A B S T R A C TObjective: To discuss hospital pharmacists' role in providing pharmaceutical care for hospitalized patients with COVID-19 to promote patient care and management during the pandemic. Method: Based on the method of evidence-based pharmacy, clinical evidence of therapeutical drugs for COVID-19 were retrieved and summarized. Based on clinical experience Chinese hospital pharmacists gained from providing pharmaceutical care services during COVID-19 pandemic, taking COVID-19 hospitalized patients' needs into consideration, the methods and strategies hospital pharmacists shall use to provide pharmaceutical care were analyzed and summarized. Results: Hospital pharmacists shall support pharmaceutical care services by participating in making evidence-based decisions for medication, monitoring and evaluation of medication safety and efficacy, providing strengthened care for special population and patients with combined underlying diseases, monitoring and management of convalescent plasma therapy, providing emotional counselling and psychological support, and providing scientific information about COVID-19 vaccines. Conclusion: The need of pharmaceutical care services in COVID-19 hospitalized patients during this pandemic was quite distinguished from the past. Hospital pharmacists shall join the collaborative multidisciplinary team to improve COVID-19 patients' outcome and reduce mortality, and to facilitate the pandemic control.

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We study the exclusive decays of B meson into P-wave charmonium states χ cJ (J = 0, 1) in the QCD factorization approach with light-cone distribution functions describing the mesons in the processes. For B → χ c1 K decay, we find that there are logarithmic divergences arising from nonfactorizable spectator interactions even at twist-2 order and the decay rate is too small to accommodate the experimental data. For B → χ c0 K decay, we find that aside from the logarithmic divergences arising from spectator interactions at leading-twist order, more importantly, the factorization will break down due to the infrared divergence arising from nonfactorizable vertex corrections, which is independent of the specific form of the light-cone distribution functions. Our results may indicate that QCD factorization in the present form may not be safely applied to B-meson exclusive decays to charmonium states. PACS numbers: 13.25.Hw; 14.40.GxExclusive nonleptonic B-meson decays provide a important opportunity to determine the parameters of the Cabibbo-Kobayashi-Maskawa (CKM) matrix, to explore CP violation and to observe new physics effects. Recently, B physics has received extensive experimental attention such as from high-energy experiments at the Tevatron and at the e + e − B factories. On the other hand, although the underlying weak decay of the b quark is simple, quantitative understanding of nonleptonic B-meson decays is difficult due to the complicated strong-interaction effects.Beneke et al. have considered two-body nonleptonic B-meson decays extensively including light-light as well as heavy-light final states within the QCD factorization approach [1,2,3]. The general idea is that in the heavy quark limit m b ≫ Λ QCD , the transition matrix elements of operators in the hadronic decay B → M 1 M 2 with M 1 being the recoiled meson and M 2 being the emitted meson can be calculated in an expansion in 1/m b and α s . The leading term in 1/m b assumes a simple form[2]:where M 2 is a light meson or a quarkonium and F BM 1 is the B → M 1 transition form factor; φ M is meson light-cone distribution amplitude and T I,II are perturbatively calculable hard scattering kernels. If we neglect strong interaction corrections, eq.(1) reproduces the result of naive factorization. However, hard gluon exchange between M 2 and BM 1 system implies a nontrivial convolution of hard scattering kernels T I,II with the light-cone distribution amplitude 1

In the framework of QCD factorization, we study the B meson exclusive decays B → χcJ K where the spin-triplet P-wave charmonium states χcJ (J = 0, 1, 2) are described by the color-singlet nonrelativistic wave functions. We find that for these decays (except χc1) there are infrared divergences arising from nonfactorizable vertex corrections as well as logarithmic end-point singularities arising from nonfactorizable spectator interactions at leading-twist order. The infrared divergences due to vertex corrections will explicitly break down QCD factorization within the color-singlet model for charmonia. Unlike in the inclusive decays where the higher Fock states with color-octet cc pair and soft gluon can make contributions to remove the infrared divergences, their contributions can not be accommodated in the exclusive two body decays. As a result, the infrared divergences encountered in exclusive processes involving charmonia may raise a new question to the QCD factorization and NRQCD factorization in B exclusive decays.

The authors confirm that the PI for this paper is Rongsheng Zhao and that he had direct clinical responsibility for patients included in the study investigating the patients' willingness on individualized medication of high-dose methotrexate.

The study aims to determine whether light microscopy can be used to accurately measure the diameters of intercellular spaces between squamous epithelial cells in the lower esophagus, and whether changes in this outcome measure can be used as a diagnostic marker for gastroesophageal reflux disease (GERD). The study has two parts. Part 1 involves 42 asymptomatic controls and 119 patients with typical symptoms of GERD, including 58 with erosive esophagitis (EE), and 61 patients with nonerosive gastroesophageal reflux disease (NERD). All biopsies were taken from the lower esophagus. All samples were observed using an immersion objective, after which diameters were measured by computer-assisted morphometry. Part 2 involves 61 individuals who were randomly selected from part 1, including 19 controls, 13 with NERD and 29 with EE. Diameter measurements using both light microscopy and transmission electron microscopy (TEM) were performed for samples of 61 individuals. Samples from a total of 61 individuals (31 male, 30 female, mean age 44.3 ± 16.0 years) were observed using both light microscopy and TEM. Both methods showed significant differences between control and disease groups; the outcomes from the two methods had a certain correlation (r = 0.605, P = 0.000). Morphometric analysis of all 161 individuals (83 males, 78 females, mean age 41.4 ± 15.7) showed mean diameters from light microscopy to be 0.58 ± 0.16 µm for controls, 1.07 ± 0.30 µm for NERD, and 1.29 ± 0.20 µm for EE; differences between control and disease groups were significant (P<0.05). The optimal cut-off value from receiver operator characteristic analysis was 0.85 µm. Diagnoses were validated using the combination of symptoms of GERD, endoscopy, and 24 h ambulatory pH monitoring as the gold standard. At the optimal cutoff, sensitivity was 93.3% and specificity was 100%. The diameters of the intercellular spaces in squamous epithelium of lower esophagus from controls and in patients with GERD can be quantitatively measured using light microscopy. Dilated diameters can serve as a sensitive, specific, and objective indicator for diagnosis of GERD.

The voltage-dependent anion channel 1 (VDAC1), a pore protein located in the outer mitochondrial membrane, has been confirmed to be related to cancer in cell or animal evidence. However, there is no available pan-cancer analysis of VDAC1. Herein, we investigated the potential roles of VDAC1 in tumorigenesis and progression based on the Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Clinical Proteomic Tumor Analysis Consortium (CPTAC) datasets. The expression of VDAC1 increased in most cancers, and the upregulation of VDAC1 distinctly correlated with the poor prognosis in patients, including breast invasive carcinoma, cervical squamous cell carcinoma, pancreatic adenocarcinoma, lung adenocarcinoma, and skin cutaneous melanoma. We also found VDAC1 S104 phosphorylation raised in various cancers, such as breast cancer, colon cancer, and lung adenocarcinoma. Moreover, the expression of VDAC1 was related to the estimated infiltration value of cancer-associated fibroblasts in bladder urothelial carcinoma, colon adenocarcinoma, kidney renal papillary cell carcinoma, and testicular germ cell tumors. At last, we showed that VDAC1-related oxidative phosphorylation and metabolic regulation may partially explain its association with tumorigenesis and progression. Taken together, this pan-cancer analysis provides relatively comprehensive information on the potential value of VDAC1 as a prognostic biomarker and therapeutic target.

Objective: High-dose methotrexate (HDMTX) is a mainstay therapeutic agent for the treatment of diverse hematological malignancies, and it plays a significant role in interindividual variability regarding the pharmacokinetics and toxicity. The genetic association of HDMTX has been widely investigated, but the conflicting results have complicated the clinical utility. Therefore, this systematic review aims to determine the role of gene variants within the HDMTX pathway and to fill the gap between knowledge and clinical practice.Methods: Databases including EMBASE, PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), and the Clinical Trials.gov were searched from inception to November 2020. We included twelve single-nucleotide polymorphisms (SNPs) within the HDMTX pathway, involving RFC1, SLCO1B1, ABCB1, FPGS, GGH, MTHFR, DHFR, TYMS, and ATIC. Meta-analysis was conducted by using Cochrane Collaboration Review Manager software 5.3. The odds ratios (ORs) or hazard ratios (HRs) with 95% confidence interval (95% CI) were analyzed to evaluate the associations between SNPs and clinical outcomes. This study was performed according to the PRISMA guideline.Results: In total, 34 studies with 4102 subjects were identified for the association analysis. Nine SNPs involving MTHFR, RFC1, ABCB1, SLCO1B1, TYMS, FPGS, and ATIC genes were investigated, while none of studies reported the polymorphisms of GGH and DHFR yet. Two SNPs were statistically associated with the increased risk of HDMTX toxicity: MTHFR 677C&gt;T and hepatotoxicity (dominant, OR=1.52, 95% CI=1.03-2.23; recessive, OR=1.68, 95% CI=1.10–2.55; allelic, OR=1.41, 95% CI=1.01–1.97), mucositis (dominant, OR=2.11, 95% CI=1.31–3.41; allelic, OR=1.91, 95% CI=1.28–2.85), and renal toxicity (recessive, OR=3.54, 95% CI=1.81–6.90; allelic, OR=1.89, 95% CI=1.18–3.02); ABCB1 3435C&gt;T and hepatotoxicity (dominant, OR=3.80, 95% CI=1.68-8.61), whereas a tendency toward the decreased risk of HDMTX toxicity was present in three SNPs: TYMS 2R&gt;3R and mucositis (dominant, OR=0.66, 95% CI=0.47–0.94); RFC1 80A&gt;G and hepatotoxicity (recessive, OR=0.35, 95% CI=0.16–0.76); and MTHFR 1298A&gt;C and renal toxicity (allelic, OR=0.41, 95% CI=0.18–0.97). Since the data of prognosis outcomes was substantially lacking, current studies were underpowered to investigate the genetic association.Conclusions: We conclude that genotyping of MTHFR and/or ABCB1 polymorphisms prior to treatment, MTHFR 677C&gt;T particularly, is likely to be potentially useful with the aim of tailoring HDMTX therapy and thus reducing toxicity in patients with hematological malignancies.