Vesicocutaneous fistula: An unusual complication of inguinoscrotal hernia

Involvement of the urinary bladder in an inguinal hernia is common, but massive bladder hernia is rare. Most urinary bladder herniations are discovered and repaired during surgery. We report a case of large incarcerated inguino-scrotal hernia, which was reduced only to present as a scrotal abscess and vesicocutaneous fistula; an unusual complication. The patient was managed conservatively due to underlying comorbidities.     

Functional dyspepsia: New insights into the pathophysiology

Abstract The pathogenesis of functional dyspepsia remains poorly understood. There is increasing evidence pointing to a predominant role of gastroduodenal visceral hypersensitivity in the pathogenesis, where patients have abnormally reduced gastric and small intestinal sensory thresholds. Motor abnormalities observed in subgroups of patients include delayed gastric emptying, antral hypomotility, gastric dysrhythmias, abnormal gastrointestinal reflexes and small intestinal dysmotility, but these may be secondary pheno nena. The central nervous system modifies peripheral visceral afferent pathways and, hente, psychological factors may possibly alter symptom status. Other putative mechanisms include Helicobacter pylori gastritis and gastric acid hypersecretion or sensitivity, but the role of these remain controversial.     

Recognition of Dementia in General Practice: Comparison of General Practitioners' Opinions with Assessments Using the Mini-Mental State Examination and the Blessed Dementia Rating Scale

Mant A, Eyland E A, Pond D C, Saunders N A and Chancellor AH B. Recognition of dementia in general practice: comparisonof general practitioners' opinions with assessments using themini-mental state examination and the Blessed dementia ratingscale. Family Practice 1988; 5: 184–188. In a study of 226 elderly residents in a retirement villagein Sydney, Australia, general practitioners' opinions aboutdementia status had high positive and negative predictive valuesand high specificity, but low sensitivity when evaluated againstthe mini-mental state examination and the Blessed dementia ratingscale. General practitioners were found to disagree with thesetwo measures more often when patients were in advanced old age,and when they considered the patients to be depressed. We concludethat the general practitioner can increase his or her sensitivityto dementia in the elderly by use of either measure.     

Stem Cell Migration and Proliferation During Severe Anemia

The pluripotential stem cell (CFU) compartment of marrow and spleen wasevaluated in mice subjected to an intense erythroid stimulus associated withphenylhydrazine-induced anemia. Erythroid hyperplasia occurred in both marrow and spleen. CFU in the marrowgradually declined to approximately 50per cent of control levels (day 5) whiletheir numbers in the spleen increased(fourfold) by day 3 and were maintainedat this level for several days. Thesechanges in numbers of marrow andsplenic CFU were not associated withCFU proliferation. Thereafter, CFU inthe marrow, but not in the spleen, entered active cell cycle. The data suggestthat CFU migrate from marrow to spleenduring the demands of severe anemia.The induction of marrow CFU into cyclefurther suggests a negative feedback,which, perhaps through cell-cell interaction, maintains stem cells at a criticalcompartment size. The failure of splenicCFU to cycle may reflect the converseeffect, i.e. an inhibition on stem cell proliferation in the wake of an expandedstem cell pool.

Submitted on March 17, 1970 Revised on May 14, 1970 Accepted on June 9, 1970     

LATE ONSET HUNTINGTON'S DISEASE AS A CAUSE OF DEMENTIA: WHERE SHOULD THE CLINICIAN'S INDEX OF SUSPICION LIE?

Our experience with two genetically confirmed cases of late onset Huntington's disease (HD) in a longitudinal dementia research study suggested that clinical misdiagnosis can easily occur. We therefore undertook genetic testing for HD in a further 84 elderly subjects, 81 of whom had come to postmortem; 75 subjects had dementia and nine were normal controls. A quarter of the demented group had demonstrated extrapyramidal symptoms in life but in none had HD formed part of the differential diagnosis. Although no genetically confirmed cases were found in this second group, the original cases serve as a reminder that late onset HD is a cause of dementia. Genetic confirmation should be sought when the condition forms part of the final differential diagnosis. Further studies conducted in the routine clinical setting are now required since it is in this environment that late onset HD is likely to be misdiagnosed in favour of other forms of dementia.     

The Renin–Angiotensin System Mediates the Effects of Stretch on Conduction Velocity,Connexin43 Expression,and Redistribution in Intact Ventricle

Effect of Stretch on Conduction and Cx43 . Introduction: In disease states such as heart failure, myocardial infarction, and hypertrophy, changes in the expression and location of Connexin43 (Cx43) occur (Cx43 remodeling), and may predispose to arrhythmias. Stretch may be an important stimulus to Cx43 remodeling; however, it has only been investigated in neonatal cell cultures, which have different physiological properties than adult myocytes. We hypothesized that localized stretch in vivo causes Cx43 remodeling, with associated changes in conduction, mediated by the renin–angiotensin system (RAS). Methods and Results: In an open‐chest canine model, a device was used to stretch part of the right ventricle (RV) by 22% for 6 hours. Activation mapping using a 312‐electrode array was performed before and after stretch. Regional stretch did not change longitudinal conduction velocity (post‐stretch vs baseline: 51.5 ± 5.2 vs 55.3 ± 8.1 cm/s, P = 0.24, n = 11), but significantly reduced transverse conduction velocity (28.7 ± 2.5 vs 35.4 ± 5.4 cm/s, P < 0.01). It also reduced total Cx43 expression, by Western blotting, compared with nonstretched RV of the same animal (86.1 ± 32.2 vs 100 ± 19.4%, P < 0.02, n = 11). Cx43 labeling redistributed to the lateral cell borders. Stretch caused a small but significant increase in the proportion of the dephosphorylated form of Cx43 (stretch 9.95 ± 1.4% vs control 8.74 ± 1.2%, P < 0.05). Olmesartan, an angiotensin II blocker, prevented the stretch‐induced changes in Cx43 levels, localization, and conduction. Conclusion: Myocardial stretch in vivo has opposite effects to that in neonatal myocytes in vitro. Stretch in vivo causes conduction changes associated with Cx43 remodeling that are likely caused by local stretch‐induced activation of the RAS. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1276‐1283, November 2010)     

NASPE POLICY STATEMENT The NASPE* BPEG** Defibrillator Code

BERNSTEIN, A.D., et al .: The NASPE/BPEG Defibrillator Code. A new generic code, patterned after and compatible with the NASPE/BPEG Generic Pacemaker Code (NBG Code) was adopted by the NASPE Board of Trustees on January 23, 1993. It was developed by the NASPE Mode Code Committee, including members of the North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG). It is abbreviated as the NBD (for NASPE/BPEG Defibrillator) Code. It is intended for describing the capabilities and operation of implanted cardioverter defibrillators (ICDs) in conversation, record keeping, and device labeling, and incorporates four positions designating: (1) shock location; (2) antitachycardia pacing location; (3) means of tachycardia detection; and (4) antibradycardia pacing location. An additional Short Form, intended only for use in conversation, was defined as a concise means of distinguishing devices capable of shock alone, shock plus antibradycardia pacing, and shock plus antitachycardia and antibradycardia pacing. (PACE, Vol. 16, September 1993)     

The kinetics of metaphase arrest in human psoriatic epidermis: an examination of optimal experimental conditions for determining the birth rate

The optimum experimental conditions have been investigated for the measurement of the birth-rate in human psoriatic epidermis using the vinca alkaloids vinblastine and vincristine. The dose response characteristics of the two drugs were assessed over a 2.5 h collection period; although the dose response characteristics differed between the two agents, a dose of 1μg injected intradermally was considered to be optimal for both. The linearity of metaphase correction was assessed for both agents, taking biopsies for up to 10 h after injection. It was found that there was a delay period for up to an hour which must be avoided during the analysis to prevent an underestimate of the birth rate. However, linearity was then demonstrated for up to 4 h after injection. Metaphase degeneration was assessed by isolating a cohort of unlabelled cells in the G₂ phase and tracing their fate over the next 10 h. It was found that the minimum life of an arrested metaphase was of the order of 4 h, and then metaphases degenerated at the rate of approximately 0.4% per hour. It is recommended that metaphase arrest experiments in psoriatic epidermis be confined to 4 h although, if required, correction factors are available to correct for experiments which are lengthened. Finally it is shown that flux into DNA synthesis exceeds the flux into mitosis by four or five times; several explanations are considered, and it is thought that the most likely explanation involves the death of psoriatic cells in the G₂ phase.     

Essential fatty acid deficient hairless mouse: the effects of topical agents on the epidermis

Essential fatty acid deficient (EFA deficient) hairless mice were used to test the ability of topical agents to reduce the high epidermal DNA synthesis and acanthosis present in EFA deficiency. An established therapeutic agent known to be effective in psoriasis (betamethasone 17-valerate) significantly reduced the epidermal DNA synthesis, mitotic count and epidermal cell thickness. Linoleic acid reduced DNA synthesis and returned epidermal histology towards that of normal skin. Prostaglandin E₂ analogue (15 (S)-15-methyl PGE₂ methyl ester) reduced epidermal DNA synthesis both in treated and distant skin sites. Prostaglandin E₂ was less effective than the analogue but slightly reduced epidermal DNA synthesis and thickness. Prostaglandin F_2α had no obvious effect on the epidermis. Chlorambucil reduced epidermal DNA synthesis and thickness. Vitamin A acid increased DNA synthesis and epidermal cell thickness but reduced the hypcrkcratosis of EFA deficiency. A rapid epidermal cell transit was found in EFA deficient mice, approximately three times faster than in normal mouse epidermis.