Whole-genome sequencing and analysis of Chryseobacterium arthrosphaerae from Rana nigromaculata.

Chryseobacterium arthrosphaerae strain FS91703 was isolated from Rana nigromaculata in our previous study. To investigate the genomic characteristics, pathogenicity-related genes, antimicrobial resistance, and phylogenetic relationship of this strain, PacBio RS II and Illumina HiSeq 2000 platforms were used for the whole genome sequencing. The genome size of strain FS91703 was 5,435,691 bp and GC content was 37.78%. A total of 4,951 coding genes were predicted; 99 potential virulence factors homologs were identified. Analysis of antibiotic resistance genes revealed that strain FS91703 harbored 10 antibiotic resistance genes in 6 categories and 2 multidrug-resistant efflux pump genes, including adeG and farA. Strain FS91703 was sensitive to ß-lactam combination drugs, cephem, monobactam and carbapenems, intermediately resistant to phenicol, and resistant to penicillin, aminoglycosides, tetracycline, fluoroquinolones, and folate pathway inhibitors. Phylogenetic analysis revealed that strain FS91703 and C. arthrosphaerae CC-VM-7T were on the same branch of the phylogenetic tree based on 16 S rRNA; the ANI value between them was 96.99%; and the DDH values were 80.2, 72.2 and 81.6% by three default calculation formulae. These results suggested that strain FS91703 was a species of C. arthrosphaerae. Pan-genome analysis showed FS91703 had 566 unique genes compared with 13 other C. arthrosphaerae strains, and had a distant phylogenetic relationship with the other C. arthrosphaerae strains of the same branch in phylogenetic tree based on orthologous genes. The results of this study suggest that strain FS91703 is a multidrug-resistant and highly virulent bacterium, that differs from other C. arthrosphaerae strains at the genomic level. The knowledge about the genomic characteristics and antimicrobial resistance of strain FS91703 provides valuable insights into this rare species, as well as guidance for the treatment of the disease caused by FS91703 in Rana nigromaculata.

Investigation of optical polarization characteristics of ultraviolet-C AlGaN multiple quantum wells by angle-resolved cathodoluminescence.

AlGaN-based ultraviolet-C (UV-C) light-emitting diodes (LEDs) face challenges related to their extremely low external quantum efficiency, which is predominantly attributed to the remarkably inadequate transverse magnetic (TM) light extraction efficiency (LEE). In this study, we employ angle-resolved cathodoluminescence (ARCL) spectroscopy to assess the optical polarization of (0001)-oriented AlGaN multiple quantum well (MQW) structures in UV-C LEDs, in conjunction with a focused ion beam and scanning electron microscopy (FIB/SEM) system to etch samples with various inclination angles (θ) of sidewall. This technique effectively distinguishes the spatial distribution of TM- and transverse electric (TE)-polarized photons contributing to the luminescence of the MQW structure. CL spectroscopy confirms that UV-C LEDs with a θ of 35° exhibit the highest CL signal compared to samples with other θ. Furthermore, we establish a model using finite difference time domain (FDTD) simulation to validate the mechanism of the outcomes. The complementary contribution of TM and TE photons at different specific angles are distinguished by ARCL and confirmed by simulation. At angles near the sidewall, the CL is dominated by the TM photons, which mainly contribute to the increased LEE and the decreased degree of polarization (DOP) to make the spatial distribution of CL more uniform. Additionally, this method allows us to analyze the polarization of light without the need for polarizers, enabling the differentiation of TE and TM modes. This distinction provides flexibility for selecting different emission mode based on various application requirements. The presented approach not only opens up new opportunities for enhanced UV-C light extraction but also provides valuable insights for future endeavors in device fabrication and epitaxial film growth.

Spatially resolved current density distribution in GaN-based flip-chip green mini-LEDs by microscopic hyperspectral imaging and modified two-level modeling.

A modified two-level model is proposed to study the spatially resolved current density distribution of GaN-based green miniaturized light-emitting diodes (mini-LEDs), combining with microscopic hyperspectral imaging. We found that the spatially resolved current density distribution reveals both the radiative and non-radiative recombination mappings, which can also be provided separately by this model. In addition, higher current density is not necessarily correlated with higher photon emission, especially for the regions around the electrode edges, where the high current density suggests current crowding and defect-related non-radiative recombination. The current density distribution of mini-LEDs is further verified by the laser-beam-induced current (LBIC) and the spatially resolved mappings of peak wavelength and FWHM. The modified two-level model also offers radiative/non-radiative mappings and is proved to be beneficial to determine the micro-zone current density distribution and to reveal the intrinsic radiative/non-radiative recombination mechanism of mini-LEDs.

InP-based tunnel junctions for ultra-high concentration photovoltaics.

To enhance the performance of multi-junction photovoltaics, we investigated three different InP-based tunnel junction designs: p++-InGaAs/n++-InP tunnel junction, p++-InGaAs/i-InGaAs-/n++-InP tunnel junction, and p++-InGaAs/i-InGaAs/n++-InGaAs tunnel junction. The p++-InGaAs/i-InGaAs/n++-InGaAs tunnel junction demonstrated a peak tunneling current density of 495 A/cm2 and a resistivity of 9.3 × 10-4 Ωcm2, allowing the tunnel junction device to operate at a concentration over 30000 suns. This was achieved by inserting an undoped InGaAs quantum well at the p++-InGaAs/n++InGaAs junction interfaces, which enhanced its stability within the operating temperature range of multi-junction solar cells. Moreover, the p++-InGaAs/i-InGaAs/n++-InGaAs tunnel junction exhibited the lowest resistance.

LED Junction Temperature Measurement: From Steady State to Transient State.

In this review, we meticulously analyze and consolidate various techniques used for measuring the junction temperature of light-emitting diodes (LEDs) by examining recent advancements in the field as reported in the literature. We initiate our exploration by delineating the evolution of LED technology and underscore the criticality of junction temperature detection. Subsequently, we delve into two key facets of LED junction temperature assessment: steady-state and transient measurements. Beginning with an examination of innovations in steady-state junction temperature detection, we cover a spectrum of approaches ranging from traditional one-dimensional methods to more advanced three-dimensional techniques. These include micro-thermocouple, liquid crystal thermography (LCT), temperature sensitive optical parameters (TSOPs), and infrared (IR) thermography methods. We provide a comprehensive summary of the contributions made by researchers in this domain, while also elucidating the merits and demerits of each method. Transitioning to transient detection, we offer a detailed overview of various techniques such as the improved T3ster method, an enhanced one-dimensional continuous rectangular wave method (CRWM), and thermal reflection imaging. Additionally, we introduce novel methods leveraging high-speed camera technology and reflected light intensity (h-SCRLI), as well as micro high-speed transient imaging based on reflected light (µ_HSTI). Finally, we provide a critical appraisal of the advantages and limitations inherent in several transient detection methods and offer prognostications on future developments in this burgeoning field.

PSMC5 regulates microglial polarization and activation in LPS-induced cognitive deficits and motor impairments by interacting with TLR4.

Luteolin is a flavonoid found in high concentrations in celery and green pepper, and acts as a neuroprotectant. PSMC5 (proteasome 26S subunit, ATPase 5) protein levels were reduced after luteolin stimulation in activated microglia. We aimed to determine whether regulating PSMC5 expression could inhibit neuroinflammation, and investigate the underlying mechanisms.BV2 microglia were transfected with siRNA PSMC5 before the addition of LPS (lipopolysaccharide, 1.0 µg/ml) for 24 h in serum free DMEM. A mouse model of LPS-induced cognitive and motor impairment was established to evaluate the neuroprotective effects of shRNA PSMC5. Intracerebroventricular administration of shRNA PSMC5 was commenced 7 days prior to i.p. injection of LPS (750 µg/kg). Treatments and behavioral experiments were performed once daily for 7 consecutive days. Behavioral tests and pathological/biochemical assays were performed to evaluate LPS-induced hippocampal damage. Molecular dynamics simulation was used to confirm the interaction between PSMC5 and TLR4 (Toll-like receptor 4) in LPS-stimulated BV2 microglia. SiRNA PSMC5 inhibited BV2 microglial activation, and suppressed the release of inflammatory factors (IL-1ß, COX-2, PGE2, TNF-α, and iNOS) upon after LPS stimulation in BV2 microglia. LPS increased IκB-α and p65 phosphorylation, which was attenuated by siRNA PSMC5. Behavioral tests and pathological/biochemical assays showed that shRNA PSMC5 attenuated LPS-induced cognitive and motor impairments, and restored synaptic ultrastructure and protein levels in mice. ShRNA PSMC5 reduced pro-inflammatory cytokine (TNF-α, IL-1ß, PGE2, and NO) levels in the serum and brain, and relevant protein factors (iNOS and COX-2) in the brain. Furthermore, shRNA PSMC5 upregulated the anti-inflammatory mediators interleukin IL-4 and IL-10 in the serum and brain, and promoted a pro-inflammation-to-anti-inflammation phenotype shift in microglial polarization. Mechanistically, shRNA PSMC5 significantly alleviated LPS-induced TLR4 expression. The polarization of LPS-induced microglial pro-inflammation phenotype was abolished by TLR4 inhibitor and in the TLR-4-/- mouse, as in shRNA PSMC5 treatment. PSMC5 interacted with TLR4 via the amino sites Glu284, Met139, Leu127, and Phe283. PSMC5 site mutations attenuated neuroinflammation and reduced pro-inflammatory factors by reducing TLR4-related effects, thereby reducing TLR4-mediated MyD88 (myeloid differentiation factor 88)-dependent activation of NF-κB. PSMC5 could be an important therapeutic target for treatment of neurodegenerative diseases involving neuroinflammation-associated cognitive deficits and motor impairments induced by microglial activation.

Optical power degradation mechanisms in 271†nm AlGaN-based deep ultraviolet light-emitting diodes.

The degradation of AlGaN-based UVC LEDs under constant temperature and constant current stress for up to 500 hrs was analyzed in this work. During each degradation stage, the two-dimensional (2D) thermal distributions, I-V curves, optical powers, combining with focused ion beam and scanning electron microscope (FIB/SEM), were thoroughly tested and analyzed the properties and failure mechanisms of UVC LEDs. The results show that: 1) the opto-electrical characteristics measured before/during stress indicate that the increased leakage current and the generation of stress-induced defects increase the non-radiative recombination in the early stress stage, resulting in a decrease in optical power; 2) the increase of temperature caused by the deterioration of the Cr/Al layer of p-metal after 48 hrs of stress aggravates the optical power in UVC LEDs. The 2D thermal distribution in conjunction with FIB/SEM provide a fast and visual way to precisely locate and analyze the failure mechanisms of UVC LEDs.

Impacts of p-GaN layer thickness on the photoelectric and thermal performance of AlGaN-based deep-UV LEDs.

The effects of different p-GaN layer thickness on the photoelectric and thermal properties of AlGaN-based deep-ultraviolet light-emitting diodes (DUV-LEDs) were investigated. The results revealed that appropriate thinning of the p-GaN layer enhances the photoelectric performance and thermal stability of DUV-LEDs, reducing current crowding effects that affect the external quantum efficiency and chip heat dissipation. The ABC + f(n) model was used to analyse the EQE, which helped in identifying the different physical mechanisms for DUV-LEDs with different p-GaN layer thickness. Moreover, the finite difference time domain simulation results revealed that the light-extraction efficiency of the DUV-LEDs exhibits a trend similar to that of damped vibration as the thickness of the p-GaN layer increases. The AlGaN-based DUV-LED with a p-GaN layer thickness of 20 nm exhibited the best photoelectric characteristics and thermal stability.

Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization.

The regulation of muscle glucose utilization has significant potential for the treatment of type 2 diabetes mellitus (T2DM) and obesity. Heat shock factor 1 (HSF1) is involved in cellular metabolism and regulation of muscle metabolism. However, it is unclear how HSF1 regulates muscle glucose metabolism. In the present study, the development of obesity in mice was associated with HSF1 downregulation. Serum samples and muscle biopsies were obtained from obese and healthy humans. Fasting glucose and insulin levels and the homeostasis model assessment of insulin resistance value showed that obesity was associated with insulin resistance. The skeletal muscle level of HSF1 was decreased in obese and ob/ob mice. HSF1 was selectively over-expressed in the skeletal muscles of high fat diet (HFD)-fed mice. Muscle HSF1 over-expression successfully triggered glycolytic-to-oxidative myofiber switch and increased fatty acid metabolism and insulin sensitivity in the skeletal muscles of HFD-fed mice. Moreover, HSF1 improved energy expenditure and blocked muscle accumulation of triglycerides in HFD-fed mice. Consequently, muscle HSF1 mitigated the impaired muscle insulin signaling and insulin resistance in HFD-fed mice. In conclusion, T2DM and obesity in HFD-fed mice may be treated with selective HSF1-directed programming of exercise-like effects in skeletal muscle. These findings may aid the development of a new therapeutic approach for obesity and T2DM.

Pacenta polypeptide injection alleviates the fibrosis and inflammation in cigarette smoke extracts-induced BEAS-2B cells by modulating MMP-9/TIMP-1 signaling.

Chronic obstructive pulmonary disease (COPD) has high morbidity and mortality. Here, we aimed to explore the roles and potential correlation of placenta polypeptide injection (PPI) and MMP-9/TIMP-1 signaling pathway in COPD. BEAS-2B cells were treated with cigarette smoke extract (CSE) to establish a COPD cell model in vitro. The cell survival and cytotoxic effect were measured by CCK-8, LDH release and flow cytometry assays. The inflammatory responses were determined by western blot and ELISA assay. Cell fibrosis was assessed by immunofluorescence and western blot assays. PPI treatment had no cytotoxic effect on BEAS-2B cells until the final concentration reached to 10%. In the range of 0%-8% final concentration, PPI treatment weakened CSE-induced the decrease of cell viability and the increase of LDH level in a concentration-dependent manner. Four percent PPI treatment enhanced cell viability and decreased cell apoptosis of CSE-treated cells in a time-dependent manner. Moreover, 4% PPI treatment significantly decreased inflammatory responses and fibrosis induced by CSE, while AMPA (MMPs agonist) had opposite effects. Notably, AMPA reversed the protective roles of PPI on CSE-induced inflammation and fibrosis. Mechanistically, 4% PPI treatment significantly suppressed MMP-1, MMP-2, MMP-3, MMP-9, MMP-13, and MMP-19 levels, but enhanced TIMP-1, TIMP-2, TIMP-3, and TIMP-4 levels. Among them, MMP-9 and TIMP-1 might be the main target of PPI. PPI effectively attenuated CSE-induced inflammation and fibrosis in vitro by regulating MMP-9/TIMP-1 signaling pathway.

Transient 2D Junction Temperature Distribution Measurement by Short Pulse Driving and Gated Integration with Ordinary CCD Camera.

The time resolution of the transient process is usually limited by the minimum exposure time of the high-speed camera. In this work, we proposed a method that can achieve nanosecond temporal resolution with an ordinary CCD camera by driving the LED under test with a periodic short-pulse signal and multiple-cycle superposition to obtain two-dimensional transient junction temperature distribution of the heating process. The temporal resolution is determined by the pulse width of the drive source. In the cooling process, the Boxcar gated integration principle is adopted to complete the two-dimensional transient junction temperature distribution with temporal resolution subject to the minimum exposure time of the CCD camera, i.e., 1 µs in this case. To demonstrate the validity of this method, we measured the two-dimensional transient junction temperature distribution of the blue LEDs according to the principle of thermoreflectance and compared it with the thermal imaging method.

On the exciton-assisted radiative recombination via impurity trap levels in AlGaN deep ultraviolet light-emitting diodes.

For decades, problems of parasitic emissions have been ubiquitously encountered in nearly all deep ultraviolet light-emitting diodes (DUV-LEDs). In this work, 450 nm parasitic peaks in 275 nm AlGaN DUV-LEDs have been studied in details. Upon careful comparisons and analyses on the electroluminescence and photoluminescence spectra at various injection levels and different temperatures, we have discovered a mechanism of exciton-assisted radiative recombination, namely, the reinforcement on radiative recombination via other impurity-trap levels (ITLs) by excitons that are generated in the midst of the band gap. For DUV-LED samples under investigation herein, a system of radiative ITLs within the band gap cannot be neglected. It includes two types of impurities located at two different energy levels, 3.80 eV and 2.75 eV, respectively. The former, establishing a sub-band edge, which behaves like an energy entrance to this system, contains a series of hydrogen-like excitons at a temperature lower than 100 K, which behaves like an energy entrance to this system. On the one hand, these excitons absorb carriers from band-edge and reduce the band-edge recombination. On the other hand they transfer the energy to lower impurity levels, enhancing the radiative recombination and giving rise to the 450 nm parasitic peak.

USP8 protects against lipopolysaccharide-induced cognitive and motor deficits by modulating microglia phenotypes through TLR4/MyD88/NF-κB signaling pathway in mice.

Ubiquitin-specific protease 8 (USP8) regulates inflammation in vitro; however, the mechanisms by which USP8 inhibits neuroinflammation and its pathophysiological functions are not completely understood. In this study, we aimed to determine whether USP8 exerts neuroprotective effects in a mouse model of lipopolysaccharide (LPS)-induced cognitive and motor impairment. We commenced intracerebroventricular USP8 administration 7 days prior to i.p. injection of LPS (750 µg/kg). All treatments and behavioral experiments were performed once per day for 7 consecutive days. Behavioral tests and pathological/biochemical assays were performed to evaluate LPS-induced hippocampal damage. USP8 attenuated LPS-induced cognitive and motor impairments in mice. Moreover, USP8 downregulated several pro-inflammatory cytokines [nitric oxide (NO), tumor necrosis factor α (TNF-α), prostaglandin E2 (PGE2), and interleukin-1ß (IL-1ß)] in the serum and brain, and the relevant protein factors [inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2)] in the brain. Furthermore, USP8 upregulated the anti-inflammatory mediators interleukin (IL)-4 and IL-10 in the serum and brain, and promoted a shift from pro-inflammatory to anti-inflammatory microglial phenotypes. The LPS-induced microglial pro-inflammatory phenotype was abolished by TLR4 inhibitor and in TLR4-/- mice; these effects were similar to those of USP8 treatment. Mechanistically, we found that USP8 increased the expression of neuregulin receptor degradation protein-1 (Nrdp1), potently downregulated the expression of TLR4 and myeloid differentiation primary response protein 88 (MyD88) protein, and inhibited the phosphorylation of IκB kinase (IKK) ß and kappa B-alpha (IκBα), thereby reducing nuclear translocation of p65 by inhibiting the activation of the nuclear factor-kappaB (NF-κB) signaling pathway in LPS-induced mice. Our results demonstrated that USP8 exerts protective effects against LPS-induced cognitive and motor deficits in mice by modulating microglial phenotypes via TLR4/MyD88/NF-κB signaling.

Salvianolic acid B ameliorates psoriatic changes in imiquimod-induced psoriasis on BALB/c mice by inhibiting inflammatory and keratin markers via altering phosphatidylinositol-3-kinase/protein kinase B signaling pathway.

Salvianolic acid B (SAB) is an active phytocomponent of a popular Chinese herb called Radix Salvia militiorrhiza with numerous biological properties. The anti-psoriasis activity of SAB was examined by evaluating various psoriasis inflammatory and keratin markers against imiquimod (IMQ)-induced psoriasis on BALB/c mice. Totally 50 healthy BALB/c mice were evenly divided into 5 groups including control, drug control (SAB; 40 mg/kg), IMQ-induced psoriasis (5%), IMQ exposure and treated with SAB (40 mg/kg), or standard methotrexate (MTX; 1 mg/kg). Mice supplemented with either SAB or MTX significantly lowered the values of psoriasis area severity index (PASI), erythema, scaling, skin thickness, inflammatory markers (interleukin [IL]-22/23/17A/1ß/6) and lipid peroxidation product (malondialdehyde). Also, IMQ exposed BALB/c mice treated with SAB or MTX display lesser histopathological changes with enhanced antioxidant activities (catalase, superoxide dismutase). Moreover, the protein expression of keratin markers (K16 and K17) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling proteins (pAkt/Akt and pPI3K/PI3K) were significantly downregulated after administration with SAB and MTX as compared with IMQ induced mice. Taking together, SAB and MTX significantly ameliorate psoriatic changes by inhibiting psoriatic inflammatory and keratin markers through abolishing PI3K/Akt signaling pathway. However, further studies (clinical trials) are needed to confirm the anti-psoriatic property of SAB before recommending to psoriasis patients.

Two-dimensional temperature distribution measurement of light-emitting diodes by micro-hyperspectral imaging-based reflected light method.

We propose a non-contact measurement method for determining two-dimensional (2D) temperature distribution of light-emitting diodes (LEDs). This method is based on both micro-hyperspectral imaging technology and reflected light method, owning merits of both high efficiency and high spatial resolution. Blue and green bare LEDs are used as LED under test, while red and near-infrared LEDs provide incident light to avoid spectral overlapping so as to reduce measurement error. During data processing, the convolution linear filtering algorithm is employed to improve the measurement accuracy. This proposed method is compared with the micro-thermocouple and infrared thermal imaging, with their respective comparison results in fairly good agreements. For spatial resolution of 2D temperature distribution, this method increases at least one order of magnitude compared with the thermal imaging method.

Lycopene protects against t-BHP-induced neuronal oxidative damage and apoptosis via activation of the PI3K/Akt pathway.

Oxidative stress is a key factor of and closely implicated in the pathogenesis of Alzheimer's disease (AD). We herein used tert-butyl hydroperoxide (t-BHP) to induce oxidative stress and mimic oxidative neurotoxicity in vitro. Lycopene is a natural antioxidant that has a strong ability to eliminate free radicals and shows effective protection in some neurodegenerative disease models. However, the effect of lycopene on t-BHP-induced neuronal damage in primary mouse neurons is unknown. This study aimed to investigate the effects of lycopene on t-BHP-induced neuronal damage and the related mechanisms. We found that lycopene pretreatment effectively enhanced the cell viability, improved the neuron morphology, increased the GSH/GSSG level, restored the mitochondrial membrane potential (ΔΨm) and decreased reactive oxygen species generation. Furthermore, lycopene reduced the ratios of Bax:Bcl-2 and cleaved caspase-3:caspase-3 and the level of cytochrome C, increased the levels of synaptophysin (SYP) and postsynaptic density 95 (PSD95) and activated the PI3K/Akt pathway. In conclusion, lycopene attenuated oxidative stress and reduced t-BHP-induced cell apoptosis, and the mechanism is likely related to activation of the PI3K/Akt pathway. Therefore, lycopene is a potential agent for preventing oxidative stress-mediated AD.

D14-SCF(D3)-dependent degradation of D53 regulates strigolactone signalling.

Strigolactones (SLs), a newly discovered class of carotenoid-derived phytohormones, are essential for developmental processes that shape plant architecture and interactions with parasitic weeds and symbiotic arbuscular mycorrhizal fungi. Despite the rapid progress in elucidating the SL biosynthetic pathway, the perception and signalling mechanisms of SL remain poorly understood. Here we show that DWARF 53 (D53) acts as a repressor of SL signalling and that SLs induce its degradation. We find that the rice (Oryza sativa) d53 mutant, which produces an exaggerated number of tillers compared to wild-type plants, is caused by a gain-of-function mutation and is insensitive to exogenous SL treatment. The D53 gene product shares predicted features with the class I Clp ATPase proteins and can form a complex with the α/ß hydrolase protein DWARF 14 (D14) and the F-box protein DWARF 3 (D3), two previously identified signalling components potentially responsible for SL perception. We demonstrate that, in a D14- and D3-dependent manner, SLs induce D53 degradation by the proteasome and abrogate its activity in promoting axillary bud outgrowth. Our combined genetic and biochemical data reveal that D53 acts as a repressor of the SL signalling pathway, whose hormone-induced degradation represents a key molecular link between SL perception and responses.

Immune correlates of clinical benefit in a phase I study of hyperthermia with adoptive T cell immunotherapy in patients with solid tumors.

Purpose: To characterize the T cell receptor (TCR) repertoire, serum cytokine levels, peripheral blood T lymphocyte populations, safety, and clinical efficacy of hyperthermia (HT) combined with autologous adoptive cell therapy (ACT) and either salvage chemotherapy (CT) or anti-PD-1 antibody in patients with previously treated advanced solid tumors.Materials and methods: Thirty-three (33) patients with ovarian, pancreatic, gastric, colorectal, cervical, or endometrial cancer were recruited into the following therapeutic groups: HT + ACT (n = 10), HT + ACT + anti-PD-1 inhibitor (pembrolizumab) (n = 11) and HT + ACT + CT (n = 12). Peripheral blood was collected to analyze TCR repertoire, measurements of cytokines levels and lymphocyte sub-populations before and after treatment.Results: The objective response rate (ORR) was 30% (10/33), including three complete responses (CR) (9.1%) and seven partial responses (PR) (21.2%) and a disease control rate (DCR = CR + PR + SD) of 66.7% (22 of 33). The most common adverse reactions, blistering, subcutaneous fat induration, local heat-related pain, vomiting and sinus tachycardia, were observed in association with HT. IL-2, IL-4, TNF-α, and IFN-γ levels in peripheral blood were significantly increased among the clinical responders (p < 0.05) while IL-6 and IL-10 were elevated among those with progressive disease (p < 0.05). Peripheral blood CD8+/CD28+ T cells increased (p = 0.002), while the CD4+/CD25+/CD127+Treg cells decreased after therapy (p = 0.012). TCR diversity was substantially increased among the clinical responders.Conclusions: Combining HT with ACT plus either CT or anti-PD-1 antibody was safe, generated clinical responses in previously treated advanced cancers, and promoted TCR repertoire diversity and favorable changes in serum IL-2, IL-4, TNF-α, and IFN-γ levels in clinical responders.

Parental Engagement and Early Interactions With Preterm Infants Reduce Risk of Late Postpartum Depression.

Recent studies have shown that preterm delivery is a risk factor for the development of postpartum depression, which not only impairs maternal-infant interactions, leading to infant developmental delay and social interaction difficulties in affected children, but also increases the risk of depression in the mother. Hence, this article aims to study the effects of parental engagement and early interactions with preterm infants on subsequent infant development and behavior, maternal adjustment, and mother-infant relationship. A total of 151 infants/mothers were enrolled in our study. Infants were randomized either to receive early parent interaction or standard care. The early parent interaction program was performed in addition to routine standard of care, Kangaroo Mother Care, during the neonatal intensive care unit stay based on PremieStart Protocol. The behavioral competencies of preterm infants were assessed, as were their mothers' adjustment (depression and coping) and competencies (knowledge of child development). At 12 months of postnatal age, child competencies (development and behavior) were assessed, together with maternal adjustment (parenting stress and depression). Mother-infant interaction was also observed. Early parent interaction did not alter early or later infant development. Furthermore, early parent interaction did not alter early maternal adjustment or late mother-infant relationship, but it reduced the risk of late postpartum depression. Taken together, these studies provide a strong basis for interventions that support parents in the parenting role and guide parents in developmentally appropriate interactions with their preterm babies. These interventions have the potential to lessen the adverse impact of preterm birth on babies and mothers. In addition, the positive benefits of reduced stress can improve parent mental health outcomes and ultimately may further improve parents' relationships with their babies.