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Objective: To understand the epidemiological characteristics of COVID-19 epidemic in Ejina banner, Inner Mongolia, in October 2021 and provide evidence for the improvement of COVID-19 prevention and control. Methods: The information about the time, area and population distributions of COVID-19 cases in Ejina before November 13, 2021 and the gene sequencing result of the isolates were collected for a statistical descriptive analysis. Results: The first COVID-19 case in Ejina occurred on 7 October, 2021. A total of 164 COVID-19 cases were reported from October 19 to November 12. Most cases were distributed in 6 communities in Darahub (156 cases, 95.12%). The result of full gene sequencing of the isolates indicted that the pathogen was Delta variant (B.1.617.2). The male to female ratio of the cases was 1.3∶1. The age of cases ranged from 1 to 85 years, and the cases aged 20-59 years accounted for 78.66%. The main clinical symptoms were sore throat (91 cases, 91.92%), cough (49 cases, 49.49%) and fever (23 cases, 23.23%). Most cases were ordinary ones (81 cases, 49.39%) and mild ones (68 cases, 41.46%). The cases were mainly detected at the isolation points (84 cases, 51.22%) and through population based nucleic acid testing (62 cases, 37.80%). The basic reproduction number ( R 0 ) of COVID-19 was 5.3, the average incubation period was 3.9 days. The local government rapidly started Ⅳ level emergency response and conducted 10 rounds of nucleic acid tests. The transferring of travelers reduced the risk for the further spread of COVID-19 in Ejina. Conclusions: The epidemic of COVID-19 in Ejina characterized by strong transmission, short incubation period, herd susceptibility and case clustering. Delta variant (B.1.617.2) was the pathogen, which might be imported from Zeke port. Comprehensive prevention and control measures, such as closed-loop management and vaccination, should be continued. The successful transferring of the patients and travelers provided evidence for the effective and precise prevention and control of COVID-19 in a routine manner.

The interaction between 20(S)-protopanaxatriol (PPT) and bovine serum albumin ( BSA) was studied with fluorescence quenching technique and ultra-violet absorption spectroscopy. The results indicated that PPT led to the intrinsic fluorescence quenching of BSA through a static quenching process .The binding constants of PPT with BSA obtained with fluorescence quenching method were calculated as 0.926 3×10(3) (298 K), 0.618 2×10(3) (308 K), 0.414 4×10(3) L·mol(-1)(318 K), respectively; while the number binding sites n were close to unity. The results showed that the driving force of the interaction between PPT and BSA was hydrogen bond and Van der Waals force. The result of synchronous fluorescence spectra showed that binding of PPT with BSA could induce conformational changes in BSA, that the part of tryptophan became more closely. According to Föster fluorescence resonance energy transfer theory, the binding distance r and energy-transfer efficiency E were respectively 26.2 nm and 0.32.

Aim: To investigate the effect of compound nutrients on Th1/Th2 imbalance caused by changes in cytokines of Th cell subsets, interleukin (IL)-2, IL-6 and TNF-α, in rats with acute immobilization and cold water-immersion stress., Methods: Male SD rats were randomly assigned to three groups including normal control group (C), acute stress group (S) and acute stress+compound nutrients group (S+CN). Stress procedure was the acute immobilization and cold water-immersion. The stress rats were fed water (Group S) or compound nutrient liquid (Group S+CN) by a feeding needle 1 week before acute stress, and then restrained and immersed in cold water for 30 min. The control rats were given water in the same way without stress stimulation. The rats were killed and blood samples were collected 0, 30, 60 and 120 min after stress, respectively. Serum was separated by centrifugation and stored at -70 DegreesCelsius until assayed. The serum levels of IL-2, IL-6 and TNF-α were analyzed by an enzyme-linked immunosorbent assay (ELISA) kit., Results: Acute immobilization and cold water-immersion stress reduced IL-2 level, and increased IL-6 and TNF-α level at different time points (0, 30, 60 and 120 min) after stress, which was most obvious at 30 min. Oral administration (gavage) of compound nutrients was found to moderate the acute immobilization and cold water-immersion stress-induced changes in serum IL-2, IL-6 and TNF-α, which was also most significant at 30 min after stress., Conclusion: Complex nutrients can significantly alleviate the changes of Th1/Th2 cytokines in stress rats, including IL-2, IL-6 and TNF-α, which suggests that compound nutrients can improve the immune regulation function of stress rats and restore Th1/Th2 balance. Compound nutrients might enhance the body's anti-stress ability and lighten the stress-related damage, thus being a possible candidate for the therapeutic modulation of stress.

A new ligand N, N-bis[(diphenylphosphino)methyl]-2-pyridinylamine (L) and its luminescent dinuclear copper(I) complex [CuBrL]1 (1) were synthesized and characterized by mass spectrometry, elemental analysis, NMR and electronic spectroscopies. The structure of complex 1 was determined by X-ray crystal analysis to be a dinuclear complex with a pseudo-tetrahedral geometry. The complex 1 crystallizes in a triclinic space group P-1 and has two copper(I ) centers bridged by two halogen ligands to form the dinuclear structure with a four-membered Cu2 Br2 ring. The Cu-Cu distance in complex 1 is 0.306 0 nm which is longer than a sum of Van der Waals radius of two copper( I ) atoms. Therefore there is no substantial interaction between the two copper(I) centers in complex 1. DFT calculations indicate that the electron density of HOMO is distributed mainly over the copper, bromine and phosphorus atoms, while that of LUMO is localized on the ligand. Our work shows that there are two mechanisms to form the the lowest excited state of complex 1, i.e. the metal-to-ligand charge transfer (MLCT) and halogen-to-ligand charge transfer (XLCT).

The molecular geometries of four 2,4-dimethyl-7-amino-1,8-naphthyridine derivatives were optimized with B3LYP/6-31G(d) method. The energies of their frontier molecular orbitals and the molecular structures were investigated theoretically. The theoretical electronic spectra were calculated with TD-DFT in gas phase, PCM-TD-B3LYP/6-31 + G(d) and semiempirical ZINDO in CH2 Cl2 solution. The influences of solvent model and calculation methods on the electronic absorption spectra were also probed. The calculated results show that delocalized pi bonds exist in the four 1,8-naphthyridine derivatives, and their energy gaps (deltaE) between HOMO and LUMO are relatively small. The variation in their deltaE values gives a consistent trend with that of their electronic absorption with lambda(max). Theoretical spectra achieved prove that their absorptions are red-shifted when the delocalization of pi electrons is enhanced or the capability to donate electron by a substituted group is increased. The maximum absorption peaks of the four derivatives originate from pi (HOMO) --> pi * (LUMO) transition. The spectra calculated at the PCM-B3LYP/6-31 + G(d) level have little difference from experimental results: the differences in wavelength are 2.6, 10.3, 5.3 and 6.9 nm, whereas those in energies are 0.03, 0.09, 0.04 and 0.08 eV, respectively. The obtained results suggest that electronic spectra calculated by TD-DFT on the bases of geometries optimized with B3LYP/6-31(d) are in agreement with experimental ones, and can account for the different spectroscopic properties of the four 1,8-naphthyridine derivatives.

In order to investigate the effect of leptin on the secretion of rat pituitary adenoma GH3 cell and its mechanisms, we observed the effect of leptin on the growth hormone secretion, proliferation and apoptosis of GH3 cells. The results indicated that leptin at 1, 10, and 100 nmol/L could inhibit the basal growth hormone secretion of GH3 cells in a dose dependent manner (P<0.05). Short-term treatment of leptin (10 nmol/L) for 30 min, 1 and 3 h did not affect basal GH secretion. However, treatment of the GH3 cells with leptin (10 nmol/L) for 1 d or longer resulted in an inhibition of GH secretion (P<0.05). We used MTT method and flow cytometery (FCM) to study the effect of leptin on the proliferation and apoptosis of GH3 cells. We found that leptin inhibited proliferation of GH3 cells with a dose-dependent manner. And leptin reduced the proportion of cells in S phase, increased the proportion of cells in G1, and increased the proportion of GH3 cells in 2 and 4 phase. These results demonstrate that leptin inhibits the basal GH secretion of GH3 cells, which may be due to the inhibition of DNA synthesis and advanced apoptosis of GH3 cells.

Aim: To observe the expression of Leptin receptors (OB-R) in male rat anterior pituitary, and study the influence of Leptin on the level of intracellular free Ca2+ ([Ca2+]i) in the cultured growth hormone (GH) cell of male rat pituitary., Methods: RT-PCR method was used to observe the expression of Leptin receptors (OB-R) in male rat anterior pituitary. We used grade centrifuging method to get growth hormone (GH) cell, and [Ca2+]i in GH cell was examined by laser scanning confocal system., Results: OB-R mRNA were expressed in male rat anterior pituitary, including OB-R (common form), OB-Ra (short form) and OB-Rb (long form). There were about 70% or 80% GH cell by grade centrifuging. Leptin at 10(-8)mol/L could decrease the level intracellular free Ca2+ ([Ca2+]i) in cultured GH cell., Conclusion: There are three subtypes of Leptin receptors expressions in male rat anterior pituitary, and Leptin could reduce intracellular free Ca2+ level of GH cell markedly.

We found previously that ACh can significantly inhibit the proliferation of cultured human pituitary adenoma cells. In order to make a further investigation of the mechanism of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, we observed the levels of protein kinase C (PKC), [Ca(2+)](i) and cAMP/cGMP in cultured pituitary adenoma cells after treatment with ACh. The results demonstrate that (1) compared with control, PMA, a PKC activator, increased the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells. However, after a 15-min treatment with ACh (10 micromol/L), a significant reduction of the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells was observed, and the reduction effect could be blocked by atropine. (2) The level of [Ca(2+)](i) of single adenoma cells was found to decrease immediately on the addition of ACh (10 micromol/L), which could also be blocked by atropine. (3) ACh increased the amount of cAMP in the cytoplasm of human pituitary adenoma cells, but had no effect on that of cGMP. These data provide an important clue to explore the molecular mechanisms of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, and suggest that the modulating effect of ACh on the proliferation of pituitary adenoma cells results from the interactions of several cellular signaling pathways.

Aim: To observe the expression of estrogen receptors alpha and beta in human tongue squamous cancer line Tca8113 cell, and to study the influence of beta-estradiol (beta-E2) on the proliferation and cell cycle of cultured Tca8113 cell., Methods: Immunocytochemistry and RT-PCR methods were used to observe the expression of estrogen receptors (ER) in human tongue squamous carcinoma line Tca8113 cell. 3H-TdR incorporation and cell cycle analysis were used to examine the change of proliferation and DNA synthesis of Tca8113 cell., Results: ER-alpha and ER-beta mRNA were expressed in human tongue squamous cancer cell, and the expression of ER-beta was weaker than that of ER-alpha. beta-Estradiol at 10(-8) mol/L - 10(-6) mol/L could increase the proliferation of human tongue squamous carcinoma cell in a dose dependent manner (P < 0.01). beta-E2 (10(-6) mol/L) could increase the proportion of cells in S phase and G2 phase from 23.5% up to 37.7%. The effect of estradiol on the proliferation of cultured human tongue squamous cancer line Tca8113 cell could be inhibited by Tamoxifen., Conclusion: There are ER-alpha and ER-beta expression in human tongue squamous cancer line Tca8113 cell, and beta-estradiol promotes the proliferation and cell cycle of cultured human Tca8113 cell.

In order to elucidate the effect of acetylcholine (ACh) on the occurrence and development of human pituitary adenoma, it was firstly observed whether there exists choline acetyl transferase (ChAT) which is necessary for the synthesis of acetylcholine in the cells of human pituitary adenoma, and then MTT method, (3)H TdR incorporation, cell cycle analysis and TUNEL were employed to estimate the influence of ACh on the proliferation, DNA synthesis and apoptosis of three kinds of human pituitary adenoma (human prolactinoma, somatotropinoma and non-functional tumor) cells cultured in vitro. The results showed that (1) the positive staining of ChAT was obviously observed in the cells of the three kinds of human pituitary adenoma, however, it was lower than that in normal human pituitary gland; (2) ACh had a similar effect on the proliferation of the three kinds of human pituitary adenoma cells. ACh at 0.1-10 micromol/L decreased the (3)H TdR incorporation and the MTT A value in a dose-dependent manner. At the same time, ACh decreased the ratio of S or G(2) phase pituitary adenoma cells significantly, but increased the ratio of G(1) phase pituitary tumour cells markedly; (3) the effect of acetylcholine on the proliferation of human pituitary adenoma cells was inhibited by atropine, but not by tubocurarine; (4) ACh had no effect on the apoptosis of human pituitary adenoma cells cultured in vitro. These data suggest that ACh may have a significant modulating effect on the proliferation of pituitary adenoma cells by means of paracrine or autocrine, and the effect is mediated by muscarinic receptor.

Aim: To study the influence of genistein (GST) on the proliferation and apoptosis of cultured human prolactinoma cells., Methods: MTT method and 3H-TdR incorporation and cell cycle analysis were used to examine the changes of proliferation and DNA synthesis of human prolactinoma cells under influence of GST and beta-estradiol (E2). Tdt-mediated dUTP nick end labeling (TUNEL) were employed to observe the effect of GST and E2 on the apoptosis of human prolactinoma cells., Results: In a dose dependent manner, GST of different concentration could significantly inhibit the proliferation of human prolactinoma cells cultured in vitro. GST(10(-5) mol/L) could increase the proportion of cells in G1 phase from 55.3% up to 90.3%. E2 of different concentration could dose-dependently increase the proliferation of human prolactinoma cells. E (10(-5) mol/L) could increase the proportion of cells in G2 phase from 15.6% up to 41.8%. However, a lower suppressive proliferation of cultured human prolactinoma cells was observed with GST and E2 together. GST, not E2, could significantly induce the apoptosis of human prolactinoma cells cultured in vitro., Conclusion: GST inhibits the proliferation, DNA synthesis and cell cycle of cultured human pituitary cells, and induces its apoptosis. E2 decreases partly the effect of GST on the suppression of proliferation, not apoptotic induction, of human prolactinoma cells cultured in vitro.

Aim: To study the influence of acetylcholine on the proliferation, DNA synthesis and cell cycle of cultured human pituitary tumour cells., Methods: MTT method, 3H-TdR incorporation and cell cycle analysis were used to examine the changes of proliferation and DNA synthesis of human pituitary tumour cells., Results: Ach at 10(-7) mol/L - 10(-5) mol/L could decrease the 3H-TdR incorporation and the MTT A value in a dose dependent manner (P < 0.01), and the ratio of G1 phase of pituitary tumour cells increased markedly (P < 0.01). The effect of acetylcholine on the proliferation of cultured human pituitary tumour cells could be inhibited by atropine., Conclusion: Ach inhibited the proliferation, DNA synthesis and cell cycle of cultured human pituitary tumour cells, and the inhibitory effect was mediated by acetylcholine receptor.