The association of ABO and Rhesus blood type with the risks of developing SARS-CoV-2 infection: A meta-analysis.

Coronavirus Disease 2019 (COVID-19) has been spreading like a wildfire everywhere in the globe. It has been challenging the global health care system ever since the end of 2019, with its virulence and pathogenicity. Recent studies have shown the association between ABO blood group, Rhesus blood type and susceptibility to COVID-19 infection. Various studies and few meta-analyses have been done and some might be inconsistent; therefore, this meta-analysis was done to assess the relationship between different ABO and Rhesus blood types on the susceptibility to COVID-19 infections. This meta-analysis assessed the odds ratio of COVID-19 infection of different ABO and Rhesus blood types. Subgroup analyses according to (1) age and gender matched; (2) different blood group antigens; (3) Rhesus positive and negative of each blood group were carried out. Publication bias and Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) were also done to assess the risk of bias in these publications. It was found that blood group A showed significant difference in odds ratio of COVID-19 infection (OR, 1.16; 95% CI, 1.08-1.24). Blood group AB showed significant difference in odds ratio when studies with lower QUADAS-2 score were removed. This means that populations with blood group A and AB are more likely to be infected with COVID-19. As there is a higher tendency that blood group A and AB to be infected with COVID- 19, precautious care should be taken by these populations.

Novel fiber Bragg grating fabrication system for long gratings with independent apodization and with local phase and wavelength control.

We proposed and demonstrated a novel practical fiber Bragg grating (FBG) fabrication setup constructed with high performance linear stages, piezoelectric translation (PZT) stages, and a highly stable continuous wave laser. The FBG fabrication system enables writing of long FBGs by a continuous translate-and-write process and allows implementation of arbitrary chirp and apodization. A key innovation is that the local Bragg wavelength is controlled by a simple movement of the phase mask by a PZT in the direction perpendicular to its surface. The focus position of the two writing beams is not changed during the Bragg wavelength change, an intrinsic feature of the design, ensuring simplicity, robustness and stability. Apodization can be achieved by vibrating the phase mask in the direction parallel to its surface by a PZT. Phase steps can also be inserted in FBGs at any desired locations by stepping the same PZT. A long uniform FBG and a linearly chirped FBG are written to demonstrate the performance of the setup.

Observation of symmetrical reflection sidebands in a silica suspended-core fiber Bragg grating.

We have observed symmetrical sidebands in reflection from Bragg grating written in a silica suspended-core fiber, which are caused by longitudinal periodic refractive index modulation in the Ge-doped suspended-core fiber with a core diameter of approximately 1.3 microm. Our simulation shows that the effective refractive index of the guided mode varied by 0.023% along the fiber with a period of approximately 650 microm. The periodic index variation can lead to amplitude modulation of fiber Bragg gratings, which can be studied by observing the spectra of a fiber Bragg grating written in the Ge-doped core. In addition, we have also characterized the temperature and strain responses of the fiber Bragg gratings, and showed that both responses in the suspended-core fiber are 20 to 25% lower than that of a fiber Bragg grating written on a conventional fiber.

Pretreatment with cholera or pertussis toxin differentially modulates morphine- and beta-endorphin-induced antinociception in the mouse formalin test.

The present study was designed to examine the possible involvement of supraspinal CTX- and PTX-sensitive G-proteins in an opioid-induced antinociception in the formalin test. Morphine (1 microg) and beta-endorphin (1 microg) given i.c.v. displayed near-maximal inhibitory effects against the formalin response in the first (0-5 min) and the second (20-40 min) phases. CTX (0.1-0.5 microg) pretreated i.c.v. produced antinociceptive effects in both phases of the formalin responses. Its effect was more pronounced in the first phase. However, PTX (0.05-0.5 microg) injected i.c.v produced the antinociceptive effect only in the first, but not the second, phase. Both CTX (0.5 microg) and PTX (0.5 microg), at the dose which had no intrinsic effect, significantly reversed the beta-endorphin-induced antinociceptive effect observed during the second, but not the first, phase. However, the antinociceptive effect by morphine failed to be affected by the same dose of treatment with CTX or PTX. Our results indicate that, at the supraspinal level, CTX- and PTX-sensitive G-proteins appear to be involved in the modulation of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin pain model.

Hepatitis C virus nonstructural protein 5A contains potential transcriptional activator domains.

Hepatitis C virus (HCV), a major etiologic agent of transfusion associated hepatitis, is a positive, single-stranded RNA virus and is also known to be implicated in liver cirrhosis and hepatocellular carcinoma. Nonstructural protein 5A (NS5A) of HCV contains acidic and proline-rich amino acids in its carboxy-terminal half. These structural features resemble eukaryotic transcription activators. In this report, we show that NS5A functions as a potent transcriptional activator when fused to the yeast (Saccharomyces cerevisiae) GAL4 DNA-binding domain (1-147). The potential transcriptional activator maps to the C-terminal half of NS5A in the yeast cell. Therefore, our data provides the first evidence that NS5A may modulate host cell function at the transcriptional level.

Differential effects of forskolin and phorbol-13-myristate injected intrathecally or intracerebroventricularly on antinociception induced by morphine or beta-endorphin administered intracerebroventricularly in the mouse.

The effects of forskolin or phorbol-13-myristate (PMA) injected intrathecally (i.t.) or intracerebroventricularly (i.c.v.) on the inhibition of the tail-flick and hotplate responses induced by morphine or beta-endorphin administered i.c.v. were studied. Animals pretreated with forskolin (20 micrograms) i.t. for 10 min had an attenuated inhibition of the tail-flick response induced by i.c.v. administered morphine (2 micrograms) or beta-endorphin (1 microgram). However, i.t. pretreatment with PMA (100 ng) was not effective in reducing the inhibition of the tail-flick response induced by morphine or beta-endorphin administered i.c.v. In addition, i.t. pretreatment with either forskolin or PMA did not affect the inhibition of the hotplate response induced by morphine or beta-endorphin administered i.c.v. Forskolin pretreatment i.c.v. for 10 min attenuated the inhibition of the tail-flick and hotplate responses induced by i.c.v. administered morphine or beta-endorphin. However, i.c.v. pretreatment with PMA was not effective in reducing the inhibition of the tail-flick or hotplate responses induced by morphine or beta-endorphin administered i.c.v. Our results suggest that activation of adenylate cyclase located at both spinal and supraspinal sites appears to be involved in antagonizing antinociception induced by morphine and beta-endorphin administered supraspinally. However, spinal or supraspinal protein kinase C may not be involved in antagonizing antinociception induced by morphine or beta-endorphin administered supraspinally.

Nicotine enhances morphine- and beta-endorphin-induced antinociception at the supraspinal level in the mouse.

The effect of nicotine administered supraspinally on antinociception induced by supraspinally administered opioids was examined in ICR mice. The intracerebroventricular (i.c.v.) injection of nicotine alone at doses from 1 to 12 micrograms produced only a minimal inhibition of the tail-flick response. Morphine (0.2 micrograms), beta-endorphin (0.1 microgram), D-Pen2.5-enkephalin (DPDPE; 0.5 microgram), trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl] benzeocetamide (U50, 488H; 6 micrograms) caused only slight inhibition of the tail-flick response. Nicotine dose dependently enhanced inhibition of the tail-flick response induced by i.c.v. administered morphine (0.2 microgram) or beta-endorphin (0.1 microgram). The degree of enhancing effect of nicotine toward beta-endorphin-induced inhibition of the tail-flick response was greater than toward morphine-induced inhibition of the tail-flick response. However, i.c.v. administered nicotine at the same doses was not effective in enhancing the inhibition of the tail-flick response induced by DPDPE (0.5 microgram) or U50, 488H (6 micrograms) administered i.c.v. Our results suggest that stimulation of supraspinal nicotinic receptors may enhance antinociception induced by morphine (a mu-opioid receptor agonist) and beta-endorphin (an epsilon-opioid receptor agonist) administered supraspinally. However, the activation of nicotinic receptors at supraspinal sites may not be involved in enhancing the antinociception induced by DPDPE (a delta-opioid receptor agonist) or U50, 488H (a kappa-opioid receptor agonist) administered supraspinally.

Differential modulation by baclofen on antinociception induced by morphine and beta-endorphin administered intracerebroventricularly in the formalin test.

Our previous studies have demonstrated that supraspinal GABAergic receptors are differentially involved in the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) in the tail-flick and hot-plate tests. These two models employed a phasic, thermal nociceptive stimulus. The present study was designed to examine the possible involvement of supraspinal GABAergic receptors in opioid-induced antinociception in the formalin test. Morphine (1 microg) and beta-endorphin (1 microg) given i.c.v. displayed the almost complete inhibitory effects against the hyperalgesic response in both phases. Muscimol (75-100 ng) and baclofen (5-10 ng) injected i.c.v. produced the hypoalgesic response in the both phases. The hypoalgesic response induced by muscimol and baclofen observed during the second phase was more pronounced than that observed during the second phase. Baclofen (2.5 ng), at the dose which did not affect the hyperalgesic response, resulted in a significant reversal of the i.c.v. administered beta-endorphin-induced hypoalgesic response observed during the second, but not the first, phase. However, the hypoalgesic response induced by i.c.v. administered morphine was not changed by the same dose of muscimol or baclofen injected i.c.v. Our results indicate that, at the supraspinal level, GABA(B)receptors appear to be involved in the modulation of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin test model.

Effects of histamine receptor antagonists injected intrathecally on antinociception induced by opioids administered intracerebroventricularly in the mouse.

The present study was designed to investigate the modulatory effects of blockade of spinal histamine receptors on antinociception induced by supraspinally administered mu-epsilon-, delta-, and kappa-opioid receptor agonists. The effects of intrathecal (i.t.) injections with cyproheptadine [a histamine-1 (H1) receptor antagonist], ranitidine (a H2 receptor antagonist), or thioperamide (a H3 receptor antagonist) injected i.t., on the antinociception induced by morphine (a mu-receptor antagonist), beta-endorphin (an epsilon-receptor agonist), D-Pen(2,5)-enkephalin (DPDPE, a delta-receptor agonist) or trans-3, 4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohxyl] benzeocetamide (U50,488H, a kappa-receptor agonist) injected intracerebroventricularly (i.c.v.) were studied. The antinociception was assayed using the tail-flick test. The i.t. injection of cyproheptadine (from 0.31 to 62 nmole), ranitidine (from 0.28 to 56 nmole), or thioperamide (from 0.24 to 48 nmole) alone did not show any antinociceptive effect. The i.t. pretreatment with cyproheptadine or thioperamide dose-dependently attenuated the inhibition of the tail-flick response induced by i.c.v. administered morphine (0.6 nmole), b-endorphin (0.03 nmole), DPDPE (1.5 nmole), and U50,488H (130 nmole). In addition, the i.t. pretreatment with ranitidine dose-dependently attenuated the inhibition of the tail-flick response induced by morphine, b-endorphin and U50,488H without affecting DPDPE-induced response. Our results suggest that spinal histamine H1 and H3 receptors may involved in the production of antinociception induced by supraspinally applied morphine, b-endorphin, DPDPE and U50,488H. Spinal H2 receptors appear to be involved in supraspinally administered morphine, b-endorphin- and U50,488H-induced antinociception but not DPDPE-induced antinociception.

Supraspinal NMDA and non-NMDA receptors are differentially involved in the production of antinociception by morphine and beta-endorphin administered intracerebroventricularly in the formalin pain model.

Our previous studies have demonstrated that supraspinal glutamate receptors are differentially involved in the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) in the tail-flick and hot-plate tests. The formalin pain test was used in the present study. Injection of mice with formalin solution (2%, 10 microl) into the hindpaw intraplantarly produced the first (0-5 min) and second (20-40 min) phases of formalin responses. The formalin responses in the both phases were attenuated dose-dependently by morphine (0.125-1 microg) or beta-endorphin (0.125-1 microg) administered i.c.v. 5 min before. The antinociceptive effect of morphine was slightly more potent in the second phase whereas the effect of beta-endorphin was more pronounced in the first phase. MK-801 (0.1-1 microg), a non-competitive NMDA receptor antagonist, and CNQX (0.05-0.5 microg), a non-NMDA antagonist, given i.c.v., produced antinociceptive effect in the both phases, but only in a partial manner. Both MK-801 (0.05 microg) and CNQX (0.01 microg), at the dose which had no intrinsic effect, reversed the antinociceptive effect of beta-endorphin (1 microg) observed during the second, but not the first, phase partially but significantly. However, the antinociceptive effect of morphine (1 microg) was not affected by the same dose of MK-801 or CNQX given i.c.v. Our results indicate that, at the supraspinal level, both NMDA and non-NMDA receptors are involved in the production of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin pain model.

Differential modulatory roles of cholera toxin and pertussis toxin in the regulation of pain responses induced by excitatory amino acids administered intrathecally in mice.

The present study was designed to characterize the possible roles of spinally located cholera toxin (CTX)- and pertussis toxin (PTX)-sensitive G-proteins in excitatory amino acids induced pain response. Intrathecal (i.t.) injection of glutamate (20 microg), N-methyl-D-aspartic acid (NMDA; 60 ng), alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 13 ng), and kainic acid (12 ng) showed pain response. Pretreatment with CTX (0.05 and 0.5 microg, i.t.) attenuated pain response induced by glutamate, NMDA, AMPA and kainic acid administered i.t. in a dose-dependent manner. On the other hand, i.t. pretreatment with PTX further increased the pain response induced by glutamate, NMDA, AMPA and kainic acid administered i.t., especially at the dose of 0.5 microg. Our results suggest that, at the spinal cord level, CTX- and PTX-sensitive G-proteins appear to play opposite roles in modulating the pain response induced by spinally administered. Furthermore, CTX- and PTX-sensitive G-proteins appear to modulate pain response induced by stimuli of both NMDA and non-NMDA glutamate receptors.

Effects of intrathecal or intracerebroventricular pretreatment with pertussis toxin on antinociception induced by beta-endorphin or morphine administered intracerebroventricularly in mice.

We have previously demonstrated that beta-endorphin and morphine, when administered supraspinally, produce antinociception by activating different descending pain inhibitory systems in both rats and mice. However, the signal transduction mechanisms involved in the descending pain-inhibitory systems that are activated by beta-endorphin and morphine administered intracerebroventricularly (i.c.v.) have not been characterized. Therefore, in the present study, the effects of intrathecal (i.t.) and i.c.v. pretreatments with pertussis toxin (PTX) on antinociception induced by beta-endorphin or by morphine administered i.c.v. were studied in ICR mice. Antinociception was assessed by the tail-flick assay and by the hot-plate assay. Intrathecal pretreatment with PTX (0.5 microgram) for 6 days effectively reduced the inhibition of the tail-flick response induced by beta-endorphin (1 microgram) or by morphine (1 microgram) administered i.c.v. However, i.t. pretreatment with PTX was not effective in reducing the inhibition of the hot-plate response induced by beta-endorphin or by morphine administered i.c.v. Intracerebroventricular pretreatment with PTX (0.5 microgram) for 6 days effectively reduced the inhibition of the tail-flick and hot-plate responses induced by morphine (1 microgram), but not that induced by beta-endorphin (1 microgram), administered i.c.v. Our results suggest that there are PTX-sensitive G proteins coupled to the spinal descending pain inhibitory systems that are activated by beta-endorphin and morphine administered i.c.v. At a supraspinal level, i.c.v. morphine- but not beta-endorphin-induced antinociception is mediated by PTX-sensitive G proteins.

Differential roles of spinal cholera toxin- and pertussis toxin-sensitive G proteins in nociceptive responses caused by formalin, capsaicin, and substance P in mice.

The aim of the present study is to characterize the roles of spinal cholera toxin (CTX)- and pertussis toxin (PTX)-sensitive G proteins in the regulation of various nociceptive responses. The effects of intrathecal (i.t.) pretreatments with CTX and PTX on the formalin (subcutaneous)-, capsaicin (i.t.)-, and substance P (SP; i.t.)-induced nociceptive behaviours were examined in mice. Pretreatment with CTX (i.t.; 24 h before) significantly and dose-dependently (0.05-0.5 microg) suppressed both the first and second phases of the formalin-induced nociceptive behaviour. On the other hand, pretreatment with PTX (i.t., 6 days before) at the same doses (0.05-N0.5 microg) did not affect the formalin-induced response. Capsaicin (i.t., 0.5 microg)- and SP (i.t., 0.7 microg)-induced nociceptive behaviours were attenuated by the pretreatment with CTX. In addition, SP-induced nociceptive response was also attenuated by the pretreatment with PTX. However, the capsaicin-induced nociceptive response was not influenced by PTX pretreatment. These findings suggest that, at the spinal cord level, CTX-sensitive G-proteins are involved in the formalin-, capsaicin-, and SP-induced nociceptive behavioural responses, whereas PTX-sensitive G proteins are involved in SP-induced nociceptive response.

Clinical evaluation of a biodegradable collagen membrane in guided tissue regeneration.

A bio-resorbable type I collagen membrane was investigated as a barrier for guided tissue regeneration. Ten human subjects with at least one pair of contralateral periodontal lesions with probing pocket depths of greater than or equal to 5 mm and radiographic evidence of greater than or equal to 40% bone loss were included. Each patient underwent contralateral surgical flap procedures. A collagen barrier was adapted to the tooth in the experimental defect and the flap replaced and sutured. The controls consisted of the same procedure without the placement of the barrier. Standardized measurements of change in probing attachment levels and fill of intrabony defects were obtained at the time of surgery and 1 year later at the time of surgical re-entry. The differences in change of probing attachment levels and amount of bone fill between individual test and control sites were compared utilizing the student's t-test for paired samples. The mean probing attachment gain in the test sites was 0.56 +/- 0.57 mm, and there was a mean probing attachment loss of 0.71 +/- 0.91 mm in the control sites (P less than 0.01). The gain of bone in test lesions was 1.16 +/- 0.95 mm, while no gain was observed in the control lesions (P less than 0.01). The results of this study demonstrated that sites treated with a collagen barrier comprised of cross-linked bovine Type I collagen exhibited significantly better healing as compared to control sites over the 1-year period of the study.

Splenic injury following colonoscopy.

Splenic injury following colonoscopy is rare but can be fatal and easily overlooked. A case of colonoscopic splenic injury is presented to highlight its potentially fatal complication. The risk factors, underlying mechanism, possible measures of prevention, diagnosis, and treatment are also discussed.

Acute appendicitis---a recent audit of an old problem.

We conducted a retrospective review of all patients who had an appendicectomy performed at the Queen Elizabeth Hospital, Hong Kong, from January 1993 through December 1994. The diagnostic accuracy for true appendicitis was 74%. Nine per cent of patients had other pathologies, which also needed exploration. The diagnostic accuracy in female patients was 66%, compared with 82% for male patients (P<0.0001). Female patients aged between 15 to 40 years were diagnosed accurately 62% of the time, which has significantly lower than the rate for other female patients (P=0.016). the overall morbidity and mortality rates were 9.2% and 3%, respectively. Complicated appendicitis had a higher morbidity rate of 21%, compared with 9% for uncomplicated appendicitis (P<0.0001). Results for patients who were operated on the day of admission were compared with those who were operated on the day after admission. No significant difference in diagnostic accuracy (P=0.46), percentage of complicated appendicitis (P=0.7), and morbidity rate (P=0.8) was found.

Molecular and cellular biology research in periodontal regeneration and its clinical implication.

The mechanisms by which new periodontium is established on root surfaces previously exposed by periodontal disease have been an area of active research interest. Recently, histological examination of periodontal regeneration has revealed a complex process orchestrated by temporo-spatial specific cell-matrix interactions. Advances in cell and molecular biology techniques have provided invaluable tools to investigate the cascade of events occurring during periodontal regeneration. This paper will provide an overview of current understanding of the cellular and molecular aspects of periodontal repair and regeneration and its implication in applied research resulting in clinical application.

The association of ABO and Rhesus blood type with the risks of developing SARS-CoV-2 infection: A meta-analysis

@#Coronavirus Disease 2019 (COVID-19) has been spreading like a wildfire everywhere in the globe. It has been challenging the global health care system ever since the end of 2019, with its virulence and pathogenicity. Recent studies have shown the association between ABO blood group, Rhesus blood type and susceptibility to COVID-19 infection. Various studies and few meta-analyses have been done and some might be inconsistent; therefore, this meta-analysis was done to assess the relationship between different ABO and Rhesus blood types on the susceptibility to COVID-19 infections. This meta-analysis assessed the odds ratio of COVID-19 infection of different ABO and Rhesus blood types. Subgroup analyses according to (1) age and gender matched; (2) different blood group antigens; (3) Rhesus positive and negative of each blood group were carried out. Publication bias and Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) were also done to assess the risk of bias in these publications. It was found that blood group A showed significant difference in odds ratio of COVID-19 infection (OR, 1.16; 95% CI, 1.08-1.24). Blood group AB showed significant difference in odds ratio when studies with lower QUADAS-2 score were removed. This means that populations with blood group A and AB are more likely to be infected with COVID-19. As there is a higher tendency that blood group A and AB to be infected with COVID19, precautious care should be taken by these populations.