Long-term monitoring of a winter bat assemblage revealed large fluctuations and trends in species abundance

Monitoring studies in Strzaliny, one of the greatest hibernacula in Poland, comprised 31 annual bat censuses (1989–2019). The abundance peaked in 2002 for Myotis myotis, 2009 for Myotis nattereri and 2008 for the whole assemblage. Comparison of the maximum abundance in the monitoring period with that from 1980 to 1982 showed an almost fourfold increase for the whole assemblage, tenfold increase for M. nattereri and fourfold increase for M. myotis. In 1989–2019, the numbers of M. myotis, M. nattereri, Myotis daubentonii and Plecotus auritus were fluctuating, but most of the recorded changes could not be explained by methodological problems or a direct human impact. Therefore, the cumulative results largely reflected the real trends in the species abundance. A long-term upward trend in the whole bat assemblage was recognisable, but with a stable or slightly decreasing phase in the last decade. An upward trend in M. nattereri was even stronger and has only slightly flattened recently. In M. myotis, the trend was clearly upwards up to the early 2000s, but weakly downwards in the following years. In M. daubentonii and P. auritus, no significant trend was determined. In strongly fluctuating M. daubentonii, the numbers were mostly moderate or high, and even increasing, up to 2008 and only moderate or low in the following years. In P. auritus, an increase occurred in the 1980s and early 1990s, and then, after the stochastic human-induced drop in 1994, its abundance remained relatively stable. The population trends in Strzaliny largely reflected the general trends assessed for a large part of Europe. This suggests that the general population trends may be recognisable even in one large winter assemblage if it is reliably and consistently monitored through a long period. In this context, the hibernaculum in Strzaliny appeared to be a model object for such studies

Electronic structure and optical properties of Sn and SnGe quantum dots

Self-assembled quantum dots in a Si–Ge–Sn system attract research attention as possible direct band gap materials, compatible with Si-based technology, with potential applications in optoelectronics. In this work, the electronic structure near the point and interband optical matrix elements of strained Sn and SnGe quantum dots in a Si or Ge matrix are calculated using the eight-band k·p method, and the competing L-valley conduction band states were found by the effective mass method. The strain distribution in the dots was found with the continuum mechanical model. The parameters required for the k·p or effective mass calculation for Sn were extracted by fitting to the energy band structure calculated by the nonlocal empirical pseudopotential method. The calculations show that the self-assembled Sn/Si dots, sized between 4 and 12 nm, have indirect interband transition energies between 0.8 and 0.4 eV and direct interband transitions between 2.5 and 2.0 eV. In particular, the actually grown, approximately cylindrical Sn dots in Si with a diameter and height of about 5 nm are calculated to have an indirect transition (to the L valley) of about 0.7 eV, which agrees very well with experimental results. Similar good agreement with the experiment was also found for SnGe dots grown on Si. However, neither of these is predicted to be direct band gap materials, in contrast to some earlier expectations

Bi-allelic Variants in TKFC Encoding Triokinase/FMN Cyclase Are Associated with Cataracts and Multisystem Disease

We report an inborn error of metabolism caused by TKFC deficiency in two unrelated families. Rapid trio genome sequencing in family 1 and exome sequencing in family 2 excluded known genetic etiologies, and further variant analysis identified rare homozygous variants in TKFC. TKFC encodes a bifunctional enzyme involved in fructose metabolism through its glyceraldehyde kinase activity and in the generation of riboflavin cyclic 4′,5′-phosphate (cyclic FMN) through an FMN lyase domain. The TKFC homozygous variants reported here are located within the FMN lyase domain. Functional assays in yeast support the deleterious effect of these variants on protein function. Shared phenotypes between affected individuals with TKFC deficiency include cataracts and developmental delay, associated with cerebellar hypoplasia in one case. Further complications observed in two affected individuals included liver dysfunction and microcytic anemia, while one had fatal cardiomyopathy with lactic acidosis following a febrile illness. We postulate that deficiency of TKFC causes disruption of endogenous fructose metabolism leading to generation of by-products that can cause cataract. In line with this, an affected individual had mildly elevated urinary galactitol, which has been linked to cataract development in the galactosemias. Further, in light of a previously reported role of TKFC in regulating innate antiviral immunity through suppression of MDA5, we speculate that deficiency of TKFC leads to impaired innate immunity in response to viral illness, which may explain the fatal illness observed in the most severely affected individual

Search for a new gauge boson in the A′A' Experiment (APEX)

We present a search at Jefferson Laboratory for new forces mediated by sub-GeV vector bosons with weak coupling $\alpha'$ to electrons. Such a particle $A'$ can be produced in electron-nucleus fixed-target scattering and then decay to an $e^+e^-$ pair, producing a narrow resonance in the QED trident spectrum. Using APEX test run data, we searched in the mass range 175--250 MeV, found no evidence for an $A'\to e^+e^-$ reaction, and set an upper limit of $\alpha'/\alpha \simeq 10^{-6}$. Our findings demonstrate that fixed-target searches can explore a new, wide, and important range of masses and couplings for sub-GeV forces.Comment: 5 pages, 5 figures, references adde

Measurement of the branching ratios of the Z0 into heavy quarks

We measure the hadronic branching ratios of the Z0 boson into heavy quarks: Rb=Gamma(Z0->bb)/Gamma(Z0->hadrons) and Rc=Gamma(Z0->cc/Gamma(Z0->hadrons) using a multi-tag technique. The measurement was performed using about 400,000 hadronic Z0 events recorded in the SLD experiment at SLAC between 1996 and 1998. The small and stable SLC beam spot and the CCD-based vertex detector were used to reconstruct bottom and charm hadron decay vertices with high efficiency and purity, which enables us to measure most efficiencies from data. We obtain, Rb=0.21604 +- 0.00098(stat.) +- 0.00073(syst.) -+ 0.00012(Rc) and, Rc= 0.1744 +- 0.0031(stat.) +- 0.0020(syst.) -+ 0.0006(Rb)Comment: 37 pages, 8 figures, to be submitted to Phys. Rev. D version 2: changed title to ratios, used common D production fractions for Rb and Rc and corrected Zgamma interference. Identical to PRD submissio

Direct Measurements of A_b and A_c using Vertex/Kaon Charge Tags at SLD

Exploiting the manipulation of the SLC electron-beam polarization, we present precise direct measurements of the parity violation parameters A_c and A_b in the Z boson - c quark and Z boson - b quark coupling. Quark/antiquark discrimination is accomplished via a unique algorithm that takes advantage of the precise SLD CCD vertex detector, employing the net charge of displaced vertices as well as the charge of kaons that emanate from those vertices. From the 1996-98 sample of 400,000 Z decays, produced with an average beam polarization of 73.4%, we find A_c = 0.673 +/- 0.029 (stat.) +/- 0.023 (syst.) and A_b = 0.919 +/- 0.018 (stat.) +/- 0.017 (syst.).Comment: 11 pages, 2 figures, 2 tables, to be submitted to Physical Review Letters; version 2 reflects changes suggested by the refere

Loss of myelin-associated glycoprotein in kearns-sayre syndrome

OBJECTIVE: To explore myelin components and mitochondrial changes within the central nervous system in patients with well-characterized mitochondrial disorders due to nuclear DNA or mitochondrial DNA (mtDNA) mutations. DESIGN: Immunohistochemical analysis, histochemical analysis, mtDNA sequencing, and real-time and long-range polymerase chain reaction were used to determine the pathogenicity of mtDNA deletions. SETTING: Department of Clinical Pathology, Columbia University Medical Center, and Newcastle Brain Tissue Resource. PATIENTS: Seventeen patients with mitochondrial disorders and 7 controls were studied from August 1, 2009, to August 1, 2010. MAIN OUTCOME MEASURE: Regions of myelin-associated glycoprotein (MAG) loss. RESULTS: Myelin-associated glycoprotein loss in Kearns-Sayre syndrome was associated with oligodendrocyte loss and nuclear translocation of apoptosis-inducing factor, whereas inflammation, neuronal loss, and axonal injury were minimal. In a Kearns-Sayre syndrome MAG loss region, high levels of mtDNA deletions together with cytochrome- c oxidase–deficient cells and loss of mitochondrial respiratory chain subunits (more prominent in the white than gray matter and glia than axons) confirmed the pathogenicity of mtDNA deletions. CONCLUSION: Primary mitochondrial respiratory chain defects affecting the white matter, and unrelated to inflammation, are associated with MAG loss and central nervous system demyelination

Microangiopathy in the cerebellum of patients with mitochondrial DNA disease

Neuropathological findings in mitochondrial DNA disease vary and are often dependent on the type of mitochondrial DNA defect. Many reports document neuronal cell loss, demyelination, gliosis and necrotic lesions in post-mortem material. However, previous studies highlight vascular abnormalities in patients harbouring mitochondrial DNA defects, particularly in those with the m.3243A>G mutation in whom stroke-like events are part of the mitochondrial encephalopathy lactic acidosis and stroke-like episodes syndrome. We investigated microangiopathic changes in the cerebellum of 16 genetically and clinically well-defined patients. Respiratory chain deficiency, high levels of mutated mitochondrial DNA and increased mitochondrial mass were present within the smooth muscle cells and endothelial cells comprising the vessel wall in patients. These changes were not limited to those harbouring the m.3243A>G mutation frequently associated with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, but were documented in patients harbouring m.8344A>G and autosomal recessive polymerase (DNA directed), gamma (POLG) mutations. In 8 of the 16 patients, multiple ischaemic-like lesions occurred in the cerebellar cortex suggestive of vascular smooth muscle cell dysfunction. Indeed, changes in vascular smooth muscle and endothelium distribution and cell size are indicative of vascular cell loss. We found evidence of blood–brain barrier breakdown characterized by plasma protein extravasation following fibrinogen and IgG immunohistochemistry. Reduced immunofluorescence was also observed using markers for endothelial tight junctions providing further evidence in support of blood–brain barrier breakdown. Understanding the structural and functional changes occurring in central nervous system microvessels in patients harbouring mitochondrial DNA defects will provide an important insight into mechanisms of neurodegeneration in mitochondrial DNA disease. Since therapeutic strategies targeting the central nervous system are limited, modulating vascular function presents an exciting opportunity to lessen the burden of disease in these patients

Effects of GnRH vaccination in wild and captive African Elephant bulls (Loxodonta africana) on reproductive organs and semen quality

OBJECTIVES: Although the African elephant (Loxodonta africana) is classified as endangered by the International Union for Conservation of Nature (IUCN), in some isolated habitats in southern Africa, contraception is of major interest due to local overpopulation. GnRH vaccination has been promoted as a non-invasive contraceptive measure for population management of overabundant wildlife. We tested the efficacy of this treatment for fertility control in elephant bulls. METHODS: In total, 17 male African elephants that were treated with a GnRH vaccine were examined in two groups. In the prospective study group 1 (n = 11 bulls, ages: 8±36 years), semen quality, the testes, seminal vesicles, ampullae and prostate, which were all measured by means of transrectal ultrasound, and faecal androgen metabolite concentrations were monitored over a three-year period. Each bull in the prospective study received 5 ml of Improvac® (1000 μg GnRH conjugate) intramuscularly after the first examination, followed by a booster six weeks later and thereafter every 5±7 months. In a retrospective study group (group 2, n = 6, ages: 19±33 years), one examination was performed on bulls which had been treated with GnRH vaccine for 5±11 years. RESULTS: In all bulls of group 1, testicular and accessory sex gland sizes decreased significantly after the third vaccination. In six males examined prior to vaccination and again after more than five vaccinations, the testis size was reduced by 57.5%. Mean testicular height and length decreased from 13.3 ± 2.6 cm x 15.2 ± 2.8 cm at the beginning to 7.6 ± 2.1 cm x 10.2 ± 1.8 cm at the end of the study. Post pubertal bulls (>9 years, n = 6) examined prior to vaccination produced ejaculates with viable spermatozoa (volume: 8±175 ml, sperm concentration: 410-4000x106/ml, total motility: 0±90%), while after 5±8 injections, only 50% of these bulls produced ejaculates with a small number of immotile spermatozoa. The ejaculates of group 2 bulls (vaccinated >8 times) were devoid of spermatozoa. Faecal androgen metabolite concentrations measured in captive males decreased significantly after the fourth vaccination. None of the males entered musth during the treatment period. CONCLUSIONS: Our results showed a marked decrease in semen quality, testicle and secondary sex gland sizes following repeated GnRH vaccinations. After 2±4 years of continuous treatment every 5±7 months, the effects were similar to surgical castration.ISIScopu