Pfizer-BioNTech COVID-19 Vaccine (BNT162b2) Side Effects: A Systematic Review.

Vaccinations prevented severe clinical complications of COVID-19. It was considered a vital component of living endemically with COVID-19. The Pfizer-BioNTech vaccine is the first mRNA-based vaccination that enhances immunity. Resulting in various adverse effects that may emerge after vaccination. This systematic review was undertaken to assess the Pfizer-BioNTech vaccine side effects by reviewing the previous studies. A total of 107 PubMed and Google Scholar publications were screened for Pfizer-BioNTech COVID-19 vaccine side effects. Fourteen articles met the study inclusion criteria. The included searching terms were a combination of "Pfizer vaccine and Side effects," "BioNTech vaccine and side effects," and "BNT162b2 vaccine and side effects," as well as all synonyms. The total number of participants in the 14 studies was 10,632 participants. Average of the most frequent side effects of 14 studies were injection site pain 77.34%, fatigue 43%, muscle pain 39.67%, local swelling 33.57%, headache 33.27%, joint pain 25.75%, chills 18.34%, fever 18%, itching 9.38%, lymph nodes swelling 7.86%, nausea 7.58%, dyspnea 7.86%,and diarrhea 6.36%. The average side effects after the first dose were 79% compared with 84% after the second dose. The average occurs side effects in females at 69.8% compared with males 30.2%. Our study reveals that side effects after the Pfizer-BioNTech vaccine are common, but they are usually mild and self-limited. Local reactions like pain at the injection site are the most common. Anaphylactic shock or severe reactions are rare. We hope that our results will reassure the public that the benefits of vaccination far exceed the dangers. Also, help reduce vaccine hesitancy among individuals worried about vaccine safety and possible adverse effects.

Medullasin enhances human natural killer cell activity.

Medullasin, a new serine protease found in bone marrow cells, increased markedly human natural killer cell activity. Whereas the natural killer cell activity measured immediately after the treatment with medullasin remained almost on the same level as the control, an incubation at 37 degrees C for several hours increased markedly the natural killer cell activity of the lymphocytes treated with medullasin. Enhancement of the natural cytotoxicity was caused by the treatment with physiologic concentrations of the protease (5-20 micrograms/ml). Inhibitors of medullasin such as phenylmethylsulfonyl fluoride and elastatinal prevented the activation of natural cytotoxicity. Depletion of lymphocytes bearing Fc receptors for IgG abolished the enhancement of natural killer cell activity by medullasin. Interferon activity was not detected in the supernatant of lymphocyte cultures stimulated with medullasin. The medullasin enhanced further the natural killer cell activity of lymphocytes stimulated with interferon. Medullasin activity was detected neither in unstimulated nor stimulated (by concanavalin A or phytohemagglutinin) human lymphocytes. The protease was released easily from human mature granulocytes into culture medium. It is considered from these results that the level of human natural killer cell activity is regulated by medullasin released by mature granulocytes.

Mid-infrared Photoconductive Response in AlGaN/GaN Step Quantum Wells.

AlGaN/GaN quantum structure is an excellent candidate for high speed infrared detectors based on intersubband transitions. However, fabrication of AlGaN/GaN quantum well infrared detectors suffers from polarization-induced internal electric field, which greatly limits the carrier vertical transport. In this article, a step quantum well is proposed to attempt solving this problem, in which a novel spacer barrier layer is used to balance the internal electric field. As a result, a nearly flat band potential profile is obtained in the step barrier layers of the AlGaN/GaN step quantum wells and a bound-to-quasi-continuum (B-to-QC) type intersubband prototype device with detectable photocurrent at atmosphere window (3-5 µm) is achieved in such nitride semiconductors.

Mutations in the human mannose-binding protein gene: frequencies in several population groups.

Mannose-binding protein (MBP; mannan-binding protein, mannan-binding lectin) is a member of the collectin family of proteins and is thought to be important in innate immunity. We have previously shown high frequencies of two distinct mutations in codon 54 and codon 57 of exon 1 of the MBP gene in non-African and African populations, respectively. These result in low levels of the protein and an opsonic deficiency but the frequencies also suggest some selective advantage for low MBP levels. A third mutation in codon 52 occurs at a much lower frequency. We have now extended our earlier studies to other populations. In the south-west Pacific (Papua New Guinea and Vanuatu) neither the codon 52 nor the codon 57 mutation was detected and the codon 54 mutation was significantly less common (gene frequencies of 0.07 and 0.01, respectively) than in other non-African populations (gene frequencies 0.11-0.16). This could be explained by relatively recent admixture. The ancestral Melanesian population probably diverged some 50,000-60,000 years ago and our data suggest that the codon 54 mutation may have occurred after that even but before the divergence of European-Asian groups (40,000 years ago). Two further sub-Saharan populations were also studied: a group of Xhosa from South Africa were similar to Gambians, with a high gene frequency for the codon 57 mutation (0.27) and no evidence of the codon 52 or 54 mutations. In contrast, San Bushmen from Namibia had low frequencies of both the codon 57 mutation (0.07) and the codon 54 mutation (0.03). Again the codon 52 mutation was not found. This pattern is unique amongst sub-Saharan populations studied to date and suggests that this population may have been subjected to different selective pressures.

Noninfectious doughnut-shaped human immunodeficiency virus type 1 can induce syncytia mediated by fusion of the particles with CD4-positive cells.

A defective doughnut-shaped human immunodeficiency virus type 1 (HIV-1)-producing cell clone (designated as L-2) was isolated from persistently HIV-1-infected MT-4 cells. The syncytium-forming capacity of the cell and virus particle fractions was examined in human CD4-positive T cells. Several cell lines producing infectious HIV-1 particles, such as persistently HIV-1-infected MOLT-4 (MOLT-4/HIV-1) cells, were used as controls. Syncytia were formed within 20 h by the cell fraction of both L-2 and MOLT-4/HIV-1 and the virus particle fraction of L-2, but not MOLT-4/HIV-1. These formations were not affected by 3'-azido-3'-deoxythymidine (ZDV). In contrast, similar syncytium formation was first observed 2 days after the incubation of the virus particle fraction of MOLT-4/LAV-1 and this syncytium formation mediated by the cell fractions of MOLT-4/HIV-1 and L-2 or the virus particle fraction of L-2 differently.

Identical point mutation leading to low levels of mannose binding protein and poor C3b mediated opsonisation in Chinese and Caucasian populations.

A common opsonic defect occurring in 7% of the Caucasian population is associated with low serum levels of the lectin mannose binding protein (MBP). This study sought to determine whether the deficiency was also present in a Chinese population using sera obtained from 100 healthy Chinese children (age range 6 weeks-16 years). The distribution profiles of MBP levels and C3b/C3bi fragments binding to mannan coated plates were both bimodal and similar to the corresponding Caucasian profiles. Serum MBP levels were low in 9% of the Chinese children and all of these sera generated low levels of C3b/C3bi fragments. Overall there was a high significant correlation between MBP levels and C3b opsonin generation (r = 0.77; P less than 0.001). By analogy with similar findings in a Caucasian population we believe this correlation to be a reflection of antibody independent complement activation by MBP. In a pilot study of DNA obtained from three adult Chinese with low MBP levels the point mutation causing MBP deficiency in Caucasians was identified in all three cases.

Mannose binding protein deficiency is not associated with malaria, hepatitis B carriage nor tuberculosis in Africans.

We retrospectively studied MBP genotypes in patients with malaria, tuberculosis (TB), and persistent hepatitis B virus (HBV) carriage, in clinics and hospitals in The Gambia. Children under 10 years with cerebral malaria and/or severe malarial anaemia, were compared with children with symptomatic, mild malaria, and controls of the same age and ethnicity. Adult TB cases with smear-positive pulmonary TB were compared with healthy blood donors from the same ethnic groups. Malaria cases and controls were tested for hepatitis B core antibody (anti-HBc) and surface antigen (HBsAg). TB patients were tested for HIV antibodies. Genotyping used sequence-specific oligonucleotide analysis to identify MBP variant alleles. Overall, 46% (944/2041) of patients and controls were homozygous for the wild-type MBP allele, 45% (922/2041) were carriers of a single variant allele and 8.6% (175/2041) had two variant alleles. Neither homozygotes nor heterozygotes for MBP variants were at increased risk of clinical malaria, persistent HBV carriage or TB. The most common mutation in Africans, the codon 57 variant allele, was weakly associated with resistance to TB (221/794 in TB cases and 276/844 in controls, p = 0.037). MBP deficiency is not a significant risk factor for persistent HBV, severe malaria nor pulmonary TB in West Africa.

PIP: Low serum mannose-binding protein (MBP), a calcium-dependent serum lectin that acts as an opsonin to promote phagocytosis, has been characterized as the most common immune deficiency. It has been suggested that MBP acts as a binding protein for mycobacteria and other intracellular pathogens, enabling them to enter host macrophages. The present study investigated the association between variant MBP alleles and malaria, tuberculosis, and hepatitis B virus (HBV) in adults and children in The Gambia. Of the 2041 Gambians screened for MBP mutations, 944 (46%) were homozygous for the wild-type allele, 922 (45%) were carriers of a single variant allele, and 175 (8.6%) possessed 2 mutant alleles. Compared to healthy controls, neither homozygotes nor heterozygotes for MBP genotypes were at increased risk of severe malaria (n = 504), HBV carriage (n = 337), or tuberculosis (n = 397). Stratification of patients by ethnic group did not alter this lack of relationship. However, the most common mutation in Africans--the codon 57 variant allele--was weakly associated with resistance to tuberculosis in both cases and controls. Although MBP deficiency may predispose to recurrent infections, this study failed to provide evidence that such a deficiency is a major risk factor for infectious diseases.

Increase of cytokine production by pulmonary artery endothelial cells induced by supernatants from monocytes stimulated with autoantibodies against U1-ribonucleoprotein.

OBJECTIVE: To clarify the pathogenetic role of autoantibodies against U1-RNP (ribonucleoprotein) (anti-U1-RNP) in mixed connective tissue disease (MCTD), we examined whether supernatants of monocytes which were stimulated with anti-U1-RNP could induce the production of proinflammatory cytokines by human pulmonary artery endothelial cells (HPAECs). METHODS: Monocytes from MCTD patients (n = 11) and normal volunteers (n = 11) were stimulated with purified antibodies against U1-RNP or double-stranded DNA and their supernatants were added to cultures of HPAECs. Cell-associated cytokines were assayed by an enzyme-linked immunosorbent assay. RESULTS: The supernatants of anti-U1-RNP-stimulated MCTD monocytes significantly up-regulated the cell-associated production of IL-1 alpha (p < 0.01) and IL-6 (p < 0.01) by HPAECs compared with their production by normal IgG-stimulated MCTD monocytes, whereas the cell-associated production of IL-1 beta and TNF-alpha by HPAECs was not up-regulated. The supernatants of anti-U1-RNP-stimulated monocytes from normal volunteers similarly up-regulated the cell-associated production by HPAECs of IL-1 alpha (p < 0.01) and IL-6 (p < 0.01), but not of IL-1 beta and TNF-alpha. Supernatants of monocytes stimulated with the F(ab')2 preparation of anti-U1-RNP antibodies enhanced the amounts of both Il-1 alpha and IL-6 associated with HPAECs almost as effectively as those stimulated with intact autoantibody molecules. Inhibition experiments employing specific anti-cytokine antibodies of anti-U1-RNP-stimulated monocyte supernatants suggested that soluble factors, including cytokines, in monocyte supernatants could enhance the cytokine association with HPAECs. CONCLUSION: Up-regulation by anti-U1-RNP autoantibodies of proinflammatory cytokines associated with vascular endothelial cells may play a role in the immunopathological processes leading to proliferative vasculopathy, a characteristic of MCTD.

Progressive multifocal leukoencephalopathy resembling central nervous system systemic lupus erythematosus.

A 21-year-old woman with a 6-year history of SLE presented with a speech disturbance and right hand clumsiness along with manifestations of active disease suggesting central nervous system SLE. Despite aggressive treatment for SLE, her neurological condition worsened. MRI demonstrated low intensity in T1-weighted images and high intensity in T2-weighted images in the white matter of the bilateral cerebrum and cerebellum, compatible with progressive multifocal leukoencephalopathy (PML). Intraspinal administration of interferon-beta seemed to slow the deterioration of her MRI and neurological findings. However, she eventually developed decerebrate rigidity and died due to candidemia. DNA of the JC virus was detected in the autopsied brain by the polymerase chain reaction technique. PML should always be borne in mind when examining patients with SLE showing neurological abnormalities.

Increased levels of matrix metalloproteinase-3 in sera from patients with active lupus nephritis.

OBJECTIVE: To determine the matrix metalloproteinase-3 (MMP-3) levels in sera from patients with systemic lupus erythematosus (SLE) and to analyse the relationships between MMP-3 and clinical and laboratory features. METHODS: Serum MMP-3 levels were measured by an enzyme immunoassay in 124 patients with SLE and 237 patients with other systemic rheumatic diseases. RESULTS: The frequencies of patients with high MMP-3 levels were 76% in SLE and 82% in rheumatoid arthritis (RA). The level of MMP-3 in the SLE patients was 193.0 +/- 171.5 ng/ml (mean +/- SD) and was almost equal to the level in the RA patients (259.5 +/- 255.6 ng/ml). The MMP-3 levels were significantly higher in SLE patients who had a history of the following abnormalities: persistent proteinuria, cellular casts, anti-double stranded DNA antibodies, decreased C3, decreased creatinine clearance (p < 0.001), circulating immune complex (p < 0.01), malar rash, hypoalbuminemia, or decreased C4 (p < 0.05). The serum MMP-3 level in patients with SLE at admission showed direct correlations with serum uric acid, total cholesterol (p < 0.001), triglyceride, the white blood cell count, and the neutrophil count (p < 0.05), as well as inverse correlations with the total protein (p < 0.01), and IgG (p < 0.05). In SLE patients with active renal disease, the median MMP-3 level at admission and that at 6 months after admission were significantly higher than that at 6 months before admission. CONCLUSIONS: The increased level of serum MMP-3 in SLE is closely associated with clinical features relevant to lupus nephritis, suggesting that it plays a role in the pathogenesis of this condition.

Clinical significance of the serum lipoprotein(a) level in patients with systemic lupus erythematosus: its elevation during disease flare.

OBJECTIVE: To determine the clinical significance of serum lipoprotein(a) [Lp(a)] levels in patients with systemic lupus erythematosus (SLE). METHODS: Serum Lp(a) levels in 77 patients with SLE were measured by turbidimetric immunoassay. RESULTS: The median serum Lp(a) levels in all the SLE patients (14.4 mg/dl) and in those with active disease (Group A; 19.6 mg/dl, n = 39) at admission were significantly higher than those in healthy subjects (11.9 mg/dl, p < 0.05 and p < 0.001, respectively). The serum Lp(a) levels in SLE patients correlated directly with the serum cholesterol (p < 0.001) and urinary protein (p < 0.001) levels and inversely with the serum albumin levels (p < 0.02). Analysis limited to Group A patients with renal disease (Group A + RD, n = 28) revealed that the median serum Lp(a) level at the time of admission (OM) was significantly higher than those at 6 months before (-6M, p < 0.01) and at 6 months after admission (+6M, p < 0.01). Moreover, the serum Lp(a) level decrease from 0M to +6M in Group A+RD correlated significantly with the serum albumin level increase (p < 0.05). Multiple regression analysis demonstrated that the serum albumin level increment, the SLEDAI score decrement, the cholesterol level at 0M and the total dose of oral corticosteroids administered during the 0M to +6M period contributed independently and significantly to the serum Lp(a) level decrement from 0M to +6M in Group A + RD. CONCLUSION: Our study is the first to reveal that hypoalbuminemia appearing during disease flare plays an important role in increasing the serum Lp(a) levels in lupus patients with renal disease and shows that corticosteroid treatment reduced the elevated serum Lp(a) levels almost to original levels.

Mannose-binding protein in HIV-seropositive patients does not contribute to disease progression or bacterial infections.

This study set out to investigate whether plasma mannose-binding protein (MBP) deficiency caused by mutations in the MBP gene associates with pyogenic or opportunistic infections in HIV-infected patients. Plasma samples were selected randomly from 131 HIV-infected patients followed prospectively for a period not exceeding 12 months or until death. Plasma MBP concentrations were measured by an ELISA and genotyping was determined by amplification of exon 1 of the MBP gene by polymerase chain reaction (PCR) technology, followed by restriction enzyme analysis and Southern blotting using sequence-specific oligonucleotide probes. Neither MBP concentration nor genotype was found to associate with disease progression or opportunistic infection rate. There was an unexpected increased bacterial infection rate in patients with MBP levels greater than 100 ng/ml and wild type genotype. Thus, MBP does not appear to play a role in HIV infection. MBP is an acute phase reactant and this may explain the higher levels in those with more frequent pyogenic infections.

Iodine-131 and other radionuclides in environmental samples collected from Ibaraki/Japan after the Chernobyl accident.

Measurements were made of 131I, 137Cs, 134Cs and 103Ru in environmental samples collected from Ibaraki-Prefecture, Japan, after the Chernobyl accident. The highest values of 131I obtained in May 1986 were 98 Bq l-1 (2.7 nCi l-1) for rain water (collected at the beginning of the rainfall), 400 Bq kg-1 (11 nCi kg-1) for pine needles (wet), 160 Bq kg-1 (4.3 nCi kg-1) for vegetables (wet) and 52 Bq kg-1 (1.4 nCi kg-1) for seaweed (wet). Most of the radioiodine in rain water was present as IO3- and I-. The proportion of IO3- in fresh rain water was higher than that of I-, but the IO3- was converted to I- during storage. About 10% of 131I was removed from leaf vegetables by washing, and about 70% by boiling.

Concentrations of radiocesium and potassium in basidiomycetes collected in Japan.

Concentrations of 137Cs, 134Cs and 40K in about 60 mushroom samples (fruit bodies of basidiomycetes) belonging to 25 species collected in Japan have been studied. The levels of 137Cs varied very widely, ranging from less than 3 to 1520 Bq kg-1 (dry wt), while those of 40K were relatively constant. Concentrations of 137Cs in common edible mushrooms of Japan such as Lentinus edodes, Flammulina velutipes, Pleurotus ostreatus and Pholiota nameko were low (normally less than 50 Bq kg-1, dry wt). Concentrations of 134Cs in many samples were below the limit of detection (usually less than 5 Bq kg-1, dry wt). The median concentrations of 137Cs and 40K were 41 (dry wt) and 1150 Bq kg-1 (dry wt), respectively. From the 137Cs/40K ratios it was found that cesium rather than potassium was selectively taken up from the soils by fungi such as Suillus granulatus and Lactarius hatsudake. The 134Cs/137Cs ratios in mushrooms are related to the depth of the mycelium in the soil. The effective dose equivalent due to the dietary intake of radiocesium through mushrooms was estimated to be only 1.6 x 10(-7) Sv.

Biological half-life of gaseous elemental iodine deposited onto rice grains.

In order to obtain the biological half-life (Tb) of iodine deposited on rough rice grains, rice plants of four different growing stages--heading, milky, dough, and yellow ripe--were exposed to elemental gaseous iodine. After the exposure, the rough rice samples were collected at different intervals and analyzed for iodine to estimate the value of Tb. The average value of Tb obtained by the experiments at the dough and yellow ripe stages was about 200 d. This value is considerably larger than those for pasture grass and leafy vegetables.

Deposition velocity of gaseous organic iodine from the atmosphere to rice plants.

To obtain parameter values for the assessment of 129I transfer from the atmosphere to rice, deposition of CH3I to rice plants has been studied. The mass normalized deposition velocity (VD) of CH3I for rough (unhulled) rice was 0.00048 cm3 g-1 s-1, which is about 1/300 of that of I2. Translocation of iodine, deposited as CH3I on leaves and stems, to rice grain was negligibly small. Distribution of iodine between hull and inner part of the grain was found to depend also on the chemical forms of atmospheric iodine to be deposited. The ratio of the iodine distribution in a grain exposed to CH3I was as follows: rough rice:brown rice (hulled rice):polished rice = 1.0:0.49:0.38. The distribution ratio in polished grains for CH3I exposed rice was about 20 times higher than that for I2.

Deposition velocity of gaseous I to rice grains.

Among the routes of gaseous I transfer to rice grains, direct deposition to the hull of rice plants and the subsequent transfer to brown rice and polished rice should be more critical than leaf absorption-translocation. A grain number normalized deposition velocity (Vs) is recommended as a key parameter to assess the amount of gaseous I deposited on the rough rice. This parameter is given as "iodine content per unit number of grain per unit time" divided by "iodine concentration per unit volume of the air." After the heading period the surface area of rough rice is almost constant but weight increases with time. Therefore, mass normalized deposition velocity (VD) varies with time. By introducing Vs instead of VD, the variations could be converged into narrow ranges. The contribution of gaseous I from the atmosphere to rough rice, brown rice and polished rice were estimated using Vs values obtained experimentally and gaseous I concentration in the air.

Association of mutations in mannose binding protein gene with childhood infection in consecutive hospital series.

OBJECTIVE: To determine the extent to which mutations in the mannose binding protein gene predispose to childhood infection. DESIGN: Clinical details and genotype of mannose binding protein determined in consecutive children attending a paediatric department. SETTING: Inner city hospital paediatric service in London. SUBJECTS: 617 children attending hospital between October 1993 and August 1995. MAIN OUTCOME MEASURE: Infection as the cause for attendance or admission in relation to mutations in the mannose binding protein gene. RESULTS: The prevalence of mutations in the mannose binding protein gene in children with infection (146/345) was about twice that in children without infection (64/272) (P < 0.0001). Increased susceptibility to infection was found in both heterozygotic and homozygotic children. 13 out of 17 children homozygotic for variant alleles presented with strikingly severe infections, including 6 with septicaemia. CONCLUSIONS: The findings suggest that mutations in the mannose binding protein gene are an important risk factor for infections in children. Screening for such mutations should be included in the investigation of severe or frequent infections.