Enhanced Bone Regeneration Using Porcine Small Intestinal Submucosa

Small instestinal submucosa (SIS) is an easily produced material that has been used experimentally for tissue engineering. To evaluate the ability of SIS to facilitate bone growth within a long-bone defect, a segment of the radius was surgically removed in adult, female Sprague-Dawley rats. The defect was either left unfilled or implanted with SIS, demineralized cortical bone (DMCB), or ovalbumin. The defect was evaluated radiographically and histologically after 3, 6, 12, and 24 weeks. Tissue remodeling within the defect was evident by week 3 in SIS- and DMCB-treated rats. Filling was characterized initially by infiltration of mononuclear cells and extracellular material in SIS-implanted rats and multifocal remodeling bone particles and cartilage formation in DMCB implanted rats. Cartilage was observed as early as 3 weeks and bone as early as 6 weeks in SIS-implanted rats. Filling of the defect arose from multiple foci in DMCB-implanted rats, but was contiguous with and parallel to the ulnar shaft in SIS-implanted rats, suggesting that defect repair by SIS may be conductive rather than inductive. Rats in which the defect was left unfilled demonstrated slow but progressive filling of the defect, characterized by mononuclear cell infiltrates and fibrous extracellular material. In summary, SIS facilitated rapid filling of a longbone defect. These results suggest that SIS may be useful as a bone repair material.     

The role of mast cells in neuroinflammation

Mast cells (MCs) are densely granulated perivascular resident cells of hematopoietic origin and well known for their pathogenetic role in allergic and anaphylactic reactions. In addition, they are also involved in processes of innate and adaptive immunity. MCs can be activated in response to a wide range of stimuli, resulting in the release of not only pro-inflammatory, but also anti-inflammatory mediators. The patterns of secreted mediators depend upon the given stimuli and microenvironmental conditions, accordingly MCs have the ability to promote or attenuate inflammatory processes. Their presence in the central nervous system (CNS) has been recognized for more than a century. Since then a participation of MCs in various pathological processes in the CNS has been well documented. They can aggravate CNS damage in models of brain ischemia and hemorrhage, namely through increased blood–brain barrier damage, brain edema and hemorrhage formation and promotion of inflammatory responses to such events. In contrast, recent evidence suggests that MCs may have a protective role following traumatic brain injury by degrading pro-inflammatory cytokines via specific proteases. In neuroinflammatory diseases such as multiple sclerosis, the role of MCs seems to be ambiguous. MCs have been shown to be damaging, neuroprotective, or even dispensable, depending on the experimental protocols used. The role of MCs in the formation and progression of CNS tumors such as gliomas is complex and both positive and negative relationships between MC activity and tumor progression have been reported. In summary, MCs and their secreted mediators modulate inflammatory processes in multiple CNS pathologies and can thereby either contribute to neurological damage or confer neuroprotection. This review intends to give a concise overview of the regulatory roles of MCs in brain disease.     

Endovenous Glue-Induced Thrombosis in Nonthermal Glue Closure Therapy for Greater Saphenous Vein Insufficiency: A Single-Center Experience

A retrospective analysis of endovenous glue-closure therapy (EVGC) performed in 76 greater saphenous veins (GSVs) from February 2016 to December 2017 was conducted to assess the incidence and characteristics of endovenous glue-induced thrombosis (EGIT), a phenomenon unique to nonthermal EVGC for GSV insufficiency. Kabnick and Lawrence classifications for endovenous heat-induced thrombosis were adopted. Seven instances of EGIT were detected among 54 patients (13%), with median/mode Kabnick and Lawrence classifications of 2/2 and 4/5, respectively. EGIT resolved with observation within an average of 5.2 wk after detection (range, 2–8 wk) without deep vein thrombosis or pulmonary embolism. EGIT was associated with significantly greater mean age (+7.75 y; P = .0308).     

Studies on the effect of vanadate on endocytosis and shape changes in human red blood cells and ghosts

When amphipathic cationic drugs are added to intact human RBCs, the RBCs first undergo a stomatocytic shape change and then, if relatively large amounts of drug are added and if the metabolic state of the RBC is appropriate, endocytic vacuoles form. Vanadate has a structural similarity to the transition state of phosphate, which presumably accounts for its ability to inhibit phosphohydrolases, although other actions of vanadate have been described. Vanadate inhibited three forms of drug-induced endocytosis in intact RBCs despite the fact that the three drugs chosen (primaquine, chlorpromazine, and vinblastine) are known to have differing requirements for RBC ATP. Vanadate also inhibited the stomatocytic shape change produced by primaquine, chlorpromazine, and vinblastine, but not the stomatocytosis produced by low pH. Vanadate had no effect on RBC echinocytosis produced by lysophosphatidylcholine. In studying endocytosis in hypotonic, leaky, "white" ghosts, we discovered that vanadate inhibited only the endocytosis produced by Mg-ATP and not the endocytosis produced by manipulations that directly attack the cytoskeletal proteins. These findings suggest that ATP hydrolysis has a role in some forms of amphipathic cation-induced stomatocytosis and endocytosis in intact RBCs. In addition, studies in ghosts support the idea that Mg-ATP does indeed produce "energized" endocytosis dependent on utilization or hydrolysis of ATP.     

Molecular characterization of a high A2 beta thalassemia by direct sequencing of single strand enriched amplified genomic DNA

Two families, one of Anglo-Saxon-Dutch descent, and the other, West Indian black, have an atypical beta thalassemia characterized by an unusually high level of Hb A2 in the heterozygous state. Restriction endonuclease mapping showed a deletion of about 1.35 kilobase (kb) in the 5' region of the beta globin gene. Direct sequencing of a specific region of genomic DNA amplified by a new modification of the polymerase chain reaction defined the deletion to be 1,393 base pairs (bp) and to be the same in both families. The deletion extends from 485 bp 5' to the mRNA CAP site to the middle of the second intervening sequence. This deletion, together with three others previously described that remove the 5' end of the beta gene but leave the delta gene intact, are all associated with unusually high levels of Hb A2 in the heterozygous state.     

Lunar soil simulants alter macrophage survival and function

Lunar regolith samples collected during previous Apollo missions were found to contain components that were established to be toxic to humans; however, the health effects due to inhalation of lunar soil as a whole are still unknown. Macrophages residing in the alveolar sacs of the lungs constitute one of the last lines of defense against inhaled particulates before entry into the bloodstream. Here, we examine the macrophage response to lunar simulants that are similar in chemical composition to the lunar regolith. We assess cytotoxicity, cellular morphology, phagocytosis of simulants and expression of inflammatory markers. Overall, the exposure of macrophages to lunar simulants results in moderate cytotoxicity and marked alteration of cell morphology and uptake of the simulants. Interestingly, simulant exposure decreased proinflammatory gene expression, but may induce an anti‐inflammatory phenotype in the cells. These results illustrate that although macrophages phagocytose lunar simulants as a protective response, the simulants do induce a degree of macrophage cell death. Our study reveals some toxicity associated with lunar simulants and supports further evaluation of the inhalation of lunar regolith to understand the risks of exposure fully.     

Neurocognitive impairment associated with predominantly early stage HIV infection in Abuja,Nigeria

Detailed neuropsychological testing was performed on 133 human immunodeficiency virus (HIV) seropositive (SP) and 77 HIV seronegative (SN) individuals, 86 % with early stage HIV infection in Nigeria, to determine the frequency of HIV-related neurocognitive impairment among the HIV-infected group. The tests were administered to assess the following seven ability domains: speed of information processing, attention/working memory, executive functioning, learning, memory, verbal fluency, and motor function motor. Demographically corrected individual test scores and scores for each domain or reflecting a global deficit (a global deficit score, or GDS) were compared for the SP and SN groups. SP participants were older, had fewer years of education, were more likely to be married, differed in ethnicity, and had higher depression scores than SN individuals. Within the seven ability domains, SP performed worse than SN with respect to speed of information processing, executive function, learning, memory, and verbal fluency and also on the global measure. SP were also more frequently impaired on tests of SIP, and there was a borderline increase in the frequency of global impairment. On the individual tests, SP performed worse than SN on four tests that assessed learning, verbal fluency, memory, and motor function (the Timed Gait). SP subjects, however, performed better than SN on the Finger-tapping test, also a motor task. Performance by SP subjects was not associated on the timed gait which showed a borderline statistically significant correlation with CD4 counts. However, there were significant correlations between viral load measurements and individual tests of speed of information processing, executive function, learning, and verbal fluency and with overall executive function and a borderline correlation with the GDS. Depression scores for SP were associated with impairment on only a single test of executive function. These results demonstrate the ability of these assessments to identify areas of impairment that may be specifically linked to a history of HIV infection among individuals in Nigeria. Confirmation of these findings awaits analyses using data from a larger number of control subjects.     

Management of ear keloids using custom-molded pressure clips: a preliminary study

Background

The application of mechanical pressure by compression devices has gained popularity in the treatment of keloid scars. In this present study, we analyze the long-term efficacy of our custom-molded pressure clip for ear keloids. Our secondary objective is to identify risk factors for the failure of the treatment in the group of the recurrence.

Methods

The patient group consisted of 9 men and 19 women with a mean age of 27 years and a mean follow-up of 8.5 years. For evaluation of the scars, scoring ratings, Patient and Observer Scar Assessment Scale (POSAS), and SF8-questionnaire have been used.

Results

Follow-up observations showed that 71 % were treated successfully. There were significant differences in the Fitzpatrick scale, cause of the ear keloids, overall opinion, and openness for re-treatment between the recurrence and nonrecurrence group. Furthermore, treatment with our custom-molded pressure ear clip resulted in a statistically significant improvement of all the item scores of the POSAS in both the patient and observer scales. Severe complications such as infections or necrosis were not noted.

Conclusions

In this study, we show that the results of adjuvant pressure therapy with our custom-molded ear clips are comparable with the recurrence rates of other studies recently published. The strength of this study is the long follow-up. Level of Evidence: Level III, therapeutic study