A chronologically reliable record of 17,000 years of biomass burning in the Lake Victoria area

Fire regimes differ across tropical and subtropical biomes depending on multiple parameters whose interactions and levels of importance are poorly understood, particularly at multidecadal and longer time scales. In the catchment of Lake Victoria, savanna, rainforest, and Afromontane vegetation have interspersed over the last 17,000 years, which may have influenced the fire regime and vice versa. However, climate and humans are most often the primary drivers of fire regime changes, and analysing their respective roles is critical for understanding current and future fire regimes. Besides a handful of radiocarbon dates on grassy charcoal, the timescales of published studies of Lake Victoria sediment chronologies rely mostly on dates of bulk sediment, and chronological disagreements persist, mainly due to variation between estimations of the 14 C reservoir effect. Here, we provide independent 14 C chronologies for three Late Glacial and Holocene lacustrine sediment cores from various water depths and compare them with the biostratigraphy to establish a new chronological framework. We present the first continuous sedimentary charcoal records from Lake Victoria; these suggest that fire activity varied substantially during the past 17,000 years. Our new pollen records reveal the long-term vegetation dynamics. The available evidence suggests that before human impact increased during the Iron Age (ca. 2400 yr BP), biomass burning was linked to climate and vegetation reorganizations, such as warming, drying, and the expansion of rainforests and savannas. Our results imply that climate can trigger substantial fire regime changes and that vegetation responses to climate change can co-determine the fire regime. For instance, biomass burning decreased significantly when the rainforest expanded in response to increasing temperatures and moisture availability. Such insights into the long-term linkages between climate, vegetation, and the fire regime may help to refine ecosystem management and conservation strategies in a changing global climate

A Protective Mechanism against Antibiotic-Induced Ototoxicity: Role of Prestin

Hearing loss or ototoxicity is one of the major side effects associated with the use of the antibiotics, particularly aminoglycosides (AGs), which are the most commonly used antibiotics worldwide. However, the molecular and cellular events involved in the antibiotic-induced ototoxicity remains unclear. In the present study, we test the possibility that prestin, the motor protein specifically expressed in the basolateral membrane of outer hair cells (OHCs) in the cochlea with electromotility responsible for sound amplification, may be involved in the process of AG-induced apoptosis in OHCs. Our results from both mice model and cultured cell line indicate a previously unexpected role of prestin, in mediating antibiotic-induced apoptosis, the effect of which is associated with its anion-transporting capacity. The observed downregulation of prestin mRNA prior to detectable apoptosis in OHCs and hearing loss in the antibiotic-treated mice is interesting, which may serve as a protective mechanism against hearing loss induced by AGs in the early stage

Measuring changes in Schlemm’s canal and trabecular meshwork in different accommodation states in myopia children: an observational study

Abstract Purpose: Studies were designed to evaluate changes in the size of the Schlemm's Canal (SC) and trabecular meshwork(TM) during accommodation stimuli and cycloplegia states in myopic children. Methods: 34 children were enrolled. A -6D accommodation stimulus was achieved by looking at an optotype through a mirror. Cycloplegia state was induced with 1% tropicamide. Two states were confirmed by measuring the central lens thickness（CLT）, the anterior chamber depth and the pupil diameter. The size of the Schlemm's Canal (SC) and Trabecular Meshwork(TM) was measured using swept-source optical coherence tomography. And the associations between the change of the SC and the CLT were analyzed. Results: When compared with the relaxation state, under -6D accommodation stimuli, the size of SC increased significantly: the SC area (SCA) amplified from 6371±2517μm2 to 7824±2727 μm2; the SC length (SCL) from 249±10 μm to 295±12 μm, and SC width (SCW) from 27±9 μm to 31±8 μm. Under cycloplegia state, the SCA reduced to 5009±2028 μm2; the SCL to 212±μm and the SCW to 22±5 μm. In addition, the changed areas of SCA (r=0. 35; P=0.0007), SCL (r=0. 251; P=0.0172), and SCW (r=0. 253; P=0.016) were significantly correlated with the change in CLT. However, the size of TM did not change substantially when compared with the relaxation state. Only the TM length (TML) increased from 562±45μm to 587±47μm after -6D accommodation stimulus. Conclusion: SC size enlarges after -6D accommodation stimuli and shrinks under cycloplegia. However, for TM, only the TM length increase under accommodation stimulus state. KEYWORDS: Schlemm’s Canal, Trabecular Meshwork, accommodatio

Differential effects of alprazolam and clonazepam on the immune system and blood vessels of non-stressed and stressed adult male albino rats

Benzodiazepines belongs to one of the most commonly used anxiolytic and anticonvulsant drugs in the world. Full description of toxic effects on different organs is lacking for nearly all the current benzodiazepines. The aim of the current work was to study the immunologic and vascular changes induced by sub-chronic administration of alprazolam and clonazepam in non-stressed and stressed adult male albino rats. Forty-two adult male albino rats were divided into 6 groups (I): (Ia) Negative control rats, (Ib): Positive control rats received distilled water, (II): Stressed rats, (III): Non-stressed rats received daily oral dose of clonazepam (0.5 mg/kg), (IV): Stressed rats received daily oral dose of clonazepam (0.5 mg/kg), (V): Non-stressed rats received daily oral dose of alprazolam (0.3 mg/kg). (VI): Stressed rats received daily oral dose of alprazolam (0.3 mg/kg). At the end of the 4th week, total leukocyte count (WBCs) and differential count were determined, anti-sheep RBC antibody (Anti-SRBC) titer and interleukin-2 (IL-2) level were assessed, thymus glands, lymph nodes, spleens and abdominal aortae were submitted to histopathological examination. Alprazolam was found to induce a significant increase in neutrophil count and a significant decrease in lymphocytes, anti-SRBC titer and IL-2 level with severe depletion of the splenic, thymal and nodal lymphocytes, accompanied by congestion and eosinophilic vasculitis of all organs tested in comparison to clonazepam treated rats. Stress enhanced the toxic effects. It was concluded that the immune system and blood vessels can be adversely affected to a greater extent by short-term chronic administration of alprazolam than by clonazepam, and these toxic effects are aggravated by stress

Role of Interaction and Nucleoside Diphosphate Kinase B in Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator Function by cAMP-Dependent Protein Kinase A

Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-dependent protein kinase A (PKA) and ATP-regulated chloride channel. Here, we demonstrate that nucleoside diphosphate kinase B (NDPK-B, NM23-H2) forms a functional complex with CFTR. In airway epithelia forskolin/IBMX significantly increases NDPK-B co-localisation with CFTR whereas PKA inhibitors attenuate complex formation. Furthermore, an NDPK-B derived peptide (but not its NDPK-A equivalent) disrupts the NDPK-B/CFTR complex in vitro (19-mers comprising amino acids 36-54 from NDPK-B or NDPK-A). Overlay (Far-Western) and Surface Plasmon Resonance (SPR) analysis both demonstrate that NDPK-B binds CFTR within its first nucleotide binding domain (NBD1, CFTR amino acids 351-727). Analysis of chloride currents reflective of CFTR or outwardly rectifying chloride channels (ORCC, DIDS-sensitive) showed that the 19-mer NDPK-B peptide (but not its NDPK-A equivalent) reduced both chloride conductances. Additionally, the NDPK-B (but not NDPK-A) peptide also attenuated acetylcholine-induced intestinal short circuit currents. In silico analysis of the NBD1/NDPK-B complex reveals an extended interaction surface between the two proteins. This binding zone is also target of the 19-mer NDPK-B peptide, thus confirming its capability to disrupt NDPK-B/CFTR complex. We propose that NDPK-B forms part of the complex that controls chloride currents in epithelia

Diversity of Cl− Channels

Cl− channels are widely found anion pores that are regulated by a variety of signals and that play various roles. On the basis of molecular biologic findings, ligand-gated Cl− channels in synapses, cystic fibrosis transmembrane conductors (CFTRs) and ClC channel types have been established, followed by bestrophin and possibly by tweety, which encode Ca2+-activated Cl− channels. The ClC family has been shown to possess a variety of functions, including stabilization of membrane potential, excitation, cellvolume regulation, fluid transport, protein degradation in endosomal vesicles and possibly cell growth. The molecular structure of Cl− channel types varies from 1 to 12 transmembrane segments. By means of computer-based prediction, functional Cl− channels have been synthesized artificially, revealing that many possible ion pores are hidden in channel, transporter or unidentified hydrophobic membrane proteins. Thus, novel Cl−-conducting pores may be occasionally discovered, and evidence from molecular biologic studies will clarify their physiologic and pathophysiologic roles

Electrogenic sodium-bicarbonate cotransport in human ciliary muscle cells

We investigated membrane voltage and intracellular pH (pHi) in cultured human ciliary muscle cells using a cell line (H7CM) and primary-cultured human ciliary muscle cells. 1) Resting potential was 58.9 +/- 1.0 mV in H7CM cells and 61.9 +/- 1.4 mV in primary cultures. The following data are from H7CM cells, but results from primary cultures were basically similar. 2) In HCO3(-)-CO2-buffered solution, removal of extracellular sodium resulted in a depolarization [change in membrane resistance (delta V) = 31.3 +/- 2.8 mV] that was less marked in the absence of HCO3(-)-CO2 (delta V = 0.5 +/- 2.6 mV) and reduced by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (delta V = 19.3 +/- 1.9 mV). 3) Removal of extracellular HCO3(-)-CO2 led to a depolarization (delta V = 13.2 +/- 0.8 mV) that was abolished in the absence of extracellular sodium and inhibited by DIDS. 4) Intracellular alkalinization led to a depolarization (delta V = 24.7 +/- 2.3 mV), and intracellular acidification resulted in a hyperpolarization (delta V = 9.4 +/- 1.1 mV) that was inhibited by DIDS and dependent on extracellular HCO3(-)-CO2 and sodium. 5) pHi backregulation after an acid load occurred in both the presence and absence of extracellular bicarbonate but not in the absence of extracellular sodium. Our data are consistent with an electrogenic Na(+)-HCO3- cotransport in human ciliary muscle cells, which is activated by intracellular acidification