'Fracture' of the penis: a case series.

OBJECTIVES: To examine the epidemiology of penile 'fracture' and its presenting characteristics in the local population. DESIGN: Retrospective study. SETTING: District hospital, Hong Kong. PATIENTS: Patients with a discharge diagnosis of 'fractured' penis during a 7-year period from August 1998 to August 2005. MAIN OUTCOME MEASURES: Age, time of attendance, cause, symptoms, signs, emergency department diagnosis, site of rupture, operative findings, and final outcome. RESULTS: A total of 11 patients were identified. The mean age was 44 years (range, 30-63 years). The interval between time of injury and presentation ranged from 17 minutes to 7 days. Seven (64%) cases were attributed to sexual intercourse, three (27%) to penile manipulation, and one (9%) to rolling over the erect penis during sleep. Ten patients underwent surgery; all had primary suturing of the tunica tear, while two also required primary urethral repair. At follow-up, three (27%) patients had erectile dysfunction, one had mild penile deformity and one had a mild urethral stricture. CONCLUSION: Emergency physicians and surgeons, as well as family physicians, should be familiar with the presentation of 'fractured' penis, as prompt diagnosis and early surgical repair are instrumental in ensuring a successful outcome with minimal complications. The public should also be educated to seek medical attention immediately, as delay or failure to report may result in permanent physical and psychological disabilities that could otherwise have been avoided.

A selective regional response of cultured astrocytes to methamphetamine.

Methamphetamine (METH) has long-lasting neurotoxic effects on the dopamine and forebrain serotonin systems. It was reported that METH would induce the release of glutamate within the striatum and that it also caused astrogliosis. The mechanisms of this release and subsequent neurotoxicity are not well defined. The aim of this study was to examine the response of cultured astrocytes after METH-induced injury. Astrocytes were cultured from neonatal C57B1/6 mice brains. Cells were obtained from the mesencephalon, striatum and cortex in order to examine any regional differences. Cells were treated with 4mM METH for 4, 8, 12, 24 and 48 hr. Lactate dehydrogenase (LDH) levels were used as a measure of cell viability. At various time points, Western blot analyses were performed to study the change in GFAP and vimentin (markers for astrogliosis) levels. Change in glutamine synthase (GS), the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia in astrocytes, was also examined. The results showed that METH caused marked astrogliosis in striatal and mesencephalic astrocytes. Cells were transformed from protoplasmic (inactive) to fibrous (reactive) form after 48 hr treatment. There were also large amounts of vacuoles present in the cytoplasm of these cells. LDH results showed that there was only slight increase in enzyme levels after 48 hr treatment suggesting that the astrogliosis observed was not due to the decrease in cell viability. The amount of GS were depleted more rapidly in striatal astrocytes (50% of control by 8 hr treatment) followed by mesencephalic astrocytes (reaching 10% of control by 48 hr treatment). Cortical astrocytes showed only a 48% depletion by 48 hr treatment, indicating that they are more resistant to METH-induced toxicity. The rapid depletion of GS obtained in striatal and mesencephalic astrocytes suggested that astrocytes of the dopaminergic system are more sensitive to METH-induced injury. This may be due to the direct effects of METH-induced oxidative stress on the mitochondria of these cells resulting in GS depletion and astrogliosis.

A Selective Regional Response of Cultured Astrocytes to Methamphetaminea.

Methamphetamine (METH) has long-lasting neurotoxic effects on the dopamine and forebrain serotonin systems. It was reported that METH would induce the release of glutamate within the striatum and that it also caused astrogliosis. The mechanisms of this release and subsequent neurotoxicity are not well defined. The aim of this study was to examine the response of cultured astrocytes after METH-induced injury. Astrocytes were cultured from neonatal C57B1/6 mice brains. Cells were obtained from the mesencephalon, striatum and cortex in order to examine any regional differences. Cells were treated with 4 mM METH for 4, 8, 12, 24 and 48 hr. Lactate dehydrogenase (LDH) levels were used as a measure of cell viability. At various time points, Western blot analyses were performed to study the change in GFAP and vimentin (markers for astrogliosis) levels. Change in glutamine synthase (GS), the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia in astrocytes, was also examined. The results showed that METH caused marked astrogliosis in striatal and mesencephalic astrocytes. Cells were transformed from protoplasmic (inactive) to fibrous (reactive) form after 48 hr treatment. There were also large amounts of vacuoles present in the cytoplasm of these cells. LDH results showed that there was only slight increase in enzyme levels after 48 hr treatment suggesting that the astrogliosis observed was not due to the decrease in cell viability. The amount of GS were depleted more rapidly in striatal astrocytes (50% of control by 8 hr treatment) followed by mesencephalic astrocytes (reaching 10% of control by 48 hr treatment). Cortical astrocytes showed only a 48% depletion by 48 hr treatment, indicating that they are more resistant to METH-induced toxicity. The rapid depletion of GS obtained in striatal and mesencephalic astrocytes suggested that astrocytes of the dopaminergic system are more sensitive to METH-induced injury. This may be due to the direct effects of METH-induced oxidative stress on the mitochondria of these cells resulting in GS depletion and astrogliosis.