Water soluble cadmium selenide quantum dots for ultrasensitive detection of organic,inorganic and elemental mercury in biological fluids and live cells

Mercury exists in organic, inorganic, and elemental forms; all of them are highly toxic. A sensor which could detect all forms of mercury below the permissible level in environmental and biological samples would be advantageous. A facile method to synthesize N-acetyl cysteine capped cadmium selenide quantum dots (CdSe QDs) with an emission at 554 nm was reported. CdSe QDs showed high sensitivity and selectivity toward Hg in aqueous media as well as biological fluids like simulated cerebrospinal fluid, saliva, and urine, and also in natural fluids like juices of tomato, sugarcane, and lime. The sensing mechanism is attributed to the interactions between Hg and CdSe QDs inducing fluorescence quenching. The limit of detection is 1.62, 0.75, and 1.27 ppb for organic, inorganic and elemental mercury, respectively, which is below WHO guidelines. The suitability of the sensor for estimating Hg in biological fluids was demonstrated by recovery experiments. Besides sensing, a two color cell imaging method was developed employing CdSe QDs and acridine orange. Using this method, the uptake of Hg in living cells was demonstrated.

CdSe QDs fluorescence is highly selective and sensitive to mercury.     

Proving the robustness of a PEDOT:PSS-based thermistor via functionalized graphene oxide–poly(vinylidene fluoride) composite encapsulation for food logistics

The instability of poly(3,4-ethylenedioxythiophene):polystyrene sulfonate (PEDOT:PSS) under a humid condition is the major limitation in the practical development of a flexible thermistor. Here, we introduced a functionalized graphene oxide–polyvinylidene fluoride (FGO–PVDF) composite as an encapsulation layer to prove the reliability of PEDOT:PSS thermistors under high-humidity conditions. The FGO–PVDF-encapsulated thermistor exhibited good linearity, a resolution of 1272.57 Ω per °C, a temperature coefficient of resistance equal to −3.95 × 10⁻³ per °C, stable performance, and an acceptable response time (∼40 s per °C) calibrated in the temperature range between −10 °C and 30 °C, resembling the temperature of a cold chain system. For applications in a food cold chain system, this thermistor was integrated into a roll-to-roll (R2R) gravure-printed NFC antenna, a microcontroller-embedded Si-chip transponder, and a printed battery to work as a smart label to wirelessly monitor the time–temperature history (TTH) of a food package. A proof-of-concept study was demonstrated by attaching an NFC-enabled hybrid TTH logger, a smart label, in a chicken package.

We introduced a FGO–PVDF composite as an encapsulation layer to prove the reliability of PEDOT:PSS thermistors under high-humidity conditions to realize an NFC-enabled smart label for monitoring time-temperature history of a food item along the cold chain.     

Concurrent Pancreatic and Renal Leukemic Cell Infiltration

Pancreatic involvement in acute lymphoblastic leukemia (ALL) is uncommon more so in adults. It can present as obstructive jaundice, pancreatitis or can be asymptomatic. We report here the clinical and imaging features in a 28 years old man with B cell ALL with simultaneous involvement of pancreas and bilateral kidneys. Computed tomography of abdomen showed diffuse infiltration of pancreas by multiple tiny hypodense lesions and multiple hypodense lesions in both kidneys. Although leukemic involvement of pancreas is unusual and our patient was asymptomatic, one should consider the possibility of pancreatic infiltration in a leukemic patient presenting with pancreatic enlargement, cholestatic jaundice or pancreatitis.     

Impact of acute kidney injury on renal allograft survival

Background: Acute kidney injury (AKI) is one of the major determinants of graft survival in kidney transplantation (KTx). Renal Transplant recipients are more vulnerable to develop AKI than general population. AKI in the transplant recipient differs from community acquired, in terms of risk factors, etiology and outcome. Our aim was to study the incidence, risk factors, etiology, outcome and the impact of AKI on graft survival.

Methods: A retrospective analysis of 219 renal transplant recipients (both live and deceased donor) was done.

Results: AKI was observed in 112 (51.14%) recipients, with mean age of 41.5?±?11.2 years during follow-up of 43.2?±?12.5 months. Etiologies of AKI were infection (47.32%), rejection (26.78%), calcineurin inhibitor (CNI) toxicity (13.39%), and recurrence of native kidney disease (NKD) (4.46%). New Onset Diabetes After Transplant (NODAT) and deceased donor transplant were the significant risk factors for AKI. During follow-up 70.53% (p?=?.004) of AKI recipients progressed to chronic kidney disease (CKD) in contrast to only 11.21% (p?=?.342) of non AKI recipients. Risk factors for CKD were AKI within first year of transplant (HR: 7.32, 95%CI: 4.37–15.32, p?=?.007), multiple episodes of AKI (HR: 6.92, 95%CI: 3.92–9.63, p?=?.008), infection (HR: 3.62, 95%CI: 2.8–5.75, p?=?.03) and rejection (HR: 9.92 95%CI: 5.56–12.36, p?=?.001).

Conclusion: Renal transplant recipients have high risk for AKI and it hampers long-term graft survival.     

Protective effect of Terminalia chebula against lysosomal enzyme alterations in isoproterenol-induced cardiac damage in rats

BACKGROUND:

Terminalia chebula is an ayurvedic drug recommended for the treatment of heart diseases. Earlier studies by the authors validated the beneficial cardioprotective effect of T chebula against isoproterenol-induced myocardial infarction.

OBJECTIVES:

To evaluate the therapeutic efficacy of T chebula in protecting against isoproterenol-induced lysosomal membrane damage.

METHODS:

Lysosomal enzyme activities from the serum, heart and lysosomal fractions were determined. The triphenyltetrazolium chloride assay was used to confirm the protective effect of T chebula on the myocardium.

RESULTS:

Isoproterenol administration produced significant cardiac damage (as seen by the triphenyltetrazolium chloride assay) and significantly altered lysosomal enzyme activities. Pretreatment with an ethanol extract of T chebula was found to retain near normal activities of lysosomal enzymes in rats given T chebula or T chebula plus isoproterenol compared with rats given isoproterenol alone.

CONCLUSIONS:

Pretreatment with T chebula extract stabilizes the lysosomal membrane and, thus, may have prevented myocardial damage.     

Influence of experimental type 1 diabetes on the pulmonary effects of diesel exhaust particles in mice

Epidemiologically, exposure to particulate air pollution is associated with increases in morbidity and mortality, and diabetics are especially vulnerable to effects of particles. This study was carried out to determine the respiratory effect of diesel exhaust particles (DEP; 0.4 mg/kg) on mice rendered diabetic by the injection of streptozotocin or vehicle (control). Four weeks following induction of diabetes, the animals were intratracheally instilled (i.t.) with DEP (0.4 mg/kg) or saline. 24 h later, the measurement of airway reactivity to methacholine in vivo by a forced oscillation technique showed a significant and dose-dependent increase in airway resistance in non-diabetic mice exposed to DEP versus non-diabetic mice exposed to saline. Similarly, the airway resistance was significantly increased in diabetic mice exposed to DEP versus diabetic mice exposed to saline. Nevertheless, there was no difference in the airway resistance between diabetic and non-diabetic mice after i.t. administration of DEP. Following DEP administration there were neutrophil polymorphs infiltration of pulmonary interalveolar septae and the alveolar spaces with many macrophages containing DEP in both diabetic and non-diabetic mice. Interestingly, apoptotic cells were only found in the examined lung sections from diabetic mice exposed to DEP. Total proteins and albumin concentrations in bronchoalveolar lavage (BAL) fluid, markers for increase of epithelial permeability, were significantly increased in diabetic mice exposed to DEP compared to saline-treated diabetic and DEP-treated non diabetic mice. Superoxide dismutase activity and reduced glutathione concentration in BAL were significantly decreased in diabetic mice exposed to DEP compared to saline-treated diabetic and DEP-treated non diabetic mice. Moreover, tumor necrosis factor α (TNFα) concentrations were significantly increased in diabetic mice exposed to DEP compared to saline-treated diabetic and DEP-treated non diabetic mice. We conclude that, at the dose and time point investigated, DEP equally increased airway resistance and caused infiltration of inflammatory cells in the lung of both diabetic and non-diabetic mice. However, the occurrence of oxidative stress, the presence lung apoptotic cells and the increase of total proteins, albumin and TNFα in BAL fluid were only seen in DEP-exposed diabetic mice suggesting an increased respiratory susceptibility to particulate air pollution.     

Midbrain dopaminergic innervation of the hippocampus is sufficient to modulate formation of aversive memories

Aversive memories are important for survival, and dopaminergic signaling in the hippocampus has been implicated in aversive learning. However, the source and mode of action of hippocampal dopamine remain controversial. Here, we utilize anterograde and retrograde viral tracing methods to label midbrain dopaminergic projections to the dorsal hippocampus. We identify a population of midbrain dopaminergic neurons near the border of the substantia nigra pars compacta and the lateral ventral tegmental area that sends direct projections to the dorsal hippocampus. Using optogenetic manipulations and mutant mice to control dopamine transmission in the hippocampus, we show that midbrain dopamine potently modulates aversive memory formation during encoding of contextual fear. Moreover, we demonstrate that dopaminergic transmission in the dorsal CA1 is required for the acquisition of contextual fear memories, and that this acquisition is sustained in the absence of catecholamine release from noradrenergic terminals. Our findings identify a cluster of midbrain dopamine neurons that innervate the hippocampus and show that the midbrain dopamine neuromodulation in the dorsal hippocampus is sufficient to maintain aversive memory formation.

Dopaminergic signaling regulates a diverse array of behaviors in the mammalian central nervous system (1). In addition to its well-established role in the control of movement (2, 3), motivation (4, 5), and reward processing (6, 7), dopamine (DA) also modulates hippocampus-dependent learning and memory (8–10). This heterogeneity of effects depends strongly on the target as well as the origin of the dopaminergic signal. Recent studies indicate that certain subpopulations of midbrain DA neurons located in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) send projections to specific target areas in the ventral and dorsal striatum, amygdala, prefrontal cortex, and other forebrain structures (11, 12). Surprisingly, very limited information exists about midbrain dopaminergic projections to the hippocampus.Studies from the 1990s in the rat suggested that dopaminergic projections from the midbrain (VTA, SNc, and retrorubral field) are the main source of hippocampal DA (13–15). Those observations found support in more recent studies showing that these projections can modulate synaptic responses in hippocampal CA1 (16), regulate drug-induced in vivo synaptic plasticity (17), and facilitate spatial memory retention (18). Nevertheless, the discrepancy between the low density of dopaminergic fibers and the high expression of D1/D5 receptors (19–21) suggested the existence of other sources of DA in the rodent hippocampus (22, 23). In fact, it was shown that the optogenetic activation of tyrosine hydroxylase (TH)–positive neurons in the locus coeruleus (LC) also enhances spatial memory (24, 25). Those neurons synthesize DA as a precursor of norepinephrine (NE), and they corelease both neurotransmitters in the hippocampus, acting as an alternative source of DA (22, 24, 25). The higher density of TH innervation from the LC has led to the expectation that DA from the midbrain may be relatively insignificant. Strikingly, however, both midbrain dopaminergic and LC projections to the dorsal hippocampus (dHip) can promote the consolidation of spatial memory in different tasks (18, 24). Furthermore, NE itself has been shown to play an important role in hippocampus-dependent memory processes (26, 27). Thus, there are considerable complications surrounding the source and function of hippocampal DA in different mnemonic processes.In addition to its role in the regulation of spatial memory retention, DA has been strongly associated with the formation of aversive memories. It is known that aversive stimuli (28, 29), as well as threat-predictive cues (30, 31), can trigger the firing of a subpopulation of midbrain dopaminergic neurons and elevate DA levels in the forebrain (32–34). In the hippocampus, it has been shown that dopaminergic transmission is necessary for aversive learning and associated synaptic plasticity, and inhibition of D1/D5 receptors in the dorsal CA1 (dCA1) impairs performance in a passive avoidance task (10, 35). Even though there is considerable evidence supporting the notion that the inhibition of hippocampal DA signaling impairs aversive learning, the source of the DA signals and the way DA contributes to this process remain understudied and unresolved.In this study, we used complementary retrograde and anterograde tracing techniques to show the dopaminergic innervation of dCA1 and to identify a population of dopaminergic neurons in VTA/SNc that projects directly to the hippocampus. Next, we utilized contextual fear conditioning (cFC) as a paradigm to test the effects of midbrain dopaminergic transmission on aversive memory formation in the hippocampus. Using optogenetics to enhance midbrain DA transmission and pharmacology to inhibit DA signaling in dCA1, we found that DA can bidirectionally regulate context-dependent, associative fear learning. Finally, by genetic ablation of catecholamine production exclusively in NE neurons, we showed that midbrain DA (with no LC DA contribution) is sufficient to maintain normal contextual fear memory formation.     

Cyanobacterial metabolites as novel drug candidates in corona viral therapies: A review

Most of the medical and nonmedical research labs, all around the world, are racing against time to produce an effective vaccine or an antiviral medicine for coronavirus disease 2019 (COVID‐19). Conventional medicines and novel nano‐materials including chemical and herbal‐based compounds are all into positive trials toward coronaviruses and other pandemic infections. Among them, natural immune boosters have attracted physicians because of their longevity and reliability for fewer side effects. This is a review article with a detailed picture of an unexplored antiviral source with maximum potency in curing viral infections. Cyanobacteriae have been known for centuries and are rich in secondary metabolites of proteins, biopeptides, and polysaccharides for prominent antiviral action against chest infections. But detailed exploratory research is required to purify, scale‐up, and commercialize the pharmacologically active agents from these drug reserves.