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To the Editor: Only a small amount of studies were reported about paraurethral duct infection in males.[1,2,3] To investigate the pathogens causing paraurethral duct infection and the secondary paraurethral duct dilation in males, and to understand the clinical characteristics and treatment options in paraurethral duct dilation, we retrospectively analyzed the data of male patients with paraurethral duct infection and subsequent paraurethral duct dilation who were treated at the Department of Dermatology of Changshu First People's Hospital from January 2000 to October 2013. Twenty-three patients (age range, 17–65 years; mean age, 31.5 years) with paraurethral duct infection and subsequent paraurethral duct dilation were enrolled in this study. All were presented with erythematous swelling of the external urethral orifice with a pinhead-like ostium at the center of the swollen area, through which pus could be expressed with pressure. The mean duration of paraurethral duct infection symptoms was 17 days (range: 9–39 days). All lesions were solitary. All the patients experienced tenderness, and 17 felt spontaneous pain. Among the purulent excretion specimens from the patients’ paraurethral ducts, 10 had detectable gonococci, 6 had Staphylococcus aureus, 5 had Chlamydia trachomatis, and 2 had Escherichia coli. Rapid plasma reagin test, Treponema pallidum hemagglutination assay, and human immunodeficiency virus antibody test results were also negative in all the patients. Patients with gonococcal infection were given intramuscular ceftriaxone sodium (1 g once daily for 5 days). Patients with S. aureus infection were treated with levofloxacin (0.5 g once daily for 8 days). Patients with C. trachomatis infection were treated with azithromycin (0.5 g once daily for 5 days). Patients with E. coli infection were treated with nitrofurantoin (0.1 g 3 times a day for 10 days). Re-evaluation was performed after 6 weeks and results showed that erythematous swelling of the external urethral orifice and the purulent excretion from the ostium were eliminated. However, the ostium did not close and transparent liquid could be expressed with pressure [Figure ​[Figure1a1a and ​andb].b]. None of the patients felt pain or had tenderness. Figure 1 (a) A pinhead-like ostium was present at the 8 o’clock position on the right side of the external urethral orifice. (b) The ostium did not close, and an overflow of transparent liquid was still visible after squeezing the lesion. The discharge from paraurethral duct was re-collected for Gram-staining. The discharge results were negative for trichomonads and Gram-negative diplococci were not visible within phagocytes, direct microscopic fungi tests were negative, and cultures for general bacteria, gonococci, Ureaplasma urealyticum, and fungi showed negative results. Fluorescence quantitative polymerase chain reaction for the DNA of gonococci, C. trachomatis, U. urealyticum, and herpes simplex virus types 1 and 2 also yielded negative results. All lesions were examined using an ultrasound system (ACUSON X300®, Siemens, Erlangen, Germany) with a probe frequency of 7.5–10.0 MHz. All patients’ examinations showed a tubular hypoechoic area with well-defined borders and smooth margins. One end was blind and the other was open to the environment. The mean lumen diameter was 1.1 ± 0.1 mm (range: 0.96–1.4 mm), and the mean length was 8.2 ± 0.8 mm (range: 7.1–11.7 mm). Thirteen patients were elected to undergo surgical treatment. Wedge excision was performed to remove the lesion. Postoperative histopathological examination revealed a tubular structure in the dermis connected to the epidermis and lined with stratified squamous epithelium. The peripheral stroma was fibrous and infiltrated by inflammatory cells. In all the 13 patients, the ostium had disappeared at 6-month follow-up and the glans penis showed no defects. Ten patients did not undergo excision; their lesions did not resolve over 6 months, and there continued to be a discharge of transparent liquid from the ostium with pressure. The male paraurethral duct is lined with columnar epithelium.[4] However, postoperative pathological examination in the current study showed that paraurethral ducts were all lined with squamous epithelium, and it is possible that the columnar epithelium had been destroyed by pathogens and replaced by squamous epithelium.[4] The present study showed that in addition to gonococci, S. aureus, C. trachomatis, and E. coli also infected the paraurethral duct and caused secondary paraurethral duct dilation. In the present study, two patients infected with E. coli had a history of anal intercourse before symptom onset. E. coli that had colonized the intestinal tract might have been transferred to the paraurethral ducts by anal intercourse and caused paraurethral duct infection. We consider local excision[1] to be a reasonable treatment strategy if the patient finds the symptoms distressing or if the dilated paraurethral duct is persistently infected. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Although bipolar disorder (BD) often presents in young adulthood, most individuals experience recurrent mood episodes, psychosocial deficits and high utilization of health services that persist into later life.1 Bipolar depression represents the predominant and least successfully treated phase of this illness. Individuals with BD spend more time ill with depressive symptoms than with manic/hypomanic or with cycling/mixed symptoms,2-4 and the proportion of time spent in depressive episodes to time spent in manic episodes increases with age. The few medications (quetiapine, lurasidone, olanzapine-fluoxetine) FDA-approved for treatment of bipolar depression were studied in predominantly middle-adult-aged cohorts. The clinical management of bipolar disorder in later life is also complicated by medical co-morbidity, cognitive impairment and polypharmacy.5 Furthermore, the neurobiological mechanisms that underlie bipolar depression may change with age and resistance to current treatments is high.6,7 Over the past decade there has been increasing evidence8 that implicates alterations in bioenergetic metabolism and enhanced oxidative stress in the neurobiology of bipolar disorder.9 Although the degree of mitochondrial dysfunction does not produce a substantial systemic metabolic disorder, it is likely sufficient to impact the CNS, as the brain requires twenty-fold the energy production of the rest of the body.9 Furthermore, the efficiency of mitochondrial energy production declines with age, an effect seen both in CNS and peripheral tissue. Successful treatment strategies for late life bipolar disorder may depend on developing novel ways to address reduced mitochondrial ATP (adenosine triphosphate) production. Coenzyme Q10 (CoQ10) is present in the phospholipid bilayers of mitochondria,10 shuttling electrons within the mitochondrial electron transport chain to generate ATP and serving as a potent antioxidant.11 CoQ10has been studied as a treatment for disorders implicating mitochondrial impairment, including congestive heart failure, diabetes, and degenerative neurological conditions.12-15 We now present the results from an open-label study of CoQ10 (added to existing treatment at a dosage of 800 mg/day for 4 weeks) for the treatment of older adults with a current episode of bipolar depression. We hypothesized that CoQ10 would reduce depressive symptoms as measured by the Montgomery Asberg Depression Rating Scale (MADRS).

Parkinson’s disease (PD) is a common neurodegenerative disorder for which genetic causes and susceptibility factors have been identified using linkage and association studies [1]. Many candidate genes have been investigated as risk factors for PD (www.pdgene.org) and several genome-wide association studies (GWAS) as well as three meta-analyses have been reported [5, 9, 10]. All GWAS indicate a strong association to several polymorphisms within the alpha-Synuclein (SNCA) gene, encoding a protein highly concentrated at presynaptic nerve terminals [13]. Most studies also confirm an association with the H1/H2 haplotype of the microtubule-associated protein tau (MAPT) gene that is enriched in axons [6]. In addition, the S18Y (rs5030732) polymorphism in the ubiquitin carboxyl-terminal hydrolase L1 (UCHL1), a neuron-specific enzyme that is involved in protein degradation, has been shown to modify enzymatic activity and to protect against PD [7]. N-acetyl transferase 2 (NAT2) is an enzyme responsible for the biotransformation of neurotoxins. An inherited defect, which results in a slower rate of metabolism can lead to greater vulnerability to neurotoxins and to a higher susceptibility of PD.[3] However, to date, all known risk factors explain only part of the heritability of PD and thus suggest additional genetic contributions. This might include interactions of genetic risk factors. After obtaining informed consent, we included 400 Caucasian PD patients enrolled in a clinical study in the US [12] and 353 controls from the US from the NINDS Human Genetics DNA Repository at the Coriell Institute for Medical Research. For diagnosis, the presence of bradykinesia was required in combination with at least one other cardinal symptom, i. e. rigidity, resting tremor or postural instability [2]. All patients were diagnosed within five years of enrollment. The study was approved by the local ethics committees and performed in accordance with the Declaration of Helsinki. We genotyped seven polymorphisms in six genes (Table 1A) previously reported as common genetic risk factors for PD.2 Genotyping methods included polyacrylamide gel electrophoresis, melting curve analysis, PCR fragment length determination and direct sequencing. NAT2 metabolizer phenotype was inferred using a validated discriminator [4]. PD risk attributable to each gene and their two-way interactions were estimated by logistic regression controlling for age and gender. Two-tailed p-values for the seven single-gene effects and for the 21 possible two-gene interactions were adjusted for multiple comparisons using a step-down Bonferroni correction. Table 1 Influence of genetic risk factors and the interaction of NAT2 and UCHL1 on PD risk, adjusted for age and gender. Consistent with the current literature [9], a significant association of PD risk was detected for both SNCA polymorphisms (Table 1A). No single gene association was found for any of the other genes including MAPT. Of note, the association of MAPT and PD depends on ethnicity [14]. Interestingly, we observed a significant interaction between NAT2 and UCHL1 genotypes (p = 0.013; Table 1B). The combination of either a slow NAT2 metabolizer genotype plus a UCHL1 A/A or A/C genotype, or an intermediate or rapid NAT2 metabolizer gentoype plus a UCHL1 C/C genotype, was significantly associated with an increased risk of PD but the alternative combinations were not associated with increased risk (Table 1B). There is increasing evidence that PD is not caused by a single factor, but rather by a complex interaction of genetic and environmental factors [11]. Single association studies in UCHL1 or NAT2 in Caucasians have resulted in contradictory results, i. e. demonstrating an association in only a third of the studies [8]. These inconsistencies may be explained, at least partly, by the interaction of the genotypes of these two genes as shown in the present study thus providing one more piece of the puzzle in the etiology of PD. Our results warranting further research to confirm this and elucidate other relevant interactions of genetic risk factors.

We carried out a chart review study to determine the rate of diagnosis of dystocia (abnormal progress) and the use of cesarean section to treat dystocia among 3887 primiparous women who gave birth to a single baby in the vertex presentation at four hospitals in Ottawa-Carleton in 1984. Of the 3740 women who had some labour 1127 (30.1%) were given a diagnosis of dystocia. Cesarean section for dystocia was done during all phases of labour (41% of procedures in the latent phase, 38% in the active phase and 21% in the second stage). The cesarean section rate varied among the hospitals from 11.8% to 19.6%. A total of 75% of the cesarean sections were for dystocia, disproportion or failed induction. The findings suggest that cesarean section is being done for disproportion without a trial of labour beyond the latent phase and for dystocia in the absence of fetal distress. If these practices were modified the cesarean section rate could be reduced from 16% to about 8%, the rate found in some other centres and that observed in Canada in the early 1970s.

Sixty infants (median gestational age 29 weeks) with acute and 60 infants (median gestational age 25 weeks) with chronic respiratory distress were randomised to be extubated either directly into a headbox or onto 3 cm H2O nasal continuous positive airway pressure (CPAP). Our aim was to test the hypothesis that extubation onto nasal CPAP rather than directly into a headbox was more likely to be associated with successful extubation in infants with acute rather than chronic respiratory distress. Overall the failure rate of extubation was approximately 33%, with no significant difference between the infants with acute and chronic respiratory distress. There was no significant difference in the failure rate of extubation among infants randomised to receive nasal CPAP or headbox oxygen in either the acute or chronic respiratory distress groups.