Melatonin increases brown adipose tissue mass and function in Zücker diabetic fatty rats: implications for obesity control

Melatonin limits obesity in rodents without affecting food intake and activity, suggesting a thermogenic effect. Previously we demonstrated that melatonin browns subcutaneous fat in Zücker diabetic fatty (ZDF) rats. Other works pointed to melatonin as a signal that increases brown adipose tissue (BAT) mass and function in rodents. However, direct proof of thermogenic properties (uncoupled mitochondria) of the newly recruited BAT in response to melatonin is still lacking. Therefore, in this work, we investigated if melatonin recruits thermogenic BAT in ZDF rats. Zücker lean (ZL) and ZDF animals were subdivided into two groups, control (C) and treated with oral melatonin (M) for 6 weeks. Mitochondrial mass, activity of citrate synthase (CS), and respiratory chain complexes I and IV were lower in C‐ZDF than in C‐ZL animals (P < .001). Melatonin treatment increased BAT weight in ZDF rats (P < .001). Also, it rose mitochondrial mass (P < .01) and activities of CS and complexes I and IV (P < .001) in both, ZDF and ZL rats. Uncoupling protein 1 (UCP1) mRNA and protein were 50% lower in BAT from obese rats. Also, guanosine diphosphate (GDP) binding was lower in ZDF than in lean rats (P < .01). Melatonin treatment of obese rats restored the expression of UCP1 and GDP binding to levels of lean rats and sensitized the thermogenic response to cold exposure. These data demonstrated that melatonin recruits thermogenic BAT in ZDF rats. This may contribute to melatonin's control of body weight and its metabolic benefits.     

Nutritional status of schoolgirls in Isfahan,Iran: Anthropometric and hematological measurements

Weights, heights and other anthropometric measurements are presented for seven year old schoolgirls belonging to different socioeconomic groups in Iran. It was found that measurements of the children of professional people were indistinguishable from internationally accepted standards. The measurements of girls in the lower socioeconomic strata were lower. Hematological measurements indicated lack of anemia in any of the children. Possible reasons for these findings are discussed in relation to previously published reports of nutritional problems in Iran.     

The Orthogeriatrics Model of Care: Systematic Review of Predictors of Institutionalization and Mortality in Post-Hip Fracture Patients and Evidence for Interventions

Hip fracture is a common serious complication of osteoporosis, which is associated with high morbidity and mortality. In nursing home residents, incidence rates of hip fractures are at least twice to three times higher than in community-dwellers of the same age and sex. Older adults with hip fracture have a 5- to 8-fold increased risk for all-cause mortality and much higher risk of institutionalization. Therefore, interventions to prevent institutionalization, prevent a second fracture in institutionalized patients, and decrease mortality after a hip fracture are highly needed. The orthogeriatrics model of care is a shared-care approach to patients after suffering a hip fracture. This program, which has been studied in models run by geriatricians with the assistance of a multidisciplinary team, includes a comprehensive medical and nursing admission assessment focusing on the patient’s premorbid function, cognition, comorbidities, and risks is followed by a comprehensive care plan design. This systematic review describes and analyzes the interrelation between hip fracture and nursing home placement taking into consideration those evidence-based interventions to prevent later complications and future institutionalization.     

Ultra-Violet Light Emission from HPV-G Cells Irradiated with Low Let Radiation From 90Y; Consequences for Radiation Induced Bystander Effects

In this study, we aimed to establish the emission of UV photons when HPV-G cells and associated materials (such as the cell substrate and cell growth media) are exposed to low LET radiation. The potential role of UV photons in the secondary triggering of biological processes led us to hypothesize that the emission and absorption of photons at this wavelength explain some radiation induced “bystander effects” that have previously been thought to be chemically mediated. Cells were plated in Petri-dishes of two different sizes, having different thicknesses of polystyrene (PS) substrate, and were exposed to β-radiation from ⁹⁰Y produced by the McMaster Nuclear Reactor. UV measurements were performed using a single photon counting system employing an interference-type filter for selection of a narrow wavelength range, 340±5 nm, of photons. Exposure of the cell substrates (which were made of polystyrene) determined that UV photons were being emitted as a consequence of β particle irradiation of the Petri-dishes. For a tightly collimated β-particle beam exposure, we observed 167 photons in the detector per unit μCi in the shielded source for a 1.76 mm thick substrate and 158 photons/μCi for a 0.878 mm thick substrate. A unit μCi source activity was equivalent to an exposure to the substrate of 18 β-particles/cm² in this case. The presence of cells and medium in a Petri-dish was found to significantly increase (up to a maximum of 250%) the measured number of photons in a narrow band of wavelengths of 340±5 nm (i.e. UVA) as compared to the signal from an empty control Petri-dish. When coloured growth medium was added to the cells, it reduced the measured count rate, while the addition of transparent medium in equal volume increased the count rate, compared to cells alone. We attribute this to the fact that emission, scattering and absorption of light by cells and media are all variables in the experiment. Under collimated irradiation conditions, it was observed that increasing cell density in medium of fixed volume resulted in a decrease in the observed light output. This followed a roughly exponential decline. We suggest that this may be due to increased scattering at the cell boundary and absorption of the UV in the cells. We conclude that we have measured UVA emitted by cells, cell medium and cell substrates as a consequence of their irradiation by low LET β-particle radiation. We suggest that these secondary UV photons could lead to effects in non-targetted cells. Some effects that had previously been attributed to a chemically mediated “bystander effect” may in fact be due to secondary UV emission. Some radiation bystander effect studies may require re-interpretation as this phenomenon of UV emission is further investigated.     

A multi-resolution textural approach to diagnostic neuropathology reporting

Journal of Neuro-Oncology - We present a computer aided diagnostic workflow focusing on two diagnostic branch points in neuropathology (intraoperative consultation and p53 status in tumor biopsy...     

Misdiagnosis of trigger finger? Flexor seed ganglion masquerading as closed FDS rupture

The authors present the case of a 25-year-old right-handed female warehouse worker who presented to the emergency department complaining of an inability to flex her left index finger and an associated painful lump on the volar surface of her left index finger over the metacarpal–phalangeal joint following a hyperextension injury. Clinical examination suspected a closed flexor digitorum superficialis (FDS) injury; however, on surgical exploration, the FDS tendon to the left index finger was intact. A flexor sheath seed ganglion was identified. This case, although rare, identifies the modality of specialist ultrasound scan (USS) by those with an interest in musculoskeletal radiology to be used in cases where the history is unclear or diagnosis in doubt. Level of Evidence: Level V, diagnostic study.     

A Novel Nonsense Mutation in RSPO4 Gene Underlies Autosomal Recessive Congenital Anonychia in a Pakistani Family

Abstract: Congenital anonychia is an inherited autosomal recessive disorder characterized by complete absence of fingernails or toenails, or both. In the present study, we have described a consanguineous Pakistani family having a family member affected with congenital anonychia. Genotyping using polymorphic microsatellite markers showed linkage of the family to gene RSPO4 encoding R‐spondin and mapped on human chromosome 20p13. Deoxyribonucleic acid sequence analysis of the gene identified a novel nonsense mutation (c.18C>A; p.Cys6X) in the affected family member.