +/- 38.76 g, respectively, in the familial BPH group whereas the same parameters were measured as 68.13 +/- 7.68 years, 24.74 +/- 3.73, 4.52 +/- 0.85, 5.93 +/- 4.75 ng/ml, 4.6 +/- 1.71 ml/s and 70.87 +/- 53.21 g, respectively. No significant difference was present between familial and sporadic BPH cases in any of the studied parameters. CONCLUSION: The clinical features of familial BPH did not differ significantly from those of sporadic BPH.     

Modeling phasic insulin release: immediate and time-dependent effects of glucose

The cellular and molecular mechanisms of insulin secretion are being intensively investigated, yet most researchers are seemingly unaware of the complexity of the dynamic regulation of the secretion. In this article, we summarize studies of the physiology of insulin secretion performed over several decades. The insulin response of perifused islets of rats, perfused rat pancreas, or that of a human, to a square-wave glucose stimulus is biphasic, a transient first-phase response of 4- to 10-min duration followed by a gradual rise in secretion rates (second-phase response). Several hypotheses have been proposed to account for the phasic nature of insulin secretion; they are briefly discussed in this review. We have favored the hypothesis that nutrient stimulators such as glucose, in addition to a primary and almost immediate secretory signal, with time induce both stimulatory and inhibitory messages in the beta-cell, and those messages modulate the primary insulinogenic signal. Indeed, studies in the rat pancreas and in humans have demonstrated that short stimulations with glucose generate a state of refractoriness of the insulin secretion, which we have termed time-dependent inhibition (TDI). Nonnutrient secretagogues such as arginine induce strong TDI independent of the duration of stimulation. Once the agent is removed, TDI persists for a considerable period. In contrast, prolonged stimulations with glucose (and other nutrients) lead to the amplification of the insulin response to subsequent stimuli; this can be demonstrated in the perfused rat pancreas, in perifused islets from several rodents, and in humans. We have termed this stimulatory signal time-dependent potentiation (TDP). The generation of TDP requires higher glucose concentrations and prolonged stimulation; the effect is retained for some time after cessation of the stimulus. Of major interest is the observation that, while the acute insulin response to glucose is severely reduced in glucose-intolerant animals and humans, TDP seems to be intact. The cellular mechanisms of TDI and TDP are poorly understood, but data reviewed here suggest that they are distinct from those that lead to the acute insulin response to stimuli. A model is proposed whereby the magnitude and kinetics of the insulin response to a given stimulus reflect the balance between TDP and TDI. Researchers studying the cellular and molecular mechanisms of insulin release are urged to take into consideration these complex and opposing factors which regulate insulin secretion.