Anatomical variations of the vein of Labbé: an angiographic study

Purpose

Little attention has been paid to the superficial anastomotic veins but severe post-operative complications can be related to iatrogenic venous damage. The importance of the position of VL (vein of Labbé) relates with the lateral accesses to skull base and medial tentorial lesions by posterior temporal approaches. The aim of this study was to characterize and deepen knowledge on the VL anatomy.

Methods

We reviewed retrospectively 101 hemispheres from cerebral angiographic studies in 59 patients (42 patients with bilateral angiography).

Results

VL duplication was found in 13 patients (31 %) and it was predominant on the left side. The absence of VL was rare (3 of 101 hemispheres). The mean location of the VL entry point in the transverse sinus was almost the middle of the distance between the inion and external acoustic meatus. The mean angle for this entry point was 69°. The mean VL caliber for the patients studied was 3.2 mm. Regarding the relation between VL and vein of Trolard, we found VL dominance in 31 % of the cases. About left–right intrapersonal variability we found a tendency for left VL dominance.

Conclusions

We emphasized not only the interindividual differences but also the great intrapersonal variability of VL anatomy. The adequate study of the cerebral venous system particularities is of crucial importance for pre-operative planning to avoid severe complications.     

Depression of theα-rhythm as an indication of underlying nervous processes

Summary A study was made of the changes of cerebral electrical activity in connection with the elaboration of motor conditioned reflexes in man. It was shown that secondary generalized reactions of the cortical rhythms, manifested as a depression of the-rhythms, occurred under the influence of both positive and inhibitory stimuli. In complex differentiation between a positive and an inhibitory signal the response was more prolonged than it was with simple differentiation.(Presented by Active Member AMN SSSR V. V. Parin) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 53, No. 2, pp. 27–31, February, 1962     

Evaluation of the vectorial capacity of Anopheles arabiensis (Diptera:Culicidae) on the island of Réunion: an approach to the health risk of malaria importation in an area of eradication]

Following intensive control measures, malaria was eradicated from La Réunion Island (Indian Ocean) in 1979. However, potential vectors remain in coastal areas and, each year Public Health Services detect some imported cases from surrounding countries. Anopheles arabiensis is the only species which can be responsible for local transmission though its brief life cycle and its exophilic and zoophilic behaviour were found to be key elements in maintaining the eradication status of the disease on the island. Its vectorial capacity was measured at different seasons and in different areas with a view to assessing the health risks due to imported malaria and suggesting a more pertinent strategy of vector control.     

Development of an immunochromatographic strip for the rapid detection of 10 β-agonists based on an ultrasensitive monoclonal antibody

A sensitive monoclonal antibody, 3G10, derived from a mouse immunized with an immunogen of salbutamol hapten conjugated to keyhole limpet hemocyanin was developed against β-agonists, with a view to establishing a rapid gold nanoparticle immunochromatographic strip. The antibody displayed a 50% inhibitory concentration (IC₅₀) of 1.04?ng/mL for salbutamol and simultaneously detected nine other β-agonists (clenbuterol, cimatero, brombuterol, mabuterol, terbutaline, clenpenterol, carbuterol, mapenterol, pirbuterol) with uniform cross-reactivity. The immunochromatographic strip had cut-off values of 5?ng/mL for salbutamol and clenbuterol, 20?ng/mL for cimaterol, brombuterol and mabuterol, and 50?ng/mL for terbutaline, clenpenterol, carbuterol, mapenterol and pirbuterol. The collective advantages of the newly developed strip, such as high affinity, sensitivity and rapidity, support its utility in detecting β-agonists from actual biological samples, such as urine.     

Can medication education improve the drug compliance of the elderly? Evaluation of an in hospital program

We report the evaluation of a pharmacist-led medication education program for the elderly. The program consisted of a single group-based education session followed by individual pre-discharge counseling. Patients also received an individual medication record card. The study design was a nonrandomised trial. Patients in the control group received a "dummy" intervention conducted on alternate months to the medication program. Drug compliance was assessed by interviewer-administered questionnaire in the patients' homes at 1 and 3 months post-discharge. The main outcome factor of interest was severe noncompliance with essential medications. This meant taking 80% or less or conversely 120% or more of those medications prescribed for the control of the patient's medical condition. At 1 and 3 months post-discharge, no effect of the program was detected. However, among the sub-group of patients taking four drugs or more the effect of the program was evident at 3 months post-discharge. Among this group at 3 months post-discharge, 55% of control group patients were severely noncompliant with essential medications as compared to 32% of the education group (a difference of 23%, 95% confidence interval 4-42%). This effect was not accounted for by possible confounding factors such as age, sex, number of medications and the patient's living arrangements.     

Suppression of EEG gamma activity — an informative measure of spreading depression waves in the neocortex of the conscious rabbit

Spreading depression can arise spontaneously in convulsions, migraine attacks, vascular lesions, and other pathological brain states. However, the methodological complexity of recording a direct current potential in the neocortex in humans and conscious animals significantly limits studies of the functional consequences of spreading depression. The present report describes a detailed analysis of the EEG dynamics at the moment of development of spreading depression waves and identifies specific signs allowing spreading depression to be recorded without recording changes in the direct current potential. At the moment of arrival of spreading depression, the interhemisphere equilibrium is highly disturbed because of large decreases in high-frequency activity. The time parameters of the dynamics of the gamma-1 and gamma-2 ranges were the most informative features of the development of spreading depression waves. Increases in power in the delta range developed with some delay on the background of a deep inhibition of high-frequency activity and are in essence a consequence of spreading depression. The encephalographic criteria of spreading depression waves identified here can significantly simplify the detection of this phenomenon both in experimental and clinical conditions in a number of pathological brain states. __________ Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 55, No. 4, pp. 437–443, July–August, 2005.     

Bridging the transmission gap: an end to an important mystery of attachment research?

The authors provide a context for this special section by arguing that the attachment relationships of infancy fulfil an evolutionary role in ensuring that the brain structures that come to subserve social cognition are appropriately organised and prepared to equip the individual for the collaborative existence with other people for which his or her brain was designed. Processes as fundamental as gene expression or changes in receptor densities can be seen as direct functions of the extent of understanding of mental states provided by the caregiving environment. If the attachment relationship is indeed a major organiser of brain development, it is even more important to understand the processes that underpin the transgenerational transmission of attachment patterns. The contributions of the papers in the special section to understanding the role of reflective function in the development of attachment and social cognition are reviewed, and the implications for the development of both theory and practice are explored.     

Is the Ala12 variant of the PPARG gene an "unthrifty allele"?

Background: The thrifty genotype hypothesis proposes that genetic susceptibility to type 2 diabetes results from the positive selection of "thrifty" alleles in the past. A corollary of this hypothesis is that genetic variants protecting against the development of diabetes are "unthrifty" and thus subject to negative selection during human evolution. Methods: It was assessed whether age estimates of the diabetes protective PPARG Ala12 allele indicate effects of natural selection. Based on published data from four populations, the date of origin of the diabetes protective PPARG Ala12 variant was estimated using both allele frequency and linkage disequilibrium (LD) with the C1431T single nucleotide polymorphism in exon 6 of the PPARG gene. Results: The best LD based estimate of the age of the Ala12 allele gave an average of ∼32 000 years with a maximum upper bound of ∼58 000 years. Assuming a population with a growth rate of r = 0.01 per generation, the frequency based estimate of the age of the Ala12 variant gave an average of ∼27 000 years with a maximum upper bound of ∼42 000 years. Discussion: The similarity of both time estimates is consistent with selective equivalence of the diabetes protective PPARG Ala12 allele and the diabetes susceptible PPARG Pro12 allele.     

Review of the “X chromosome-nucleolus nexus” hypothesis of autoimmune diseases with an update explaining disruption of the nucleolus

Immunologic Research - The “X chromosome-nucleolus nexus” hypothesis provides a comprehensive explanation of how autoantibodies can develop following cellular stress. The hypothesis...     

A test of the immunoreactive theory of the origin of neurodevelopmental disorders: Is there an antecedent brother effect?

Gualtieri and Hicks (1985) proposed that male vulnerability to neurodevelopmental disorders (NDs) could be explained by maternal immune attack on the male fetus, especially among children whose mothers had previously conceived boys as opposed to girls. This antecedent brother effect was attributed to the build‐up of maternal antibodies against previous male fetuses. Our sample consisted of 11,578 mother‐child pairs who were followed up until 7 years old. For only one ND—mental retardation—was there a true antecedent brother effect: Mentally retarded boys were significantly more likely to have antecedent brothers than sisters, whereas mentally retarded girls did not show this effect. Moreover, the incidence of mental retardation was elevated significantly among boys with at least two, as opposed to one, antecedent brothers. This did not occur among boys with antecedent sisters or in girls irrespective of antecedent sibling gender or number. This supports Gualtieri and Hicks's immunoreactive theory for the origin of NDs for only one specific ND: mental retardation.     

Is GnRH self-priming an obligatory feature of the reproductive cycle?

Insufficient suppression of LH (premature elevation) and FSH (prolonged release) give rise to blood concentrations which may cause damaging effects on oocyte viability and too many follicles respectively. During the surge, LH rises from low to high threshold values to initiate processes from initiation of the resumption of oocyte meiosis to the induction of ovulation. In general, it is thought that a dramatic increase in LH concentration is required to attain the high threshold for ovulation. A self-priming mechanism, by which gonadotrophin-releasing hormone (GnRH) enhances the LH (and FSH) responses to its own action, was thought to be responsible. However, normal LH surges in rats consist of <2-7% of the maximal pituitary releasing capacity. The physiological roles of LH and FSH favour a control mechanism that restrains their blood concentrations during most of the cycle. Ovarian proteins, e.g. inhibin and putative gonadotrophin-surge-inhibiting factor/attenuating factor (GnSIF/AF), are involved in this process. We argue that the increased pituitary LH responsiveness during the mid-cycle surge is not the result of a self-priming process that 'dramatically' increases the LH releasing capacity of the pituitary gland. This is probably due to elimination by GnRH of the inhibitory action of the putative ovarian proteins GnSIF/AF.     

Duodeno-jejunal junction: a histoanatomical study with the concept of the existence of an “anatomical” sphincter

Background Duodenojejunal junction (DJJ) pressure decreased on duodenal contraction and increased on jejunal contraction. These findings postulated potential existence of anatomical sphincter at DJJ. Methods DJJ was studied by direct dissection in 34 cadavers and histologically in 24. Transverse and longitudinal sections across DJJ were cut and stained. Results DJJ was narrower than duodenum or jejunum and had one or two grooves occupied by arterial branch derived from superior mesenteric artery and we call it “duodenojejunal junction artery”. DJJ was thicker on palpation than duodenum or jejunum. Its mucous membrane was crowded into “DJJ rosette”. DJJ length varied in adults from 0.75 to 0.9 cm. Microscopically, circular muscle layer was thickened at DJJ. Conclusion The thickened circular muscle, mucosal rosette and narrowing at DJJ point to possible existence of anatomical sphincter at DJJ. Together with presence of high-pressure zone at DJJ, these findings would support such postulation.     

Does an ultra violet photooxidation of the manganese-loaded/copper-depleted prion protein in the retina initiate the pathogenesis of TSE?

Ecosystems supporting clusters of sporadic transmissible spongiform encephalopathy (TSE) are characterized by common properties of high-manganese/low-copper, zinc, selenium mineral status, and high-altitude/snow-covered/pre-cambrian mountain terrain where above-average intensities of ultra violet/ozone oxidants are prevalent. Cell culture trials have confirmed the hypothesis that manganese (Mn) substitutes at Prion Protein’s (PrP’s) vacated copper (Cu) domain, whereupon PrP loses its Cu-mediated antioxidant function, transforming into a protease-resistant misfolded isoform that aggregates into fibril ‘tombstone’ structures – the key hallmark distinguishing TSE central nervous system (CNS) pathology. The cellular localisation of PrP suggests PrP serves a ‘front line’ contributory role in neutralizing radicals generated by incoming environmental oxidants, whilst an intensive expression of PrP messenger ribonucleic acid (mRNA) in the retina, melanocytes, epidermis, etc., suggests PrP performs a key antioxidant role as a ‘photooxidative shock absorber’; binding of porphyrin IX, Congo red and other photosensitisers to PrPc suggests PrPc serves as an integral associate of the porphyrin/melanin chromophore electron transfer chain; thereby serving as a quencher of singlet O₂/superoxide generated by photoenergised chromophores/xeno photosensitisers. It is proposed that sporadic TSE pathogenesis is initiated in the retina of environmentally/genetically predisposed individuals via a two-stage chronic toxic process – Mn substitution at PrP’s Cu domain forming a stable Mn2+-PrP complex, followed by an ultra violet in situ photo-oxidization of the Mn2+ component; whereby the latent ‘Jekyll and Hyde’ capacity of the Mn2+-PrP conjugate is activated into the fully fledged, ‘infectious’ lethal auto-oxidizing, Mn3+-PrP ‘prion’ agent. Thus, PrPc’s Cu-mediated antioxidant function is replaced by a Mn3+-mediated autooxidant dysfunction. Could the UK’s increased loading of a cocktail of environmental oxidants that penetrated the CNS of the UK bovine (ultra violet microwaves/ozone/systemic cu-chelating insecticides) account for a more virulent Mn4+ mediated acceleration of the TSE degenerative process in Mn-contaminated/genetically predisposed individuals, manifesting as the widespread emergence of new-variant bovine spongiform encephalopathy (BSE)/variant Creutzfeldt–Jacob disease (VCJD)/FSE in younger mammals?