Ultrahigh Photo-Responsivity and Detectivity in 2D Bismuth Sulfide Photodetector for Vis-NIR Radiation.

Bismuth sulfide (Bi2S3) exhibits a direct energy bandgap and an exceptional optical absorption capability over a broadband radiation, thus presents a novel class of 2D photodetector material. The field effect transistor (FET) photodetector device is fabricated from 2D Bi2S3. An anomalous variation in the transport characteristics of 2D Bi2S3 is observed with the variation in temperature. The electrical resistance reduces by 99.26% at 10 K compared to the response at 300 K. Defects due to the bismuth and sulfur vacancies play a critical role in the dramatic behavior, which is confirmed using photoluminescence, time-resolved photoluminescence, Hall measurements, and energy dispersive X-ray spectroscopy. The density functional theory calculations provide a significant insight into the thermodynamic properties of intrinsic defects in Bi2S3. Moreover, the effect of gate bias on responsivity additionally confirms its invariance at low temperature. The Bi2S3 based FET photodetector achieves ultrahigh responsivity in the order of ≈106 A W-1 and detectivity of ≈1014 Jones. Moreover, the external quantum efficiency of ≈107% is measured in a wide spectrum of optical illumination (532 to 1064 nm) with a noise-equivalent power of 3.5 × 10-18 W/√Hz at a bias of 0.2 V. The extraordinary performance of Bi2S3 photodetector outstands 2D photodetectors.

Comparing the Reliability of the Glomerular Filtration Rate Estimated with 99m-Technetium Diethylene-Triamine-Pentaacetate versus the Effective Renal Plasma Flow Obtained with 99m-Technetium Ethylene Dicysteine: A Prospective Observational Study.

The glomerular filtration rate (GFR) is important for assessing renal function and must be calculated reliably and reproducibly. This study aimed to compare the reliability and accuracy of GFR estimated with 99m-technetium diethylene-triamine-pentaacetate (99mTc-DTPA) versus that calculated from the effective renal plasma flow (ERPF) (GFR is 20% of ERPF) determined by the 99m-technetium ethylene dicysteine (99mTc-EC) technique. Forty-five patients suffering from cancer requiring platinum compound-based chemotherapy or from chronic renal failure were recruited. The patients were divided into two cohorts: (1) those with normal serum creatinine (SCr) levels (≤2 mg/dL) and (2) deranged SCr levels (>2 mg/dL). For all patients, the relative renal function was estimated by the 99mTc-DTPA and 99mTc-EC methods, 2-4 days apart. A 24-h urine sample for estimating 24-h creatinine clearance (CrCl) was obtained. GFR was also calculated using the Modification of Diet in Renal Disease (MDRD) formula. The GFR estimated via 24-h urine CrCl, 99mTc-DTPA, and ERPF obtained with 99mTc-EC were examined by quantile comparison plots, and all showed evidence of following a non-Gaussian distribution. For SCr values ≤2 mg/dL, the GFR estimated by the MDRD formula consistently shows significantly higher values than the GFR estimated with 99mTc-DTPA or 99mTc-EC. We found a high degree of correlation between the 99mTc-DTPA and 99mTc-EC radionuclide methods of estimating GFR. However, in patients with renal dysfunction, GFR estimated through Gates' method using a gamma camera overestimated the GFR; in these patients, calculating the GFR from the ERPF obtained with 99mTc-EC is more accurate.

Unwinding the modalities of necrosome activation and necroptosis machinery in neurological diseases.

Necroptosis, a regulated form of cell death, is involved in the genesis and development of various life-threatening diseases, including cancer, neurological disorders, cardiac myopathy, and diabetes. Necroptosis initiates with the formation and activation of a necrosome complex, which consists of RIPK1, RIPK2, RIPK3, and MLKL. Emerging studies has demonstrated the regulation of the necroptosis cell death pathway through the implication of numerous post-translational modifications, namely ubiquitination, acetylation, methylation, SUMOylation, hydroxylation, and others. In addition, the negative regulation of the necroptosis pathway has been shown to interfere with brain homeostasis through the regulation of axonal degeneration, mitochondrial dynamics, lysosomal defects, and inflammatory response. Necroptosis is controlled by the activity and expression of signaling molecules, namely VEGF/VEGFR, PI3K/Akt/GSK-3ß, c-Jun N-terminal kinases (JNK), ERK/MAPK, and Wnt/ß-catenin. Herein, we briefly discussed the implication and potential of necrosome activation in the pathogenesis and progression of neurological manifestations, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, traumatic brain injury, and others. Further, we present a detailed picture of natural compounds, micro-RNAs, and chemical compounds as therapeutic agents for treating neurological manifestations.

Protein S-sulfhydration: Unraveling the prospective of hydrogen sulfide in the brain, vasculature and neurological manifestations.

Hydrogen sulfide (H2S) and hydrogen polysulfides (H2Sn) are essential regulatory signaling molecules generated by the entire body, including the central nervous system. Researchers have focused on the classical H2S signaling from the past several decades, whereas the last decade has shown the emergence of H2S-induced protein S-sulfhydration signaling as a potential therapeutic approach. Cysteine S-persulfidation is a critical paradigm of post-translational modification in the process of H2S signaling. Additionally, studies have shown the cross-relationship between S-sulfhydration and other cysteine-induced post-translational modifications, namely nitrosylation and carbonylation. In the central nervous system, S-sulfhydration is involved in the cytoprotection through various signaling pathways, viz. inflammatory response, oxidative stress, endoplasmic reticulum stress, atherosclerosis, thrombosis, and angiogenesis. Further, studies have demonstrated H2S-induced S-sulfhydration in regulating different biological processes, such as mitochondrial integrity, calcium homeostasis, blood-brain permeability, cerebral blood flow, and long-term potentiation. Thus, protein S-sulfhydration becomes a crucial regulatory molecule in cerebrovascular and neurodegenerative diseases. Herein, we first described the generation of intracellular H2S followed by the application of H2S in the regulation of cerebral blood flow and blood-brain permeability. Further, we described the involvement of S-sulfhydration in different biological and cellular functions, such as inflammatory response, mitochondrial integrity, calcium imbalance, and oxidative stress. Moreover, we highlighted the importance of S-sulfhydration in cerebrovascular and neurodegenerative diseases.

Free radical biology in neurological manifestations: mechanisms to therapeutics interventions.

Recent advancements and growing attention about free radicals (ROS) and redox signaling enable the scientific fraternity to consider their involvement in the pathophysiology of inflammatory diseases, metabolic disorders, and neurological defects. Free radicals increase the concentration of reactive oxygen and nitrogen species in the biological system through different endogenous sources and thus increased the overall oxidative stress. An increase in oxidative stress causes cell death through different signaling mechanisms such as mitochondrial impairment, cell-cycle arrest, DNA damage response, inflammation, negative regulation of protein, and lipid peroxidation. Thus, an appropriate balance between free radicals and antioxidants becomes crucial to maintain physiological function. Since the 1brain requires high oxygen for its functioning, it is highly vulnerable to free radical generation and enhanced ROS in the brain adversely affects axonal regeneration and synaptic plasticity, which results in neuronal cell death. In addition, increased ROS in the brain alters various signaling pathways such as apoptosis, autophagy, inflammation and microglial activation, DNA damage response, and cell-cycle arrest, leading to memory and learning defects. Mounting evidence suggests the potential involvement of micro-RNAs, circular-RNAs, natural and dietary compounds, synthetic inhibitors, and heat-shock proteins as therapeutic agents to combat neurological diseases. Herein, we explain the mechanism of free radical generation and its role in mitochondrial, protein, and lipid peroxidation biology. Further, we discuss the negative role of free radicals in synaptic plasticity and axonal regeneration through the modulation of various signaling molecules and also in the involvement of free radicals in various neurological diseases and their potential therapeutic approaches. The primary cause of free radical generation is drug overdosing, industrial air pollution, toxic heavy metals, ionizing radiation, smoking, alcohol, pesticides, and ultraviolet radiation. Excessive generation of free radicals inside the cell R1Q1 increases reactive oxygen and nitrogen species, which causes oxidative damage. An increase in oxidative damage alters different cellular pathways and processes such as mitochondrial impairment, DNA damage response, cell cycle arrest, and inflammatory response, leading to pathogenesis and progression of neurodegenerative disease other neurological defects.

Association Between Obesity and Cancer Mortality: An Internal Medicine Outpatient Clinic Perspective.

BACKGROUND: Obesity is one of the leading preventable causes of cancer that has a causal relationship with cancers of esophagus, breast and colon. Paradoxically, there are studies demonstrating that obesity is associated with improved survival in cancer patients. The aim of our study was to investigate the association of obesity and cancer mortality in adult patients. METHODS: Retrospective medical record review of 784 adult patients was performed who had a diagnosis of cancer and who were seen in our outpatient Internal Medicine Clinic between January 1, 2019 and December 31, 2019. RESULTS: Forty-three (5.2%) patients were cancer non-survivors and 741 (94.8%) were cancer survivors. The mean age of the cancer non-survivors group was significantly higher than that of the cancer survivors (78.7 vs. 68.0 years, respectively; P < 0.001). For every unit increase in age, there was 7.6% increased odds of cancer death (95% confidence interval (CI): 3-12%) (P = 0.001). Average body mass index (BMI) of the patients in the cancer non-survivors group was significantly lower than that of the cancer survivors group (25.0 vs. 28.1 kg/m2; P = 0.008). Non-obese patients had 4.9 times greater odds of cancer death (95% CI: 1.51 - 15.81) (P = 0.008). The mean glycosylated hemoglobin (HbA1c) was significantly higher in the cancer non-survivors group compared to the cancer survivors group (7.1% vs. 6.0%; P < 0.001), and for every unit increase in HbA1c there was 1.6 times greater odds of cancer death (95% CI: 1.14 - 2.23) (P = 0.006). Patients with peripheral artery disease (PAD) had 3.5 times greater odds of cancer death compared to those without PAD (95% CI: 1.18 - 10.19) (P = 0.023). CONCLUSIONS: Non-obese patients with cancer had higher odds of cancer death. Rising HbA1c, increasing age, and presence of PAD were associated with increased cancer mortality.

Protective role of anticancer drugs in neurodegenerative disorders: A drug repurposing approach.

The disease heterogeneity and little therapeutic progress in neurodegenerative diseases justify the need for novel and effective drug discovery approaches. Drug repurposing is an emerging approach that reinvigorates the classical drug discovery method by divulging new therapeutic uses of existing drugs. The common biological background and inverse tuning between cancer and neurodegeneration give weight to the conceptualization of repurposing of anticancer drugs as novel therapeutics. Many studies are available in the literature, which highlights the success story of anticancer drugs as repurposed therapeutics. Among them, kinase inhibitors, developed for various oncology indications evinced notable neuroprotective effects in neurodegenerative diseases. In this review, we shed light on the salient role of multiple protein kinases in neurodegenerative disorders. We also proposed a feasible explanation of the action of kinase inhibitors in neurodegenerative disorders with more attention towards neurodegenerative disorders. The problem of neurotoxicity associated with some anticancer drugs is also highlighted. Our review encourages further research to better encode the hidden potential of anticancer drugs with the aim of developing prospective repurposed drugs with no toxicity for neurodegenerative disorders.

Paclitaxel Encapsulation into Dual-Functionalized Multi-Walled Carbon Nanotubes.

This work reports the synthesis of multi-walled carbon nanotubes (CNTs) from xylene/ferrocene using catalytic chemical vapor deposition technique. Following characterization using transmission electron microscopy (TEM), energy-dispersive X-ray (EDX), and Raman spectroscopy, CNT surface was dual-functionalized using ethylenediamine and phenylboronic acid groups. Average diameter of CNTs was calculated to be 16.5 nm. EDX spectra confirmed the existence of carbonaceous deposits on the tube's surface. Scattered electron diffraction and X-ray peak broadening calculations showed consistent inter-planer distance of the grown CNTs. Chemical functionalization, confirmed from FT-IR and Raman spectra, showed an enhanced dispersibility of CNTs in water. We describe the changes in the first- and second-order regions of the Raman spectra following the encapsulation of an anti-cancer drug, paclitaxel (PLX), into the free volume of functionalized CNTs. High PLX loading, achieved through its non-covalent π-π stacking within the CNT interior, is confirmed through the blue-shifted, softened G band in the Raman spectrum. While not addressed here, we will exploit this dual functionalization tactic to elaborate the relative role of attached moieties in the affinity interaction of CNTs with extra-cellular sialic acid, a biological target showing metastatic stage-dependent over-expression in colon cancer cells.

Functionalized graphene nanosheets with improved dispersion stability and superior paclitaxel loading capacity.

This study reports our attempt of improving dispersibility of reduced graphene oxide (rGO) through differential functionalization of carboxyl moieties with ethylene diamine (EDA) and folic acid (FA) using carbodimide chemistry. Successful covalent linkage was demonstrated through FT-IR, Raman and energy dispersive X-ray spectroscopy. Functionalized nanosheets (GNs) produced a stable dispersion up to 0.1 wt% which remained unaffected against salt- and protein-induced aggregation. Hemolysis test showed negligible toxicity of GNs in murine erythrocytes up to 100 µg/ml. Non-covalent hydrophobic and п-п stacking interactions between GNs and paclitaxel (PLX) offered a superior loading (95.07%) capacity. The latter could substantially minimize the incidence of disruptive protein-carrier interactions and thus, inflate the biomedical potential of graphene materials. Besides, the attached FA groups can be exploited for target-selective delivery of PLX to folate receptor over-expressing tumor cells.

Greenhouse gas emissions and energy exchange in wet and dry season rice: eddy covariance-based approach.

Lowland tropical rice-rice system has a unique micrometrological characteristic that affects both energy component and net ecosystem energy. Periodic and seasonal variations of methane (CH4), carbon dioxide (CO2), and energy exchange from irrigated lowland rice-rice ecosystem were studied using open-path eddy covariance (EC) system during the dry (DS) and wet (WS) seasons in 2015. Concurrently, the manual chamber method was employed in nitrous oxide (N2O) measurement efflux. Cumulative net ecosystem carbon exchange (NEE) was observed highest (- 232.55 g C m-2) during the WS and lowest (- 14.81 g C m-2) during wet fallow (WF). Similarly, the cumulative net ecosystem methane exchange (NEME) was found highest (13,456.5 mg CH4 m-2) during the WS and lowest (2014.3 mg CH4 m-2) during the WF. Surface energy fluxes, i.e., sensible (Hs) and latent heat (LE) fluxes, showed a similar trend. With the advancement of time, the ratio of ecosystem respiration (Re) and gross primary production (GPP) increased. The cumulative global warming potential (GWP) for the two cropping seasons including two fallows was 13,224.1 kg CO2 equivalent ha-1. The GWP and NEME showed a similar trend as soil enzymes and labile carbon pools in both seasons (except GWP at the harvesting stage in the wet season). The mean NEE exhibited a more negative value with decrease in labile pools from panicle initiation to harvesting stage in the WS. Soil labile C and soil enzymes can be used as an indicator of NEE, NEME, and GWP in lowland rice ecology. Graphical abstract Schematic presentation of GHG emission and energy exchange in lowland rice.

Rehabilitation of hemi-maxillectomy with a definite one piece hollow bulb obturator.

Maxillary intraoral defects due to surgical resection create an open link between the oral and nasal cavities causing difficulty in deglutition, speech, and an unaesthetic appearance. Prosthetic innervention is required to restore the needs of speech, mastication as well as closing the oroantral communication. This article shows a case report of systematic approach for fabrication of immediate plate just after surgery, followed by interim feeding plate 2 weeks after surgery, and finally definitive one piece hollow bulb obturator 6 months after surgery.

Methotrexate: a detailed review on drug delivery and clinical aspects.

INTRODUCTION: Uses of methotrexate (MTX) are well established for the treatment of various types of malignancy, psoriasis, rheumatological diseases and the medical termination of pregnancy. Formulation and targeting approaches for MTX with controlled release carriers, multiparticulate systems, prodrug and drug conjugates have been found to improve bioavailability, reduce adverse effects and maximize clinical efficacy, compared with conventional methods. AREAS COVERED: This exhaustive literature survey on different electronic databases covers drug delivery and clinical trials on MTX. This review deals with the challenges and achievements of controlled release, multiparticulate, prodrug and drug conjugate systems of MTX. EXPERT OPINION: Therapeutic drug monitoring of MTX is crucial to attain a good efficacy. In spite of the advantages of multiparticulate, prodrug and drug conjugates, clinical applications of such formulations of MTX are still under infancy. These drug delivery systems require the special attention of medical experts for its wider clinical usage, and pharmaceutical experts for its scale-up. The combination of MTX with other antineoplastic and immunosuppressants should also be subjected to clinical trials, such as the combination of misoprostol with MTX in abortion.