Physical disability contributes to caregiver stress in dementia caregivers

BACKGROUND: Previous findings of studies on the impact of physical illness on caregiver health have been inconsistent. The authors wanted to determine whether physical disability, as determined by the SF-12 survey that provides information on both physical and mental health problems, contributes to caregiver stress. METHODS: The authors interviewed 91 primary caregivers (aged 38-85 years) of persons with dementia who had been referred by their family physicians for the first time for formal support services or memory evaluation. Caregivers completed the SF-12 version of the Medical Outcomes Study Short Form Health Survey that generates Mental Component Summary (MCS) and Physical Component Summary (PCS) scores and reported on caregiver stress and concurrent medical conditions and medications. RESULTS: Most caregivers reported stress (76.9%), having medical conditions (72.4%), or taking medications (67%). The MCS but not the PCS scores were significantly lower than community norms, indicating an excess of disability due to mental health problems. Nevertheless, 40.7% had PCS scores indicating some degree of physical disability. Using multiple logistic regression analysis, PCS scores but not the presence of medical problems were independently associated with caregiver stress. CONCLUSIONS: Chronic disability as assessed by SF-12 PCS scores is independently associated with caregiver stress. These data suggest that caregivers of persons with dementia should be assessed for disabling physical conditions and mental health problems. In addition, reducing the impact of physical disability could ameliorate caregiver stress.     

Polyarteritis nodosa in children: radiological aspects and diagnostic correlation

The radiological findings in 14 children with polyarteritis nodosa (PN) were evaluated in relation to clinical, laboratory, and histological findings. In this series, there were two major groups of radiological findings, one associated with renal insufficiency and the other with intestinal vascular insufficiency. No radiographic finding was pathognomonic. Two patients were suspected of having small bowel intussusception (SBI), and SBI was documented at laparotomy in a third patient. The diagnosis and management of PN in children is dependent upon the correlation of clinical and laboratory findings. Associated pertinent radiological features which may be useful in the management of children with PN are reviewed.     

Melatonin Rhythms in Quail: Regulation by Photoperiod and Circadian Pacemakers

The profile of melatonin in the eyes, pineal, and blood of Japanese quail was assessed in birds held under LD 16:8 and LD 6: 18 photoperiods. Melatonin levels in all three tissues showed a robust daily rhythm with higher levels occurring at night. The amplitude of the rhythm was depressed and its duration lengthened on LD 6: 18 relative to LD 16:8. The blood melatonin rhythm precisely reflected the rhythms shown by the pineal and eyes, supporting the idea that the blood rhythm is a result of melatonin secretion by both the eyes and pineal.
The ocular melatonin rhythm continued after sectioning of the optic nerve, was reentrainable to a shift in the phase of the LD cycle, and persisted for at least 2 days in constant darkness. It was concluded that either (1) an intraocular circadian clock drives the ocular melatonin rhythm, or (2) an extraocular clock drives the ocular melatonin rhythm via a route other than the efferent innervation (which enters the eye via the optic tract).     

Citrobacter koseri and Citrobacter amalonaticus isolates carry highly divergent beta-lactamase genes despite having high levels of biochemical similarity and 16S rRNA sequence homology

OBJECTIVES: Isolates previously identified as Citrobacter diversus are now known as Citrobacter koseri. We measured sequence variation at the beta-lactamase structural gene among a group of clinical isolates originally identified as C. diversus by API 20E profiling. METHODS: beta-Lactamase and 16S rRNA genes were amplified by PCR and sequenced by standard methods. beta-Lactamase induction was attempted in liquid-grown cultures using cefoxitin. Nitrocefin hydrolysis assays were performed using a spectrophotometer. RESULTS: Analysis of 16S rRNA gene sequences showed that Citrobacter spp. isolates with an inducible beta-lactamase gene, cdiA, closely related to 'C. koseri ' NF85 and ULA27 are actually Citrobacter amalonaticus. C. koseri isolates, whose identities were confirmed by 16S rRNA sequencing, produce a class A beta-lactamase, Cko, constitutively at low levels. The cko and cdiA beta-lactamase genes share <45% identity. CONCLUSIONS: We have confirmed that cko is a beta-lactamase gene carried by C. koseri, and that isolates previously identified as 'C. koseri ', but carrying the cdiA beta-lactamase gene are C. amalonaticus. Thus, beta-lactamase-gene-specific PCR may provide a valuable tool to differentiate these biochemically homogeneous Citrobacter species.     

HER2/neu gene amplification and protein overexpression in G3 pT2 transitional cell carcinoma of the bladder: a role for anti-HER2 therapy?

HER2/neu is an oncogene encoding a type 1 tyrosine kinase growth factor receptor. Polysomy 17, gene amplification and HER2/neu protein overexpression are associated with a poor prognosis in transitional cell carcinomas (TCC) of the bladder. Due to the application of different laboratory techniques, the exact incidence of HER/neu abnormalities remains uncertain in TCC. Standardised laboratory techniques are therefore important in the determination of the HER2/neu status if an assessment of the potential value of anti-HER2/neu treatments in the clinical management of patients with TCC is to be made. In this study, 75 TCCs with evidence of detrusor muscle invasion at first clinical presentation were included. Gene amplification, polysomy 17 and HER2 copy number were assessed using fluorescence in situ hybridisation (FISH), with separate probes for chromosome 17 and HER2/neu. Protein overexpression was assessed using immunohistochemistry (IHC), with the CB11 antibody and a scoring system evaluating only membranous staining as positive. The mean patient age was 69.5 years (range 42-93 years) and the median survival was 15 months (range 1-156 months). Polysomy 17 occurred in 97%, increased HER/neu copy number in 92% and HER2/neu gene amplification in 7%. Protein overexpression occurred in 57% of cases. Polysomy 17 and HER2/neu protein overexpression are common in G3 pT2 TCCs of the bladder. However, gene amplification is uncommon. Mechanisms other than gene amplification may be responsible for protein overexpression in this tumour type. Evidence from breast cancer suggests that only tumours with HER2/neu gene amplification respond to the anti-HER2/neu therapy trastuzumab (Herceptin). If this were true for bladder cancer, only 4/75 (5%) of G3 pT2 TCCs would be suitable for treatment. The role of trastuzumab in these tumours remains untested at present.     

Congenital methemoglobinemia: a rare cause of cyanosis in the newborn--a case report

Cyanosis is a physical finding that can occur at any age but presents the greatest challenge when it occurs in the newborn. The cause is multiple, and it usually represents an ominous sign, especially when it occurs in association with neonatal sepsis, cyanotic congenital heart disease, and airway abnormalities. Cyanosis caused by abnormal forms of hemoglobin can also be life-threatening, and early recognition is mandatory to prevent unnecessary investigations and delay in management. Abnormal hemoglobin, such as hemoglobin M, is traditionally discovered by electrophoresis, so the newborn screen, which is mandatory in several states, is a useful tool for the diagnosis. Although acquired methemoglobinemia, caused by environmental oxidizing agents, is common, congenital deficiency of the innate reducing enzyme is so rare that only a few cases are documented in the medical literature around the world. We present a neonate with cyanosis as a result of congenital deficiency of the reduced nicotinamide adenine dinucleotide-cytochrome b5 reductase enzyme. This infant was found to be blue at a routine newborn follow-up visit. Sepsis, structural congenital heart disease, prenatal administration, and ingestion of oxidant dyes were excluded as a cause of the cyanosis by history and appropriate tests. Chocolate discoloration of arterial blood provided a clue to the diagnosis. A normal newborn screen and hemoglobin electrophoresis made the diagnosis of hemoglobin M unlikely as the cause of the methemoglobinemia (Hb A 59.4%, A2 1.8%, and F 38.8%). Red blood cell enzyme activity and DNA analysis revealed a homozygous form of the cytochrome b5 reductase enzyme deficiency. He responded very well to daily methylene blue and ascorbic acid administration, and he has normal growth and developmental parameters, although he shows an exaggerated increase in his methemoglobin level with minor oxidant stress such as diarrhea.