The leftward deletion alpha-thal-2 haplotype in a black subject with hemoglobin SS

We have identified a black individual with homozygous sickle cell anemia who is the silent carrier of alpha-thalassemia (genotype - alpha/alpha alpha) due to heterozygosity for the leftward deletion alpha-thal-2 haplotype. This deletion has not been described previously in a black subject and is the only leftward deletion that we have found among 255 alpha-thal-2 chromosomes from sickle cell subjects. Its effects on the clinical, hematologic, biosynthetic, and cellular pathology of sickle cell anemia resemble those reported for the common alpha-thalassemia genotypes of the black population.     

Bearing exchange in the management of pseudotumours

Introduction

Soft tissue reactions following metal-on-metal (MoM) arthroplasty of the hip have been under considerable discussion. These reactions are seen following both hip resurfacing and MoM total hip arthroplasty (THA). The phenomenon may arise owing to shedding of metal particles in high wear states, hypersensitivity with normal metal wear rates or a combination of the two.

Methods

Three patients were identified who had developed a soft tissue reaction (pseudotumour) following MoM hip resurfacing procedures. The prostheses were revised to ceramic-on-ceramic (CoC) THA with only minimal debridement of the pseudotumour. Pre and postoperative magnetic resonance imaging was performed to assess the size of the lesions.

Results

Progressive and satisfactory resolution of the associated pseudotumours was identified following revision of the prostheses to CoC THA.

Conclusions

In the early stages of pseudotumour formation following MoM hip resurfacing, this potentially devastating condition can be managed adequately with revision to a CoC bearing THA with minimal soft tissue excision.     

假细锥香茶菜新二萜成分——假细锥甲素的结构

从假细锥香茶菜(Rabdosia coetsoides C.Y.Wu)叶分离得到新二萜成分,根据紫外光谱、红外光谱、质谱、核磁共振氢谱及碳谱等分析,推定了化学结构,并经X-射线衍射确证,命名为假细锥甲素。     

The immunohistology of follicle lysis in lymph node biopsies from homosexual men

Follicle lysis is a characteristic alteration of B cell follicles described recently in lymph node biopsies from homosexual men. It consists of disruption of germinal centers by aggregates of small mature lymphocytes variably associated with erythrocyte extravasation. We studied the immunohistology of follicle lysis identified in lymph node biopsies from 11 homosexual men. The results indicate that follicle lysis has two principal immunohistologic features: (1) intrafollicular aggregates of small lymphocytes predominantly of polytypic mantle B cell phenotype (T015+/Leu-8+/mu+/delta+/k+ or lambda+), and (2) disruption of the normal, unified follicular meshwork of R4/23+ dendritic reticulum cells by these B cell aggregates. These structural alterations may affect the functional integrity of the germinal center as it pertains to the abnormal B cell effector function and the increased prevalence of B cell lymphoma recently documented in the acquired immunodeficiency syndrome and related disorders. Because dendritic reticulum cells weakly express the Leu-3 (T4) antigen, which is known to be an essential component of the receptor for human T- lymphotropic virus type III/lymphadenopathy-associated virus (HTLV- III/LAV) retrovirus infection, it is possible that retroviral infection of dendritic reticulum cells may play a role in the pathogenesis of follicle lysis.     

Effect of green tea-loaded chitosan nanoparticles on leathery dentin microhardness

The purpose of this study was to assess the effect of a chitosan-based nanoformulation containing green tea on leathery (remaining) dentin subsurface microhardness. Size distribution, polydispersity index (PDI) and zeta potential (mV) of nanoformulations were previously determined by dynamic light scattering (DLS). Human dentin specimens were exposed to Streptococcus mutans for 14 d. Soft dentin were selectively removed by Er:YAG laser (n?=?30) or bur (n?=?30). Remaining dentin was biomodified with chitosan nanoparticles (Nchi, n?=?10) or green tea-loaded chitosan nanoparticles (Gt?+?Nchi, n?=?10) for 1 min. Control group (n?=?10) did not receive any treatment. Subsurface microhardness (Knoop) was evaluated in hard (sound) and soft dentin, and then, in leathery dentin and after its biomodification, at depths of 30, 60 and 90 μm from the surface. Nchi reached an average size of?≤?300 nm, PDI varied between 0.311 and 0.422, and zeta potential around?+?30 mV. Gt?+?Nchi reached an average size of?≤?350 nm, PDI?<?0.45, and zeta potential around?+?40 mV. Soft dentin showed significantly reduced microhardness at all depths (p?>?0.05). The subsurface microhardness was independent of choice of excavation method (p?>?0.05). At 30 µm from the surface, Gt?+?Nchi increased the leathery dentin microhardness compared to untreated group (p?<?0.05). Nchi promoted intermediate values (p?>?0.05). Both nanoformulations showed an average size less than 350 nm with nanoparticles of different sizes and stability along the 90-day period evaluated. Subsurface microhardness of bur-treated and laser-irradiated dentin was similar. At 30 µm, the biomodification with Gt?+?Nchi improved the microhardness of leathery dentin, independently of caries excavation method used.

     

Neuropeptide Y Attenuates Stress‐Induced Bone Loss Through Suppression of Noradrenaline Circuits

Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress‐induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress‐induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6‐week restraint, or cold‐stress protocol, Npy‐null mice exhibit three‐fold greater bone loss compared to wild‐type mice, owing to suppression of osteoblast activity. This stress‐protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin‐releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy‐null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy‐null mice blocks the increase in circulating noradrenaline and the stress‐induced bone loss. Thus, NPY protects against excessive stress‐induced bone loss, through Y2 receptor‐mediated modulation of central and peripheral noradrenergic neurons. © 2014 American Society for Bone and Mineral Research.