Ab Initio Transcorrelated Method enabling accurate Quantum Chemistry on near-term Quantum Hardware

Quantum computing is emerging as a new computational paradigm with the potential to transform several research fields, including quantum chemistry. However, current hardware limitations (including limited coherence times, gate infidelities, and limited connectivity) hamper the straightforward implementation of most quantum algorithms and call for more noise-resilient solutions. In quantum chemistry, the limited number of available qubits and gate operations is particularly restrictive since, for each molecular orbital, one needs, in general, two qubits. In this study, we propose an explicitly correlated Ansatz based on the transcorrelated (TC) approach, which transfers -- without any approximation -- correlation from the wavefunction directly into the Hamiltonian, thus reducing the number of resources needed to achieve accurate results with noisy, near-term quantum devices. In particular, we show that the exact transcorrelated approach not only allows for more shallow circuits but also improves the convergence towards the so-called basis set limit, providing energies within chemical accuracy to experiment with smaller basis sets and, therefore, fewer qubits. We demonstrate our method by computing bond lengths, dissociation energies, and vibrational frequencies close to experimental results for the hydrogen dimer and lithium hydride using just 4 and 6 qubits, respectively. Conventional methods require at least ten times more qubits for the same accuracy

Minimum Two-Year Follow-Up of Cases with Recurrent Disc Herniation Treated with Microdiscectomy and Posterior Dynamic Transpedicular Stabilisation

The objective of this article is to evaluate two-year clinical and radiological follow-up results for patients who were treated with microdiscectomy and posterior dynamic transpedicular stabilisation (PDTS) due to recurrent disc herniation. This article is a prospective clinical study. We conducted microdiscectomy and PDTS (using a cosmic dynamic screw-rod system) in 40 cases (23 males, 17 females) with a diagnosis of recurrent disc herniation. Mean age of included patients was 48.92 ± 12.18 years (range: 21-73 years). Patients were clinically and radiologically evaluated for follow-up for at least two years. Patients’ postoperative clinical results and radiological outcomes were evaluated during the 3rd, 12th, and 24th months after surgery. Forty patients who underwent microdiscectomy and PDTS were followed for a mean of 41 months (range: 24-63 months). Both the Oswestry and VAS scores showed significant improvements two years postoperatively in comparison to preoperative scores (p<0.01). There were no significant differences between any of the three measured radiological parameters (α, LL, IVS) after two years of follow-up (p > 0.05). New recurrent disc herniations were not observed during follow-up in any of the patients. We observed complications in two patients. Performing microdiscectomy and PDTS after recurrent disc herniation can decrease the risk of postoperative segmental instability. This approach reduces the frequency of failed back syndrome with low back pain and sciatica

SIVcol and SIVolc Nef fail to efficiently downmodulate the T cell receptor CD3.

<p>(A) Human PBMCs were transduced with VSV-G pseudotyped NL4-3 constructs coexpressing the indicated Nef proteins and eGFP via an IRES. 72 hr post-transduction, CD3 surface expression was quantified by flow cytometry. Mean values of six infections ± SEM are shown on the left. The panel on the right shows examples for primary flow cytometry data. (B) Due to the lack of an antibody detecting SIVcol and SIVolc Nef, counteraction of human SERINC5 was analyzed to verify functional Nef expression. HEK293T cells were cotransfected with increasing amounts of a SERINC5 expression plasmid and the NL4-3-based proviral constructs also used in (A). 40 hr post-transfection, infectious virus yield was quantified by infection of TZM-bl reporter cells. Mean values of three independent experiments in triplicates ± SEM are shown. (C) HEK293T cells were cotransfected with the proviral constructs described in (A) and expression vectors for CD3-CD8 fusion proteins comprising the cytoplasmic domain of human or colobus CD3ζ and the extracellular and transmembrane domain of human CD8. 40 hr post transfection, CD3ζ downmodulation was determined by monitoring CD8 surface levels via flow cytometry. Mean values of three to four independent experiments ± SEM are shown. In (A) and (C), asterisks indicate statistically significant differences compared to the <i>nef</i>-defective control (**p < 0.01; ***p < 0.001).</p

Vpr-mediated modulation of NF-κB activity and immune activation in infected T cells.

<p>(A) Genomic organization of a chimeric infectious molecular clone (IMC) of HIV-1 M CH293.1 expressing heterologous <i>vpr</i> alleles. The CH293 <i>vpr</i> open reading frame was replaced by XbaI and MluI restriction sites (green), allowing the insertion of heterologous AU1-tagged <i>vpr</i> alleles (yellow). The original <i>vpr</i> start codon in <i>vif</i> was silenced (blue) to prevent expression of a truncated CH293 Vpr. Expression of Vpu was abrogated by inserting a premature stop codon (pink). (B) Expression of heterologous Vpr proteins from the CH293.1 chimeras described in (A). HEK293T cells were cotransfected with CH293.1 IMCs encoding the indicated <i>vpr</i> alleles. 40 hr post-transfection, cells and supernatants were harvested and virions in the supernatant were purified by centrifugation through a sucrose cushion. Subsequently, Western blotting was performed to detect AU1-tagged Vpr, Env and Gag. Detection of GAPDH served as loading control. (C) HEK293T cells were cotransfected with the indicated CH293.1 chimeras, a firefly luciferase reporter construct under the control of three NF-κB binding sites, and a <i>Gaussia</i> luciferase construct for normalization. Luciferase activities were determined 40 hr post-transfection. Mean values of three independent experiments in triplicates ± SEM are shown. (D) The SupD1 NF-κB reporter cell line was transduced with the indicated VSV-G pseudotyped CH293.1 chimeras. Cells were harvested at various time points post-transduction to determine the activation levels of NF-κB. The mean values of triplicate infections ± SD of a representative experiment are shown. (E) PBMCs of three different donors were transduced with VSV-G pseudotyped CH293.1 chimeras encoding the indicated <i>vpr</i> alleles. Cells were harvested 72 hr post-transduction and total cellular RNA was isolated and reversely transcribed. IFNβ mRNA levels were determined by quantitative RT-PCR and normalized to GAPDH mRNA. The mean values ± SEM are shown. In (C) to (E), asterisks indicate statistically significant differences compared to CH293.1 wild type transfected or infected cells (*p < 0.05; **p < 0.01; ***p < 0.001).</p

NF-κB inhibition by SIVolc and SIVcol Vpr reduces LTR-driven gene expression.

<p>(A, B) HEK293T cells were cotransfected with the indicated <i>vpr</i> alleles, a firefly luciferase reporter construct under the control of the HIV-1 M, SIVcol or SIVolc LTR promoter, and a <i>Gaussia</i> luciferase construct for normalization. Cells were (A) stimulated with TNFα or (B) cotransfected with a constitutively active mutant of IKKβ (c.a. IKKβ). Luciferase activities were determined 40 hr post-transfection. Mean values of four independent experiments in triplicates ± SEM are shown (*p<0.05; **p < 0.01; ***p < 0.001).</p